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Patient Navigators for Serious Illnesses Can Now Bill Under New Medicare Codes

Article Type
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In a move that acknowledges the gauntlet the US health system poses for people facing serious and fatal illnesses, Medicare will pay for a new class of workers to help patients manage treatments for conditions like cancer and heart failure.

The 2024 Medicare physician fee schedule includes new billing codes, including G0023, to pay for 60 minutes a month of care coordination by certified or trained auxiliary personnel working under the direction of a clinician.

A diagnosis of cancer or another serious illness takes a toll beyond the physical effects of the disease. Patients often scramble to make adjustments in family and work schedules to manage treatment, said Samyukta Mullangi, MD, MBA, medical director of oncology at Thyme Care, a Nashville, Tennessee–based firm that provides navigation and coordination services to oncology practices and insurers.

 

Thyme Care
Dr. Samyukta Mullangi

“It just really does create a bit of a pressure cooker for patients,” Dr. Mullangi told this news organization.

Medicare has for many years paid for medical professionals to help patients cope with the complexities of disease, such as chronic care management (CCM) provided by physicians, nurses, and physician assistants.

The new principal illness navigation (PIN) payments are intended to pay for work that to date typically has been done by people without medical degrees, including those involved in peer support networks and community health programs. The US Centers for Medicare and Medicaid Services(CMS) expects these navigators will undergo training and work under the supervision of clinicians.

The new navigators may coordinate care transitions between medical settings, follow up with patients after emergency department (ED) visits, or communicate with skilled nursing facilities regarding the psychosocial needs and functional deficits of a patient, among other functions.

CMS expects the new navigators may:

  • Conduct assessments to understand a patient’s life story, strengths, needs, goals, preferences, and desired outcomes, including understanding cultural and linguistic factors.
  • Provide support to accomplish the clinician’s treatment plan.
  • Coordinate the receipt of needed services from healthcare facilities, home- and community-based service providers, and caregivers.

Peers as Navigators

The new navigators can be former patients who have undergone similar treatments for serious diseases, CMS said. This approach sets the new program apart from other care management services Medicare already covers, program officials wrote in the 2024 physician fee schedule.

“For some conditions, patients are best able to engage with the healthcare system and access care if they have assistance from a single, dedicated individual who has ‘lived experience,’ ” according to the rule.

The agency has taken a broad initial approach in defining what kinds of illnesses a patient may have to qualify for services. Patients must have a serious condition that is expected to last at least 3 months, such as cancer, heart failure, or substance use disorder.

But those without a definitive diagnosis may also qualify to receive navigator services.

In the rule, CMS cited a case in which a CT scan identified a suspicious mass in a patient’s colon. A clinician might decide this person would benefit from navigation services due to the potential risks for an undiagnosed illness.

“Regardless of the definitive diagnosis of the mass, presence of a colonic mass for that patient may be a serious high-risk condition that could, for example, cause obstruction and lead the patient to present to the emergency department, as well as be potentially indicative of an underlying life-threatening illness such as colon cancer,” CMS wrote in the rule.

Navigators often start their work when cancer patients are screened and guide them through initial diagnosis, potential surgery, radiation, or chemotherapy, said Sharon Gentry, MSN, RN, a former nurse navigator who is now the editor in chief of the Journal of the Academy of Oncology Nurse & Patient Navigators.

The navigators are meant to be a trusted and continual presence for patients, who otherwise might be left to start anew in finding help at each phase of care.

The navigators “see the whole picture. They see the whole journey the patient takes, from pre-diagnosis all the way through diagnosis care out through survival,” Ms. Gentry said.

Journal of Oncology Navigation & Survivorship
Sharon Gentry



Gaining a special Medicare payment for these kinds of services will elevate this work, she said.

Many newer drugs can target specific mechanisms and proteins of cancer. Often, oncology treatment involves testing to find out if mutations are allowing the cancer cells to evade a patient’s immune system.

Checking these biomarkers takes time, however. Patients sometimes become frustrated because they are anxious to begin treatment. Patients may receive inaccurate information from friends or family who went through treatment previously. Navigators can provide knowledge on the current state of care for a patient’s disease, helping them better manage anxieties.

“You have to explain to them that things have changed since the guy you drink coffee with was diagnosed with cancer, and there may be a drug that could target that,” Ms. Gentry said.
 

 

 

Potential Challenges

Initial uptake of the new PIN codes may be slow going, however, as clinicians and health systems may already use well-established codes. These include CCM and principal care management services, which may pay higher rates, Mullangi said.

“There might be sensitivity around not wanting to cannibalize existing programs with a new program,” Dr. Mullangi said.

In addition, many patients will have a copay for the services of principal illness navigators, Dr. Mullangi said.

While many patients have additional insurance that would cover the service, not all do. People with traditional Medicare coverage can sometimes pay 20% of the cost of some medical services.

“I think that may give patients pause, particularly if they’re already feeling the financial burden of a cancer treatment journey,” Dr. Mullangi said.

Pay rates for PIN services involve calculations of regional price differences, which are posted publicly by CMS, and potential added fees for services provided by hospital-affiliated organizations.

Consider payments for code G0023, covering 60 minutes of principal navigation services provided in a single month.

A set reimbursement for patients cared for in independent medical practices exists, with variation for local costs. Medicare’s non-facility price for G0023 would be $102.41 in some parts of Silicon Valley in California, including San Jose. In Arkansas, where costs are lower, reimbursement would be $73.14 for this same service.

Patients who get services covered by code G0023 in independent medical practices would have monthly copays of about $15-$20, depending on where they live.

The tab for patients tends to be higher for these same services if delivered through a medical practice owned by a hospital, as this would trigger the addition of facility fees to the payments made to cover the services. Facility fees are difficult for the public to ascertain before getting a treatment or service.

Dr. Mullangi and Ms. Gentry reported no relevant financial disclosures outside of their employers.
 

A version of this article first appeared on Medscape.com.

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In a move that acknowledges the gauntlet the US health system poses for people facing serious and fatal illnesses, Medicare will pay for a new class of workers to help patients manage treatments for conditions like cancer and heart failure.

The 2024 Medicare physician fee schedule includes new billing codes, including G0023, to pay for 60 minutes a month of care coordination by certified or trained auxiliary personnel working under the direction of a clinician.

A diagnosis of cancer or another serious illness takes a toll beyond the physical effects of the disease. Patients often scramble to make adjustments in family and work schedules to manage treatment, said Samyukta Mullangi, MD, MBA, medical director of oncology at Thyme Care, a Nashville, Tennessee–based firm that provides navigation and coordination services to oncology practices and insurers.

 

Thyme Care
Dr. Samyukta Mullangi

“It just really does create a bit of a pressure cooker for patients,” Dr. Mullangi told this news organization.

Medicare has for many years paid for medical professionals to help patients cope with the complexities of disease, such as chronic care management (CCM) provided by physicians, nurses, and physician assistants.

The new principal illness navigation (PIN) payments are intended to pay for work that to date typically has been done by people without medical degrees, including those involved in peer support networks and community health programs. The US Centers for Medicare and Medicaid Services(CMS) expects these navigators will undergo training and work under the supervision of clinicians.

The new navigators may coordinate care transitions between medical settings, follow up with patients after emergency department (ED) visits, or communicate with skilled nursing facilities regarding the psychosocial needs and functional deficits of a patient, among other functions.

CMS expects the new navigators may:

  • Conduct assessments to understand a patient’s life story, strengths, needs, goals, preferences, and desired outcomes, including understanding cultural and linguistic factors.
  • Provide support to accomplish the clinician’s treatment plan.
  • Coordinate the receipt of needed services from healthcare facilities, home- and community-based service providers, and caregivers.

Peers as Navigators

The new navigators can be former patients who have undergone similar treatments for serious diseases, CMS said. This approach sets the new program apart from other care management services Medicare already covers, program officials wrote in the 2024 physician fee schedule.

“For some conditions, patients are best able to engage with the healthcare system and access care if they have assistance from a single, dedicated individual who has ‘lived experience,’ ” according to the rule.

The agency has taken a broad initial approach in defining what kinds of illnesses a patient may have to qualify for services. Patients must have a serious condition that is expected to last at least 3 months, such as cancer, heart failure, or substance use disorder.

But those without a definitive diagnosis may also qualify to receive navigator services.

In the rule, CMS cited a case in which a CT scan identified a suspicious mass in a patient’s colon. A clinician might decide this person would benefit from navigation services due to the potential risks for an undiagnosed illness.

“Regardless of the definitive diagnosis of the mass, presence of a colonic mass for that patient may be a serious high-risk condition that could, for example, cause obstruction and lead the patient to present to the emergency department, as well as be potentially indicative of an underlying life-threatening illness such as colon cancer,” CMS wrote in the rule.

Navigators often start their work when cancer patients are screened and guide them through initial diagnosis, potential surgery, radiation, or chemotherapy, said Sharon Gentry, MSN, RN, a former nurse navigator who is now the editor in chief of the Journal of the Academy of Oncology Nurse & Patient Navigators.

The navigators are meant to be a trusted and continual presence for patients, who otherwise might be left to start anew in finding help at each phase of care.

The navigators “see the whole picture. They see the whole journey the patient takes, from pre-diagnosis all the way through diagnosis care out through survival,” Ms. Gentry said.

Journal of Oncology Navigation & Survivorship
Sharon Gentry



Gaining a special Medicare payment for these kinds of services will elevate this work, she said.

Many newer drugs can target specific mechanisms and proteins of cancer. Often, oncology treatment involves testing to find out if mutations are allowing the cancer cells to evade a patient’s immune system.

Checking these biomarkers takes time, however. Patients sometimes become frustrated because they are anxious to begin treatment. Patients may receive inaccurate information from friends or family who went through treatment previously. Navigators can provide knowledge on the current state of care for a patient’s disease, helping them better manage anxieties.

“You have to explain to them that things have changed since the guy you drink coffee with was diagnosed with cancer, and there may be a drug that could target that,” Ms. Gentry said.
 

 

 

Potential Challenges

Initial uptake of the new PIN codes may be slow going, however, as clinicians and health systems may already use well-established codes. These include CCM and principal care management services, which may pay higher rates, Mullangi said.

“There might be sensitivity around not wanting to cannibalize existing programs with a new program,” Dr. Mullangi said.

In addition, many patients will have a copay for the services of principal illness navigators, Dr. Mullangi said.

While many patients have additional insurance that would cover the service, not all do. People with traditional Medicare coverage can sometimes pay 20% of the cost of some medical services.

“I think that may give patients pause, particularly if they’re already feeling the financial burden of a cancer treatment journey,” Dr. Mullangi said.

Pay rates for PIN services involve calculations of regional price differences, which are posted publicly by CMS, and potential added fees for services provided by hospital-affiliated organizations.

Consider payments for code G0023, covering 60 minutes of principal navigation services provided in a single month.

A set reimbursement for patients cared for in independent medical practices exists, with variation for local costs. Medicare’s non-facility price for G0023 would be $102.41 in some parts of Silicon Valley in California, including San Jose. In Arkansas, where costs are lower, reimbursement would be $73.14 for this same service.

Patients who get services covered by code G0023 in independent medical practices would have monthly copays of about $15-$20, depending on where they live.

The tab for patients tends to be higher for these same services if delivered through a medical practice owned by a hospital, as this would trigger the addition of facility fees to the payments made to cover the services. Facility fees are difficult for the public to ascertain before getting a treatment or service.

Dr. Mullangi and Ms. Gentry reported no relevant financial disclosures outside of their employers.
 

A version of this article first appeared on Medscape.com.

 

In a move that acknowledges the gauntlet the US health system poses for people facing serious and fatal illnesses, Medicare will pay for a new class of workers to help patients manage treatments for conditions like cancer and heart failure.

The 2024 Medicare physician fee schedule includes new billing codes, including G0023, to pay for 60 minutes a month of care coordination by certified or trained auxiliary personnel working under the direction of a clinician.

A diagnosis of cancer or another serious illness takes a toll beyond the physical effects of the disease. Patients often scramble to make adjustments in family and work schedules to manage treatment, said Samyukta Mullangi, MD, MBA, medical director of oncology at Thyme Care, a Nashville, Tennessee–based firm that provides navigation and coordination services to oncology practices and insurers.

 

Thyme Care
Dr. Samyukta Mullangi

“It just really does create a bit of a pressure cooker for patients,” Dr. Mullangi told this news organization.

Medicare has for many years paid for medical professionals to help patients cope with the complexities of disease, such as chronic care management (CCM) provided by physicians, nurses, and physician assistants.

The new principal illness navigation (PIN) payments are intended to pay for work that to date typically has been done by people without medical degrees, including those involved in peer support networks and community health programs. The US Centers for Medicare and Medicaid Services(CMS) expects these navigators will undergo training and work under the supervision of clinicians.

The new navigators may coordinate care transitions between medical settings, follow up with patients after emergency department (ED) visits, or communicate with skilled nursing facilities regarding the psychosocial needs and functional deficits of a patient, among other functions.

CMS expects the new navigators may:

  • Conduct assessments to understand a patient’s life story, strengths, needs, goals, preferences, and desired outcomes, including understanding cultural and linguistic factors.
  • Provide support to accomplish the clinician’s treatment plan.
  • Coordinate the receipt of needed services from healthcare facilities, home- and community-based service providers, and caregivers.

Peers as Navigators

The new navigators can be former patients who have undergone similar treatments for serious diseases, CMS said. This approach sets the new program apart from other care management services Medicare already covers, program officials wrote in the 2024 physician fee schedule.

“For some conditions, patients are best able to engage with the healthcare system and access care if they have assistance from a single, dedicated individual who has ‘lived experience,’ ” according to the rule.

The agency has taken a broad initial approach in defining what kinds of illnesses a patient may have to qualify for services. Patients must have a serious condition that is expected to last at least 3 months, such as cancer, heart failure, or substance use disorder.

But those without a definitive diagnosis may also qualify to receive navigator services.

In the rule, CMS cited a case in which a CT scan identified a suspicious mass in a patient’s colon. A clinician might decide this person would benefit from navigation services due to the potential risks for an undiagnosed illness.

“Regardless of the definitive diagnosis of the mass, presence of a colonic mass for that patient may be a serious high-risk condition that could, for example, cause obstruction and lead the patient to present to the emergency department, as well as be potentially indicative of an underlying life-threatening illness such as colon cancer,” CMS wrote in the rule.

Navigators often start their work when cancer patients are screened and guide them through initial diagnosis, potential surgery, radiation, or chemotherapy, said Sharon Gentry, MSN, RN, a former nurse navigator who is now the editor in chief of the Journal of the Academy of Oncology Nurse & Patient Navigators.

The navigators are meant to be a trusted and continual presence for patients, who otherwise might be left to start anew in finding help at each phase of care.

The navigators “see the whole picture. They see the whole journey the patient takes, from pre-diagnosis all the way through diagnosis care out through survival,” Ms. Gentry said.

Journal of Oncology Navigation & Survivorship
Sharon Gentry



Gaining a special Medicare payment for these kinds of services will elevate this work, she said.

Many newer drugs can target specific mechanisms and proteins of cancer. Often, oncology treatment involves testing to find out if mutations are allowing the cancer cells to evade a patient’s immune system.

Checking these biomarkers takes time, however. Patients sometimes become frustrated because they are anxious to begin treatment. Patients may receive inaccurate information from friends or family who went through treatment previously. Navigators can provide knowledge on the current state of care for a patient’s disease, helping them better manage anxieties.

“You have to explain to them that things have changed since the guy you drink coffee with was diagnosed with cancer, and there may be a drug that could target that,” Ms. Gentry said.
 

 

 

Potential Challenges

Initial uptake of the new PIN codes may be slow going, however, as clinicians and health systems may already use well-established codes. These include CCM and principal care management services, which may pay higher rates, Mullangi said.

“There might be sensitivity around not wanting to cannibalize existing programs with a new program,” Dr. Mullangi said.

In addition, many patients will have a copay for the services of principal illness navigators, Dr. Mullangi said.

While many patients have additional insurance that would cover the service, not all do. People with traditional Medicare coverage can sometimes pay 20% of the cost of some medical services.

“I think that may give patients pause, particularly if they’re already feeling the financial burden of a cancer treatment journey,” Dr. Mullangi said.

Pay rates for PIN services involve calculations of regional price differences, which are posted publicly by CMS, and potential added fees for services provided by hospital-affiliated organizations.

Consider payments for code G0023, covering 60 minutes of principal navigation services provided in a single month.

A set reimbursement for patients cared for in independent medical practices exists, with variation for local costs. Medicare’s non-facility price for G0023 would be $102.41 in some parts of Silicon Valley in California, including San Jose. In Arkansas, where costs are lower, reimbursement would be $73.14 for this same service.

Patients who get services covered by code G0023 in independent medical practices would have monthly copays of about $15-$20, depending on where they live.

The tab for patients tends to be higher for these same services if delivered through a medical practice owned by a hospital, as this would trigger the addition of facility fees to the payments made to cover the services. Facility fees are difficult for the public to ascertain before getting a treatment or service.

Dr. Mullangi and Ms. Gentry reported no relevant financial disclosures outside of their employers.
 

A version of this article first appeared on Medscape.com.

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How to explain physician compounding to legislators

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Changed

 

In Ohio, new limits on drug compounding in physicians’ offices went into effect in April and have become a real hindrance to care for dermatology patients. The State of Ohio Board of Pharmacy has defined compounding as combining two or more prescription drugs and has required that physicians who perform this “compounding” must obtain a “Terminal Distributor of Dangerous Drugs” license. Ohio is the “test state,” and these rules, unless vigorously opposed, will be coming to your state.

[polldaddy:9779752]

The rules state that “compounded” drugs used within 6 hours of preparation must be prepared in a designated clean medication area with proper hand hygiene and the use of powder-free gloves. “Compounded” drugs that are used more than 6 hours after preparation, require a designated clean room with access limited to authorized personnel, environmental control devices such as a laminar flow hood, and additional equipment and training of personnel to maintain an aseptic environment. A separate license is required for each office location.

The state pharmacy boards are eager to restrict physicians – as well as dentists and veterinarians – and to collect annual licensing fees. Additionally, according to an article from the Ohio State Medical Association, noncompliant physicians can be fined by the pharmacy board.

We are talking big money, power, and dreams of clinical relevancy (and billable activities) here.

What can dermatologists do to prevent this regulatory overreach? I encourage you to plan a visit to your state representative, where you can demonstrate how these restrictions affect you and your patients – an exercise that should be both fun and compelling. All you need to illustrate your case is a simple kit that includes a syringe (but no needles in the statehouse!), a bottle of lidocaine with epinephrine, a bottle of 8.4% bicarbonate, alcohol pads, and gloves.

First, explain to your audience that there is a skin cancer epidemic with more than 5.4 million new cases a year and that, over the past 20 years, the incidence of skin cancer has doubled and is projected to double again over the next 20 years. Further, explain that dermatologists treat more than 70% of these cases in the office setting, under local anesthesia, at a huge cost savings to the public and government (it costs an average of 12 times as much to remove these cancers in the outpatient department at the hospital). Remember, states foot most of the bill for Medicaid and Medicare gap indigent coverage.

Take the bottle of lidocaine with epinephrine and open the syringe pack (Staffers love this demonstration; everyone is fascinated with shots.). Put on your gloves, wipe the top of the lidocaine bottle with an alcohol swab, and explain that this medicine is the anesthetic preferred for skin cancer surgery. Explain how it not only numbs the skin, but also causes vasoconstriction, so that the cancer can be easily and safely removed in the office.

Then explain that, in order for the epinephrine to be stable, the solution has to be very acidic (a pH of 4.2, in fact). Explain that this makes it burn like hell unless you add 0.1 cc per cc of 8.4% bicarbonate, in which case the perceived pain on a 10-point scale will drop from 8 to 2. Then pick up the bottle of bicarbonate and explain that you will no longer be able to mix these two components anymore without a “Terminal Distributor of Dangerous Drugs” license because your state pharmacy board considers this compounding. Your representative is likely to give you looks of astonishment, disbelief, and then a dawning realization of the absurdity of the situation.

Follow-up questions may include “Why can’t you buy buffered lidocaine with epinephrine from the compounding pharmacy?” Easy answer: because each patient needs an individual prescription, and you may not know in advance which patient will need it, and how much the patient will need, and it becomes unstable once it has been buffered. It also will cost the patient $45 per 5-cc syringe, and it will be degraded by the time the patient returns from the compounding pharmacy. Explain further that it costs you only 84 cents to make a 5-cc syringe of buffered lidocaine; that some patients may need as many as 10 syringes; and that these costs are all included in the surgery (free!) if the physician draws it up in the office.

A simple summary is – less pain, less cost – and no history of infections or complications.

It is an eye-opener when you demonstrate how ridiculous the compounding rules being imposed are for physicians and patients. I’ve used this demonstration at the state and federal legislative level, and more recently, at the Food and Drug Administration.

If you get the chance, when a state legislator is in your office, become an advocate for your patients and fellow physicians. Make sure physician offices are excluded from these definitions of com

Dr. Brett M. Coldiron
pounding.

This column was updated June 22, 2017. 

 

 

Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and several book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at dermnews@frontlinemedcom.com.

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In Ohio, new limits on drug compounding in physicians’ offices went into effect in April and have become a real hindrance to care for dermatology patients. The State of Ohio Board of Pharmacy has defined compounding as combining two or more prescription drugs and has required that physicians who perform this “compounding” must obtain a “Terminal Distributor of Dangerous Drugs” license. Ohio is the “test state,” and these rules, unless vigorously opposed, will be coming to your state.

[polldaddy:9779752]

The rules state that “compounded” drugs used within 6 hours of preparation must be prepared in a designated clean medication area with proper hand hygiene and the use of powder-free gloves. “Compounded” drugs that are used more than 6 hours after preparation, require a designated clean room with access limited to authorized personnel, environmental control devices such as a laminar flow hood, and additional equipment and training of personnel to maintain an aseptic environment. A separate license is required for each office location.

The state pharmacy boards are eager to restrict physicians – as well as dentists and veterinarians – and to collect annual licensing fees. Additionally, according to an article from the Ohio State Medical Association, noncompliant physicians can be fined by the pharmacy board.

We are talking big money, power, and dreams of clinical relevancy (and billable activities) here.

What can dermatologists do to prevent this regulatory overreach? I encourage you to plan a visit to your state representative, where you can demonstrate how these restrictions affect you and your patients – an exercise that should be both fun and compelling. All you need to illustrate your case is a simple kit that includes a syringe (but no needles in the statehouse!), a bottle of lidocaine with epinephrine, a bottle of 8.4% bicarbonate, alcohol pads, and gloves.

First, explain to your audience that there is a skin cancer epidemic with more than 5.4 million new cases a year and that, over the past 20 years, the incidence of skin cancer has doubled and is projected to double again over the next 20 years. Further, explain that dermatologists treat more than 70% of these cases in the office setting, under local anesthesia, at a huge cost savings to the public and government (it costs an average of 12 times as much to remove these cancers in the outpatient department at the hospital). Remember, states foot most of the bill for Medicaid and Medicare gap indigent coverage.

Take the bottle of lidocaine with epinephrine and open the syringe pack (Staffers love this demonstration; everyone is fascinated with shots.). Put on your gloves, wipe the top of the lidocaine bottle with an alcohol swab, and explain that this medicine is the anesthetic preferred for skin cancer surgery. Explain how it not only numbs the skin, but also causes vasoconstriction, so that the cancer can be easily and safely removed in the office.

Then explain that, in order for the epinephrine to be stable, the solution has to be very acidic (a pH of 4.2, in fact). Explain that this makes it burn like hell unless you add 0.1 cc per cc of 8.4% bicarbonate, in which case the perceived pain on a 10-point scale will drop from 8 to 2. Then pick up the bottle of bicarbonate and explain that you will no longer be able to mix these two components anymore without a “Terminal Distributor of Dangerous Drugs” license because your state pharmacy board considers this compounding. Your representative is likely to give you looks of astonishment, disbelief, and then a dawning realization of the absurdity of the situation.

Follow-up questions may include “Why can’t you buy buffered lidocaine with epinephrine from the compounding pharmacy?” Easy answer: because each patient needs an individual prescription, and you may not know in advance which patient will need it, and how much the patient will need, and it becomes unstable once it has been buffered. It also will cost the patient $45 per 5-cc syringe, and it will be degraded by the time the patient returns from the compounding pharmacy. Explain further that it costs you only 84 cents to make a 5-cc syringe of buffered lidocaine; that some patients may need as many as 10 syringes; and that these costs are all included in the surgery (free!) if the physician draws it up in the office.

A simple summary is – less pain, less cost – and no history of infections or complications.

It is an eye-opener when you demonstrate how ridiculous the compounding rules being imposed are for physicians and patients. I’ve used this demonstration at the state and federal legislative level, and more recently, at the Food and Drug Administration.

If you get the chance, when a state legislator is in your office, become an advocate for your patients and fellow physicians. Make sure physician offices are excluded from these definitions of com

Dr. Brett M. Coldiron
pounding.

This column was updated June 22, 2017. 

 

 

Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and several book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at dermnews@frontlinemedcom.com.

 

In Ohio, new limits on drug compounding in physicians’ offices went into effect in April and have become a real hindrance to care for dermatology patients. The State of Ohio Board of Pharmacy has defined compounding as combining two or more prescription drugs and has required that physicians who perform this “compounding” must obtain a “Terminal Distributor of Dangerous Drugs” license. Ohio is the “test state,” and these rules, unless vigorously opposed, will be coming to your state.

[polldaddy:9779752]

The rules state that “compounded” drugs used within 6 hours of preparation must be prepared in a designated clean medication area with proper hand hygiene and the use of powder-free gloves. “Compounded” drugs that are used more than 6 hours after preparation, require a designated clean room with access limited to authorized personnel, environmental control devices such as a laminar flow hood, and additional equipment and training of personnel to maintain an aseptic environment. A separate license is required for each office location.

The state pharmacy boards are eager to restrict physicians – as well as dentists and veterinarians – and to collect annual licensing fees. Additionally, according to an article from the Ohio State Medical Association, noncompliant physicians can be fined by the pharmacy board.

We are talking big money, power, and dreams of clinical relevancy (and billable activities) here.

What can dermatologists do to prevent this regulatory overreach? I encourage you to plan a visit to your state representative, where you can demonstrate how these restrictions affect you and your patients – an exercise that should be both fun and compelling. All you need to illustrate your case is a simple kit that includes a syringe (but no needles in the statehouse!), a bottle of lidocaine with epinephrine, a bottle of 8.4% bicarbonate, alcohol pads, and gloves.

First, explain to your audience that there is a skin cancer epidemic with more than 5.4 million new cases a year and that, over the past 20 years, the incidence of skin cancer has doubled and is projected to double again over the next 20 years. Further, explain that dermatologists treat more than 70% of these cases in the office setting, under local anesthesia, at a huge cost savings to the public and government (it costs an average of 12 times as much to remove these cancers in the outpatient department at the hospital). Remember, states foot most of the bill for Medicaid and Medicare gap indigent coverage.

Take the bottle of lidocaine with epinephrine and open the syringe pack (Staffers love this demonstration; everyone is fascinated with shots.). Put on your gloves, wipe the top of the lidocaine bottle with an alcohol swab, and explain that this medicine is the anesthetic preferred for skin cancer surgery. Explain how it not only numbs the skin, but also causes vasoconstriction, so that the cancer can be easily and safely removed in the office.

Then explain that, in order for the epinephrine to be stable, the solution has to be very acidic (a pH of 4.2, in fact). Explain that this makes it burn like hell unless you add 0.1 cc per cc of 8.4% bicarbonate, in which case the perceived pain on a 10-point scale will drop from 8 to 2. Then pick up the bottle of bicarbonate and explain that you will no longer be able to mix these two components anymore without a “Terminal Distributor of Dangerous Drugs” license because your state pharmacy board considers this compounding. Your representative is likely to give you looks of astonishment, disbelief, and then a dawning realization of the absurdity of the situation.

Follow-up questions may include “Why can’t you buy buffered lidocaine with epinephrine from the compounding pharmacy?” Easy answer: because each patient needs an individual prescription, and you may not know in advance which patient will need it, and how much the patient will need, and it becomes unstable once it has been buffered. It also will cost the patient $45 per 5-cc syringe, and it will be degraded by the time the patient returns from the compounding pharmacy. Explain further that it costs you only 84 cents to make a 5-cc syringe of buffered lidocaine; that some patients may need as many as 10 syringes; and that these costs are all included in the surgery (free!) if the physician draws it up in the office.

A simple summary is – less pain, less cost – and no history of infections or complications.

It is an eye-opener when you demonstrate how ridiculous the compounding rules being imposed are for physicians and patients. I’ve used this demonstration at the state and federal legislative level, and more recently, at the Food and Drug Administration.

If you get the chance, when a state legislator is in your office, become an advocate for your patients and fellow physicians. Make sure physician offices are excluded from these definitions of com

Dr. Brett M. Coldiron
pounding.

This column was updated June 22, 2017. 

 

 

Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and several book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at dermnews@frontlinemedcom.com.

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Sheila Fallon Friedlander, MD 
Professor of Clinical Dermatology & Pediatrics 
Director, Pediatric Dermatology Fellowship Training Program 
University of California at San Diego School of Medicine 
Rady Children’s Hospital, 
San Diego, California

Dr. Friedlander was compensated for her participation in the development of this article.

CeraVe is a registered trademark of Valeant Pharmaceuticals International, Inc. or its affiliates.

 

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A supplement to Dermatology News. This advertising supplement is sponsored by Valeant Pharmaceuticals.

Topics
  • Reinforcing the Skin Barrier
  • NEA Seal of Acceptance
  • A Preventative Approach to Dry, Cracked Skin
  • CeraVe Ointment in the Clinical Setting

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Sheila Fallon Friedlander, MD 
Professor of Clinical Dermatology & Pediatrics 
Director, Pediatric Dermatology Fellowship Training Program 
University of California at San Diego School of Medicine 
Rady Children’s Hospital, 
San Diego, California

Dr. Friedlander was compensated for her participation in the development of this article.

CeraVe is a registered trademark of Valeant Pharmaceuticals International, Inc. or its affiliates.

 

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Rural dermatology is not as simple as it seems. For some, it means being the only dermatologist in a county where patients drive 3 hours for an appointment; for others, it means practicing in a mid-sized town and serving as both community doctor and regional referral point. Too often, rural dermatology is dismissed as isolating or career limiting, but the truth is very different. Rural dermatologists see plenty of common conditions such as acne and eczema, but they also see complex inflammatory diseases and advanced skin cancers that reflect delays in care for patients living in rural communities in the United States. Careers in rural dermatology can be flexible and creative, ranging from private practice to hospital employment to hybrid models that blend community and academic life.

The myths persist: You will lack colleagues. Your practice will be thin. You must sacrifice academic engagement. In reality, rural practice offers variety, leadership opportunities, and the chance to influence the health of entire communities in profound ways. In this article, we aim to unpack what rural dermatology actually looks like as a potential career path for residents, with a focus on private-academic hybrid and hospital-based practice models.

What Does Rural Really Mean?

Definitions of the term rural vary. For the US Census Bureau, it is synonymous with nonurban, and for the Office of Management and Budget, the term ­nonmetropolitan is preferred. The US Department of Agriculture’s ­Rural-Urban Commuting Area codes recognize a continuum of classifications from micropolitan to remote. In practice, the term rural covers a wide spectrum: the rolling farmlands of the Midwest, the mountains of Montana, the bayous of the South, the Native American reservations in New Mexico, and everything in between. It is not one uniform reality—rural America is diverse, resilient, and deeply connected.

A Day in Rural Practice

Daily clinic flow may look familiar: a full schedule, a mix of new and established patients, and frequent simple procedures such as biopsies and corticosteroid injections. But the scope of practice is wider. You become the dermatologist for hundreds of miles in every direction, managing most conditions locally while referring select cases to subspecialty centers.

Case variety is striking. Neglected tumors, unusual inflammatory presentations, pediatric conditions, and occupational dermatoses/injuries appear alongside the routine. Each day requires flexibility, judgment, confidence, and the ability to think outside the box. You must consider how a patient’s seasonal work, such as ranching or farming, and/or their total commute time impacts the risk-benefit discussion around treatment recommendations.

Matthew P. Shaffer, MD (Salina, Kansas), who has practiced rural dermatology for more than 20 years, explained that the breadth of dermatologic cases in which he served as the expert was both exciting and intimidating, but it became clear that this was the right professional path for him (email communication, September 5, 2025). In small communities, your role extends beyond the clinic walls. You will see patients at the grocery store, the library, and school events. That continuity fosters loyalty and accountability in ways that are hard to quantify.

Hybrid Partnerships and Hospital-Based Practice

Many practice structures exist: independent clinics, multispecialty groups, hospital employment, and increasingly, hybrid partnerships with academic centers.

Academic institutions have recognized the importance of rural exposure, and many now collaborate with rural dermatologists. For example, Heartland Dermatology in Salina, Kansas, where 2 of the authors (B.R.L. and T.G.) practice, partners with St. Louis University in Missouri to provide a residency track and rotations in rural clinics.

Rural-based hospital systems can create similar structures. Monument Health Dermatology in Spearfish, South Dakota, is integrated into the fabric of the community’s larger rural health care model. The physician (M.E.L.) collaborates daily with primary care providers, surgeons, and oncologists through a shared electronic health record (sometimes even through telephone speed-dial given the close collegiality of small-town providers). Patients come from across 4 states, some driving 6 hours each way. Patients who once doubted whether dermatology was worth the trip will consistently return for follow-up care once trust is earned. The stability of hospital employment supports volunteer faculty positions and a free satellite clinic in partnership with a local Lakota Tribal health center. There is never a dull day: the providers see urgent add-ons daily, which keeps them on their toes but in exchange brings immense reward. This includes a recent case from rural Wyoming: a complex mixed infantile hemangioma on the mid face just entering the rapid proliferation phase. Propranolol was started immediately, as opposed to months later when it was too late—a common complication for the majority of rural patients by the time to get to a dermatologist.

The Hub-and-Spoke Model

Complex cases can overwhelm rural practices, and this is when the hub-and-spoke model is invaluable. Dermatologists embed in local communities as spokes, while subspecialty services such as pediatric dermatology, dermatopathology, or Mohs micrographic surgery remain centralized at hubs. The hubs can be but do not have to be academic institutions; for Heartland Dermatology in Kansas, private practices fulfill both hub and spoke roles. With that said, 10 states do not have academic dermatology programs.1 Mohs surgeons and pediatric dermatologists still can establish robust and successful independent rural subspecialty practices outside academic hubs. Christopher Gasbarre, DO (Spearfish, South Dakota), a board-certified, fellowship-trained Mohs surgeon in rural practice, advises residents to be confident in their abilities and to trust their training, noting that they often will be asked to manage complicated cases because of patient travel and cost constraints; however, clinicians should recognize their own limitations and those of nearby specialists and develop a referral network for cases that require multidisciplinary care (text communication, September 14, 2025).

The hub-and-spoke models—whether they entail an academic center as the hub with private practices as the spokes, or a network of private practices that include rural subspecialists—allows rural dermatologists to remain trusted local experts while ensuring that patients can access advanced care via a more streamlined referral process/network. The challenge is triage: what can be managed locally and what must patients travel for? As Dr. Shaffer explained, decisions about whether care is managed locally or referred to a hub often depend on the experience and comfort level of both the physician and the patient (email communication, September 5, 2025). Ultimately, continuity and trust are central. Patients rely on their local dermatologist to guide these decisions, and that guidance makes the model effective.

Finding the Right Fit

The idea that rural practice means being stuck in a small solo clinic is outdated. Multiple pathways exist, each with strengths and challenges. Independent private practice offers maximum autonomy and deep community integration, though financial and staffing risks are yours to manage. Hospital employment with outreach clinics provides stability, benefits, and collegiality, but bureaucracy can limit innovation and efficiency. Private equity platforms supply resources and rapid growth, but alignment with mission and autonomy must be weighed carefully. Hybrid joint ventures with hospitals combine private control and institutional support, but contracts can be complex. Locum tenens–to-permanent arrangements let you try rural life with minimal commitment, but continuity with patients may be sacrificed. A self-screener can clarify your path: How much autonomy do I want? Do I prefer predictability or variety? How important are procedures, teaching, or community roles? Answer these questions honestly and pair that insight with mentor guidance.

Getting Started: A 90-Day Outline

Launching a rural dermatology clinic is equal parts vision and structure. A focused 90-day plan can make the difference between a smooth opening and early frustration. Think in 4 domains: site selection, employment and licensing, credentialing and contracting, and operations. Even in a compressed timeline, dozens of small but crucial tasks may surface. There are resources—such as the Medical Group Management Association’s practice start-up checklist—that can provide a roadmap, ensuring no detail is overlooked as you transform a vision into a functioning clinic.2

Site Selection—First, determine whether you are opening a new standalone clinic, extending an existing practice, or creating a part-time satellite. Referral mapping with local primary care providers is essential, as is a scan of payer mix and dermatologist density in the region to ensure sustainability.

Employment and Licensing—Confirm state licensure and Drug Enforcement Administration registration and initiate hospital privileges early. These processes can stretch across the entire 90-day window, so starting immediately is critical.

Credentialing and Contracting—Applications with commercial and federal payers, along with Council for Affordable Quality Healthcare updates, often consume weeks if not months. If you plan to perform office microscopy or establish a dermatopathology laboratory, begin the Clinical Laboratory Improvement Amendments certification process in parallel.

Operations—Once the regulatory wheels are in motion, shift to building your practice infrastructure. Secure space, weigh lease vs purchase, and consider partnerships with local hospitals for shared clinic facilities. Recruit staff with dermatology-specific skills such as clinical photography and biopsy assistance. Implement an electronic health record, set up payroll and malpractice insurance, and establish supply chains for everything from liquid nitrogen to surgical trays. Decide whether revenue cycle management will be in-house or outsourced and finalize dermatopathology workflows including courier and transport agreements.

Compensation and Career Sustainability

Compensation in rural dermatology mirrors that of other clinical settings: base salary with productivity bonuses, revenue pooling, or relative value unit structures. Financial planning is crucial. Develop a pro forma that models patient volume, expenses, and realistic growth. Risks exist, including payer mix, staffing, and competition, but the demand for care in underserved areas often offsets these, and communities may support practices with reduced overhead and strong loyalty. Hospital systems may add stipends for supervising advanced practitioners or outreach travel. Loan repayment programs, tax credits, and grants can further enhance packages. Consider checking with the state’s Office of Rural Health.

Career sustainability ultimately depends on more than finances. Geography, amenities, schedule flexibility, autonomy in medical decision-making, work-life balance, the value of being part of and serving a community, and other personal values will shape your “best-fit” practice model. Ask whether you can envision yourself thriving in the community you would be serving.

Broader Efforts and Community

No one builds a rural dermatology practice alone. That is why one of the authors (M.E.L.) created the Rural Access to Dermatology Society (https://www.radsociety.org/), a nonprofit organization connecting dermatologists, residents, and medical students with a shared mission. The organization supports residents through scholarships, mentorship, and telementoring. Faculty can contribute through advocacy, residency track development, and outreach to uniquely underserved rural populations such as Native American reservations where access to dermatology care remains severely limited. Joining can be as simple as attending a webinar, finding a mentor, or volunteering at a free clinic. You do not need to launch your own clinic to get involved; you can begin by connecting with a network already laying the foundation.

Teledermatology and Academic Tracks

Teledermatology and academic initiatives enhance rural care but do not replace in-person practice. Store-and-forward consultations extend reach but cannot match the continuity and trust of long-term patient relationships. Academic rural tracks prepare residents for unique challenges, but someone must staff the clinics. Private and hybrid models remain the backbone of rural access, where dermatologists take on the responsibility and the joy of being the local expert.

Final Thoughts

At its heart, rural dermatology is about trust and presence. Patients will share stories of delayed care, of driving hours for an appointment, of feeling invisible in the health care system. When you choose this path, you are not just filling a workforce gap, you are changing trajectories of lives, families, and communities. The rewards are not easily measured in relative value units or contracts; they show up in the loyalty of patients who return year after year, in the gratitude of families who no longer have to travel to “the big city,” and in the satisfaction of building something bigger than yourself. As Dr. Shaffer noted, he views success primarily in relational terms, reflected in long-term patient trust and continuity of care, particularly when individuals with serious conditions return over many years and entrust him with their ongoing management (email communication, September 5, 2025).

So here’s the invitation: bring one question to your mentor about rural practice and identify one rural site you could visit. The road less traveled in dermatology is closer than you think—and it might just be your path.

References
  1. Association of American Medical Colleges. ERAS Directory: Dermatology. Accessed December 11, 2025. https://systems.aamc.org/eras/erasstats/par/display.cfm?NAV_ROW=PAR&SPEC_CD=080
  2. Medical Group Management Association. Large group or organization practice startup checklist. Accessed December 11, 2025. https://www.mgma.com/member-tools/large-group-or-organization -practice-startup-checklist
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Dr. Logue is from the Department of Dermatology, Monument Health, Spearfish, South Dakota, and the Department of Dermatology, University of New Mexico, Albuquerque. Dr. Litzner and Tara Gillespie are from Heartland Dermatology, Salina, Kansas. Dr. Litzner also is from the Department of Dermatology, School of Medicine, Saint Louis University, Missouri.

The authors have no relevant financial disclosures to report.

Correspondence: Mary E. Logue, MD, 810 N Main St, PMB #138, Spearfish, SD, 57783 (admin@radsociety.org).

Cutis. November 2025;116(5):E20-E22. doi:10.12788/cutis.1318

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Dr. Logue is from the Department of Dermatology, Monument Health, Spearfish, South Dakota, and the Department of Dermatology, University of New Mexico, Albuquerque. Dr. Litzner and Tara Gillespie are from Heartland Dermatology, Salina, Kansas. Dr. Litzner also is from the Department of Dermatology, School of Medicine, Saint Louis University, Missouri.

The authors have no relevant financial disclosures to report.

Correspondence: Mary E. Logue, MD, 810 N Main St, PMB #138, Spearfish, SD, 57783 (admin@radsociety.org).

Cutis. November 2025;116(5):E20-E22. doi:10.12788/cutis.1318

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Dr. Logue is from the Department of Dermatology, Monument Health, Spearfish, South Dakota, and the Department of Dermatology, University of New Mexico, Albuquerque. Dr. Litzner and Tara Gillespie are from Heartland Dermatology, Salina, Kansas. Dr. Litzner also is from the Department of Dermatology, School of Medicine, Saint Louis University, Missouri.

The authors have no relevant financial disclosures to report.

Correspondence: Mary E. Logue, MD, 810 N Main St, PMB #138, Spearfish, SD, 57783 (admin@radsociety.org).

Cutis. November 2025;116(5):E20-E22. doi:10.12788/cutis.1318

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Rural dermatology is not as simple as it seems. For some, it means being the only dermatologist in a county where patients drive 3 hours for an appointment; for others, it means practicing in a mid-sized town and serving as both community doctor and regional referral point. Too often, rural dermatology is dismissed as isolating or career limiting, but the truth is very different. Rural dermatologists see plenty of common conditions such as acne and eczema, but they also see complex inflammatory diseases and advanced skin cancers that reflect delays in care for patients living in rural communities in the United States. Careers in rural dermatology can be flexible and creative, ranging from private practice to hospital employment to hybrid models that blend community and academic life.

The myths persist: You will lack colleagues. Your practice will be thin. You must sacrifice academic engagement. In reality, rural practice offers variety, leadership opportunities, and the chance to influence the health of entire communities in profound ways. In this article, we aim to unpack what rural dermatology actually looks like as a potential career path for residents, with a focus on private-academic hybrid and hospital-based practice models.

What Does Rural Really Mean?

Definitions of the term rural vary. For the US Census Bureau, it is synonymous with nonurban, and for the Office of Management and Budget, the term ­nonmetropolitan is preferred. The US Department of Agriculture’s ­Rural-Urban Commuting Area codes recognize a continuum of classifications from micropolitan to remote. In practice, the term rural covers a wide spectrum: the rolling farmlands of the Midwest, the mountains of Montana, the bayous of the South, the Native American reservations in New Mexico, and everything in between. It is not one uniform reality—rural America is diverse, resilient, and deeply connected.

A Day in Rural Practice

Daily clinic flow may look familiar: a full schedule, a mix of new and established patients, and frequent simple procedures such as biopsies and corticosteroid injections. But the scope of practice is wider. You become the dermatologist for hundreds of miles in every direction, managing most conditions locally while referring select cases to subspecialty centers.

Case variety is striking. Neglected tumors, unusual inflammatory presentations, pediatric conditions, and occupational dermatoses/injuries appear alongside the routine. Each day requires flexibility, judgment, confidence, and the ability to think outside the box. You must consider how a patient’s seasonal work, such as ranching or farming, and/or their total commute time impacts the risk-benefit discussion around treatment recommendations.

Matthew P. Shaffer, MD (Salina, Kansas), who has practiced rural dermatology for more than 20 years, explained that the breadth of dermatologic cases in which he served as the expert was both exciting and intimidating, but it became clear that this was the right professional path for him (email communication, September 5, 2025). In small communities, your role extends beyond the clinic walls. You will see patients at the grocery store, the library, and school events. That continuity fosters loyalty and accountability in ways that are hard to quantify.

Hybrid Partnerships and Hospital-Based Practice

Many practice structures exist: independent clinics, multispecialty groups, hospital employment, and increasingly, hybrid partnerships with academic centers.

Academic institutions have recognized the importance of rural exposure, and many now collaborate with rural dermatologists. For example, Heartland Dermatology in Salina, Kansas, where 2 of the authors (B.R.L. and T.G.) practice, partners with St. Louis University in Missouri to provide a residency track and rotations in rural clinics.

Rural-based hospital systems can create similar structures. Monument Health Dermatology in Spearfish, South Dakota, is integrated into the fabric of the community’s larger rural health care model. The physician (M.E.L.) collaborates daily with primary care providers, surgeons, and oncologists through a shared electronic health record (sometimes even through telephone speed-dial given the close collegiality of small-town providers). Patients come from across 4 states, some driving 6 hours each way. Patients who once doubted whether dermatology was worth the trip will consistently return for follow-up care once trust is earned. The stability of hospital employment supports volunteer faculty positions and a free satellite clinic in partnership with a local Lakota Tribal health center. There is never a dull day: the providers see urgent add-ons daily, which keeps them on their toes but in exchange brings immense reward. This includes a recent case from rural Wyoming: a complex mixed infantile hemangioma on the mid face just entering the rapid proliferation phase. Propranolol was started immediately, as opposed to months later when it was too late—a common complication for the majority of rural patients by the time to get to a dermatologist.

The Hub-and-Spoke Model

Complex cases can overwhelm rural practices, and this is when the hub-and-spoke model is invaluable. Dermatologists embed in local communities as spokes, while subspecialty services such as pediatric dermatology, dermatopathology, or Mohs micrographic surgery remain centralized at hubs. The hubs can be but do not have to be academic institutions; for Heartland Dermatology in Kansas, private practices fulfill both hub and spoke roles. With that said, 10 states do not have academic dermatology programs.1 Mohs surgeons and pediatric dermatologists still can establish robust and successful independent rural subspecialty practices outside academic hubs. Christopher Gasbarre, DO (Spearfish, South Dakota), a board-certified, fellowship-trained Mohs surgeon in rural practice, advises residents to be confident in their abilities and to trust their training, noting that they often will be asked to manage complicated cases because of patient travel and cost constraints; however, clinicians should recognize their own limitations and those of nearby specialists and develop a referral network for cases that require multidisciplinary care (text communication, September 14, 2025).

The hub-and-spoke models—whether they entail an academic center as the hub with private practices as the spokes, or a network of private practices that include rural subspecialists—allows rural dermatologists to remain trusted local experts while ensuring that patients can access advanced care via a more streamlined referral process/network. The challenge is triage: what can be managed locally and what must patients travel for? As Dr. Shaffer explained, decisions about whether care is managed locally or referred to a hub often depend on the experience and comfort level of both the physician and the patient (email communication, September 5, 2025). Ultimately, continuity and trust are central. Patients rely on their local dermatologist to guide these decisions, and that guidance makes the model effective.

Finding the Right Fit

The idea that rural practice means being stuck in a small solo clinic is outdated. Multiple pathways exist, each with strengths and challenges. Independent private practice offers maximum autonomy and deep community integration, though financial and staffing risks are yours to manage. Hospital employment with outreach clinics provides stability, benefits, and collegiality, but bureaucracy can limit innovation and efficiency. Private equity platforms supply resources and rapid growth, but alignment with mission and autonomy must be weighed carefully. Hybrid joint ventures with hospitals combine private control and institutional support, but contracts can be complex. Locum tenens–to-permanent arrangements let you try rural life with minimal commitment, but continuity with patients may be sacrificed. A self-screener can clarify your path: How much autonomy do I want? Do I prefer predictability or variety? How important are procedures, teaching, or community roles? Answer these questions honestly and pair that insight with mentor guidance.

Getting Started: A 90-Day Outline

Launching a rural dermatology clinic is equal parts vision and structure. A focused 90-day plan can make the difference between a smooth opening and early frustration. Think in 4 domains: site selection, employment and licensing, credentialing and contracting, and operations. Even in a compressed timeline, dozens of small but crucial tasks may surface. There are resources—such as the Medical Group Management Association’s practice start-up checklist—that can provide a roadmap, ensuring no detail is overlooked as you transform a vision into a functioning clinic.2

Site Selection—First, determine whether you are opening a new standalone clinic, extending an existing practice, or creating a part-time satellite. Referral mapping with local primary care providers is essential, as is a scan of payer mix and dermatologist density in the region to ensure sustainability.

Employment and Licensing—Confirm state licensure and Drug Enforcement Administration registration and initiate hospital privileges early. These processes can stretch across the entire 90-day window, so starting immediately is critical.

Credentialing and Contracting—Applications with commercial and federal payers, along with Council for Affordable Quality Healthcare updates, often consume weeks if not months. If you plan to perform office microscopy or establish a dermatopathology laboratory, begin the Clinical Laboratory Improvement Amendments certification process in parallel.

Operations—Once the regulatory wheels are in motion, shift to building your practice infrastructure. Secure space, weigh lease vs purchase, and consider partnerships with local hospitals for shared clinic facilities. Recruit staff with dermatology-specific skills such as clinical photography and biopsy assistance. Implement an electronic health record, set up payroll and malpractice insurance, and establish supply chains for everything from liquid nitrogen to surgical trays. Decide whether revenue cycle management will be in-house or outsourced and finalize dermatopathology workflows including courier and transport agreements.

Compensation and Career Sustainability

Compensation in rural dermatology mirrors that of other clinical settings: base salary with productivity bonuses, revenue pooling, or relative value unit structures. Financial planning is crucial. Develop a pro forma that models patient volume, expenses, and realistic growth. Risks exist, including payer mix, staffing, and competition, but the demand for care in underserved areas often offsets these, and communities may support practices with reduced overhead and strong loyalty. Hospital systems may add stipends for supervising advanced practitioners or outreach travel. Loan repayment programs, tax credits, and grants can further enhance packages. Consider checking with the state’s Office of Rural Health.

Career sustainability ultimately depends on more than finances. Geography, amenities, schedule flexibility, autonomy in medical decision-making, work-life balance, the value of being part of and serving a community, and other personal values will shape your “best-fit” practice model. Ask whether you can envision yourself thriving in the community you would be serving.

Broader Efforts and Community

No one builds a rural dermatology practice alone. That is why one of the authors (M.E.L.) created the Rural Access to Dermatology Society (https://www.radsociety.org/), a nonprofit organization connecting dermatologists, residents, and medical students with a shared mission. The organization supports residents through scholarships, mentorship, and telementoring. Faculty can contribute through advocacy, residency track development, and outreach to uniquely underserved rural populations such as Native American reservations where access to dermatology care remains severely limited. Joining can be as simple as attending a webinar, finding a mentor, or volunteering at a free clinic. You do not need to launch your own clinic to get involved; you can begin by connecting with a network already laying the foundation.

Teledermatology and Academic Tracks

Teledermatology and academic initiatives enhance rural care but do not replace in-person practice. Store-and-forward consultations extend reach but cannot match the continuity and trust of long-term patient relationships. Academic rural tracks prepare residents for unique challenges, but someone must staff the clinics. Private and hybrid models remain the backbone of rural access, where dermatologists take on the responsibility and the joy of being the local expert.

Final Thoughts

At its heart, rural dermatology is about trust and presence. Patients will share stories of delayed care, of driving hours for an appointment, of feeling invisible in the health care system. When you choose this path, you are not just filling a workforce gap, you are changing trajectories of lives, families, and communities. The rewards are not easily measured in relative value units or contracts; they show up in the loyalty of patients who return year after year, in the gratitude of families who no longer have to travel to “the big city,” and in the satisfaction of building something bigger than yourself. As Dr. Shaffer noted, he views success primarily in relational terms, reflected in long-term patient trust and continuity of care, particularly when individuals with serious conditions return over many years and entrust him with their ongoing management (email communication, September 5, 2025).

So here’s the invitation: bring one question to your mentor about rural practice and identify one rural site you could visit. The road less traveled in dermatology is closer than you think—and it might just be your path.

Rural dermatology is not as simple as it seems. For some, it means being the only dermatologist in a county where patients drive 3 hours for an appointment; for others, it means practicing in a mid-sized town and serving as both community doctor and regional referral point. Too often, rural dermatology is dismissed as isolating or career limiting, but the truth is very different. Rural dermatologists see plenty of common conditions such as acne and eczema, but they also see complex inflammatory diseases and advanced skin cancers that reflect delays in care for patients living in rural communities in the United States. Careers in rural dermatology can be flexible and creative, ranging from private practice to hospital employment to hybrid models that blend community and academic life.

The myths persist: You will lack colleagues. Your practice will be thin. You must sacrifice academic engagement. In reality, rural practice offers variety, leadership opportunities, and the chance to influence the health of entire communities in profound ways. In this article, we aim to unpack what rural dermatology actually looks like as a potential career path for residents, with a focus on private-academic hybrid and hospital-based practice models.

What Does Rural Really Mean?

Definitions of the term rural vary. For the US Census Bureau, it is synonymous with nonurban, and for the Office of Management and Budget, the term ­nonmetropolitan is preferred. The US Department of Agriculture’s ­Rural-Urban Commuting Area codes recognize a continuum of classifications from micropolitan to remote. In practice, the term rural covers a wide spectrum: the rolling farmlands of the Midwest, the mountains of Montana, the bayous of the South, the Native American reservations in New Mexico, and everything in between. It is not one uniform reality—rural America is diverse, resilient, and deeply connected.

A Day in Rural Practice

Daily clinic flow may look familiar: a full schedule, a mix of new and established patients, and frequent simple procedures such as biopsies and corticosteroid injections. But the scope of practice is wider. You become the dermatologist for hundreds of miles in every direction, managing most conditions locally while referring select cases to subspecialty centers.

Case variety is striking. Neglected tumors, unusual inflammatory presentations, pediatric conditions, and occupational dermatoses/injuries appear alongside the routine. Each day requires flexibility, judgment, confidence, and the ability to think outside the box. You must consider how a patient’s seasonal work, such as ranching or farming, and/or their total commute time impacts the risk-benefit discussion around treatment recommendations.

Matthew P. Shaffer, MD (Salina, Kansas), who has practiced rural dermatology for more than 20 years, explained that the breadth of dermatologic cases in which he served as the expert was both exciting and intimidating, but it became clear that this was the right professional path for him (email communication, September 5, 2025). In small communities, your role extends beyond the clinic walls. You will see patients at the grocery store, the library, and school events. That continuity fosters loyalty and accountability in ways that are hard to quantify.

Hybrid Partnerships and Hospital-Based Practice

Many practice structures exist: independent clinics, multispecialty groups, hospital employment, and increasingly, hybrid partnerships with academic centers.

Academic institutions have recognized the importance of rural exposure, and many now collaborate with rural dermatologists. For example, Heartland Dermatology in Salina, Kansas, where 2 of the authors (B.R.L. and T.G.) practice, partners with St. Louis University in Missouri to provide a residency track and rotations in rural clinics.

Rural-based hospital systems can create similar structures. Monument Health Dermatology in Spearfish, South Dakota, is integrated into the fabric of the community’s larger rural health care model. The physician (M.E.L.) collaborates daily with primary care providers, surgeons, and oncologists through a shared electronic health record (sometimes even through telephone speed-dial given the close collegiality of small-town providers). Patients come from across 4 states, some driving 6 hours each way. Patients who once doubted whether dermatology was worth the trip will consistently return for follow-up care once trust is earned. The stability of hospital employment supports volunteer faculty positions and a free satellite clinic in partnership with a local Lakota Tribal health center. There is never a dull day: the providers see urgent add-ons daily, which keeps them on their toes but in exchange brings immense reward. This includes a recent case from rural Wyoming: a complex mixed infantile hemangioma on the mid face just entering the rapid proliferation phase. Propranolol was started immediately, as opposed to months later when it was too late—a common complication for the majority of rural patients by the time to get to a dermatologist.

The Hub-and-Spoke Model

Complex cases can overwhelm rural practices, and this is when the hub-and-spoke model is invaluable. Dermatologists embed in local communities as spokes, while subspecialty services such as pediatric dermatology, dermatopathology, or Mohs micrographic surgery remain centralized at hubs. The hubs can be but do not have to be academic institutions; for Heartland Dermatology in Kansas, private practices fulfill both hub and spoke roles. With that said, 10 states do not have academic dermatology programs.1 Mohs surgeons and pediatric dermatologists still can establish robust and successful independent rural subspecialty practices outside academic hubs. Christopher Gasbarre, DO (Spearfish, South Dakota), a board-certified, fellowship-trained Mohs surgeon in rural practice, advises residents to be confident in their abilities and to trust their training, noting that they often will be asked to manage complicated cases because of patient travel and cost constraints; however, clinicians should recognize their own limitations and those of nearby specialists and develop a referral network for cases that require multidisciplinary care (text communication, September 14, 2025).

The hub-and-spoke models—whether they entail an academic center as the hub with private practices as the spokes, or a network of private practices that include rural subspecialists—allows rural dermatologists to remain trusted local experts while ensuring that patients can access advanced care via a more streamlined referral process/network. The challenge is triage: what can be managed locally and what must patients travel for? As Dr. Shaffer explained, decisions about whether care is managed locally or referred to a hub often depend on the experience and comfort level of both the physician and the patient (email communication, September 5, 2025). Ultimately, continuity and trust are central. Patients rely on their local dermatologist to guide these decisions, and that guidance makes the model effective.

Finding the Right Fit

The idea that rural practice means being stuck in a small solo clinic is outdated. Multiple pathways exist, each with strengths and challenges. Independent private practice offers maximum autonomy and deep community integration, though financial and staffing risks are yours to manage. Hospital employment with outreach clinics provides stability, benefits, and collegiality, but bureaucracy can limit innovation and efficiency. Private equity platforms supply resources and rapid growth, but alignment with mission and autonomy must be weighed carefully. Hybrid joint ventures with hospitals combine private control and institutional support, but contracts can be complex. Locum tenens–to-permanent arrangements let you try rural life with minimal commitment, but continuity with patients may be sacrificed. A self-screener can clarify your path: How much autonomy do I want? Do I prefer predictability or variety? How important are procedures, teaching, or community roles? Answer these questions honestly and pair that insight with mentor guidance.

Getting Started: A 90-Day Outline

Launching a rural dermatology clinic is equal parts vision and structure. A focused 90-day plan can make the difference between a smooth opening and early frustration. Think in 4 domains: site selection, employment and licensing, credentialing and contracting, and operations. Even in a compressed timeline, dozens of small but crucial tasks may surface. There are resources—such as the Medical Group Management Association’s practice start-up checklist—that can provide a roadmap, ensuring no detail is overlooked as you transform a vision into a functioning clinic.2

Site Selection—First, determine whether you are opening a new standalone clinic, extending an existing practice, or creating a part-time satellite. Referral mapping with local primary care providers is essential, as is a scan of payer mix and dermatologist density in the region to ensure sustainability.

Employment and Licensing—Confirm state licensure and Drug Enforcement Administration registration and initiate hospital privileges early. These processes can stretch across the entire 90-day window, so starting immediately is critical.

Credentialing and Contracting—Applications with commercial and federal payers, along with Council for Affordable Quality Healthcare updates, often consume weeks if not months. If you plan to perform office microscopy or establish a dermatopathology laboratory, begin the Clinical Laboratory Improvement Amendments certification process in parallel.

Operations—Once the regulatory wheels are in motion, shift to building your practice infrastructure. Secure space, weigh lease vs purchase, and consider partnerships with local hospitals for shared clinic facilities. Recruit staff with dermatology-specific skills such as clinical photography and biopsy assistance. Implement an electronic health record, set up payroll and malpractice insurance, and establish supply chains for everything from liquid nitrogen to surgical trays. Decide whether revenue cycle management will be in-house or outsourced and finalize dermatopathology workflows including courier and transport agreements.

Compensation and Career Sustainability

Compensation in rural dermatology mirrors that of other clinical settings: base salary with productivity bonuses, revenue pooling, or relative value unit structures. Financial planning is crucial. Develop a pro forma that models patient volume, expenses, and realistic growth. Risks exist, including payer mix, staffing, and competition, but the demand for care in underserved areas often offsets these, and communities may support practices with reduced overhead and strong loyalty. Hospital systems may add stipends for supervising advanced practitioners or outreach travel. Loan repayment programs, tax credits, and grants can further enhance packages. Consider checking with the state’s Office of Rural Health.

Career sustainability ultimately depends on more than finances. Geography, amenities, schedule flexibility, autonomy in medical decision-making, work-life balance, the value of being part of and serving a community, and other personal values will shape your “best-fit” practice model. Ask whether you can envision yourself thriving in the community you would be serving.

Broader Efforts and Community

No one builds a rural dermatology practice alone. That is why one of the authors (M.E.L.) created the Rural Access to Dermatology Society (https://www.radsociety.org/), a nonprofit organization connecting dermatologists, residents, and medical students with a shared mission. The organization supports residents through scholarships, mentorship, and telementoring. Faculty can contribute through advocacy, residency track development, and outreach to uniquely underserved rural populations such as Native American reservations where access to dermatology care remains severely limited. Joining can be as simple as attending a webinar, finding a mentor, or volunteering at a free clinic. You do not need to launch your own clinic to get involved; you can begin by connecting with a network already laying the foundation.

Teledermatology and Academic Tracks

Teledermatology and academic initiatives enhance rural care but do not replace in-person practice. Store-and-forward consultations extend reach but cannot match the continuity and trust of long-term patient relationships. Academic rural tracks prepare residents for unique challenges, but someone must staff the clinics. Private and hybrid models remain the backbone of rural access, where dermatologists take on the responsibility and the joy of being the local expert.

Final Thoughts

At its heart, rural dermatology is about trust and presence. Patients will share stories of delayed care, of driving hours for an appointment, of feeling invisible in the health care system. When you choose this path, you are not just filling a workforce gap, you are changing trajectories of lives, families, and communities. The rewards are not easily measured in relative value units or contracts; they show up in the loyalty of patients who return year after year, in the gratitude of families who no longer have to travel to “the big city,” and in the satisfaction of building something bigger than yourself. As Dr. Shaffer noted, he views success primarily in relational terms, reflected in long-term patient trust and continuity of care, particularly when individuals with serious conditions return over many years and entrust him with their ongoing management (email communication, September 5, 2025).

So here’s the invitation: bring one question to your mentor about rural practice and identify one rural site you could visit. The road less traveled in dermatology is closer than you think—and it might just be your path.

References
  1. Association of American Medical Colleges. ERAS Directory: Dermatology. Accessed December 11, 2025. https://systems.aamc.org/eras/erasstats/par/display.cfm?NAV_ROW=PAR&SPEC_CD=080
  2. Medical Group Management Association. Large group or organization practice startup checklist. Accessed December 11, 2025. https://www.mgma.com/member-tools/large-group-or-organization -practice-startup-checklist
References
  1. Association of American Medical Colleges. ERAS Directory: Dermatology. Accessed December 11, 2025. https://systems.aamc.org/eras/erasstats/par/display.cfm?NAV_ROW=PAR&SPEC_CD=080
  2. Medical Group Management Association. Large group or organization practice startup checklist. Accessed December 11, 2025. https://www.mgma.com/member-tools/large-group-or-organization -practice-startup-checklist
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The Diagnosis: Fibroelastolytic Papulosis

Histopathology demonstrated decreased density and fragmentation of elastic fibers in the superficial reticular and papillary dermis consistent with an elastolytic disease process (Figure). Of note, elastolysis typically is visualized with Verhoeff-van Gieson stain but cannot be visualized well with standard hematoxylin and eosin staining. Additional staining with Congo red was negative for amyloid, and colloidal iron did not show any increase in dermal mucin, ruling out amyloidosis and scleromyxedema, respectively. Based on the histopathologic findings and the clinical history, a diagnosis of fibroelastolytic papulosis (FP) was made. Given the benign nature of the condition, the patient was prescribed a topical steroid (clobetasol 0.05%) for symptomatic relief. 

FIGURE. Papillary dermal elastolysis. A, Evidence suggestive of an elastolytic disease process manifesting as slight pallor of the papillary dermis with decreased connective tissue density (H&E, original magnification ×10). B, Decreased density and fragmentation of elastic fibers in the superficial reticular and papillary dermis (Verhoeff-van Gieson, original magnification ×10).

Cutaneous conditions can arise from abnormalities in the elastin composition of connective tissue due to abnormal elastin formation or degradation (elastolysis).1 Fibroelastolytic papulosis is a distinct elastolytic disorder diagnosed histologically by a notable loss of elastic fibers localized to the papillary dermis.2 Fibroelastolytic papulosis is an acquired condition linked to exposure to UV radiation, abnormal elastogenesis, and hormonal factors that commonly involves the neck, supraclavicular area, and upper back.1-3 Predominantly affecting elderly women, FP is characterized by soft white papules that often coalesce into a cobblestonelike plaque.2 Because the condition rarely is seen in men, there is speculation that it may involve genetic, hereditary, and hormonal factors that have yet to be identified.1 

Fibroelastolytic papulosis can be classified as either pseudoxanthoma elasticum–like papillary dermal elastolysis or white fibrous papulosis.2,3 White fibrous papulosis manifests with haphazardly arranged collagen fibers in the reticular and deep dermis with papillary dermal elastolysis and most commonly develops on the neck.3 Although our patient’s lesion was on the neck, the absence of thickened collagen bands on histology supported classification as the pseudoxanthoma elasticum– like papillary dermal elastolysis subtype. 

Fibroelastolytic papulosis can be distinguished from other elastic abnormalities by its characteristic clinical appearance, demographic distribution, and associated histopathologic findings. The differential diagnosis of FP includes pseudoxanthoma elasticum (PXE), anetoderma, scleromyxedema, and lichen amyloidosis. 

Pseudoxanthoma elasticum is a hereditary or acquired multisystem disease characterized by fragmentation and calcification of elastic fibers in the mid dermis.1,4 Its clinical presentation resembles that of FP, appearing as small, asymptomatic, yellowish or flesh-colored papules in a reticular pattern that progressively coalesce into larger plaques with a cobblestonelike appearance.1 Like FP, PXE commonly affects the flexural creases in women but in contrast may manifest earlier (ie, second or third decades of life). Additionally, the pathogenesis of PXE is not related to UV radiation exposure. The hereditary form develops due to a gene variation, whereas the acquired form may be due to conditions associated with physiologic and/or mechanical stress.1 

Anetoderma, also known as macular atrophy, is another condition that demonstrates elastic tissue loss in the dermis on histopathology.1 Anetoderma commonly is seen in younger patients and can be differentiated from FP by the antecedent presence of an inflammatory process. Anetoderma is classified as primary or secondary. Primary anetoderma is associated with prothrombotic abnormalities, while secondary anetoderma is associated with systemic disease including but not limited to sarcoidosis, systemic lupus erythematous, and Graves disease.1

Neither lichen myxedematosus (LM) nor lichen amyloidosis (LA) are true elastolytic conditions. Lichen myxedematosus is considered in the differential diagnosis of FP due to the associated loss of elastin observed with disease progression. An idiopathic cutaneous mucinosis, LM is a localized form of scleromyxedema, which is characterized by small, firm, waxy papules; mucin deposition in the skin; fibroblast proliferation; and fibrosis. On histologic analysis, typical findings of LM include irregularly arranged fibroblasts, diffuse mucin deposition within the upper and mid reticular dermis, increased collagen deposition, and a decrease in elastin fibers.5 

Lichen amyloidosis is a subtype of primary localized cutaneous amyloidosis, a rare condition characterized by the extracellular deposition of amyloid proteins in the skin and a lack of systemic involvement. Although it is not an elastolytic condition, LA is clinically similar to FP, often manifesting as multiple localized, pruritic, hyperpigmented papules that can coalesce into larger plaques; it tends to develop on the shins, calves, ankles, and thighs.6,7 The condition commonly manifests in the fifth and sixth decades of life; however, in contrast to FP, LA is more prevalent in men and individuals from Central and South American as well as Middle Eastern and non-Chinese Asian populations.8 Lichen amyloidosis is a keratin-derived amyloidosis with cytokeratin-based amyloid precursors that only deposit in the dermis.6 Histopathology reveals colloid bodies due to the presence of apoptotic basal keratinocytes. The etiology of LA is unknown, but on rare occasions it has been associated with multiple endocrine neoplasia 2A rearranged during transfection mutations.6 

In summary, FP is an uncommonly diagnosed elastolytic condition that often is asymptomatic or associated with mild pruritus. Biopsy is warranted to help differentiate it from mimicker conditions that may be associated with systemic disease. Currently, there is no established therapy that provides successful treatment. Research suggests unsatisfactory results with the use of topical tretinoin or topical antioxidants.3 More recently, nonablative fractional resurfacing lasers have been evaluated as a possible therapeutic strategy of promise for elastic disorders.9

References
  1. Andrés-Ramos I, Alegría-Landa V, Gimeno I, et al. Cutaneous elastic tissue anomalies. Am J Dermatopathol. 2019;41:85-117. doi:10.1097/DAD.0000000000001275
  2. Valbuena V, Assaad D, Yeung J. Pseudoxanthoma elasticum-like papillary dermal elastolysis: a single case report. J Cutan Med Surg. 2017;21:345-347. doi:10.1177/1203475417699407
  3. Dokic Y, Tschen J. White fibrous papulosis of the axillae and neck. Cureus. 2020;12:E7635. doi:10.7759/cureus.7635
  4. Recio-Monescillo M, Torre-Castro J, Manzanas C, et al. Papillary dermal elastolysis histopathology mimicking folliculotropic mycosis fungoides. J Cutan Pathol. 2023;50:430-433. doi:10.1111/cup.14402
  5. Cokonis Georgakis CD, Falasca G, Georgakis A, et al. Scleromyxedema. Clin Dermatol. 2006;24:493-497. doi:10.1016/j.clindermatol.2006.07.011
  6. Weidner T, Illing T, Elsner P. Primary localized cutaneous amyloidosis: a systematic treatment review. Am J Clin Dermatol. 2017;18:629-642. doi:10.1007/s40257-017-0278-9
  7. Ladizinski B, Lee KC. Lichen amyloidosis. CMAJ. 2014;186:532. doi:10.1503/cmaj.130698
  8. Chen JF, Chen YF. Answer: can you identify this condition? Can Fam Physician. 2012;58:1234-1235.
  9. Foering K, Torbeck RL, Frank MP, et al. Treatment of pseudoxanthoma elasticum-like papillary dermal elastolysis with nonablative fractional resurfacing laser resulting in clinical and histologic improvement in elastin and collagen. J Cosmet Laser Ther. 2018;20:382-384. doi:10.1080/14764172.2017.1358457
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Christina Asare is from Georgetown University School of Medicine, Washington, DC. Drs. Russomanno and Cardis are from MedStar Health/ Georgetown University Department of Dermatology, Chevy Chase, Maryland. 

The authors have no relevant financial disclosures to report. 

Correspondence: Michael A. Cardis, MD, Department of Dermatology,Medstar Health/Georgetown University, 5530 Wisconsin Ave, Ste 730, Chevy Chase MD 20815 (Michael.A.Cardis@medstar.net). 

Cutis. 2025 November;116(5):E17-E19. doi:10.12788/cutis.1314

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Christina Asare is from Georgetown University School of Medicine, Washington, DC. Drs. Russomanno and Cardis are from MedStar Health/ Georgetown University Department of Dermatology, Chevy Chase, Maryland. 

The authors have no relevant financial disclosures to report. 

Correspondence: Michael A. Cardis, MD, Department of Dermatology,Medstar Health/Georgetown University, 5530 Wisconsin Ave, Ste 730, Chevy Chase MD 20815 (Michael.A.Cardis@medstar.net). 

Cutis. 2025 November;116(5):E17-E19. doi:10.12788/cutis.1314

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Christina Asare is from Georgetown University School of Medicine, Washington, DC. Drs. Russomanno and Cardis are from MedStar Health/ Georgetown University Department of Dermatology, Chevy Chase, Maryland. 

The authors have no relevant financial disclosures to report. 

Correspondence: Michael A. Cardis, MD, Department of Dermatology,Medstar Health/Georgetown University, 5530 Wisconsin Ave, Ste 730, Chevy Chase MD 20815 (Michael.A.Cardis@medstar.net). 

Cutis. 2025 November;116(5):E17-E19. doi:10.12788/cutis.1314

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The Diagnosis: Fibroelastolytic Papulosis

Histopathology demonstrated decreased density and fragmentation of elastic fibers in the superficial reticular and papillary dermis consistent with an elastolytic disease process (Figure). Of note, elastolysis typically is visualized with Verhoeff-van Gieson stain but cannot be visualized well with standard hematoxylin and eosin staining. Additional staining with Congo red was negative for amyloid, and colloidal iron did not show any increase in dermal mucin, ruling out amyloidosis and scleromyxedema, respectively. Based on the histopathologic findings and the clinical history, a diagnosis of fibroelastolytic papulosis (FP) was made. Given the benign nature of the condition, the patient was prescribed a topical steroid (clobetasol 0.05%) for symptomatic relief. 

FIGURE. Papillary dermal elastolysis. A, Evidence suggestive of an elastolytic disease process manifesting as slight pallor of the papillary dermis with decreased connective tissue density (H&E, original magnification ×10). B, Decreased density and fragmentation of elastic fibers in the superficial reticular and papillary dermis (Verhoeff-van Gieson, original magnification ×10).

Cutaneous conditions can arise from abnormalities in the elastin composition of connective tissue due to abnormal elastin formation or degradation (elastolysis).1 Fibroelastolytic papulosis is a distinct elastolytic disorder diagnosed histologically by a notable loss of elastic fibers localized to the papillary dermis.2 Fibroelastolytic papulosis is an acquired condition linked to exposure to UV radiation, abnormal elastogenesis, and hormonal factors that commonly involves the neck, supraclavicular area, and upper back.1-3 Predominantly affecting elderly women, FP is characterized by soft white papules that often coalesce into a cobblestonelike plaque.2 Because the condition rarely is seen in men, there is speculation that it may involve genetic, hereditary, and hormonal factors that have yet to be identified.1 

Fibroelastolytic papulosis can be classified as either pseudoxanthoma elasticum–like papillary dermal elastolysis or white fibrous papulosis.2,3 White fibrous papulosis manifests with haphazardly arranged collagen fibers in the reticular and deep dermis with papillary dermal elastolysis and most commonly develops on the neck.3 Although our patient’s lesion was on the neck, the absence of thickened collagen bands on histology supported classification as the pseudoxanthoma elasticum– like papillary dermal elastolysis subtype. 

Fibroelastolytic papulosis can be distinguished from other elastic abnormalities by its characteristic clinical appearance, demographic distribution, and associated histopathologic findings. The differential diagnosis of FP includes pseudoxanthoma elasticum (PXE), anetoderma, scleromyxedema, and lichen amyloidosis. 

Pseudoxanthoma elasticum is a hereditary or acquired multisystem disease characterized by fragmentation and calcification of elastic fibers in the mid dermis.1,4 Its clinical presentation resembles that of FP, appearing as small, asymptomatic, yellowish or flesh-colored papules in a reticular pattern that progressively coalesce into larger plaques with a cobblestonelike appearance.1 Like FP, PXE commonly affects the flexural creases in women but in contrast may manifest earlier (ie, second or third decades of life). Additionally, the pathogenesis of PXE is not related to UV radiation exposure. The hereditary form develops due to a gene variation, whereas the acquired form may be due to conditions associated with physiologic and/or mechanical stress.1 

Anetoderma, also known as macular atrophy, is another condition that demonstrates elastic tissue loss in the dermis on histopathology.1 Anetoderma commonly is seen in younger patients and can be differentiated from FP by the antecedent presence of an inflammatory process. Anetoderma is classified as primary or secondary. Primary anetoderma is associated with prothrombotic abnormalities, while secondary anetoderma is associated with systemic disease including but not limited to sarcoidosis, systemic lupus erythematous, and Graves disease.1

Neither lichen myxedematosus (LM) nor lichen amyloidosis (LA) are true elastolytic conditions. Lichen myxedematosus is considered in the differential diagnosis of FP due to the associated loss of elastin observed with disease progression. An idiopathic cutaneous mucinosis, LM is a localized form of scleromyxedema, which is characterized by small, firm, waxy papules; mucin deposition in the skin; fibroblast proliferation; and fibrosis. On histologic analysis, typical findings of LM include irregularly arranged fibroblasts, diffuse mucin deposition within the upper and mid reticular dermis, increased collagen deposition, and a decrease in elastin fibers.5 

Lichen amyloidosis is a subtype of primary localized cutaneous amyloidosis, a rare condition characterized by the extracellular deposition of amyloid proteins in the skin and a lack of systemic involvement. Although it is not an elastolytic condition, LA is clinically similar to FP, often manifesting as multiple localized, pruritic, hyperpigmented papules that can coalesce into larger plaques; it tends to develop on the shins, calves, ankles, and thighs.6,7 The condition commonly manifests in the fifth and sixth decades of life; however, in contrast to FP, LA is more prevalent in men and individuals from Central and South American as well as Middle Eastern and non-Chinese Asian populations.8 Lichen amyloidosis is a keratin-derived amyloidosis with cytokeratin-based amyloid precursors that only deposit in the dermis.6 Histopathology reveals colloid bodies due to the presence of apoptotic basal keratinocytes. The etiology of LA is unknown, but on rare occasions it has been associated with multiple endocrine neoplasia 2A rearranged during transfection mutations.6 

In summary, FP is an uncommonly diagnosed elastolytic condition that often is asymptomatic or associated with mild pruritus. Biopsy is warranted to help differentiate it from mimicker conditions that may be associated with systemic disease. Currently, there is no established therapy that provides successful treatment. Research suggests unsatisfactory results with the use of topical tretinoin or topical antioxidants.3 More recently, nonablative fractional resurfacing lasers have been evaluated as a possible therapeutic strategy of promise for elastic disorders.9

The Diagnosis: Fibroelastolytic Papulosis

Histopathology demonstrated decreased density and fragmentation of elastic fibers in the superficial reticular and papillary dermis consistent with an elastolytic disease process (Figure). Of note, elastolysis typically is visualized with Verhoeff-van Gieson stain but cannot be visualized well with standard hematoxylin and eosin staining. Additional staining with Congo red was negative for amyloid, and colloidal iron did not show any increase in dermal mucin, ruling out amyloidosis and scleromyxedema, respectively. Based on the histopathologic findings and the clinical history, a diagnosis of fibroelastolytic papulosis (FP) was made. Given the benign nature of the condition, the patient was prescribed a topical steroid (clobetasol 0.05%) for symptomatic relief. 

FIGURE. Papillary dermal elastolysis. A, Evidence suggestive of an elastolytic disease process manifesting as slight pallor of the papillary dermis with decreased connective tissue density (H&E, original magnification ×10). B, Decreased density and fragmentation of elastic fibers in the superficial reticular and papillary dermis (Verhoeff-van Gieson, original magnification ×10).

Cutaneous conditions can arise from abnormalities in the elastin composition of connective tissue due to abnormal elastin formation or degradation (elastolysis).1 Fibroelastolytic papulosis is a distinct elastolytic disorder diagnosed histologically by a notable loss of elastic fibers localized to the papillary dermis.2 Fibroelastolytic papulosis is an acquired condition linked to exposure to UV radiation, abnormal elastogenesis, and hormonal factors that commonly involves the neck, supraclavicular area, and upper back.1-3 Predominantly affecting elderly women, FP is characterized by soft white papules that often coalesce into a cobblestonelike plaque.2 Because the condition rarely is seen in men, there is speculation that it may involve genetic, hereditary, and hormonal factors that have yet to be identified.1 

Fibroelastolytic papulosis can be classified as either pseudoxanthoma elasticum–like papillary dermal elastolysis or white fibrous papulosis.2,3 White fibrous papulosis manifests with haphazardly arranged collagen fibers in the reticular and deep dermis with papillary dermal elastolysis and most commonly develops on the neck.3 Although our patient’s lesion was on the neck, the absence of thickened collagen bands on histology supported classification as the pseudoxanthoma elasticum– like papillary dermal elastolysis subtype. 

Fibroelastolytic papulosis can be distinguished from other elastic abnormalities by its characteristic clinical appearance, demographic distribution, and associated histopathologic findings. The differential diagnosis of FP includes pseudoxanthoma elasticum (PXE), anetoderma, scleromyxedema, and lichen amyloidosis. 

Pseudoxanthoma elasticum is a hereditary or acquired multisystem disease characterized by fragmentation and calcification of elastic fibers in the mid dermis.1,4 Its clinical presentation resembles that of FP, appearing as small, asymptomatic, yellowish or flesh-colored papules in a reticular pattern that progressively coalesce into larger plaques with a cobblestonelike appearance.1 Like FP, PXE commonly affects the flexural creases in women but in contrast may manifest earlier (ie, second or third decades of life). Additionally, the pathogenesis of PXE is not related to UV radiation exposure. The hereditary form develops due to a gene variation, whereas the acquired form may be due to conditions associated with physiologic and/or mechanical stress.1 

Anetoderma, also known as macular atrophy, is another condition that demonstrates elastic tissue loss in the dermis on histopathology.1 Anetoderma commonly is seen in younger patients and can be differentiated from FP by the antecedent presence of an inflammatory process. Anetoderma is classified as primary or secondary. Primary anetoderma is associated with prothrombotic abnormalities, while secondary anetoderma is associated with systemic disease including but not limited to sarcoidosis, systemic lupus erythematous, and Graves disease.1

Neither lichen myxedematosus (LM) nor lichen amyloidosis (LA) are true elastolytic conditions. Lichen myxedematosus is considered in the differential diagnosis of FP due to the associated loss of elastin observed with disease progression. An idiopathic cutaneous mucinosis, LM is a localized form of scleromyxedema, which is characterized by small, firm, waxy papules; mucin deposition in the skin; fibroblast proliferation; and fibrosis. On histologic analysis, typical findings of LM include irregularly arranged fibroblasts, diffuse mucin deposition within the upper and mid reticular dermis, increased collagen deposition, and a decrease in elastin fibers.5 

Lichen amyloidosis is a subtype of primary localized cutaneous amyloidosis, a rare condition characterized by the extracellular deposition of amyloid proteins in the skin and a lack of systemic involvement. Although it is not an elastolytic condition, LA is clinically similar to FP, often manifesting as multiple localized, pruritic, hyperpigmented papules that can coalesce into larger plaques; it tends to develop on the shins, calves, ankles, and thighs.6,7 The condition commonly manifests in the fifth and sixth decades of life; however, in contrast to FP, LA is more prevalent in men and individuals from Central and South American as well as Middle Eastern and non-Chinese Asian populations.8 Lichen amyloidosis is a keratin-derived amyloidosis with cytokeratin-based amyloid precursors that only deposit in the dermis.6 Histopathology reveals colloid bodies due to the presence of apoptotic basal keratinocytes. The etiology of LA is unknown, but on rare occasions it has been associated with multiple endocrine neoplasia 2A rearranged during transfection mutations.6 

In summary, FP is an uncommonly diagnosed elastolytic condition that often is asymptomatic or associated with mild pruritus. Biopsy is warranted to help differentiate it from mimicker conditions that may be associated with systemic disease. Currently, there is no established therapy that provides successful treatment. Research suggests unsatisfactory results with the use of topical tretinoin or topical antioxidants.3 More recently, nonablative fractional resurfacing lasers have been evaluated as a possible therapeutic strategy of promise for elastic disorders.9

References
  1. Andrés-Ramos I, Alegría-Landa V, Gimeno I, et al. Cutaneous elastic tissue anomalies. Am J Dermatopathol. 2019;41:85-117. doi:10.1097/DAD.0000000000001275
  2. Valbuena V, Assaad D, Yeung J. Pseudoxanthoma elasticum-like papillary dermal elastolysis: a single case report. J Cutan Med Surg. 2017;21:345-347. doi:10.1177/1203475417699407
  3. Dokic Y, Tschen J. White fibrous papulosis of the axillae and neck. Cureus. 2020;12:E7635. doi:10.7759/cureus.7635
  4. Recio-Monescillo M, Torre-Castro J, Manzanas C, et al. Papillary dermal elastolysis histopathology mimicking folliculotropic mycosis fungoides. J Cutan Pathol. 2023;50:430-433. doi:10.1111/cup.14402
  5. Cokonis Georgakis CD, Falasca G, Georgakis A, et al. Scleromyxedema. Clin Dermatol. 2006;24:493-497. doi:10.1016/j.clindermatol.2006.07.011
  6. Weidner T, Illing T, Elsner P. Primary localized cutaneous amyloidosis: a systematic treatment review. Am J Clin Dermatol. 2017;18:629-642. doi:10.1007/s40257-017-0278-9
  7. Ladizinski B, Lee KC. Lichen amyloidosis. CMAJ. 2014;186:532. doi:10.1503/cmaj.130698
  8. Chen JF, Chen YF. Answer: can you identify this condition? Can Fam Physician. 2012;58:1234-1235.
  9. Foering K, Torbeck RL, Frank MP, et al. Treatment of pseudoxanthoma elasticum-like papillary dermal elastolysis with nonablative fractional resurfacing laser resulting in clinical and histologic improvement in elastin and collagen. J Cosmet Laser Ther. 2018;20:382-384. doi:10.1080/14764172.2017.1358457
References
  1. Andrés-Ramos I, Alegría-Landa V, Gimeno I, et al. Cutaneous elastic tissue anomalies. Am J Dermatopathol. 2019;41:85-117. doi:10.1097/DAD.0000000000001275
  2. Valbuena V, Assaad D, Yeung J. Pseudoxanthoma elasticum-like papillary dermal elastolysis: a single case report. J Cutan Med Surg. 2017;21:345-347. doi:10.1177/1203475417699407
  3. Dokic Y, Tschen J. White fibrous papulosis of the axillae and neck. Cureus. 2020;12:E7635. doi:10.7759/cureus.7635
  4. Recio-Monescillo M, Torre-Castro J, Manzanas C, et al. Papillary dermal elastolysis histopathology mimicking folliculotropic mycosis fungoides. J Cutan Pathol. 2023;50:430-433. doi:10.1111/cup.14402
  5. Cokonis Georgakis CD, Falasca G, Georgakis A, et al. Scleromyxedema. Clin Dermatol. 2006;24:493-497. doi:10.1016/j.clindermatol.2006.07.011
  6. Weidner T, Illing T, Elsner P. Primary localized cutaneous amyloidosis: a systematic treatment review. Am J Clin Dermatol. 2017;18:629-642. doi:10.1007/s40257-017-0278-9
  7. Ladizinski B, Lee KC. Lichen amyloidosis. CMAJ. 2014;186:532. doi:10.1503/cmaj.130698
  8. Chen JF, Chen YF. Answer: can you identify this condition? Can Fam Physician. 2012;58:1234-1235.
  9. Foering K, Torbeck RL, Frank MP, et al. Treatment of pseudoxanthoma elasticum-like papillary dermal elastolysis with nonablative fractional resurfacing laser resulting in clinical and histologic improvement in elastin and collagen. J Cosmet Laser Ther. 2018;20:382-384. doi:10.1080/14764172.2017.1358457
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A 76-year-old woman presented to the dermatology clinic for evaluation of a pruritic rash on the posterior lateral neck of several years’ duration. The rash had been slowly worsening and was intermittently symptomatic. Physical examination revealed monomorphous flesh-colored papules coalescing on the neck, yielding a cobblestonelike texture. The patient had been treated previously by dermatology with topical steroids, but symptoms persisted. A punch biopsy of the left lateral neck was performed.

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Alopecia and Pruritic Rash on the Forehead and Scalp

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Alopecia and Pruritic Rash on the Forehead and Scalp

THE DIAGNOSIS: Folliculitis Decalvans

Biopsy results revealed a brisk perifollicular and intrafollicular mixed inflammatory infiltrate comprising lymphocytes, neutrophils, and plasma cells filling the upper dermis and encircling dilated hair follicles. Elastic stain (Verhoeff-van Gieson) demonstrated loss of elastic fibers in areas of scarring. Periodic acid–Schiff with diastase staining was negative for fungal elements, while Gram staining revealed colonies of bacterial cocci in the stratum corneum and within the hair follicles. Immunofluorescence was unremarkable, and culture revealed methicillin-sensitive Staphylococcus aureus, leading to a diagnosis of folliculitis decalvans (FD). The patient was treated with doxycycline 100 mg twice daily and received intralesional triamcinolone 2.5 mg/mL (total volume, 2 mL) every 6 weeks with considerable improvement in pustules, erythema, and scaling (Figure). While not yet in complete remission, our patient demonstrated short regrowing hairs in areas of incomplete scarring and focal remaining perifollicular erythema and scale along the midline frontal scalp 5 months after initial presentation.

Gui-Figure
FIGURE. Clinical improvement of folliculitis decalvans following treatment with oral doxycycline and intralesional triamcinolone.

Folliculitis decalvans is an uncommon subtype of cicatricial alopecia that may mimic other forms of alopecia. Cicatricial alopecia often is difficult to diagnose due to its overlapping clinical characteristics, but early diagnosis is essential for appropriate management and prevention of further permanent hair loss. Traditionally classified as a primary neutrophilic cicatricial alopecia, lymphocyte-predominant variants of FD now are recognized.1

Patients with FD typically present with patchy scarring alopecia at the vertex scalp that gradually expands and may demonstrate secondary features of follicular tufting and pustules.1-3 While the epidemiology of FD is poorly characterized, Vañó-Galván et al4 reported that FD accounted for 2.8% of all alopecia cases and 10.5% of cicatricial alopecia cases in a multicenter study of 2835 patients. The pathophysiology of FD still is under investigation but is thought to result from a dysregulated immune response to a chronic bacterial infection (eg, S aureus), with resulting neutrophilpredominant inflammation in early stages.1-3 Vañó-Galván et al4 reported that, among 35 patients with FD cultured for bacteria, 74% (26/35) returned positive results, 96% (25/26) of which grew S aureus.5

A systematic review of 20 studies that included 263 patients found rifampin and clindamycin to be the most common treatments for FD; however, there is insufficient evidence to determine if this treatment is the most effective.6 In our patient, clindamycin was avoided due to its propensity to negatively alter the gut microbiome long term.7 Other therapies such as oral tetracyclines, high-potency topical steroids, and intralesional triamcinolone also can be used to achieve disease remission.5,6 Other treatments such as isotretinoin, red-light photodynamic therapy, tacrolimus, and external beam radiation have been reported in the literature but vary in efficacy.6 Our patient improved on a regimen of topical benzoyl peroxide wash, oral doxycycline, and intralesional triamcinolone.

Notably, FD may share clinical features with other causes of cicatricial alopecia. In our patient, FD mimicked other entities including discoid lupus erythematosus, frontal fibrosing alopecia, dissecting cellulitis, and erosive pustular dermatosis (Table).1-14 Discoid lupus erythematosus manifests as round hypopigmented and hyperpigmented plaques with associated atrophy, perifollicular erythema, and follicular plugging. Frontal fibrosing alopecia is a primary lymphocytic scarring alopecia that manifests in a bandlike linear distribution over the frontal scalp and may involve the temporal scalp, posterior hairline, and/or eyebrows. Isolated hairs (known as lonely hairs) often are seen. Dissecting cellulitis is characterized by boggy nodules associated with alopecia on the scalp without notable epidermal change, although pustules and sinus tracts may develop.9 Erosive pustular dermatosis is a diagnosis of exclusion but often is seen in older adults with chronic sun damage and clinically manifests with eroded plaques with adherent crusts.10

CT116005014_e-Table

While our patient presented with several overlapping clinical features, including progressive hair loss along the frontal scalp in a bandlike pattern suspicious for frontal fibrosing alopecia as well as atrophic depigmented plaques with adherent peripheral scaling suspicious for discoid lupus erythematosus, the presence of pustules was an important clue. The biopsy demonstrating a mixed infiltrate inclusive of neutrophils confirmed the diagnosis of FD.

References
  1. Olsen EA, Bergfeld WF, Cotsarelis G, et al. Summary of North American Hair Research Society (NAHRS)-sponsored Workshop on Cicatricial Alopecia, Duke University Medical Center, February 10 and 11, 2001. J Am Acad Dermatol. 2003;48:103-110. doi:10.1067/mjd.2003.68
  2. Filbrandt R, Rufaut N, Jones L. Primary cicatricial alopecia: diagnosis and treatment. CMAJ. 2013;185:1579-1585. doi:10.1503/cmaj.111570
  3. Otberg N, Kang H, Alzolibani AA, et al. Folliculitis decalvans. Dermatol Ther. 2008;21:238-244. doi:10.1111/j.1529-8019.2008.00204.x
  4. Vañó-Galván S, Saceda-Corralo D, Blume-Peytavi U, et al. Frequency of the types of alopecia at twenty-two specialist hair clinics: a multicenter study. Skin Appendage Disord. 2019;5:309-315. doi:10.1159/000496708
  5. Vañó-Galván S, Molina-Ruiz AM, Fernández-Crehuet P, et al. Folliculitis decalvans: a multicentre review of 82 patients. J Eur Acad Dermatol Venereol. 2015;29:1750-1757. doi:10.1111/jdv.12993
  6. Rambhia PH, Conic RRZ, Murad A, et al. Updates in therapeutics for folliculitis decalvans: a systematic review with evidence-based analysis. J Am Acad Dermatol. 2019;80:794-801. doi:10.1016/j.jaad.2018.07.050
  7. Zimmermann P, Curtis N. The effect of antibiotics on the composition of the intestinal microbiota - a systematic review. J Infect. 2019;79:471-489. doi:10.1016/j.jinf.2019.10.008
  8. Kanti V, Röwert-Huber J, Vogt A, et al. Cicatricial alopecia. J Dtsch Dermatol Ges. 2018;16:435-461. doi:10.1111/ddg.13498
  9. Melo DF, Slaibi EB, Siqueira TMFM, et al. Trichoscopy findings in dissecting cellulitis. An Bras Dermatol. 2019;94:608-611. doi:10.1016/j.abd.2019.09.006
  10. Anzai A, Pirmez R, Vincenzi C, et al. Trichoscopy findings of frontal fibrosing alopecia on the eyebrows: a study of 151 cases. J Am Acad Dermatol. 2021;85:1130-1134. doi:10.1016/j.jaad.2019.12.023
  11. Starace M, Loi C, Bruni F, et al. Erosive pustular dermatosis of the scalp: clinical, trichoscopic, and histopathologic features of 20 cases. J Am Acad Dermatol. 2017;76:1109-1114. doi:10.1016/j.jaad.2016.12.016
  12. Rongioletti F, Christana K. Cicatricial (scarring) alopecias: an overview of pathogenesis, classification, diagnosis, and treatment. Am J Clin Dermatol. 2012;13:247-260. doi:10.2165/11596960-000000000-00000
  13. Badaoui A, Reygagne P, Cavelier-Balloy B, et al. Dissecting cellulitis of the scalp: a retrospective study of 51 patients and review of literature. Br J Dermatol. 2016;174:421-423. doi:10.1111/bjd.13999
  14. Michelerio A, Vassallo C, Fiandrino G, et al. Erosive pustular dermatosis of the scalp: a clinicopathologic study of fifty cases. Dermatopathology (Basel). 2021;8:450-462. doi:10.3390/dermatopathology8040048
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From the Department of Dermatology, School of Medicine and Public Health, University of Wisconsin, Madison.

The authors have no relevant financial disclosures to report.

Correspondence: Michael Gui, MD, 1 S Park St, 7th Floor, Madison, WI 53715 (mgui2@wisc.edu).

Cutis. 2025 November;116(5):E14-E16. doi:10.12788/cutis.1311

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The authors have no relevant financial disclosures to report.

Correspondence: Michael Gui, MD, 1 S Park St, 7th Floor, Madison, WI 53715 (mgui2@wisc.edu).

Cutis. 2025 November;116(5):E14-E16. doi:10.12788/cutis.1311

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The authors have no relevant financial disclosures to report.

Correspondence: Michael Gui, MD, 1 S Park St, 7th Floor, Madison, WI 53715 (mgui2@wisc.edu).

Cutis. 2025 November;116(5):E14-E16. doi:10.12788/cutis.1311

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THE DIAGNOSIS: Folliculitis Decalvans

Biopsy results revealed a brisk perifollicular and intrafollicular mixed inflammatory infiltrate comprising lymphocytes, neutrophils, and plasma cells filling the upper dermis and encircling dilated hair follicles. Elastic stain (Verhoeff-van Gieson) demonstrated loss of elastic fibers in areas of scarring. Periodic acid–Schiff with diastase staining was negative for fungal elements, while Gram staining revealed colonies of bacterial cocci in the stratum corneum and within the hair follicles. Immunofluorescence was unremarkable, and culture revealed methicillin-sensitive Staphylococcus aureus, leading to a diagnosis of folliculitis decalvans (FD). The patient was treated with doxycycline 100 mg twice daily and received intralesional triamcinolone 2.5 mg/mL (total volume, 2 mL) every 6 weeks with considerable improvement in pustules, erythema, and scaling (Figure). While not yet in complete remission, our patient demonstrated short regrowing hairs in areas of incomplete scarring and focal remaining perifollicular erythema and scale along the midline frontal scalp 5 months after initial presentation.

Gui-Figure
FIGURE. Clinical improvement of folliculitis decalvans following treatment with oral doxycycline and intralesional triamcinolone.

Folliculitis decalvans is an uncommon subtype of cicatricial alopecia that may mimic other forms of alopecia. Cicatricial alopecia often is difficult to diagnose due to its overlapping clinical characteristics, but early diagnosis is essential for appropriate management and prevention of further permanent hair loss. Traditionally classified as a primary neutrophilic cicatricial alopecia, lymphocyte-predominant variants of FD now are recognized.1

Patients with FD typically present with patchy scarring alopecia at the vertex scalp that gradually expands and may demonstrate secondary features of follicular tufting and pustules.1-3 While the epidemiology of FD is poorly characterized, Vañó-Galván et al4 reported that FD accounted for 2.8% of all alopecia cases and 10.5% of cicatricial alopecia cases in a multicenter study of 2835 patients. The pathophysiology of FD still is under investigation but is thought to result from a dysregulated immune response to a chronic bacterial infection (eg, S aureus), with resulting neutrophilpredominant inflammation in early stages.1-3 Vañó-Galván et al4 reported that, among 35 patients with FD cultured for bacteria, 74% (26/35) returned positive results, 96% (25/26) of which grew S aureus.5

A systematic review of 20 studies that included 263 patients found rifampin and clindamycin to be the most common treatments for FD; however, there is insufficient evidence to determine if this treatment is the most effective.6 In our patient, clindamycin was avoided due to its propensity to negatively alter the gut microbiome long term.7 Other therapies such as oral tetracyclines, high-potency topical steroids, and intralesional triamcinolone also can be used to achieve disease remission.5,6 Other treatments such as isotretinoin, red-light photodynamic therapy, tacrolimus, and external beam radiation have been reported in the literature but vary in efficacy.6 Our patient improved on a regimen of topical benzoyl peroxide wash, oral doxycycline, and intralesional triamcinolone.

Notably, FD may share clinical features with other causes of cicatricial alopecia. In our patient, FD mimicked other entities including discoid lupus erythematosus, frontal fibrosing alopecia, dissecting cellulitis, and erosive pustular dermatosis (Table).1-14 Discoid lupus erythematosus manifests as round hypopigmented and hyperpigmented plaques with associated atrophy, perifollicular erythema, and follicular plugging. Frontal fibrosing alopecia is a primary lymphocytic scarring alopecia that manifests in a bandlike linear distribution over the frontal scalp and may involve the temporal scalp, posterior hairline, and/or eyebrows. Isolated hairs (known as lonely hairs) often are seen. Dissecting cellulitis is characterized by boggy nodules associated with alopecia on the scalp without notable epidermal change, although pustules and sinus tracts may develop.9 Erosive pustular dermatosis is a diagnosis of exclusion but often is seen in older adults with chronic sun damage and clinically manifests with eroded plaques with adherent crusts.10

CT116005014_e-Table

While our patient presented with several overlapping clinical features, including progressive hair loss along the frontal scalp in a bandlike pattern suspicious for frontal fibrosing alopecia as well as atrophic depigmented plaques with adherent peripheral scaling suspicious for discoid lupus erythematosus, the presence of pustules was an important clue. The biopsy demonstrating a mixed infiltrate inclusive of neutrophils confirmed the diagnosis of FD.

THE DIAGNOSIS: Folliculitis Decalvans

Biopsy results revealed a brisk perifollicular and intrafollicular mixed inflammatory infiltrate comprising lymphocytes, neutrophils, and plasma cells filling the upper dermis and encircling dilated hair follicles. Elastic stain (Verhoeff-van Gieson) demonstrated loss of elastic fibers in areas of scarring. Periodic acid–Schiff with diastase staining was negative for fungal elements, while Gram staining revealed colonies of bacterial cocci in the stratum corneum and within the hair follicles. Immunofluorescence was unremarkable, and culture revealed methicillin-sensitive Staphylococcus aureus, leading to a diagnosis of folliculitis decalvans (FD). The patient was treated with doxycycline 100 mg twice daily and received intralesional triamcinolone 2.5 mg/mL (total volume, 2 mL) every 6 weeks with considerable improvement in pustules, erythema, and scaling (Figure). While not yet in complete remission, our patient demonstrated short regrowing hairs in areas of incomplete scarring and focal remaining perifollicular erythema and scale along the midline frontal scalp 5 months after initial presentation.

Gui-Figure
FIGURE. Clinical improvement of folliculitis decalvans following treatment with oral doxycycline and intralesional triamcinolone.

Folliculitis decalvans is an uncommon subtype of cicatricial alopecia that may mimic other forms of alopecia. Cicatricial alopecia often is difficult to diagnose due to its overlapping clinical characteristics, but early diagnosis is essential for appropriate management and prevention of further permanent hair loss. Traditionally classified as a primary neutrophilic cicatricial alopecia, lymphocyte-predominant variants of FD now are recognized.1

Patients with FD typically present with patchy scarring alopecia at the vertex scalp that gradually expands and may demonstrate secondary features of follicular tufting and pustules.1-3 While the epidemiology of FD is poorly characterized, Vañó-Galván et al4 reported that FD accounted for 2.8% of all alopecia cases and 10.5% of cicatricial alopecia cases in a multicenter study of 2835 patients. The pathophysiology of FD still is under investigation but is thought to result from a dysregulated immune response to a chronic bacterial infection (eg, S aureus), with resulting neutrophilpredominant inflammation in early stages.1-3 Vañó-Galván et al4 reported that, among 35 patients with FD cultured for bacteria, 74% (26/35) returned positive results, 96% (25/26) of which grew S aureus.5

A systematic review of 20 studies that included 263 patients found rifampin and clindamycin to be the most common treatments for FD; however, there is insufficient evidence to determine if this treatment is the most effective.6 In our patient, clindamycin was avoided due to its propensity to negatively alter the gut microbiome long term.7 Other therapies such as oral tetracyclines, high-potency topical steroids, and intralesional triamcinolone also can be used to achieve disease remission.5,6 Other treatments such as isotretinoin, red-light photodynamic therapy, tacrolimus, and external beam radiation have been reported in the literature but vary in efficacy.6 Our patient improved on a regimen of topical benzoyl peroxide wash, oral doxycycline, and intralesional triamcinolone.

Notably, FD may share clinical features with other causes of cicatricial alopecia. In our patient, FD mimicked other entities including discoid lupus erythematosus, frontal fibrosing alopecia, dissecting cellulitis, and erosive pustular dermatosis (Table).1-14 Discoid lupus erythematosus manifests as round hypopigmented and hyperpigmented plaques with associated atrophy, perifollicular erythema, and follicular plugging. Frontal fibrosing alopecia is a primary lymphocytic scarring alopecia that manifests in a bandlike linear distribution over the frontal scalp and may involve the temporal scalp, posterior hairline, and/or eyebrows. Isolated hairs (known as lonely hairs) often are seen. Dissecting cellulitis is characterized by boggy nodules associated with alopecia on the scalp without notable epidermal change, although pustules and sinus tracts may develop.9 Erosive pustular dermatosis is a diagnosis of exclusion but often is seen in older adults with chronic sun damage and clinically manifests with eroded plaques with adherent crusts.10

CT116005014_e-Table

While our patient presented with several overlapping clinical features, including progressive hair loss along the frontal scalp in a bandlike pattern suspicious for frontal fibrosing alopecia as well as atrophic depigmented plaques with adherent peripheral scaling suspicious for discoid lupus erythematosus, the presence of pustules was an important clue. The biopsy demonstrating a mixed infiltrate inclusive of neutrophils confirmed the diagnosis of FD.

References
  1. Olsen EA, Bergfeld WF, Cotsarelis G, et al. Summary of North American Hair Research Society (NAHRS)-sponsored Workshop on Cicatricial Alopecia, Duke University Medical Center, February 10 and 11, 2001. J Am Acad Dermatol. 2003;48:103-110. doi:10.1067/mjd.2003.68
  2. Filbrandt R, Rufaut N, Jones L. Primary cicatricial alopecia: diagnosis and treatment. CMAJ. 2013;185:1579-1585. doi:10.1503/cmaj.111570
  3. Otberg N, Kang H, Alzolibani AA, et al. Folliculitis decalvans. Dermatol Ther. 2008;21:238-244. doi:10.1111/j.1529-8019.2008.00204.x
  4. Vañó-Galván S, Saceda-Corralo D, Blume-Peytavi U, et al. Frequency of the types of alopecia at twenty-two specialist hair clinics: a multicenter study. Skin Appendage Disord. 2019;5:309-315. doi:10.1159/000496708
  5. Vañó-Galván S, Molina-Ruiz AM, Fernández-Crehuet P, et al. Folliculitis decalvans: a multicentre review of 82 patients. J Eur Acad Dermatol Venereol. 2015;29:1750-1757. doi:10.1111/jdv.12993
  6. Rambhia PH, Conic RRZ, Murad A, et al. Updates in therapeutics for folliculitis decalvans: a systematic review with evidence-based analysis. J Am Acad Dermatol. 2019;80:794-801. doi:10.1016/j.jaad.2018.07.050
  7. Zimmermann P, Curtis N. The effect of antibiotics on the composition of the intestinal microbiota - a systematic review. J Infect. 2019;79:471-489. doi:10.1016/j.jinf.2019.10.008
  8. Kanti V, Röwert-Huber J, Vogt A, et al. Cicatricial alopecia. J Dtsch Dermatol Ges. 2018;16:435-461. doi:10.1111/ddg.13498
  9. Melo DF, Slaibi EB, Siqueira TMFM, et al. Trichoscopy findings in dissecting cellulitis. An Bras Dermatol. 2019;94:608-611. doi:10.1016/j.abd.2019.09.006
  10. Anzai A, Pirmez R, Vincenzi C, et al. Trichoscopy findings of frontal fibrosing alopecia on the eyebrows: a study of 151 cases. J Am Acad Dermatol. 2021;85:1130-1134. doi:10.1016/j.jaad.2019.12.023
  11. Starace M, Loi C, Bruni F, et al. Erosive pustular dermatosis of the scalp: clinical, trichoscopic, and histopathologic features of 20 cases. J Am Acad Dermatol. 2017;76:1109-1114. doi:10.1016/j.jaad.2016.12.016
  12. Rongioletti F, Christana K. Cicatricial (scarring) alopecias: an overview of pathogenesis, classification, diagnosis, and treatment. Am J Clin Dermatol. 2012;13:247-260. doi:10.2165/11596960-000000000-00000
  13. Badaoui A, Reygagne P, Cavelier-Balloy B, et al. Dissecting cellulitis of the scalp: a retrospective study of 51 patients and review of literature. Br J Dermatol. 2016;174:421-423. doi:10.1111/bjd.13999
  14. Michelerio A, Vassallo C, Fiandrino G, et al. Erosive pustular dermatosis of the scalp: a clinicopathologic study of fifty cases. Dermatopathology (Basel). 2021;8:450-462. doi:10.3390/dermatopathology8040048
References
  1. Olsen EA, Bergfeld WF, Cotsarelis G, et al. Summary of North American Hair Research Society (NAHRS)-sponsored Workshop on Cicatricial Alopecia, Duke University Medical Center, February 10 and 11, 2001. J Am Acad Dermatol. 2003;48:103-110. doi:10.1067/mjd.2003.68
  2. Filbrandt R, Rufaut N, Jones L. Primary cicatricial alopecia: diagnosis and treatment. CMAJ. 2013;185:1579-1585. doi:10.1503/cmaj.111570
  3. Otberg N, Kang H, Alzolibani AA, et al. Folliculitis decalvans. Dermatol Ther. 2008;21:238-244. doi:10.1111/j.1529-8019.2008.00204.x
  4. Vañó-Galván S, Saceda-Corralo D, Blume-Peytavi U, et al. Frequency of the types of alopecia at twenty-two specialist hair clinics: a multicenter study. Skin Appendage Disord. 2019;5:309-315. doi:10.1159/000496708
  5. Vañó-Galván S, Molina-Ruiz AM, Fernández-Crehuet P, et al. Folliculitis decalvans: a multicentre review of 82 patients. J Eur Acad Dermatol Venereol. 2015;29:1750-1757. doi:10.1111/jdv.12993
  6. Rambhia PH, Conic RRZ, Murad A, et al. Updates in therapeutics for folliculitis decalvans: a systematic review with evidence-based analysis. J Am Acad Dermatol. 2019;80:794-801. doi:10.1016/j.jaad.2018.07.050
  7. Zimmermann P, Curtis N. The effect of antibiotics on the composition of the intestinal microbiota - a systematic review. J Infect. 2019;79:471-489. doi:10.1016/j.jinf.2019.10.008
  8. Kanti V, Röwert-Huber J, Vogt A, et al. Cicatricial alopecia. J Dtsch Dermatol Ges. 2018;16:435-461. doi:10.1111/ddg.13498
  9. Melo DF, Slaibi EB, Siqueira TMFM, et al. Trichoscopy findings in dissecting cellulitis. An Bras Dermatol. 2019;94:608-611. doi:10.1016/j.abd.2019.09.006
  10. Anzai A, Pirmez R, Vincenzi C, et al. Trichoscopy findings of frontal fibrosing alopecia on the eyebrows: a study of 151 cases. J Am Acad Dermatol. 2021;85:1130-1134. doi:10.1016/j.jaad.2019.12.023
  11. Starace M, Loi C, Bruni F, et al. Erosive pustular dermatosis of the scalp: clinical, trichoscopic, and histopathologic features of 20 cases. J Am Acad Dermatol. 2017;76:1109-1114. doi:10.1016/j.jaad.2016.12.016
  12. Rongioletti F, Christana K. Cicatricial (scarring) alopecias: an overview of pathogenesis, classification, diagnosis, and treatment. Am J Clin Dermatol. 2012;13:247-260. doi:10.2165/11596960-000000000-00000
  13. Badaoui A, Reygagne P, Cavelier-Balloy B, et al. Dissecting cellulitis of the scalp: a retrospective study of 51 patients and review of literature. Br J Dermatol. 2016;174:421-423. doi:10.1111/bjd.13999
  14. Michelerio A, Vassallo C, Fiandrino G, et al. Erosive pustular dermatosis of the scalp: a clinicopathologic study of fifty cases. Dermatopathology (Basel). 2021;8:450-462. doi:10.3390/dermatopathology8040048
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Alopecia and Pruritic Rash on the Forehead and Scalp

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A 52-year-old woman presented to the dermatology department with an intermittently pruritic rash in a bandlike distribution on the left upper forehead and the frontal and temporal scalp of 4 years’ duration. The rash initially was diagnosed as psoriasis at an outside facility. Treatment over the year prior to presentation included tildrakizumab-asmn; topical crisaborole 2%; and excimer laser, which was complicated by blistering. The patient reported no history of topical or injected steroid use in the involved areas. Physical examination at the current presentation revealed arcuate erythematous plaques with follicular prominence, perifollicular scaling, pustules, and lone hairs. There also were porcelain-white atrophic plaques with loss of follicular ostia that were most prominent over the temporal scalp. A biopsy of the left lateral forehead was performed.

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Interview Tips for Dermatology Applicants From Dr. Scott Worswick

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What qualities are dermatology programs looking for that may be different from 5 years ago? 

DR. WORSWICK: Every dermatology residency program is different, and as a result, each program is looking for different qualities in its applicants. Overall, I don’t think there has been a huge change in what programs are generally looking for, though. While each program may have a particular trait it values more than another, in general, programs are looking to find residents who will be competent and caring doctors, who work well in teams, and who could be future leaders in our field. 

What are common mistakes you see in dermatology residency interviews, and how can applicants avoid them? 

DR. WORSWICK: Most dermatology applicants are highly accomplished and empathic soon-to-be physicians, so I haven’t found a lot of “mistakes” from this incredible group of people that we have the privilege of interviewing. From time to time, an applicant will lie in an interview, usually out of a desire to appear to be a certain way, and occasionally, they may be nervous and stumble over their words. The former is a really big problem when it happens, and I would recommend that applicants be honest in all their encounters. The latter is not a major problem, and in some cases, might be avoided by lots of practice in advance. 

What types of questions do you recommend applicants ask their interviewers to demonstrate genuine interest in the program? 

DR. WORSWICK: Because of the signaling system, I think that programs assume interest at baseline once an applicant has sent the signal. So, “demonstrating interest” is generally not something I would recommend to applicants during the interview day. It is important for applicants to determine on interview day if a program is a fit for them, so applicants should showcase their unique strengths and skills and find out about what makes any given program different from another. The match generally works well and gets applicants into a program that closely aligns with their strengths and interests. So, think of interview day as your time to figure out how good a fit a program is for you, and not the other way around. 

How can applicants who feel they don't have standout research or leadership credentials differentiate themselves in the interview? 

DR. WORSWICK: While leadership, and less so research experience, is a trait valued highly by most if not all dermatology programs, it is only a part of what an applicant can offer a program. Most programs employ holistic review and consider several factors, probably most commonly grades in medical school, leadership experience, mentorship, teaching, volunteering, Step 2 scores, and letters of recommendation. Any given applicant does not need to excel in all of these. If an applicant has not done a lot of research, they may not match into a research-heavy program, but it doesn’t mean they won’t match. They should determine in which areas they shine and signal the programs that align with those interests/strengths. 

How should applicants discuss nontraditional experiences in a way that adds value rather than raising red flags? 

DR. WORSWICK: In general, my recommendation would be to explain what happened leading up to the change or challenge so that someone reading the application clearly understands the circumstances of the experience, then add value to the description by explaining what was learned and how this might relate to the applicant being a dermatology resident. For example, if a resident took time off for financial reasons and had to work as a medical assitant for a year, a concise description that explains the need for the leave (financial) as well as what value was gained (a year of hands-on patient care experience that validated their choice of going into medicine) could be very helpful.

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Dr. Worswick is from the Department of Dermatology, Keck School of Medicine, University of Southern California, Los Angeles. 

Dr. Worswick is a speaker for Boehringer-Ingelheim. 

Cutis. 2025 December;116(6):222. doi:10.12788/cutis.1307

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Dr. Worswick is a speaker for Boehringer-Ingelheim. 

Cutis. 2025 December;116(6):222. doi:10.12788/cutis.1307

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Cutis. 2025 December;116(6):222. doi:10.12788/cutis.1307

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What qualities are dermatology programs looking for that may be different from 5 years ago? 

DR. WORSWICK: Every dermatology residency program is different, and as a result, each program is looking for different qualities in its applicants. Overall, I don’t think there has been a huge change in what programs are generally looking for, though. While each program may have a particular trait it values more than another, in general, programs are looking to find residents who will be competent and caring doctors, who work well in teams, and who could be future leaders in our field. 

What are common mistakes you see in dermatology residency interviews, and how can applicants avoid them? 

DR. WORSWICK: Most dermatology applicants are highly accomplished and empathic soon-to-be physicians, so I haven’t found a lot of “mistakes” from this incredible group of people that we have the privilege of interviewing. From time to time, an applicant will lie in an interview, usually out of a desire to appear to be a certain way, and occasionally, they may be nervous and stumble over their words. The former is a really big problem when it happens, and I would recommend that applicants be honest in all their encounters. The latter is not a major problem, and in some cases, might be avoided by lots of practice in advance. 

What types of questions do you recommend applicants ask their interviewers to demonstrate genuine interest in the program? 

DR. WORSWICK: Because of the signaling system, I think that programs assume interest at baseline once an applicant has sent the signal. So, “demonstrating interest” is generally not something I would recommend to applicants during the interview day. It is important for applicants to determine on interview day if a program is a fit for them, so applicants should showcase their unique strengths and skills and find out about what makes any given program different from another. The match generally works well and gets applicants into a program that closely aligns with their strengths and interests. So, think of interview day as your time to figure out how good a fit a program is for you, and not the other way around. 

How can applicants who feel they don't have standout research or leadership credentials differentiate themselves in the interview? 

DR. WORSWICK: While leadership, and less so research experience, is a trait valued highly by most if not all dermatology programs, it is only a part of what an applicant can offer a program. Most programs employ holistic review and consider several factors, probably most commonly grades in medical school, leadership experience, mentorship, teaching, volunteering, Step 2 scores, and letters of recommendation. Any given applicant does not need to excel in all of these. If an applicant has not done a lot of research, they may not match into a research-heavy program, but it doesn’t mean they won’t match. They should determine in which areas they shine and signal the programs that align with those interests/strengths. 

How should applicants discuss nontraditional experiences in a way that adds value rather than raising red flags? 

DR. WORSWICK: In general, my recommendation would be to explain what happened leading up to the change or challenge so that someone reading the application clearly understands the circumstances of the experience, then add value to the description by explaining what was learned and how this might relate to the applicant being a dermatology resident. For example, if a resident took time off for financial reasons and had to work as a medical assitant for a year, a concise description that explains the need for the leave (financial) as well as what value was gained (a year of hands-on patient care experience that validated their choice of going into medicine) could be very helpful.

What qualities are dermatology programs looking for that may be different from 5 years ago? 

DR. WORSWICK: Every dermatology residency program is different, and as a result, each program is looking for different qualities in its applicants. Overall, I don’t think there has been a huge change in what programs are generally looking for, though. While each program may have a particular trait it values more than another, in general, programs are looking to find residents who will be competent and caring doctors, who work well in teams, and who could be future leaders in our field. 

What are common mistakes you see in dermatology residency interviews, and how can applicants avoid them? 

DR. WORSWICK: Most dermatology applicants are highly accomplished and empathic soon-to-be physicians, so I haven’t found a lot of “mistakes” from this incredible group of people that we have the privilege of interviewing. From time to time, an applicant will lie in an interview, usually out of a desire to appear to be a certain way, and occasionally, they may be nervous and stumble over their words. The former is a really big problem when it happens, and I would recommend that applicants be honest in all their encounters. The latter is not a major problem, and in some cases, might be avoided by lots of practice in advance. 

What types of questions do you recommend applicants ask their interviewers to demonstrate genuine interest in the program? 

DR. WORSWICK: Because of the signaling system, I think that programs assume interest at baseline once an applicant has sent the signal. So, “demonstrating interest” is generally not something I would recommend to applicants during the interview day. It is important for applicants to determine on interview day if a program is a fit for them, so applicants should showcase their unique strengths and skills and find out about what makes any given program different from another. The match generally works well and gets applicants into a program that closely aligns with their strengths and interests. So, think of interview day as your time to figure out how good a fit a program is for you, and not the other way around. 

How can applicants who feel they don't have standout research or leadership credentials differentiate themselves in the interview? 

DR. WORSWICK: While leadership, and less so research experience, is a trait valued highly by most if not all dermatology programs, it is only a part of what an applicant can offer a program. Most programs employ holistic review and consider several factors, probably most commonly grades in medical school, leadership experience, mentorship, teaching, volunteering, Step 2 scores, and letters of recommendation. Any given applicant does not need to excel in all of these. If an applicant has not done a lot of research, they may not match into a research-heavy program, but it doesn’t mean they won’t match. They should determine in which areas they shine and signal the programs that align with those interests/strengths. 

How should applicants discuss nontraditional experiences in a way that adds value rather than raising red flags? 

DR. WORSWICK: In general, my recommendation would be to explain what happened leading up to the change or challenge so that someone reading the application clearly understands the circumstances of the experience, then add value to the description by explaining what was learned and how this might relate to the applicant being a dermatology resident. For example, if a resident took time off for financial reasons and had to work as a medical assitant for a year, a concise description that explains the need for the leave (financial) as well as what value was gained (a year of hands-on patient care experience that validated their choice of going into medicine) could be very helpful.

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Management of Facial Hair in Women

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IN PARTNERSHIP WITH THE ASSOCIATION OF MILITARY DERMATOLOGISTS

Facial hair growth in women is complex and multifaceted. It is not a disease but rather a part of normal anatomy or a symptom influenced by an underlying condition such as hypertrichosis, a hormonal imbalance (eg, hirsutism due to polycystic ovary syndrome [PCOS]), mechanical factors such as pseudofolliculitis barbae (PFB) from shaving, and perimenopausal and postmenopausal hormonal shifts. Additionally, normal facial hair patterns can vary substantially based on genetics, ethnicity, and cultural background. Some populations may naturally have more visible vellus or terminal hairs on the face, which are entirely physiologic rather than indicative of an underlying disorder. Despite this, societal expectations and beauty standards across many cultures dictate that facial hair in women is undesirable, often associating hair-free skin with femininity and attractiveness. This perception drives many women to seek treatment—not necessarily for medical reasons, but due to social pressure and aesthetic preferences.

Hypertrichosis, whether congenital or acquired, refers to excessive hair growth that is not androgen dependent and can appear on any site of the body. Causes include genetic predisposition, porphyria, thyroid disorders, internal malignancies, malnutrition, anorexia nervosa, or use of medications such as cyclosporine, prednisolone, and phenytoin.1 Hirsutism, by contrast, is characterized by the growth of terminal hairs in women at androgen-dependent sites such as the face, neck, and upper chest, where coarse hair typically grows in men.2 This condition often is associated with excess androgens produced by the ovaries or adrenal glands, most commonly due to PCOS although genetic factors may contribute. 

Before initiating treatment, a thorough history and physical examination are essential to determine the underlying cause of conditions associated with facial hair growth in women. Clinicians should assess for signs of hyperandrogenism, menstrual irregularities, virilization, medication use, and family history. In cases of a suspected endocrine disorder, further laboratory evaluation may be warranted to guide appropriate management. While each cause of facial hair growth in women has unique management considerations, the shared impact on psychosocial well-being and adherence to grooming standards in the US military warrants an all-encompassing yet targeted approach. This comprehensive review discusses management options for women with facial hair in the military based on a review of PubMed articles indexed for MEDLINE conducted in November 2024 using combinations of the following search terms: hirsutism, facial hair, pseudofolliculitis barbae, women, female, military, grooming standards, hyperandrogenism, and hair removal.

Treatment Modalities

The available treatment modalities, including their mechanisms, potential risks, and considerations are summarized in the eTable.

eTABLE. Comparison of Facial Hair Management Strategies For Women

Mechanical—Shaving remains one of the most widely utilized methods of hair removal in women due to its accessibility and ease of use. It does not disrupt the anagen phase of the hair growth cycle, making it a temporary method that requires frequent repetition (often daily), particularly for individuals with rapid hair growth. The belief that shaving causes hair to grow back thicker or faster is a common misconception. Shaving does not alter the thickness or growth rate of hair; instead, it leaves a blunt tip, making the hair feel coarser or appear thicker than uncut hair.3 Despite its relative convenience, shaving can lead to skin irritation due to mechanical trauma. Potential complications include PFB, superficial abrasions known more broadly as shaving irritation, and an increased risk for infections such as bacterial or fungal folliculitis.4

Chemical depilation, which uses thioglycolates mixed with alkali compounds, disrupts disulfide bonds in the hair, effectively breaking down the shaft without affecting the bulb. The depilatory requires application to the skin for approximately 3 to 15 minutes depending on the specific formulation and the thickness or texture of the hair. While it is a cost-effective option that easily can be done at home, the chemicals involved may trigger irritant contact dermatitis or folliculitis and produce an unpleasant odor from hydrogen disulfide gas.5 They also can lead to PFB.

Epilation removes the entire hair shaft and bulb, with results lasting approximately 6 weeks.6 Methods range from using tweezers to pluck single hairs and devices that simultaneously remove multiple hairs to hot or cold waxing, which use resin to grip and remove hair. Threading is a technique that uses twisted thread to remove the hair at the follicle level; this method may not alter hair growth unless performed during the anagen phase, during which repeated plucking can damage the matrix and potentially lead to permanent hair reduction.5 Common adverse effects include pain during removal, burns from waxing, folliculitis, PFB, postinflammatory hyperpigmentation, and scarring, particularly when multiple hairs are removed at once.

Pharmacologic—Pharmacologic therapy commonly is used to manage hirsutism and typically begins with a trial of combined oral contraceptives (COCs) containing estrogen and progestin, which are considered the first-line option unless contraindicated.7 If response to COC monotherapy is inadequate, an antiandrogen such as spironolactone may be added. Combination therapy with a COC and an antiandrogen generally is reserved for severe cases or patients who previously have shown suboptimal response to COCs alone.7 Patients should be counseled to discontinue antiandrogen therapy if they become pregnant due to the risk for fetal undervirilization observed in animal studies.8,9 Typical dosing of spironolactone, a competitive inhibitor of 5-α-reductase and androgen receptors, ranges from 100 mg to 200 mg daily.10 Reported adverse effects include polyuria, postural hypotension, menstrual irregularities, hyperkalemia, and potential liver dysfunction. Although spironolactone has demonstrated tumorigenic effects in animal studies, no such effects have been observed in humans.11

Eflornithine hydrochloride cream 13.9% is the first topical prescription medication approved by the US Food and Drug Administration for reduction of unwanted facial hair in women.12 It works by irreversibly blocking the activity of ornithine decarboxylase, an enzyme involved in the rate-limiting step of polyamine synthesis, which is essential for hair growth. In a randomized, double-blind clinical trial evaluating its effectiveness and safety, twice-daily application for 24 weeks resulted in a clinically meaningful reduction in hair length and density (measured as surface area) compared with the control group.13 When eflornithine hydrochloride cream 13.9% is discontinued, hair growth gradually returns to baseline. Studies have shown that hair regrowth typically begins within 8 weeks after treatment is stopped; within several months, hair returns to pretreatment levels.14 Adverse effects of eflornithine hydrochloride cream generally are mild and may include local irritation and acneform eruptions. In a randomized bilateral vehicle-controlled trial of 31 women, both eflornithine and vehicle creams were well tolerated, with 1 patient reporting mild tingling with eflornithine that resolved with continued use for 7 days.15

Procedural—Photoepilation therapies widely are considered by dermatologists to be among the most effective methods for reducing unwanted hair.16 Laser hair removal employs selective photothermolysis, a principle by which specific wavelengths of light target melanin in hair follicles. This method results in localized thermal damage, destroying hair follicles and reducing regrowth. Wavelengths between 600 and 1100 nm are most effective for hair removal; widely used devices include the ruby (694 nm), alexandrite (755 nm), diode (800-810 nm), and long-pulsed Nd:YAG lasers (1064 nm). Cooling mechanisms such as cryogen spray or contact cooling often are employed to minimize epidermal damage and lessen patient discomfort.

The hair matrix is most responsive to laser treatment during the anagen phase, necessitating multiple sessions to ensure all hairs are treated during this optimal growth stage. Generally, 4 to 6 sessions spaced at intervals of 4 to 6 weeks are required to achieve satisfactory results.17 Matching the laser wavelength to the absorption properties of melanin—the target chromophore—enables selective destruction of melanin-rich hair follicles while minimizing damage to surrounding skin.

The ideal laser wavelength primarily affects melanin concentrated in the hair bulb, leading to follicular destruction while reducing the risk for unintended depigmentation of the epidermis; however, competing structures in the skin (eg, epidermal pigment) also can absorb laser energy, diminishing treatment efficacy and increasing the risk for adverse effects. Shorter wavelengths are effective for lighter skin types, while longer wavelengths such as the Nd:YAG laser are safer for individuals with darker skin types as they bypass melanin in the epidermis.

It is important to note that laser hair removal is ineffective for white and gray hairs due to the lack of melanin. As a result, alternative methods such as electrolysis, which does not rely on pigment, may be more appropriate for permanent hair removal in individuals with nonpigmented hairs. Research indicates that combining topical eflornithine with alexandrite or Nd:YAG lasers improves outcomes for reducing unwanted facial hair.18

In military settings, laser hair removal is utilized for specific conditions such as PFB in male service members to assist with the reduction of hair and mitigation of symptoms.19 The majority of military dermatology clinics have devices for laser hair removal; however, dermatology services are not available at many military treatment facilities, and dermatologic care may be provided by the local civilian dermatologists. That said, laser therapy is covered in the civilian sector for active-duty service members with PFB of the face and neck under certain criteria. These include a documented safety risk in environments requiring respiratory protection, failure of conservative treatments, and evaluation by a military dermatologist who confirms the necessity of civilian-provided laser therapy when it is unavailable at a military facility.20 While such policies demonstrate the military’s recognition of laser therapy as a viable solution for certain grooming-related conditions, many are unaware that the existing laser hair removal policy also applies to women. Increasing awareness of this coverage could help female service members access treatment options that align with both medical and professional grooming needs.

Intense pulsed light (IPL) systems are nonlaser devices that emit broad-spectrum light in the 590- to 1200-nm range. They utilize a flash lamp to achieve thermal damage. Filters are used to narrow the wavelength range based on the specific target. Intense pulsed light devices are less precise than lasers but remain effective for hair reduction. In addition to hair removal, IPL devices are employed in the treatment of pigmented and vascular lesions. Common adverse effects of both laser and IPL hair removal include transient erythema, perifollicular edema, and pigmentary changes, especially in patients with darker skin types. Rare complications include blistering, scarring, and paradoxical hair stimulation in which untreated areas develop increased hair growth.

Electrolysis is recognized as the only method of truly permanent hair removal and is effective for all hair colors.21 However, the variability in technique among practitioners often leads to inconsistent results, with some patients experiencing hair regrowth. Galvanic electrolysis involves inserting a fine needle into the hair follicle and applying an electrical current to destroy the it and the rapidly dividing cells of the matrix.22 The introduction of thermolytic electrolysis, which uses a high-frequency alternating current (commonly 13.56 MHz or 27.12 MHz), has enhanced efficiency by creating heat at the needle tip to destroy the follicle. This approach is faster and now is commonly combined with galvanic electrolysis.23 While no controlled clinical trials directly compare these methods, many patients experience permanent hair removal, with approximately 15% to 25% regrowth within 6 months.22,24

Alternative Options—Home-use laser and light-based devices have become increasingly popular for managing unwanted hair due to their affordability and convenience, with most devices priced less than $1000.25 These devices utilize various technologies, including lasers (808 nm), IPL, or combinations of IPL and radiofrequency.26 Despite their accessibility, peer-reviewed research on their safety profile and effectiveness is limited, as existing data primarily come from industry-funded, uncontrolled studies with short follow-up durations—making it difficult to assess long-term outcomes.25

Psychosocial Impact

A 2023 study of active-duty female service members with PCOS highlighted the unique challenges they face while managing symptoms such as facial hair within the constraints of military service.27 Although the study focused on PCOS, the findings shed light on how facial hair specifically impacts the psychological well-being of servicewomen. Participants described facial hair as one of the most visible and stigmatizing symptoms, often leading to feelings of embarrassment and diminished confidence. Participants also highlighted the professional implications of facial hair, with some describing feelings of scrutiny and judgment from peers and leadership in public. These challenges can be more pronounced in deployments or field exercises where hygiene resources are limited. The lack of access not only affects self-perception but also can hinder the ability of servicewomen to meet implicit expectations for grooming and appearance.27 There is a notable gap in research examining the impact of facial hair on military servicewomen. Given the unique environmental challenges and professional expectations, further investigation is warranted to better understand how facial hair affects women and to optimize treatment approaches in this population.

Final Thoughts

Limited awareness and understanding of facial hair in woman contribute to stigma, often leaving affected individuals to navigate challenges in isolation. Given the impact on confidence, professional appearance, and adherence to military grooming standards, it is essential for health care practitioners to recognize and address facial hair in women. Importantly, laser hair removal is covered by TRICARE for active-duty female service members with PFB, yet many remain unaware of this benefit. Increased awareness of available mechanical, pharmacologic, and procedural treatment options allows for tailored management, ensuring that women receive appropriate medical care.

References
  1. Wendelin DS, Pope DN, Mallory SB. Hypertrichosis. J Am Acad Dermatol. 2003;48:161-181. doi:10.1067/mjd.2003.100

  2. Blume-Peytavi U, Hahn S. Medical treatment of hirsutism. Dermatol Ther. 2008;21:329-339. doi:10.1111/j.1529-8019.2008.00215.x

  3. Kang CN, Shah M, Lynde C, et al. Hair removal practices: a literature review. Skin Therapy Lett. 2021;26:6-11.

  4. Matheson E, Bain J. Hirsutism in women. Am Fam Physician. 2019;100:168-175.

  5. Shenenberger DW, Utecht LM. Removal of unwanted facial hair. Am Fam Physician. 2002;66:1907-1911.

  6. Johnson E, Ebling FJ. The effect of plucking hairs during different phases of the follicular cycle. J Embryol Exp Morphol. 1964;12:465-474.

  7. Martin KA, Anderson RR, Chang RJ, et al. Evaluation and treatment of hirsutism in premenopausal women: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2018;103:1233-1257. doi:10.1210/jc.2018-00241

  8. Barrionuevo P, Nabhan M, Altayar O, et al. Treatment options for hirsutism: a systematic review and network meta-analysis. J Clin Endocrinol Metab. 2018;103:1258-1264. doi:10.1210/jc.2017-02052

  9. Alesi S, Forslund M, Melin J, et al. Efficacy and safety of anti-androgens in the management of polycystic ovary syndrome: a systematic review and meta-analysis of randomised controlled trials. EClinicalMedicine. Published online August 9, 2023. doi:10.1016/j.eclinm.2023.102162

  10. Escobar-Morreale HF, Carmina E, Dewailly D, et al. Epidemiology, diagnosis and management of hirsutism: a consensus statement. Hum Reprod Update. 2012;18:146-170.

  11. Hussein RS, Abdelbasset WK. Updates on hirsutism: a narrative review. Int J Biomedicine. 2022;12:193-198. doi:10.21103/Article12(2)_RA4

  12. Shapiro J, Lui H. Vaniqa—eflornithine 13.9% cream. Skin Therapy Lett. 2001;6:1-5.

  13. Wolf JE Jr, Shander D, Huber F, et al. Randomized, double-blind clinical evaluation of the efficacy and safety of topical eflornithine HCl 13.9% cream in the treatment of women with facial hair. Int J Dermatol. 2007;46:94-98. doi:10.1111/j.1365-4632.2006.03079.x

  14. Balfour JA, McClellan K. Topical eflornithine. Am J Clin Dermatol. 2001;2:197-202. doi:10.2165/00128071-200102030-00009

  15. Hamzavi I, Tan E, Shapiro J, et al. A randomized bilateral vehicle-controlled study of eflornithine cream combined with laser treatment versus laser treatment alone for facial hirsutism in women. J Am Acad Dermatol. 2007;57:54-59. doi:10.1016/j.jaad.2006.09.025

  16. Goldberg DJ. Laser hair removal. In: Goldberg DJ, ed. Laser Dermatology: Pearls and Problems. Blackwell; 2008.

  17. Hussain M, Polnikorn N, Goldberg DJ. Laser-assisted hair removal in Asian skin: efficacy, complications, and the effect of single versus multiple treatments. Dermatol Surg. 2003;29:249-254. doi:10.1046/j.1524-4725.2003.29059.x

  18. Smith SR, Piacquadio DJ, Beger B, et al. Eflornithine cream combined with laser therapy in the management of unwanted facial hair growth in women: a randomized trial. Dermatol Surg. 2006;32:1237-1243. doi:10.1111/j.1524-4725.2006.32282.x

  19. Jung I, Lannan FM, Weiss A, et al. Treatment and current policies on pseudofolliculitis barbae in the US military. Cutis. 2023;112:299-302. doi:10.12788/cutis.0907

  20. TRICARE Operations Manual 6010.59-M. Supplemental Health Care Program (SHCP)—Chapter 17. Contractor Responsibilities. Military Health System and Defense Health Agency website. Revised November 5, 2021. Accessed February 13, 2024. https://manuals.health.mil/pages/DisplayManualHtmlFile/2022-08-31/AsOf/TO15/C17S3.html 

  21. Yanes DA, Smith P, Avram MM. A review of best practices for gender-affirming laser hair removal. Dermatol Surg. 2024;50:S201-S204. doi:10.1097/DSS.0000000000004441

  22. Wagner RF Jr, Tomich JM, Grande DJ. Electrolysis and thermolysis for permanent hair removal. J Am Acad Dermatol. 1985;12:441-449. doi:10.1016/s0190-9622(85)70062-x

  23. Olsen EA. Methods of hair removal. J Am Acad Dermatol. 1999;40:143-157. doi:10.1016/s0190-9622(99)70181-7

  24. Kligman AM, Peters L. Histologic changes of human hair follicles after electrolysis: a comparison of two methods. Cutis. 1984;34:169-176.

  25. Hession MT, Markova A, Graber EM. A review of hand-held, home-use cosmetic laser and light devices. Dermatol Surg. 2015;41:307-320. doi:10.1097/DSS.0000000000000283

  26. Wheeland RG. Permanent hair reduction with a home-use diode laser: safety and effectiveness 1 year after eight treatments. Lasers Surg Med. 2012;44:550-557. doi:10.1002/lsm.22051

  27. Hopkins D, Walker SC, Wilson C, et al. The experience of living with polycystic ovary syndrome in the military. Mil Med. 2024;189:E188-E197. doi:10.1093/milmed/usad241

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Author and Disclosure Information

Dr. Gutierrez is from the Burnett School of Medicine, Texas Christian University, Fort Worth. Drs. Coffel and Wong are from the Department of Dermatology, San Antonio Uniformed Services Health Education Consortium, Lackland Air Force Base, Texas.

The authors have no relevant financial disclosures to report. 

The views expressed herein are those of the authors and do not reflect the official policy or position of Brooke Army Medical Center, the US Army Medical Department, the Defense Health Agency, the US Army Office of the Surgeon General, the Department of the Army, the Department of the Air Force, the Department of Defense, or the US Government. References to non-Federal entities or products do not constitute or imply a Department of Defense endorsement. 

The eTable is available in the Appendix online at www.mdedge.com/cutis. 

Correspondence: Alejandra Gutierrez, MD (alejandra.v.gutierrez.mil@health.mil). 

Cutis. December 2025;116(6):198-201, E2. doi:10.12788/cutis.1310

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Author and Disclosure Information

Dr. Gutierrez is from the Burnett School of Medicine, Texas Christian University, Fort Worth. Drs. Coffel and Wong are from the Department of Dermatology, San Antonio Uniformed Services Health Education Consortium, Lackland Air Force Base, Texas.

The authors have no relevant financial disclosures to report. 

The views expressed herein are those of the authors and do not reflect the official policy or position of Brooke Army Medical Center, the US Army Medical Department, the Defense Health Agency, the US Army Office of the Surgeon General, the Department of the Army, the Department of the Air Force, the Department of Defense, or the US Government. References to non-Federal entities or products do not constitute or imply a Department of Defense endorsement. 

The eTable is available in the Appendix online at www.mdedge.com/cutis. 

Correspondence: Alejandra Gutierrez, MD (alejandra.v.gutierrez.mil@health.mil). 

Cutis. December 2025;116(6):198-201, E2. doi:10.12788/cutis.1310

Author and Disclosure Information

Dr. Gutierrez is from the Burnett School of Medicine, Texas Christian University, Fort Worth. Drs. Coffel and Wong are from the Department of Dermatology, San Antonio Uniformed Services Health Education Consortium, Lackland Air Force Base, Texas.

The authors have no relevant financial disclosures to report. 

The views expressed herein are those of the authors and do not reflect the official policy or position of Brooke Army Medical Center, the US Army Medical Department, the Defense Health Agency, the US Army Office of the Surgeon General, the Department of the Army, the Department of the Air Force, the Department of Defense, or the US Government. References to non-Federal entities or products do not constitute or imply a Department of Defense endorsement. 

The eTable is available in the Appendix online at www.mdedge.com/cutis. 

Correspondence: Alejandra Gutierrez, MD (alejandra.v.gutierrez.mil@health.mil). 

Cutis. December 2025;116(6):198-201, E2. doi:10.12788/cutis.1310

Article PDF
Article PDF
IN PARTNERSHIP WITH THE ASSOCIATION OF MILITARY DERMATOLOGISTS
IN PARTNERSHIP WITH THE ASSOCIATION OF MILITARY DERMATOLOGISTS

Facial hair growth in women is complex and multifaceted. It is not a disease but rather a part of normal anatomy or a symptom influenced by an underlying condition such as hypertrichosis, a hormonal imbalance (eg, hirsutism due to polycystic ovary syndrome [PCOS]), mechanical factors such as pseudofolliculitis barbae (PFB) from shaving, and perimenopausal and postmenopausal hormonal shifts. Additionally, normal facial hair patterns can vary substantially based on genetics, ethnicity, and cultural background. Some populations may naturally have more visible vellus or terminal hairs on the face, which are entirely physiologic rather than indicative of an underlying disorder. Despite this, societal expectations and beauty standards across many cultures dictate that facial hair in women is undesirable, often associating hair-free skin with femininity and attractiveness. This perception drives many women to seek treatment—not necessarily for medical reasons, but due to social pressure and aesthetic preferences.

Hypertrichosis, whether congenital or acquired, refers to excessive hair growth that is not androgen dependent and can appear on any site of the body. Causes include genetic predisposition, porphyria, thyroid disorders, internal malignancies, malnutrition, anorexia nervosa, or use of medications such as cyclosporine, prednisolone, and phenytoin.1 Hirsutism, by contrast, is characterized by the growth of terminal hairs in women at androgen-dependent sites such as the face, neck, and upper chest, where coarse hair typically grows in men.2 This condition often is associated with excess androgens produced by the ovaries or adrenal glands, most commonly due to PCOS although genetic factors may contribute. 

Before initiating treatment, a thorough history and physical examination are essential to determine the underlying cause of conditions associated with facial hair growth in women. Clinicians should assess for signs of hyperandrogenism, menstrual irregularities, virilization, medication use, and family history. In cases of a suspected endocrine disorder, further laboratory evaluation may be warranted to guide appropriate management. While each cause of facial hair growth in women has unique management considerations, the shared impact on psychosocial well-being and adherence to grooming standards in the US military warrants an all-encompassing yet targeted approach. This comprehensive review discusses management options for women with facial hair in the military based on a review of PubMed articles indexed for MEDLINE conducted in November 2024 using combinations of the following search terms: hirsutism, facial hair, pseudofolliculitis barbae, women, female, military, grooming standards, hyperandrogenism, and hair removal.

Treatment Modalities

The available treatment modalities, including their mechanisms, potential risks, and considerations are summarized in the eTable.

eTABLE. Comparison of Facial Hair Management Strategies For Women

Mechanical—Shaving remains one of the most widely utilized methods of hair removal in women due to its accessibility and ease of use. It does not disrupt the anagen phase of the hair growth cycle, making it a temporary method that requires frequent repetition (often daily), particularly for individuals with rapid hair growth. The belief that shaving causes hair to grow back thicker or faster is a common misconception. Shaving does not alter the thickness or growth rate of hair; instead, it leaves a blunt tip, making the hair feel coarser or appear thicker than uncut hair.3 Despite its relative convenience, shaving can lead to skin irritation due to mechanical trauma. Potential complications include PFB, superficial abrasions known more broadly as shaving irritation, and an increased risk for infections such as bacterial or fungal folliculitis.4

Chemical depilation, which uses thioglycolates mixed with alkali compounds, disrupts disulfide bonds in the hair, effectively breaking down the shaft without affecting the bulb. The depilatory requires application to the skin for approximately 3 to 15 minutes depending on the specific formulation and the thickness or texture of the hair. While it is a cost-effective option that easily can be done at home, the chemicals involved may trigger irritant contact dermatitis or folliculitis and produce an unpleasant odor from hydrogen disulfide gas.5 They also can lead to PFB.

Epilation removes the entire hair shaft and bulb, with results lasting approximately 6 weeks.6 Methods range from using tweezers to pluck single hairs and devices that simultaneously remove multiple hairs to hot or cold waxing, which use resin to grip and remove hair. Threading is a technique that uses twisted thread to remove the hair at the follicle level; this method may not alter hair growth unless performed during the anagen phase, during which repeated plucking can damage the matrix and potentially lead to permanent hair reduction.5 Common adverse effects include pain during removal, burns from waxing, folliculitis, PFB, postinflammatory hyperpigmentation, and scarring, particularly when multiple hairs are removed at once.

Pharmacologic—Pharmacologic therapy commonly is used to manage hirsutism and typically begins with a trial of combined oral contraceptives (COCs) containing estrogen and progestin, which are considered the first-line option unless contraindicated.7 If response to COC monotherapy is inadequate, an antiandrogen such as spironolactone may be added. Combination therapy with a COC and an antiandrogen generally is reserved for severe cases or patients who previously have shown suboptimal response to COCs alone.7 Patients should be counseled to discontinue antiandrogen therapy if they become pregnant due to the risk for fetal undervirilization observed in animal studies.8,9 Typical dosing of spironolactone, a competitive inhibitor of 5-α-reductase and androgen receptors, ranges from 100 mg to 200 mg daily.10 Reported adverse effects include polyuria, postural hypotension, menstrual irregularities, hyperkalemia, and potential liver dysfunction. Although spironolactone has demonstrated tumorigenic effects in animal studies, no such effects have been observed in humans.11

Eflornithine hydrochloride cream 13.9% is the first topical prescription medication approved by the US Food and Drug Administration for reduction of unwanted facial hair in women.12 It works by irreversibly blocking the activity of ornithine decarboxylase, an enzyme involved in the rate-limiting step of polyamine synthesis, which is essential for hair growth. In a randomized, double-blind clinical trial evaluating its effectiveness and safety, twice-daily application for 24 weeks resulted in a clinically meaningful reduction in hair length and density (measured as surface area) compared with the control group.13 When eflornithine hydrochloride cream 13.9% is discontinued, hair growth gradually returns to baseline. Studies have shown that hair regrowth typically begins within 8 weeks after treatment is stopped; within several months, hair returns to pretreatment levels.14 Adverse effects of eflornithine hydrochloride cream generally are mild and may include local irritation and acneform eruptions. In a randomized bilateral vehicle-controlled trial of 31 women, both eflornithine and vehicle creams were well tolerated, with 1 patient reporting mild tingling with eflornithine that resolved with continued use for 7 days.15

Procedural—Photoepilation therapies widely are considered by dermatologists to be among the most effective methods for reducing unwanted hair.16 Laser hair removal employs selective photothermolysis, a principle by which specific wavelengths of light target melanin in hair follicles. This method results in localized thermal damage, destroying hair follicles and reducing regrowth. Wavelengths between 600 and 1100 nm are most effective for hair removal; widely used devices include the ruby (694 nm), alexandrite (755 nm), diode (800-810 nm), and long-pulsed Nd:YAG lasers (1064 nm). Cooling mechanisms such as cryogen spray or contact cooling often are employed to minimize epidermal damage and lessen patient discomfort.

The hair matrix is most responsive to laser treatment during the anagen phase, necessitating multiple sessions to ensure all hairs are treated during this optimal growth stage. Generally, 4 to 6 sessions spaced at intervals of 4 to 6 weeks are required to achieve satisfactory results.17 Matching the laser wavelength to the absorption properties of melanin—the target chromophore—enables selective destruction of melanin-rich hair follicles while minimizing damage to surrounding skin.

The ideal laser wavelength primarily affects melanin concentrated in the hair bulb, leading to follicular destruction while reducing the risk for unintended depigmentation of the epidermis; however, competing structures in the skin (eg, epidermal pigment) also can absorb laser energy, diminishing treatment efficacy and increasing the risk for adverse effects. Shorter wavelengths are effective for lighter skin types, while longer wavelengths such as the Nd:YAG laser are safer for individuals with darker skin types as they bypass melanin in the epidermis.

It is important to note that laser hair removal is ineffective for white and gray hairs due to the lack of melanin. As a result, alternative methods such as electrolysis, which does not rely on pigment, may be more appropriate for permanent hair removal in individuals with nonpigmented hairs. Research indicates that combining topical eflornithine with alexandrite or Nd:YAG lasers improves outcomes for reducing unwanted facial hair.18

In military settings, laser hair removal is utilized for specific conditions such as PFB in male service members to assist with the reduction of hair and mitigation of symptoms.19 The majority of military dermatology clinics have devices for laser hair removal; however, dermatology services are not available at many military treatment facilities, and dermatologic care may be provided by the local civilian dermatologists. That said, laser therapy is covered in the civilian sector for active-duty service members with PFB of the face and neck under certain criteria. These include a documented safety risk in environments requiring respiratory protection, failure of conservative treatments, and evaluation by a military dermatologist who confirms the necessity of civilian-provided laser therapy when it is unavailable at a military facility.20 While such policies demonstrate the military’s recognition of laser therapy as a viable solution for certain grooming-related conditions, many are unaware that the existing laser hair removal policy also applies to women. Increasing awareness of this coverage could help female service members access treatment options that align with both medical and professional grooming needs.

Intense pulsed light (IPL) systems are nonlaser devices that emit broad-spectrum light in the 590- to 1200-nm range. They utilize a flash lamp to achieve thermal damage. Filters are used to narrow the wavelength range based on the specific target. Intense pulsed light devices are less precise than lasers but remain effective for hair reduction. In addition to hair removal, IPL devices are employed in the treatment of pigmented and vascular lesions. Common adverse effects of both laser and IPL hair removal include transient erythema, perifollicular edema, and pigmentary changes, especially in patients with darker skin types. Rare complications include blistering, scarring, and paradoxical hair stimulation in which untreated areas develop increased hair growth.

Electrolysis is recognized as the only method of truly permanent hair removal and is effective for all hair colors.21 However, the variability in technique among practitioners often leads to inconsistent results, with some patients experiencing hair regrowth. Galvanic electrolysis involves inserting a fine needle into the hair follicle and applying an electrical current to destroy the it and the rapidly dividing cells of the matrix.22 The introduction of thermolytic electrolysis, which uses a high-frequency alternating current (commonly 13.56 MHz or 27.12 MHz), has enhanced efficiency by creating heat at the needle tip to destroy the follicle. This approach is faster and now is commonly combined with galvanic electrolysis.23 While no controlled clinical trials directly compare these methods, many patients experience permanent hair removal, with approximately 15% to 25% regrowth within 6 months.22,24

Alternative Options—Home-use laser and light-based devices have become increasingly popular for managing unwanted hair due to their affordability and convenience, with most devices priced less than $1000.25 These devices utilize various technologies, including lasers (808 nm), IPL, or combinations of IPL and radiofrequency.26 Despite their accessibility, peer-reviewed research on their safety profile and effectiveness is limited, as existing data primarily come from industry-funded, uncontrolled studies with short follow-up durations—making it difficult to assess long-term outcomes.25

Psychosocial Impact

A 2023 study of active-duty female service members with PCOS highlighted the unique challenges they face while managing symptoms such as facial hair within the constraints of military service.27 Although the study focused on PCOS, the findings shed light on how facial hair specifically impacts the psychological well-being of servicewomen. Participants described facial hair as one of the most visible and stigmatizing symptoms, often leading to feelings of embarrassment and diminished confidence. Participants also highlighted the professional implications of facial hair, with some describing feelings of scrutiny and judgment from peers and leadership in public. These challenges can be more pronounced in deployments or field exercises where hygiene resources are limited. The lack of access not only affects self-perception but also can hinder the ability of servicewomen to meet implicit expectations for grooming and appearance.27 There is a notable gap in research examining the impact of facial hair on military servicewomen. Given the unique environmental challenges and professional expectations, further investigation is warranted to better understand how facial hair affects women and to optimize treatment approaches in this population.

Final Thoughts

Limited awareness and understanding of facial hair in woman contribute to stigma, often leaving affected individuals to navigate challenges in isolation. Given the impact on confidence, professional appearance, and adherence to military grooming standards, it is essential for health care practitioners to recognize and address facial hair in women. Importantly, laser hair removal is covered by TRICARE for active-duty female service members with PFB, yet many remain unaware of this benefit. Increased awareness of available mechanical, pharmacologic, and procedural treatment options allows for tailored management, ensuring that women receive appropriate medical care.

Facial hair growth in women is complex and multifaceted. It is not a disease but rather a part of normal anatomy or a symptom influenced by an underlying condition such as hypertrichosis, a hormonal imbalance (eg, hirsutism due to polycystic ovary syndrome [PCOS]), mechanical factors such as pseudofolliculitis barbae (PFB) from shaving, and perimenopausal and postmenopausal hormonal shifts. Additionally, normal facial hair patterns can vary substantially based on genetics, ethnicity, and cultural background. Some populations may naturally have more visible vellus or terminal hairs on the face, which are entirely physiologic rather than indicative of an underlying disorder. Despite this, societal expectations and beauty standards across many cultures dictate that facial hair in women is undesirable, often associating hair-free skin with femininity and attractiveness. This perception drives many women to seek treatment—not necessarily for medical reasons, but due to social pressure and aesthetic preferences.

Hypertrichosis, whether congenital or acquired, refers to excessive hair growth that is not androgen dependent and can appear on any site of the body. Causes include genetic predisposition, porphyria, thyroid disorders, internal malignancies, malnutrition, anorexia nervosa, or use of medications such as cyclosporine, prednisolone, and phenytoin.1 Hirsutism, by contrast, is characterized by the growth of terminal hairs in women at androgen-dependent sites such as the face, neck, and upper chest, where coarse hair typically grows in men.2 This condition often is associated with excess androgens produced by the ovaries or adrenal glands, most commonly due to PCOS although genetic factors may contribute. 

Before initiating treatment, a thorough history and physical examination are essential to determine the underlying cause of conditions associated with facial hair growth in women. Clinicians should assess for signs of hyperandrogenism, menstrual irregularities, virilization, medication use, and family history. In cases of a suspected endocrine disorder, further laboratory evaluation may be warranted to guide appropriate management. While each cause of facial hair growth in women has unique management considerations, the shared impact on psychosocial well-being and adherence to grooming standards in the US military warrants an all-encompassing yet targeted approach. This comprehensive review discusses management options for women with facial hair in the military based on a review of PubMed articles indexed for MEDLINE conducted in November 2024 using combinations of the following search terms: hirsutism, facial hair, pseudofolliculitis barbae, women, female, military, grooming standards, hyperandrogenism, and hair removal.

Treatment Modalities

The available treatment modalities, including their mechanisms, potential risks, and considerations are summarized in the eTable.

eTABLE. Comparison of Facial Hair Management Strategies For Women

Mechanical—Shaving remains one of the most widely utilized methods of hair removal in women due to its accessibility and ease of use. It does not disrupt the anagen phase of the hair growth cycle, making it a temporary method that requires frequent repetition (often daily), particularly for individuals with rapid hair growth. The belief that shaving causes hair to grow back thicker or faster is a common misconception. Shaving does not alter the thickness or growth rate of hair; instead, it leaves a blunt tip, making the hair feel coarser or appear thicker than uncut hair.3 Despite its relative convenience, shaving can lead to skin irritation due to mechanical trauma. Potential complications include PFB, superficial abrasions known more broadly as shaving irritation, and an increased risk for infections such as bacterial or fungal folliculitis.4

Chemical depilation, which uses thioglycolates mixed with alkali compounds, disrupts disulfide bonds in the hair, effectively breaking down the shaft without affecting the bulb. The depilatory requires application to the skin for approximately 3 to 15 minutes depending on the specific formulation and the thickness or texture of the hair. While it is a cost-effective option that easily can be done at home, the chemicals involved may trigger irritant contact dermatitis or folliculitis and produce an unpleasant odor from hydrogen disulfide gas.5 They also can lead to PFB.

Epilation removes the entire hair shaft and bulb, with results lasting approximately 6 weeks.6 Methods range from using tweezers to pluck single hairs and devices that simultaneously remove multiple hairs to hot or cold waxing, which use resin to grip and remove hair. Threading is a technique that uses twisted thread to remove the hair at the follicle level; this method may not alter hair growth unless performed during the anagen phase, during which repeated plucking can damage the matrix and potentially lead to permanent hair reduction.5 Common adverse effects include pain during removal, burns from waxing, folliculitis, PFB, postinflammatory hyperpigmentation, and scarring, particularly when multiple hairs are removed at once.

Pharmacologic—Pharmacologic therapy commonly is used to manage hirsutism and typically begins with a trial of combined oral contraceptives (COCs) containing estrogen and progestin, which are considered the first-line option unless contraindicated.7 If response to COC monotherapy is inadequate, an antiandrogen such as spironolactone may be added. Combination therapy with a COC and an antiandrogen generally is reserved for severe cases or patients who previously have shown suboptimal response to COCs alone.7 Patients should be counseled to discontinue antiandrogen therapy if they become pregnant due to the risk for fetal undervirilization observed in animal studies.8,9 Typical dosing of spironolactone, a competitive inhibitor of 5-α-reductase and androgen receptors, ranges from 100 mg to 200 mg daily.10 Reported adverse effects include polyuria, postural hypotension, menstrual irregularities, hyperkalemia, and potential liver dysfunction. Although spironolactone has demonstrated tumorigenic effects in animal studies, no such effects have been observed in humans.11

Eflornithine hydrochloride cream 13.9% is the first topical prescription medication approved by the US Food and Drug Administration for reduction of unwanted facial hair in women.12 It works by irreversibly blocking the activity of ornithine decarboxylase, an enzyme involved in the rate-limiting step of polyamine synthesis, which is essential for hair growth. In a randomized, double-blind clinical trial evaluating its effectiveness and safety, twice-daily application for 24 weeks resulted in a clinically meaningful reduction in hair length and density (measured as surface area) compared with the control group.13 When eflornithine hydrochloride cream 13.9% is discontinued, hair growth gradually returns to baseline. Studies have shown that hair regrowth typically begins within 8 weeks after treatment is stopped; within several months, hair returns to pretreatment levels.14 Adverse effects of eflornithine hydrochloride cream generally are mild and may include local irritation and acneform eruptions. In a randomized bilateral vehicle-controlled trial of 31 women, both eflornithine and vehicle creams were well tolerated, with 1 patient reporting mild tingling with eflornithine that resolved with continued use for 7 days.15

Procedural—Photoepilation therapies widely are considered by dermatologists to be among the most effective methods for reducing unwanted hair.16 Laser hair removal employs selective photothermolysis, a principle by which specific wavelengths of light target melanin in hair follicles. This method results in localized thermal damage, destroying hair follicles and reducing regrowth. Wavelengths between 600 and 1100 nm are most effective for hair removal; widely used devices include the ruby (694 nm), alexandrite (755 nm), diode (800-810 nm), and long-pulsed Nd:YAG lasers (1064 nm). Cooling mechanisms such as cryogen spray or contact cooling often are employed to minimize epidermal damage and lessen patient discomfort.

The hair matrix is most responsive to laser treatment during the anagen phase, necessitating multiple sessions to ensure all hairs are treated during this optimal growth stage. Generally, 4 to 6 sessions spaced at intervals of 4 to 6 weeks are required to achieve satisfactory results.17 Matching the laser wavelength to the absorption properties of melanin—the target chromophore—enables selective destruction of melanin-rich hair follicles while minimizing damage to surrounding skin.

The ideal laser wavelength primarily affects melanin concentrated in the hair bulb, leading to follicular destruction while reducing the risk for unintended depigmentation of the epidermis; however, competing structures in the skin (eg, epidermal pigment) also can absorb laser energy, diminishing treatment efficacy and increasing the risk for adverse effects. Shorter wavelengths are effective for lighter skin types, while longer wavelengths such as the Nd:YAG laser are safer for individuals with darker skin types as they bypass melanin in the epidermis.

It is important to note that laser hair removal is ineffective for white and gray hairs due to the lack of melanin. As a result, alternative methods such as electrolysis, which does not rely on pigment, may be more appropriate for permanent hair removal in individuals with nonpigmented hairs. Research indicates that combining topical eflornithine with alexandrite or Nd:YAG lasers improves outcomes for reducing unwanted facial hair.18

In military settings, laser hair removal is utilized for specific conditions such as PFB in male service members to assist with the reduction of hair and mitigation of symptoms.19 The majority of military dermatology clinics have devices for laser hair removal; however, dermatology services are not available at many military treatment facilities, and dermatologic care may be provided by the local civilian dermatologists. That said, laser therapy is covered in the civilian sector for active-duty service members with PFB of the face and neck under certain criteria. These include a documented safety risk in environments requiring respiratory protection, failure of conservative treatments, and evaluation by a military dermatologist who confirms the necessity of civilian-provided laser therapy when it is unavailable at a military facility.20 While such policies demonstrate the military’s recognition of laser therapy as a viable solution for certain grooming-related conditions, many are unaware that the existing laser hair removal policy also applies to women. Increasing awareness of this coverage could help female service members access treatment options that align with both medical and professional grooming needs.

Intense pulsed light (IPL) systems are nonlaser devices that emit broad-spectrum light in the 590- to 1200-nm range. They utilize a flash lamp to achieve thermal damage. Filters are used to narrow the wavelength range based on the specific target. Intense pulsed light devices are less precise than lasers but remain effective for hair reduction. In addition to hair removal, IPL devices are employed in the treatment of pigmented and vascular lesions. Common adverse effects of both laser and IPL hair removal include transient erythema, perifollicular edema, and pigmentary changes, especially in patients with darker skin types. Rare complications include blistering, scarring, and paradoxical hair stimulation in which untreated areas develop increased hair growth.

Electrolysis is recognized as the only method of truly permanent hair removal and is effective for all hair colors.21 However, the variability in technique among practitioners often leads to inconsistent results, with some patients experiencing hair regrowth. Galvanic electrolysis involves inserting a fine needle into the hair follicle and applying an electrical current to destroy the it and the rapidly dividing cells of the matrix.22 The introduction of thermolytic electrolysis, which uses a high-frequency alternating current (commonly 13.56 MHz or 27.12 MHz), has enhanced efficiency by creating heat at the needle tip to destroy the follicle. This approach is faster and now is commonly combined with galvanic electrolysis.23 While no controlled clinical trials directly compare these methods, many patients experience permanent hair removal, with approximately 15% to 25% regrowth within 6 months.22,24

Alternative Options—Home-use laser and light-based devices have become increasingly popular for managing unwanted hair due to their affordability and convenience, with most devices priced less than $1000.25 These devices utilize various technologies, including lasers (808 nm), IPL, or combinations of IPL and radiofrequency.26 Despite their accessibility, peer-reviewed research on their safety profile and effectiveness is limited, as existing data primarily come from industry-funded, uncontrolled studies with short follow-up durations—making it difficult to assess long-term outcomes.25

Psychosocial Impact

A 2023 study of active-duty female service members with PCOS highlighted the unique challenges they face while managing symptoms such as facial hair within the constraints of military service.27 Although the study focused on PCOS, the findings shed light on how facial hair specifically impacts the psychological well-being of servicewomen. Participants described facial hair as one of the most visible and stigmatizing symptoms, often leading to feelings of embarrassment and diminished confidence. Participants also highlighted the professional implications of facial hair, with some describing feelings of scrutiny and judgment from peers and leadership in public. These challenges can be more pronounced in deployments or field exercises where hygiene resources are limited. The lack of access not only affects self-perception but also can hinder the ability of servicewomen to meet implicit expectations for grooming and appearance.27 There is a notable gap in research examining the impact of facial hair on military servicewomen. Given the unique environmental challenges and professional expectations, further investigation is warranted to better understand how facial hair affects women and to optimize treatment approaches in this population.

Final Thoughts

Limited awareness and understanding of facial hair in woman contribute to stigma, often leaving affected individuals to navigate challenges in isolation. Given the impact on confidence, professional appearance, and adherence to military grooming standards, it is essential for health care practitioners to recognize and address facial hair in women. Importantly, laser hair removal is covered by TRICARE for active-duty female service members with PFB, yet many remain unaware of this benefit. Increased awareness of available mechanical, pharmacologic, and procedural treatment options allows for tailored management, ensuring that women receive appropriate medical care.

References
  1. Wendelin DS, Pope DN, Mallory SB. Hypertrichosis. J Am Acad Dermatol. 2003;48:161-181. doi:10.1067/mjd.2003.100

  2. Blume-Peytavi U, Hahn S. Medical treatment of hirsutism. Dermatol Ther. 2008;21:329-339. doi:10.1111/j.1529-8019.2008.00215.x

  3. Kang CN, Shah M, Lynde C, et al. Hair removal practices: a literature review. Skin Therapy Lett. 2021;26:6-11.

  4. Matheson E, Bain J. Hirsutism in women. Am Fam Physician. 2019;100:168-175.

  5. Shenenberger DW, Utecht LM. Removal of unwanted facial hair. Am Fam Physician. 2002;66:1907-1911.

  6. Johnson E, Ebling FJ. The effect of plucking hairs during different phases of the follicular cycle. J Embryol Exp Morphol. 1964;12:465-474.

  7. Martin KA, Anderson RR, Chang RJ, et al. Evaluation and treatment of hirsutism in premenopausal women: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2018;103:1233-1257. doi:10.1210/jc.2018-00241

  8. Barrionuevo P, Nabhan M, Altayar O, et al. Treatment options for hirsutism: a systematic review and network meta-analysis. J Clin Endocrinol Metab. 2018;103:1258-1264. doi:10.1210/jc.2017-02052

  9. Alesi S, Forslund M, Melin J, et al. Efficacy and safety of anti-androgens in the management of polycystic ovary syndrome: a systematic review and meta-analysis of randomised controlled trials. EClinicalMedicine. Published online August 9, 2023. doi:10.1016/j.eclinm.2023.102162

  10. Escobar-Morreale HF, Carmina E, Dewailly D, et al. Epidemiology, diagnosis and management of hirsutism: a consensus statement. Hum Reprod Update. 2012;18:146-170.

  11. Hussein RS, Abdelbasset WK. Updates on hirsutism: a narrative review. Int J Biomedicine. 2022;12:193-198. doi:10.21103/Article12(2)_RA4

  12. Shapiro J, Lui H. Vaniqa—eflornithine 13.9% cream. Skin Therapy Lett. 2001;6:1-5.

  13. Wolf JE Jr, Shander D, Huber F, et al. Randomized, double-blind clinical evaluation of the efficacy and safety of topical eflornithine HCl 13.9% cream in the treatment of women with facial hair. Int J Dermatol. 2007;46:94-98. doi:10.1111/j.1365-4632.2006.03079.x

  14. Balfour JA, McClellan K. Topical eflornithine. Am J Clin Dermatol. 2001;2:197-202. doi:10.2165/00128071-200102030-00009

  15. Hamzavi I, Tan E, Shapiro J, et al. A randomized bilateral vehicle-controlled study of eflornithine cream combined with laser treatment versus laser treatment alone for facial hirsutism in women. J Am Acad Dermatol. 2007;57:54-59. doi:10.1016/j.jaad.2006.09.025

  16. Goldberg DJ. Laser hair removal. In: Goldberg DJ, ed. Laser Dermatology: Pearls and Problems. Blackwell; 2008.

  17. Hussain M, Polnikorn N, Goldberg DJ. Laser-assisted hair removal in Asian skin: efficacy, complications, and the effect of single versus multiple treatments. Dermatol Surg. 2003;29:249-254. doi:10.1046/j.1524-4725.2003.29059.x

  18. Smith SR, Piacquadio DJ, Beger B, et al. Eflornithine cream combined with laser therapy in the management of unwanted facial hair growth in women: a randomized trial. Dermatol Surg. 2006;32:1237-1243. doi:10.1111/j.1524-4725.2006.32282.x

  19. Jung I, Lannan FM, Weiss A, et al. Treatment and current policies on pseudofolliculitis barbae in the US military. Cutis. 2023;112:299-302. doi:10.12788/cutis.0907

  20. TRICARE Operations Manual 6010.59-M. Supplemental Health Care Program (SHCP)—Chapter 17. Contractor Responsibilities. Military Health System and Defense Health Agency website. Revised November 5, 2021. Accessed February 13, 2024. https://manuals.health.mil/pages/DisplayManualHtmlFile/2022-08-31/AsOf/TO15/C17S3.html 

  21. Yanes DA, Smith P, Avram MM. A review of best practices for gender-affirming laser hair removal. Dermatol Surg. 2024;50:S201-S204. doi:10.1097/DSS.0000000000004441

  22. Wagner RF Jr, Tomich JM, Grande DJ. Electrolysis and thermolysis for permanent hair removal. J Am Acad Dermatol. 1985;12:441-449. doi:10.1016/s0190-9622(85)70062-x

  23. Olsen EA. Methods of hair removal. J Am Acad Dermatol. 1999;40:143-157. doi:10.1016/s0190-9622(99)70181-7

  24. Kligman AM, Peters L. Histologic changes of human hair follicles after electrolysis: a comparison of two methods. Cutis. 1984;34:169-176.

  25. Hession MT, Markova A, Graber EM. A review of hand-held, home-use cosmetic laser and light devices. Dermatol Surg. 2015;41:307-320. doi:10.1097/DSS.0000000000000283

  26. Wheeland RG. Permanent hair reduction with a home-use diode laser: safety and effectiveness 1 year after eight treatments. Lasers Surg Med. 2012;44:550-557. doi:10.1002/lsm.22051

  27. Hopkins D, Walker SC, Wilson C, et al. The experience of living with polycystic ovary syndrome in the military. Mil Med. 2024;189:E188-E197. doi:10.1093/milmed/usad241

References
  1. Wendelin DS, Pope DN, Mallory SB. Hypertrichosis. J Am Acad Dermatol. 2003;48:161-181. doi:10.1067/mjd.2003.100

  2. Blume-Peytavi U, Hahn S. Medical treatment of hirsutism. Dermatol Ther. 2008;21:329-339. doi:10.1111/j.1529-8019.2008.00215.x

  3. Kang CN, Shah M, Lynde C, et al. Hair removal practices: a literature review. Skin Therapy Lett. 2021;26:6-11.

  4. Matheson E, Bain J. Hirsutism in women. Am Fam Physician. 2019;100:168-175.

  5. Shenenberger DW, Utecht LM. Removal of unwanted facial hair. Am Fam Physician. 2002;66:1907-1911.

  6. Johnson E, Ebling FJ. The effect of plucking hairs during different phases of the follicular cycle. J Embryol Exp Morphol. 1964;12:465-474.

  7. Martin KA, Anderson RR, Chang RJ, et al. Evaluation and treatment of hirsutism in premenopausal women: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2018;103:1233-1257. doi:10.1210/jc.2018-00241

  8. Barrionuevo P, Nabhan M, Altayar O, et al. Treatment options for hirsutism: a systematic review and network meta-analysis. J Clin Endocrinol Metab. 2018;103:1258-1264. doi:10.1210/jc.2017-02052

  9. Alesi S, Forslund M, Melin J, et al. Efficacy and safety of anti-androgens in the management of polycystic ovary syndrome: a systematic review and meta-analysis of randomised controlled trials. EClinicalMedicine. Published online August 9, 2023. doi:10.1016/j.eclinm.2023.102162

  10. Escobar-Morreale HF, Carmina E, Dewailly D, et al. Epidemiology, diagnosis and management of hirsutism: a consensus statement. Hum Reprod Update. 2012;18:146-170.

  11. Hussein RS, Abdelbasset WK. Updates on hirsutism: a narrative review. Int J Biomedicine. 2022;12:193-198. doi:10.21103/Article12(2)_RA4

  12. Shapiro J, Lui H. Vaniqa—eflornithine 13.9% cream. Skin Therapy Lett. 2001;6:1-5.

  13. Wolf JE Jr, Shander D, Huber F, et al. Randomized, double-blind clinical evaluation of the efficacy and safety of topical eflornithine HCl 13.9% cream in the treatment of women with facial hair. Int J Dermatol. 2007;46:94-98. doi:10.1111/j.1365-4632.2006.03079.x

  14. Balfour JA, McClellan K. Topical eflornithine. Am J Clin Dermatol. 2001;2:197-202. doi:10.2165/00128071-200102030-00009

  15. Hamzavi I, Tan E, Shapiro J, et al. A randomized bilateral vehicle-controlled study of eflornithine cream combined with laser treatment versus laser treatment alone for facial hirsutism in women. J Am Acad Dermatol. 2007;57:54-59. doi:10.1016/j.jaad.2006.09.025

  16. Goldberg DJ. Laser hair removal. In: Goldberg DJ, ed. Laser Dermatology: Pearls and Problems. Blackwell; 2008.

  17. Hussain M, Polnikorn N, Goldberg DJ. Laser-assisted hair removal in Asian skin: efficacy, complications, and the effect of single versus multiple treatments. Dermatol Surg. 2003;29:249-254. doi:10.1046/j.1524-4725.2003.29059.x

  18. Smith SR, Piacquadio DJ, Beger B, et al. Eflornithine cream combined with laser therapy in the management of unwanted facial hair growth in women: a randomized trial. Dermatol Surg. 2006;32:1237-1243. doi:10.1111/j.1524-4725.2006.32282.x

  19. Jung I, Lannan FM, Weiss A, et al. Treatment and current policies on pseudofolliculitis barbae in the US military. Cutis. 2023;112:299-302. doi:10.12788/cutis.0907

  20. TRICARE Operations Manual 6010.59-M. Supplemental Health Care Program (SHCP)—Chapter 17. Contractor Responsibilities. Military Health System and Defense Health Agency website. Revised November 5, 2021. Accessed February 13, 2024. https://manuals.health.mil/pages/DisplayManualHtmlFile/2022-08-31/AsOf/TO15/C17S3.html 

  21. Yanes DA, Smith P, Avram MM. A review of best practices for gender-affirming laser hair removal. Dermatol Surg. 2024;50:S201-S204. doi:10.1097/DSS.0000000000004441

  22. Wagner RF Jr, Tomich JM, Grande DJ. Electrolysis and thermolysis for permanent hair removal. J Am Acad Dermatol. 1985;12:441-449. doi:10.1016/s0190-9622(85)70062-x

  23. Olsen EA. Methods of hair removal. J Am Acad Dermatol. 1999;40:143-157. doi:10.1016/s0190-9622(99)70181-7

  24. Kligman AM, Peters L. Histologic changes of human hair follicles after electrolysis: a comparison of two methods. Cutis. 1984;34:169-176.

  25. Hession MT, Markova A, Graber EM. A review of hand-held, home-use cosmetic laser and light devices. Dermatol Surg. 2015;41:307-320. doi:10.1097/DSS.0000000000000283

  26. Wheeland RG. Permanent hair reduction with a home-use diode laser: safety and effectiveness 1 year after eight treatments. Lasers Surg Med. 2012;44:550-557. doi:10.1002/lsm.22051

  27. Hopkins D, Walker SC, Wilson C, et al. The experience of living with polycystic ovary syndrome in the military. Mil Med. 2024;189:E188-E197. doi:10.1093/milmed/usad241

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Millipede Burns: An Unusual Cause of Purplish Toes

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To the Editor:

Millipedes do not have nearly as many feet as their name would suggest; most have fewer than 100.1 They are not actually insects; they are a wormlike arthropod in the Diplopoda class. Generally these harmless animals can be a welcome resident in gardens because they break down decaying plant material and rejuvenate the soil.1 However, they are less welcome in the home or underfoot because of what happens when these invertebrates are threatened or crushed.2

Millipedes, which typically have at least 30 pairs of legs, have 2 defense mechanisms: (1) body coiling to withstand external pressure, and (2) secretion of fluids with insecticidal properties from specialized glands distributed along their body.3 These secretions, which are used by the millipede to defend against predators, contain organic compounds including benzoquinone. When these secretions come into contact with skin, pigmentary changes resembling a burn or necrosis and irritation to the skin (pain, burning, itching) occur.4,5

Millipedes typically are found in tropical and temperate regions worldwide, such as the Amazon rainforest, Southeast Asia, tropical areas of Africa, forests, grasslands, and gardens in North America and Europe.6 They also are found in every US state as well as Puerto Rico.1 Millipedes are nocturnal, favor dark places, and can make their way into residential areas, including homes, basements, gardens, and yards.2,6 Although millipede burns commonly are reported in tropical regions, we present a case in China.6A 33-year-old woman presented with purplish-red discoloration on all 5 toes on the left foot. The patient recounted that she discovered a millipede in her shoe earlier in the day, removed it, and crushed it with her bare foot. That night, while taking a bath, she noticed that the toes had turned purplish-red (Figure 1). The patient brought the crushed millipede with her to the emergency department where she sought treatment. The dermatologist confirmed that it was a millipede; however, the team was unable to determine the specific species because it had been crushed (Figure 2).

FIGURE 1. A and B, Following contact with a millipede, the patient developed purplish-red discoloration on the foot that mimicked ischemia. The discoloration on the second and third toes was particularly vivid.
FIGURE 1. A and B, Following contact with a millipede, the patient developed purplish-red discoloration on the foot that mimicked ischemia. The discoloration on the second and third toes was particularly vivid. 

 

FIGURE 2. The patient crushed the millipede with her bare foot and brought it with her when she sought care.
FIGURE 2. The patient crushed the millipede with her bare foot and brought it with her when she sought care.

 

Physical examination of the affected toes showed a clear boundary and iodinelike staining. The patient did not report pain. The stained skin had a normal temperature, pulse, texture, and sensation. Dermoscopy revealed multiple black-brown patches on the toes (Figure 3). The pigmented area gradually faded over a 1-month period. Superficial damage to the toenail revealed evidence of black-brown pigmentation on both the nail and the skin underneath. The diagnosis in the dermoscopy report suggested exogenous pigmentation of the toes. The patient was advised that no treatment was needed and that the condition would resolve on its own. At 1-month follow-up, the patient’s toes had returned to their normal color (Figure 4).

FIGURE 3. Dermoscopy revealed multiple black-brown patches on the patient’s toes (original magnification ×20). The 3 white lines in the center of the image represent normal skin.
FIGURE 3. Dermoscopy revealed multiple black-brown patches on the patient’s toes (original magnification ×20). The 3 white lines in the center of the image represent normal skin.

 

FIGURE 4. A and B, One month after the patient sought treatment, the color of the toes returned to normal.
FIGURE 4. A and B, One month after the patient sought treatment, the color of the toes returned to normal.

The feet are common sites of millipede burns; other exposed areas, such as the arms, face, and eyes, also are potential sites of involvement.5 The cutaneous pigmentary changes seen on our patient’s foot were a result of the millipede’s defense mechanism—secreted toxic chemicals that stained the foot. It is important to note that the pigmentation was not associated with the death of the millipede, as the millipede was still alive upon initial contact with the patient’s foot in her shoe. 

When a patient presents with pigmentary changes, several conditions must be ruled out—notably acute arterial thrombosis. Patients with this condition will describe acute pain and weakness in the area of involvement. Physicians inspecting the area will note coldness and pallor in the affected limb as well as a diminished or absent pulse. In severe cases, the skin may exhibit a purplish-red appearance.5 Millipede burns also should be distinguished from bacterial endocarditis and cryoglobulinemia.7 All 3 conditions can manifest with redness, swelling, blisters, and purpuralike changes. Positive blood culture is an important diagnostic basis for bacterial endocarditis; in addition, routine blood tests will demonstrate a decrease in red blood cells and hemoglobin, and routine urinalysis may show proteinuria and microscopic hematuria. Patients with cryoglobulinemia will have a positive cryoglobulin assay, increased IgM, and often decreased complement.7 It also is worth noting that millipede burns might resemble child abuse in pediatric patients, necessitating further evaluation.5 

It is unusual to see a millipede burn in nontropical regions. Therefore, the identification of our patient’s millipede burn was notable and serves as a reminder to keep this diagnosis in the differential when caring for patients with pigmentary changes. An accurate diagnosis hinges on being alert to a millipede exposure history and recognizing the clinical manifestations. For affected patients, it may be beneficial to recommend they advise friends and relatives to avoid skin contact with millipedes and most importantly to avoid stepping on them with bare feet.

References
  1. Millipedes. National Wildlife Federation. Accessed October 15, 2025. https://www.nwf.org/Educational-Resources/Wildlife-Guide/Invertebrates/Millipedes

  2. Pennini SN, Rebello PFB, Guerra MdGVB, et al. Millipede accident with unusual dermatological lesion. An Bras Dermatol. 2019;94:765-767. doi:10.1016/j.abd.2019.10.003

  3. Lima CAJ, Cardoso JLC, Magela A, et al. Exogenous pigmentation in toes feigning ischemia of the extremities: a diagnostic challenge brought by arthropods of the Diplopoda Class (“millipedes“). An Bras Dermatol. 2010;85:391-392. doi:10.1590/s0365-05962910000300018

  4. De Capitani EM, Vieira RJ, Bucaretchi F, et al. Human accidents involving Rhinocricus spp., a common millipede genus observed in urban areas of Brazil. Clin Toxicol (Phila). 2011;49:187-190. doi:10.3109/15563650.2011.560855

  5. Lacy FA, Elston DM. What’s eating you? millipede burns. Cutis. 2019;103:195-196.

  6. Neto ASH, Filho FB, Martins G. Skin lesions simulating blue toe syndrome caused by prolonged contact with a millipede. Rev Soc Bras Med Trop. 2014;47:257-258. doi:10.1590/0037-8682-0212-2013

  7. Sampaio FMS, Valviesse VRGdA, Lyra-da-Silva JO, et al. Pain and hyperpigmentation of the toes: a quiz. hyperpigmentation of the toes caused by millipedes. Acta Derm Venereol. 2014;94:253-254. doi:10.2340/00015555-1645

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Author and Disclosure Information

Lu Chen and Gongliang Du are from the Department of Emergency Surgery, Shaanxi Provincial People’s Hospital, Xi’an City, China. Lu Chen also is from Xi’an Medical College, Xi’an City, Shaanxi Province, China. Haiying Hui is from the Department of Dermatology, Shaanxi Provincial People’s Hospital, China. 

The authors have no relevant financial disclosures to report. 

Correspondence: Haiying Hui, MM, No. 256, Youyi West Road, Xi’an City, Shaanxi Province, China 710068 (haiyinghui@163.com). 

Cutis. 2025 December;116(6):212-214. doi:10.12788/cutis.1299

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Lu Chen and Gongliang Du are from the Department of Emergency Surgery, Shaanxi Provincial People’s Hospital, Xi’an City, China. Lu Chen also is from Xi’an Medical College, Xi’an City, Shaanxi Province, China. Haiying Hui is from the Department of Dermatology, Shaanxi Provincial People’s Hospital, China. 

The authors have no relevant financial disclosures to report. 

Correspondence: Haiying Hui, MM, No. 256, Youyi West Road, Xi’an City, Shaanxi Province, China 710068 (haiyinghui@163.com). 

Cutis. 2025 December;116(6):212-214. doi:10.12788/cutis.1299

Author and Disclosure Information

Lu Chen and Gongliang Du are from the Department of Emergency Surgery, Shaanxi Provincial People’s Hospital, Xi’an City, China. Lu Chen also is from Xi’an Medical College, Xi’an City, Shaanxi Province, China. Haiying Hui is from the Department of Dermatology, Shaanxi Provincial People’s Hospital, China. 

The authors have no relevant financial disclosures to report. 

Correspondence: Haiying Hui, MM, No. 256, Youyi West Road, Xi’an City, Shaanxi Province, China 710068 (haiyinghui@163.com). 

Cutis. 2025 December;116(6):212-214. doi:10.12788/cutis.1299

Article PDF
Article PDF

To the Editor:

Millipedes do not have nearly as many feet as their name would suggest; most have fewer than 100.1 They are not actually insects; they are a wormlike arthropod in the Diplopoda class. Generally these harmless animals can be a welcome resident in gardens because they break down decaying plant material and rejuvenate the soil.1 However, they are less welcome in the home or underfoot because of what happens when these invertebrates are threatened or crushed.2

Millipedes, which typically have at least 30 pairs of legs, have 2 defense mechanisms: (1) body coiling to withstand external pressure, and (2) secretion of fluids with insecticidal properties from specialized glands distributed along their body.3 These secretions, which are used by the millipede to defend against predators, contain organic compounds including benzoquinone. When these secretions come into contact with skin, pigmentary changes resembling a burn or necrosis and irritation to the skin (pain, burning, itching) occur.4,5

Millipedes typically are found in tropical and temperate regions worldwide, such as the Amazon rainforest, Southeast Asia, tropical areas of Africa, forests, grasslands, and gardens in North America and Europe.6 They also are found in every US state as well as Puerto Rico.1 Millipedes are nocturnal, favor dark places, and can make their way into residential areas, including homes, basements, gardens, and yards.2,6 Although millipede burns commonly are reported in tropical regions, we present a case in China.6A 33-year-old woman presented with purplish-red discoloration on all 5 toes on the left foot. The patient recounted that she discovered a millipede in her shoe earlier in the day, removed it, and crushed it with her bare foot. That night, while taking a bath, she noticed that the toes had turned purplish-red (Figure 1). The patient brought the crushed millipede with her to the emergency department where she sought treatment. The dermatologist confirmed that it was a millipede; however, the team was unable to determine the specific species because it had been crushed (Figure 2).

FIGURE 1. A and B, Following contact with a millipede, the patient developed purplish-red discoloration on the foot that mimicked ischemia. The discoloration on the second and third toes was particularly vivid.
FIGURE 1. A and B, Following contact with a millipede, the patient developed purplish-red discoloration on the foot that mimicked ischemia. The discoloration on the second and third toes was particularly vivid. 

 

FIGURE 2. The patient crushed the millipede with her bare foot and brought it with her when she sought care.
FIGURE 2. The patient crushed the millipede with her bare foot and brought it with her when she sought care.

 

Physical examination of the affected toes showed a clear boundary and iodinelike staining. The patient did not report pain. The stained skin had a normal temperature, pulse, texture, and sensation. Dermoscopy revealed multiple black-brown patches on the toes (Figure 3). The pigmented area gradually faded over a 1-month period. Superficial damage to the toenail revealed evidence of black-brown pigmentation on both the nail and the skin underneath. The diagnosis in the dermoscopy report suggested exogenous pigmentation of the toes. The patient was advised that no treatment was needed and that the condition would resolve on its own. At 1-month follow-up, the patient’s toes had returned to their normal color (Figure 4).

FIGURE 3. Dermoscopy revealed multiple black-brown patches on the patient’s toes (original magnification ×20). The 3 white lines in the center of the image represent normal skin.
FIGURE 3. Dermoscopy revealed multiple black-brown patches on the patient’s toes (original magnification ×20). The 3 white lines in the center of the image represent normal skin.

 

FIGURE 4. A and B, One month after the patient sought treatment, the color of the toes returned to normal.
FIGURE 4. A and B, One month after the patient sought treatment, the color of the toes returned to normal.

The feet are common sites of millipede burns; other exposed areas, such as the arms, face, and eyes, also are potential sites of involvement.5 The cutaneous pigmentary changes seen on our patient’s foot were a result of the millipede’s defense mechanism—secreted toxic chemicals that stained the foot. It is important to note that the pigmentation was not associated with the death of the millipede, as the millipede was still alive upon initial contact with the patient’s foot in her shoe. 

When a patient presents with pigmentary changes, several conditions must be ruled out—notably acute arterial thrombosis. Patients with this condition will describe acute pain and weakness in the area of involvement. Physicians inspecting the area will note coldness and pallor in the affected limb as well as a diminished or absent pulse. In severe cases, the skin may exhibit a purplish-red appearance.5 Millipede burns also should be distinguished from bacterial endocarditis and cryoglobulinemia.7 All 3 conditions can manifest with redness, swelling, blisters, and purpuralike changes. Positive blood culture is an important diagnostic basis for bacterial endocarditis; in addition, routine blood tests will demonstrate a decrease in red blood cells and hemoglobin, and routine urinalysis may show proteinuria and microscopic hematuria. Patients with cryoglobulinemia will have a positive cryoglobulin assay, increased IgM, and often decreased complement.7 It also is worth noting that millipede burns might resemble child abuse in pediatric patients, necessitating further evaluation.5 

It is unusual to see a millipede burn in nontropical regions. Therefore, the identification of our patient’s millipede burn was notable and serves as a reminder to keep this diagnosis in the differential when caring for patients with pigmentary changes. An accurate diagnosis hinges on being alert to a millipede exposure history and recognizing the clinical manifestations. For affected patients, it may be beneficial to recommend they advise friends and relatives to avoid skin contact with millipedes and most importantly to avoid stepping on them with bare feet.

To the Editor:

Millipedes do not have nearly as many feet as their name would suggest; most have fewer than 100.1 They are not actually insects; they are a wormlike arthropod in the Diplopoda class. Generally these harmless animals can be a welcome resident in gardens because they break down decaying plant material and rejuvenate the soil.1 However, they are less welcome in the home or underfoot because of what happens when these invertebrates are threatened or crushed.2

Millipedes, which typically have at least 30 pairs of legs, have 2 defense mechanisms: (1) body coiling to withstand external pressure, and (2) secretion of fluids with insecticidal properties from specialized glands distributed along their body.3 These secretions, which are used by the millipede to defend against predators, contain organic compounds including benzoquinone. When these secretions come into contact with skin, pigmentary changes resembling a burn or necrosis and irritation to the skin (pain, burning, itching) occur.4,5

Millipedes typically are found in tropical and temperate regions worldwide, such as the Amazon rainforest, Southeast Asia, tropical areas of Africa, forests, grasslands, and gardens in North America and Europe.6 They also are found in every US state as well as Puerto Rico.1 Millipedes are nocturnal, favor dark places, and can make their way into residential areas, including homes, basements, gardens, and yards.2,6 Although millipede burns commonly are reported in tropical regions, we present a case in China.6A 33-year-old woman presented with purplish-red discoloration on all 5 toes on the left foot. The patient recounted that she discovered a millipede in her shoe earlier in the day, removed it, and crushed it with her bare foot. That night, while taking a bath, she noticed that the toes had turned purplish-red (Figure 1). The patient brought the crushed millipede with her to the emergency department where she sought treatment. The dermatologist confirmed that it was a millipede; however, the team was unable to determine the specific species because it had been crushed (Figure 2).

FIGURE 1. A and B, Following contact with a millipede, the patient developed purplish-red discoloration on the foot that mimicked ischemia. The discoloration on the second and third toes was particularly vivid.
FIGURE 1. A and B, Following contact with a millipede, the patient developed purplish-red discoloration on the foot that mimicked ischemia. The discoloration on the second and third toes was particularly vivid. 

 

FIGURE 2. The patient crushed the millipede with her bare foot and brought it with her when she sought care.
FIGURE 2. The patient crushed the millipede with her bare foot and brought it with her when she sought care.

 

Physical examination of the affected toes showed a clear boundary and iodinelike staining. The patient did not report pain. The stained skin had a normal temperature, pulse, texture, and sensation. Dermoscopy revealed multiple black-brown patches on the toes (Figure 3). The pigmented area gradually faded over a 1-month period. Superficial damage to the toenail revealed evidence of black-brown pigmentation on both the nail and the skin underneath. The diagnosis in the dermoscopy report suggested exogenous pigmentation of the toes. The patient was advised that no treatment was needed and that the condition would resolve on its own. At 1-month follow-up, the patient’s toes had returned to their normal color (Figure 4).

FIGURE 3. Dermoscopy revealed multiple black-brown patches on the patient’s toes (original magnification ×20). The 3 white lines in the center of the image represent normal skin.
FIGURE 3. Dermoscopy revealed multiple black-brown patches on the patient’s toes (original magnification ×20). The 3 white lines in the center of the image represent normal skin.

 

FIGURE 4. A and B, One month after the patient sought treatment, the color of the toes returned to normal.
FIGURE 4. A and B, One month after the patient sought treatment, the color of the toes returned to normal.

The feet are common sites of millipede burns; other exposed areas, such as the arms, face, and eyes, also are potential sites of involvement.5 The cutaneous pigmentary changes seen on our patient’s foot were a result of the millipede’s defense mechanism—secreted toxic chemicals that stained the foot. It is important to note that the pigmentation was not associated with the death of the millipede, as the millipede was still alive upon initial contact with the patient’s foot in her shoe. 

When a patient presents with pigmentary changes, several conditions must be ruled out—notably acute arterial thrombosis. Patients with this condition will describe acute pain and weakness in the area of involvement. Physicians inspecting the area will note coldness and pallor in the affected limb as well as a diminished or absent pulse. In severe cases, the skin may exhibit a purplish-red appearance.5 Millipede burns also should be distinguished from bacterial endocarditis and cryoglobulinemia.7 All 3 conditions can manifest with redness, swelling, blisters, and purpuralike changes. Positive blood culture is an important diagnostic basis for bacterial endocarditis; in addition, routine blood tests will demonstrate a decrease in red blood cells and hemoglobin, and routine urinalysis may show proteinuria and microscopic hematuria. Patients with cryoglobulinemia will have a positive cryoglobulin assay, increased IgM, and often decreased complement.7 It also is worth noting that millipede burns might resemble child abuse in pediatric patients, necessitating further evaluation.5 

It is unusual to see a millipede burn in nontropical regions. Therefore, the identification of our patient’s millipede burn was notable and serves as a reminder to keep this diagnosis in the differential when caring for patients with pigmentary changes. An accurate diagnosis hinges on being alert to a millipede exposure history and recognizing the clinical manifestations. For affected patients, it may be beneficial to recommend they advise friends and relatives to avoid skin contact with millipedes and most importantly to avoid stepping on them with bare feet.

References
  1. Millipedes. National Wildlife Federation. Accessed October 15, 2025. https://www.nwf.org/Educational-Resources/Wildlife-Guide/Invertebrates/Millipedes

  2. Pennini SN, Rebello PFB, Guerra MdGVB, et al. Millipede accident with unusual dermatological lesion. An Bras Dermatol. 2019;94:765-767. doi:10.1016/j.abd.2019.10.003

  3. Lima CAJ, Cardoso JLC, Magela A, et al. Exogenous pigmentation in toes feigning ischemia of the extremities: a diagnostic challenge brought by arthropods of the Diplopoda Class (“millipedes“). An Bras Dermatol. 2010;85:391-392. doi:10.1590/s0365-05962910000300018

  4. De Capitani EM, Vieira RJ, Bucaretchi F, et al. Human accidents involving Rhinocricus spp., a common millipede genus observed in urban areas of Brazil. Clin Toxicol (Phila). 2011;49:187-190. doi:10.3109/15563650.2011.560855

  5. Lacy FA, Elston DM. What’s eating you? millipede burns. Cutis. 2019;103:195-196.

  6. Neto ASH, Filho FB, Martins G. Skin lesions simulating blue toe syndrome caused by prolonged contact with a millipede. Rev Soc Bras Med Trop. 2014;47:257-258. doi:10.1590/0037-8682-0212-2013

  7. Sampaio FMS, Valviesse VRGdA, Lyra-da-Silva JO, et al. Pain and hyperpigmentation of the toes: a quiz. hyperpigmentation of the toes caused by millipedes. Acta Derm Venereol. 2014;94:253-254. doi:10.2340/00015555-1645

References
  1. Millipedes. National Wildlife Federation. Accessed October 15, 2025. https://www.nwf.org/Educational-Resources/Wildlife-Guide/Invertebrates/Millipedes

  2. Pennini SN, Rebello PFB, Guerra MdGVB, et al. Millipede accident with unusual dermatological lesion. An Bras Dermatol. 2019;94:765-767. doi:10.1016/j.abd.2019.10.003

  3. Lima CAJ, Cardoso JLC, Magela A, et al. Exogenous pigmentation in toes feigning ischemia of the extremities: a diagnostic challenge brought by arthropods of the Diplopoda Class (“millipedes“). An Bras Dermatol. 2010;85:391-392. doi:10.1590/s0365-05962910000300018

  4. De Capitani EM, Vieira RJ, Bucaretchi F, et al. Human accidents involving Rhinocricus spp., a common millipede genus observed in urban areas of Brazil. Clin Toxicol (Phila). 2011;49:187-190. doi:10.3109/15563650.2011.560855

  5. Lacy FA, Elston DM. What’s eating you? millipede burns. Cutis. 2019;103:195-196.

  6. Neto ASH, Filho FB, Martins G. Skin lesions simulating blue toe syndrome caused by prolonged contact with a millipede. Rev Soc Bras Med Trop. 2014;47:257-258. doi:10.1590/0037-8682-0212-2013

  7. Sampaio FMS, Valviesse VRGdA, Lyra-da-Silva JO, et al. Pain and hyperpigmentation of the toes: a quiz. hyperpigmentation of the toes caused by millipedes. Acta Derm Venereol. 2014;94:253-254. doi:10.2340/00015555-1645

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PRACTICE POINTS

  • Millipede burns can resemble ischemia. The most common site of a millipede burn is the feet.
  • Diagnosing a millipede burn hinges on obtaining a detailed history, viewing the site under a dermatoscope, and carefully assessing the temperature and pulse of the affected area.
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Growing Nodule on the Parietal Scalp

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Growing Nodule on the Parietal Scalp

THE DIAGNOSIS: Malignant Proliferating Trichilemmal Tumor

Biopsy revealed a squamous epithelium with cystic changes, trichilemmal differentiation, squamous eddy formation, keratinocyte atypia, focal necrotic changes, and a focus of atypical keratinocytes invading the dermis (Figure 1). Based on these findings, a diagnosis of malignant proliferating trichilemmal tumor (MPTT) was made.

Martin-DD-1
FIGURE 1. Malignant proliferating trichilemmal tumor. Lobulated intradermal mass composed of a squamous epithelium with cystic changes, squamous eddy formation, keratinocyte atypia, trichilemmal differentiation, and focal necrotic changes. Note the nests of atypical keratinocytes invading the surrounding dermis (H&E, original magnification ×4).

Malignant proliferating trichilemmal tumor is a rare adnexal tumor that develops from the outer root sheath of the hair follicle. It often arises due to malignant transformation of pre-existing trichilemmal cysts, but some cases occur de novo.1 Malignant transformation is thought to start from a trichilemmal cyst in an adenomatous histologic stage, progressing to a proliferating trichilemmal cyst (PTC) in an epitheliomatous phase, ultimately becoming carcinomatous with MPTT.2-4 This transformation has been categorized into 3 morphologic groups to predict tumor behavior, including benign PTCs (curable by excision), low-grade malignant PTCs (minor risk for local recurrence), and high-grade malignant PTCs (risk for regional spread and metastasis with cytologic atypical features and potential for aggressive growth).1

More commonly observed in women in the fourth to eighth decades of life, MPTT may manifest as a fast- growing, painless, solitary nodule or as a progressively enlarging nodule at the site of a previously stable, long-standing lesion. Malignant proliferating trichilemmal tumor manifests frequently on the scalp, face, or neck, but there are reports of MPTT manifesting on the trunk and even as multiple concurrent lesions.1-4 The variability in clinical presentation and the potential to be mistaken for benign conditions makes excisional biopsy essential for diagnosis of MPTT. Histopathology classically demonstrates trichilemmal keratinization, a high mitotic index, and cellular atypia with invasion into the dermis.4 Malignant transformation frequently follows a prior history of trauma to the area or local inflammation.

Given the locally aggressive nature of MPTT, our patient was referred to a Mohs micrographic surgeon. While both wide excision with tumor-free margins and Mohs micrographic surgery are accepted surgical procedures for MPTT, there is no consensus in the literature on a standard treatment recommendation. Following surgery, close monitoring is needed for potential recurrence and metastases intracranially to the dura and muscles,5 as well as to the lungs.6 Further imaging using computed tomography or positron emission tomography can be ordered to rule out metastatic disease.4

Pilomatrixomas are benign neoplasms that arise from hair matrix cells and have been associated with catenin beta-1 gene mutations, as well as genetic syndromes and trauma.7 Clinically, pilomatrixomas manifest as solitary, firm, painless, slow-growing nodules that commonly are found in the head and neck region. This tumor has a slight predominance in women and occurs frequently in adolescent years. The overlying skin may appear normal or show grey-bluish discoloration.8 Histopathology shows basaloid cells resembling primitive hair matrix cells with an abrupt transition to shadow cells composed of transformed keratinocytes without nuclei and calcification.7-8 This tumor can be differentiated by the presence of basaloid and shadow cells with calcification on histopathology, while MPTT will show atypical, mitotically active squamous cells with trichilemmal keratinization (Figure 2).

Martin-DD-2
FIGURE 2. Pilomatrixoma. Basophilic matrical cells with scant cytoplasm and hyperchromatic nuclei with occasional normal mitoses transitioning to eosinophilic shadow/ghost cells without nuclei. There often is surrounding granulomatous inflammation with giant cell formation (H&E; original magnification ×10).

Proliferating trichilemmal cyst is a variant of trichilemmal cyst (TC) arising from the outer root sheath cells of the hair follicle. While TCs usually are slow growing and benign, the proliferating variant can be more aggressive with malignant potential. Patients often present with a solitary, well-circumscribed, rapidly growing nodule on the scalp. The lesion may be painful, and ulceration can occur, exposing the cystic contents. Histopathologically, PTCs resemble TCs with trichilemmal keratinization but also exhibit notable epithelial proliferation within the cystic space.9 While there can be considerable histopathologic overlap between PTC and MPTT—including extensive trichilemmal keratinization, variable atypia, and mitotic activity—PTC typically should not demonstrate invasion into the surrounding soft tissue or the degree of high-grade atypia, brisk mitoses, or necrosis seen in MPTT (eFigure 1).1 Immunohistochemistry may help distinguish PTC from MPTT and squamous cell carcinoma (SCC).10-11 The pattern of Ki-67 and p53 expression may be helpful with classification of PTC/MPTT into the 3 groups (benign, low-grade malignant, and high-grade malignant) proposed by Ye et al.1 Other investigators have suggested that Ki-67 expression may correlate potential for recurrence and clinical prognosis.12 Expression of CD34 (a marker that supports outer root sheath origin) might favor PTC/MPTT over SCC; however, cases of CD34- negative MPTT have been reported, particularly those with poorly differentiated histopathology.

CT116006215-eFig-1_AB
eFIGURE 1. Proliferating trichilemmal cyst. A, Well-circumscribed dermal tumor with a pushing border that exhibits abrupt trichilemmal keratinization and has extensive epithelial proliferation within the center of the cystic space (H&E, original magnification ×4). B, Epithelial proliferation with minimal cytologic atypia (H&E, original magnification ×10).

Squamous cell carcinoma with cystic features is a histologic variant of SCC characterized by cystlike spaces containing malignant squamous epithelial cells.13 Squamous cell carcinoma with cystic features can manifest as a firm nodule with ulceration similar to MPTT or PTC but also can mimic a benign cyst.14 The diagnosis of invasive SCC with cystic features typically is straightforward and characterized by cords and nests of atypical keratinocytes extending into the dermis with areas of cystic architecture (eFigure 2). While both SCC with cystic features and MPTT may show cystic histopathologic architecture, MPTT typically shows areas of PTC, whereas SCC with cystic features lacks such areas.

Martin-DD_e_2
eFIGURE 2. Squamous cell carcinoma with cystic changes. Invasive cords and nests of atypical keratinocytes extend into the dermis with an overlying epidermal connection. The center of the tumor shows cystic architecture (H&E; original magnification ×10).

Verrucous cysts refer to infundibular cysts or less commonly pilar cysts or hybrid pilar-epidermoid cysts that exhibit superimposed human papillomavirus (HPV) cytopathic changes. Clinically, a verrucous cyst manifests as a single, asymptomatic, slow-growing, firm lesion most commonly manifesting on the face and back. Histopathologically, the cyst wall may show acanthosis, papillomatosis, hypergranulosis with coarse keratohyalin granules, and koilocytic changes (eFigure 3). These histopathologic features are believed to be induced by secondary HPV infection. While HPV-related change, characterized by koilocytic alteration, papillomatosis, and verruciform hyperplasia, more commonly affects epidermal cysts, occasionally trichilemmal (pilar) cysts are involved. In these cases, verrucous cysts should be distinguished from MPTT. Verrucous cysts may contain rare normal mitotic figures, but do not contain atypical mitosis, marked cellular pleomorphism, or an infiltrating pattern similar to MPTT.15

Martin-DD_e_3
eFIGURE 3. Verrucous cyst. Note the cyst wall with acanthosis, papillomatosis, orthokeratosis and parakeratosis, hypergranulosis with coarse keratohyalin granules, and koilocytic changes (H&E; original magnification ×10).
References
  1. Ye J, Nappi O, Swanson PE, et al. Proliferating pilar tumors: a clinicopathologic study of 76 cases with a proposal for definition of benign and malignant variants. Am J Clin Pathol. 2004;122:566-574. doi:10.1309/0XLEGFQ64XYJU4G6
  2. Saida T, Oohara K, Hori Y, et al. Development of a malignant proliferating trichilemmal cyst in a patient with multiple trichilemmal cysts. Dermatologica. 1983;166:203-208. doi:10.1159/000249868
  3. Rao S, Ramakrishnan R, Kamakshi D, et al. Malignant proliferating trichilemmal tumour presenting early in life: an uncommon feature. J Cutan Aesthet Surg. 2011;4:51-55. doi:10.4103/0974-2077.79196
  4. Kearns-Turcotte S, Thériault M, Blouin MM. Malignant proliferating trichilemmal tumors arising in patients with multiple trichilemmal cysts: a case series. JAAD Case Rep. 2022;22:42-46. doi:10.1016
  5. Karamese M, Akatekin A, Abaci M, et al. Unusual invasion of trichilemmal tumors: two case reports. Modern Plastic Surg. 2012; 2:54-57. doi:10.4236/MPS.2012.23014 /j.jdcr.2022.01.033
  6. Lobo L, Amonkar AD, Dontamsetty VV. Malignant proliferating trichilemmal tumour of the scalp with intra-cranial extension and lung metastasis-a case report. Indian J Surg. 2016;78:493-495. doi:10.1007/s12262-015-1427-0
  7. Jones CD, Ho W, Robertson BF, et al. Pilomatrixoma: a comprehensive review of the literature. Am J Dermatopathol. 2018;40:631-641. doi:10.1097/DAD.0000000000001118
  8. Sharma D, Agarwal S, Jain LS, et al. Pilomatrixoma masquerading as metastatic adenocarcinoma. A diagnostic pitfall on cytology. J Clin Diagn Res. 2014;8:FD13-FD14. doi:10.7860/JCDR/2014/9696.5064
  9. Valerio E, Parro FHS, Macedo MP, et al. Proliferating trichilemmal cyst with clinical, radiological, macroscopic, and microscopic orrelation. An Bras Dermatol. 2019;94:452-454. doi:10.1590 /abd1806-4841.20198199
  10. Joshi TP, Marchand S, Tschen J. Malignant proliferating trichilemmal tumor: a subtle presentation in an African American woman and review of immunohistochemical markers for this rare condition. Cureus. 2021;13:E17289. doi:10.7759/cureus.17289
  11. Gulati HK, Deshmukh SD, Anand M, et al. Low-grade malignant proliferating pilar tumor simulating a squamous-cell carcinoma in an elderly female: a case report and immunohistochemical study. Int J Trichology. 2011;3:98-101. doi:10.4103/0974-7753.90818
  12. Rangel-Gamboa L, Reyes-Castro M, Dominguez-Cherit J, et al. Proliferating trichilemmal cyst: the value of ki67 immunostaining. Int J Trichology. 2013;5:115-117. doi:10.4103/0974-7753.125599
  13. Asad U, Alkul S, Shimizu I, et al. Squamous cell carcinoma with unusual benign-appearing cystic features on histology. Cureus. 2023;15:E33610. doi:10.7759/cureus.33610
  14. Alkul S, Nguyen CN, Ramani NS, et al. Squamous cell carcinoma arising in an epidermal inclusion cyst. Baylor Univ Med Cent Proc. 2022;35:688-690. doi:10.1080/08998280.2022.207760
  15. Nanes BA, Laknezhad S, Chamseddin B, et al. Verrucous pilar cysts infected with beta human papillomavirus. J Cutan Pathol. 2020;47:381-386. doi:10.1111/cup.13599
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The authors have no financial disclosures to report.

Correspondence: Edidiong Kaminska, MD, 3808 N Lincoln Ave, Ste 101, Chicago, IL 60613 (edikaminska@kaminskadermatology.com).

Cutis. 2025 December;116(6):215, 220-221, E1. doi:10.12788/cutis.1309

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Correspondence: Edidiong Kaminska, MD, 3808 N Lincoln Ave, Ste 101, Chicago, IL 60613 (edikaminska@kaminskadermatology.com).

Cutis. 2025 December;116(6):215, 220-221, E1. doi:10.12788/cutis.1309

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Correspondence: Edidiong Kaminska, MD, 3808 N Lincoln Ave, Ste 101, Chicago, IL 60613 (edikaminska@kaminskadermatology.com).

Cutis. 2025 December;116(6):215, 220-221, E1. doi:10.12788/cutis.1309

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THE DIAGNOSIS: Malignant Proliferating Trichilemmal Tumor

Biopsy revealed a squamous epithelium with cystic changes, trichilemmal differentiation, squamous eddy formation, keratinocyte atypia, focal necrotic changes, and a focus of atypical keratinocytes invading the dermis (Figure 1). Based on these findings, a diagnosis of malignant proliferating trichilemmal tumor (MPTT) was made.

Martin-DD-1
FIGURE 1. Malignant proliferating trichilemmal tumor. Lobulated intradermal mass composed of a squamous epithelium with cystic changes, squamous eddy formation, keratinocyte atypia, trichilemmal differentiation, and focal necrotic changes. Note the nests of atypical keratinocytes invading the surrounding dermis (H&E, original magnification ×4).

Malignant proliferating trichilemmal tumor is a rare adnexal tumor that develops from the outer root sheath of the hair follicle. It often arises due to malignant transformation of pre-existing trichilemmal cysts, but some cases occur de novo.1 Malignant transformation is thought to start from a trichilemmal cyst in an adenomatous histologic stage, progressing to a proliferating trichilemmal cyst (PTC) in an epitheliomatous phase, ultimately becoming carcinomatous with MPTT.2-4 This transformation has been categorized into 3 morphologic groups to predict tumor behavior, including benign PTCs (curable by excision), low-grade malignant PTCs (minor risk for local recurrence), and high-grade malignant PTCs (risk for regional spread and metastasis with cytologic atypical features and potential for aggressive growth).1

More commonly observed in women in the fourth to eighth decades of life, MPTT may manifest as a fast- growing, painless, solitary nodule or as a progressively enlarging nodule at the site of a previously stable, long-standing lesion. Malignant proliferating trichilemmal tumor manifests frequently on the scalp, face, or neck, but there are reports of MPTT manifesting on the trunk and even as multiple concurrent lesions.1-4 The variability in clinical presentation and the potential to be mistaken for benign conditions makes excisional biopsy essential for diagnosis of MPTT. Histopathology classically demonstrates trichilemmal keratinization, a high mitotic index, and cellular atypia with invasion into the dermis.4 Malignant transformation frequently follows a prior history of trauma to the area or local inflammation.

Given the locally aggressive nature of MPTT, our patient was referred to a Mohs micrographic surgeon. While both wide excision with tumor-free margins and Mohs micrographic surgery are accepted surgical procedures for MPTT, there is no consensus in the literature on a standard treatment recommendation. Following surgery, close monitoring is needed for potential recurrence and metastases intracranially to the dura and muscles,5 as well as to the lungs.6 Further imaging using computed tomography or positron emission tomography can be ordered to rule out metastatic disease.4

Pilomatrixomas are benign neoplasms that arise from hair matrix cells and have been associated with catenin beta-1 gene mutations, as well as genetic syndromes and trauma.7 Clinically, pilomatrixomas manifest as solitary, firm, painless, slow-growing nodules that commonly are found in the head and neck region. This tumor has a slight predominance in women and occurs frequently in adolescent years. The overlying skin may appear normal or show grey-bluish discoloration.8 Histopathology shows basaloid cells resembling primitive hair matrix cells with an abrupt transition to shadow cells composed of transformed keratinocytes without nuclei and calcification.7-8 This tumor can be differentiated by the presence of basaloid and shadow cells with calcification on histopathology, while MPTT will show atypical, mitotically active squamous cells with trichilemmal keratinization (Figure 2).

Martin-DD-2
FIGURE 2. Pilomatrixoma. Basophilic matrical cells with scant cytoplasm and hyperchromatic nuclei with occasional normal mitoses transitioning to eosinophilic shadow/ghost cells without nuclei. There often is surrounding granulomatous inflammation with giant cell formation (H&E; original magnification ×10).

Proliferating trichilemmal cyst is a variant of trichilemmal cyst (TC) arising from the outer root sheath cells of the hair follicle. While TCs usually are slow growing and benign, the proliferating variant can be more aggressive with malignant potential. Patients often present with a solitary, well-circumscribed, rapidly growing nodule on the scalp. The lesion may be painful, and ulceration can occur, exposing the cystic contents. Histopathologically, PTCs resemble TCs with trichilemmal keratinization but also exhibit notable epithelial proliferation within the cystic space.9 While there can be considerable histopathologic overlap between PTC and MPTT—including extensive trichilemmal keratinization, variable atypia, and mitotic activity—PTC typically should not demonstrate invasion into the surrounding soft tissue or the degree of high-grade atypia, brisk mitoses, or necrosis seen in MPTT (eFigure 1).1 Immunohistochemistry may help distinguish PTC from MPTT and squamous cell carcinoma (SCC).10-11 The pattern of Ki-67 and p53 expression may be helpful with classification of PTC/MPTT into the 3 groups (benign, low-grade malignant, and high-grade malignant) proposed by Ye et al.1 Other investigators have suggested that Ki-67 expression may correlate potential for recurrence and clinical prognosis.12 Expression of CD34 (a marker that supports outer root sheath origin) might favor PTC/MPTT over SCC; however, cases of CD34- negative MPTT have been reported, particularly those with poorly differentiated histopathology.

CT116006215-eFig-1_AB
eFIGURE 1. Proliferating trichilemmal cyst. A, Well-circumscribed dermal tumor with a pushing border that exhibits abrupt trichilemmal keratinization and has extensive epithelial proliferation within the center of the cystic space (H&E, original magnification ×4). B, Epithelial proliferation with minimal cytologic atypia (H&E, original magnification ×10).

Squamous cell carcinoma with cystic features is a histologic variant of SCC characterized by cystlike spaces containing malignant squamous epithelial cells.13 Squamous cell carcinoma with cystic features can manifest as a firm nodule with ulceration similar to MPTT or PTC but also can mimic a benign cyst.14 The diagnosis of invasive SCC with cystic features typically is straightforward and characterized by cords and nests of atypical keratinocytes extending into the dermis with areas of cystic architecture (eFigure 2). While both SCC with cystic features and MPTT may show cystic histopathologic architecture, MPTT typically shows areas of PTC, whereas SCC with cystic features lacks such areas.

Martin-DD_e_2
eFIGURE 2. Squamous cell carcinoma with cystic changes. Invasive cords and nests of atypical keratinocytes extend into the dermis with an overlying epidermal connection. The center of the tumor shows cystic architecture (H&E; original magnification ×10).

Verrucous cysts refer to infundibular cysts or less commonly pilar cysts or hybrid pilar-epidermoid cysts that exhibit superimposed human papillomavirus (HPV) cytopathic changes. Clinically, a verrucous cyst manifests as a single, asymptomatic, slow-growing, firm lesion most commonly manifesting on the face and back. Histopathologically, the cyst wall may show acanthosis, papillomatosis, hypergranulosis with coarse keratohyalin granules, and koilocytic changes (eFigure 3). These histopathologic features are believed to be induced by secondary HPV infection. While HPV-related change, characterized by koilocytic alteration, papillomatosis, and verruciform hyperplasia, more commonly affects epidermal cysts, occasionally trichilemmal (pilar) cysts are involved. In these cases, verrucous cysts should be distinguished from MPTT. Verrucous cysts may contain rare normal mitotic figures, but do not contain atypical mitosis, marked cellular pleomorphism, or an infiltrating pattern similar to MPTT.15

Martin-DD_e_3
eFIGURE 3. Verrucous cyst. Note the cyst wall with acanthosis, papillomatosis, orthokeratosis and parakeratosis, hypergranulosis with coarse keratohyalin granules, and koilocytic changes (H&E; original magnification ×10).

THE DIAGNOSIS: Malignant Proliferating Trichilemmal Tumor

Biopsy revealed a squamous epithelium with cystic changes, trichilemmal differentiation, squamous eddy formation, keratinocyte atypia, focal necrotic changes, and a focus of atypical keratinocytes invading the dermis (Figure 1). Based on these findings, a diagnosis of malignant proliferating trichilemmal tumor (MPTT) was made.

Martin-DD-1
FIGURE 1. Malignant proliferating trichilemmal tumor. Lobulated intradermal mass composed of a squamous epithelium with cystic changes, squamous eddy formation, keratinocyte atypia, trichilemmal differentiation, and focal necrotic changes. Note the nests of atypical keratinocytes invading the surrounding dermis (H&E, original magnification ×4).

Malignant proliferating trichilemmal tumor is a rare adnexal tumor that develops from the outer root sheath of the hair follicle. It often arises due to malignant transformation of pre-existing trichilemmal cysts, but some cases occur de novo.1 Malignant transformation is thought to start from a trichilemmal cyst in an adenomatous histologic stage, progressing to a proliferating trichilemmal cyst (PTC) in an epitheliomatous phase, ultimately becoming carcinomatous with MPTT.2-4 This transformation has been categorized into 3 morphologic groups to predict tumor behavior, including benign PTCs (curable by excision), low-grade malignant PTCs (minor risk for local recurrence), and high-grade malignant PTCs (risk for regional spread and metastasis with cytologic atypical features and potential for aggressive growth).1

More commonly observed in women in the fourth to eighth decades of life, MPTT may manifest as a fast- growing, painless, solitary nodule or as a progressively enlarging nodule at the site of a previously stable, long-standing lesion. Malignant proliferating trichilemmal tumor manifests frequently on the scalp, face, or neck, but there are reports of MPTT manifesting on the trunk and even as multiple concurrent lesions.1-4 The variability in clinical presentation and the potential to be mistaken for benign conditions makes excisional biopsy essential for diagnosis of MPTT. Histopathology classically demonstrates trichilemmal keratinization, a high mitotic index, and cellular atypia with invasion into the dermis.4 Malignant transformation frequently follows a prior history of trauma to the area or local inflammation.

Given the locally aggressive nature of MPTT, our patient was referred to a Mohs micrographic surgeon. While both wide excision with tumor-free margins and Mohs micrographic surgery are accepted surgical procedures for MPTT, there is no consensus in the literature on a standard treatment recommendation. Following surgery, close monitoring is needed for potential recurrence and metastases intracranially to the dura and muscles,5 as well as to the lungs.6 Further imaging using computed tomography or positron emission tomography can be ordered to rule out metastatic disease.4

Pilomatrixomas are benign neoplasms that arise from hair matrix cells and have been associated with catenin beta-1 gene mutations, as well as genetic syndromes and trauma.7 Clinically, pilomatrixomas manifest as solitary, firm, painless, slow-growing nodules that commonly are found in the head and neck region. This tumor has a slight predominance in women and occurs frequently in adolescent years. The overlying skin may appear normal or show grey-bluish discoloration.8 Histopathology shows basaloid cells resembling primitive hair matrix cells with an abrupt transition to shadow cells composed of transformed keratinocytes without nuclei and calcification.7-8 This tumor can be differentiated by the presence of basaloid and shadow cells with calcification on histopathology, while MPTT will show atypical, mitotically active squamous cells with trichilemmal keratinization (Figure 2).

Martin-DD-2
FIGURE 2. Pilomatrixoma. Basophilic matrical cells with scant cytoplasm and hyperchromatic nuclei with occasional normal mitoses transitioning to eosinophilic shadow/ghost cells without nuclei. There often is surrounding granulomatous inflammation with giant cell formation (H&E; original magnification ×10).

Proliferating trichilemmal cyst is a variant of trichilemmal cyst (TC) arising from the outer root sheath cells of the hair follicle. While TCs usually are slow growing and benign, the proliferating variant can be more aggressive with malignant potential. Patients often present with a solitary, well-circumscribed, rapidly growing nodule on the scalp. The lesion may be painful, and ulceration can occur, exposing the cystic contents. Histopathologically, PTCs resemble TCs with trichilemmal keratinization but also exhibit notable epithelial proliferation within the cystic space.9 While there can be considerable histopathologic overlap between PTC and MPTT—including extensive trichilemmal keratinization, variable atypia, and mitotic activity—PTC typically should not demonstrate invasion into the surrounding soft tissue or the degree of high-grade atypia, brisk mitoses, or necrosis seen in MPTT (eFigure 1).1 Immunohistochemistry may help distinguish PTC from MPTT and squamous cell carcinoma (SCC).10-11 The pattern of Ki-67 and p53 expression may be helpful with classification of PTC/MPTT into the 3 groups (benign, low-grade malignant, and high-grade malignant) proposed by Ye et al.1 Other investigators have suggested that Ki-67 expression may correlate potential for recurrence and clinical prognosis.12 Expression of CD34 (a marker that supports outer root sheath origin) might favor PTC/MPTT over SCC; however, cases of CD34- negative MPTT have been reported, particularly those with poorly differentiated histopathology.

CT116006215-eFig-1_AB
eFIGURE 1. Proliferating trichilemmal cyst. A, Well-circumscribed dermal tumor with a pushing border that exhibits abrupt trichilemmal keratinization and has extensive epithelial proliferation within the center of the cystic space (H&E, original magnification ×4). B, Epithelial proliferation with minimal cytologic atypia (H&E, original magnification ×10).

Squamous cell carcinoma with cystic features is a histologic variant of SCC characterized by cystlike spaces containing malignant squamous epithelial cells.13 Squamous cell carcinoma with cystic features can manifest as a firm nodule with ulceration similar to MPTT or PTC but also can mimic a benign cyst.14 The diagnosis of invasive SCC with cystic features typically is straightforward and characterized by cords and nests of atypical keratinocytes extending into the dermis with areas of cystic architecture (eFigure 2). While both SCC with cystic features and MPTT may show cystic histopathologic architecture, MPTT typically shows areas of PTC, whereas SCC with cystic features lacks such areas.

Martin-DD_e_2
eFIGURE 2. Squamous cell carcinoma with cystic changes. Invasive cords and nests of atypical keratinocytes extend into the dermis with an overlying epidermal connection. The center of the tumor shows cystic architecture (H&E; original magnification ×10).

Verrucous cysts refer to infundibular cysts or less commonly pilar cysts or hybrid pilar-epidermoid cysts that exhibit superimposed human papillomavirus (HPV) cytopathic changes. Clinically, a verrucous cyst manifests as a single, asymptomatic, slow-growing, firm lesion most commonly manifesting on the face and back. Histopathologically, the cyst wall may show acanthosis, papillomatosis, hypergranulosis with coarse keratohyalin granules, and koilocytic changes (eFigure 3). These histopathologic features are believed to be induced by secondary HPV infection. While HPV-related change, characterized by koilocytic alteration, papillomatosis, and verruciform hyperplasia, more commonly affects epidermal cysts, occasionally trichilemmal (pilar) cysts are involved. In these cases, verrucous cysts should be distinguished from MPTT. Verrucous cysts may contain rare normal mitotic figures, but do not contain atypical mitosis, marked cellular pleomorphism, or an infiltrating pattern similar to MPTT.15

Martin-DD_e_3
eFIGURE 3. Verrucous cyst. Note the cyst wall with acanthosis, papillomatosis, orthokeratosis and parakeratosis, hypergranulosis with coarse keratohyalin granules, and koilocytic changes (H&E; original magnification ×10).
References
  1. Ye J, Nappi O, Swanson PE, et al. Proliferating pilar tumors: a clinicopathologic study of 76 cases with a proposal for definition of benign and malignant variants. Am J Clin Pathol. 2004;122:566-574. doi:10.1309/0XLEGFQ64XYJU4G6
  2. Saida T, Oohara K, Hori Y, et al. Development of a malignant proliferating trichilemmal cyst in a patient with multiple trichilemmal cysts. Dermatologica. 1983;166:203-208. doi:10.1159/000249868
  3. Rao S, Ramakrishnan R, Kamakshi D, et al. Malignant proliferating trichilemmal tumour presenting early in life: an uncommon feature. J Cutan Aesthet Surg. 2011;4:51-55. doi:10.4103/0974-2077.79196
  4. Kearns-Turcotte S, Thériault M, Blouin MM. Malignant proliferating trichilemmal tumors arising in patients with multiple trichilemmal cysts: a case series. JAAD Case Rep. 2022;22:42-46. doi:10.1016
  5. Karamese M, Akatekin A, Abaci M, et al. Unusual invasion of trichilemmal tumors: two case reports. Modern Plastic Surg. 2012; 2:54-57. doi:10.4236/MPS.2012.23014 /j.jdcr.2022.01.033
  6. Lobo L, Amonkar AD, Dontamsetty VV. Malignant proliferating trichilemmal tumour of the scalp with intra-cranial extension and lung metastasis-a case report. Indian J Surg. 2016;78:493-495. doi:10.1007/s12262-015-1427-0
  7. Jones CD, Ho W, Robertson BF, et al. Pilomatrixoma: a comprehensive review of the literature. Am J Dermatopathol. 2018;40:631-641. doi:10.1097/DAD.0000000000001118
  8. Sharma D, Agarwal S, Jain LS, et al. Pilomatrixoma masquerading as metastatic adenocarcinoma. A diagnostic pitfall on cytology. J Clin Diagn Res. 2014;8:FD13-FD14. doi:10.7860/JCDR/2014/9696.5064
  9. Valerio E, Parro FHS, Macedo MP, et al. Proliferating trichilemmal cyst with clinical, radiological, macroscopic, and microscopic orrelation. An Bras Dermatol. 2019;94:452-454. doi:10.1590 /abd1806-4841.20198199
  10. Joshi TP, Marchand S, Tschen J. Malignant proliferating trichilemmal tumor: a subtle presentation in an African American woman and review of immunohistochemical markers for this rare condition. Cureus. 2021;13:E17289. doi:10.7759/cureus.17289
  11. Gulati HK, Deshmukh SD, Anand M, et al. Low-grade malignant proliferating pilar tumor simulating a squamous-cell carcinoma in an elderly female: a case report and immunohistochemical study. Int J Trichology. 2011;3:98-101. doi:10.4103/0974-7753.90818
  12. Rangel-Gamboa L, Reyes-Castro M, Dominguez-Cherit J, et al. Proliferating trichilemmal cyst: the value of ki67 immunostaining. Int J Trichology. 2013;5:115-117. doi:10.4103/0974-7753.125599
  13. Asad U, Alkul S, Shimizu I, et al. Squamous cell carcinoma with unusual benign-appearing cystic features on histology. Cureus. 2023;15:E33610. doi:10.7759/cureus.33610
  14. Alkul S, Nguyen CN, Ramani NS, et al. Squamous cell carcinoma arising in an epidermal inclusion cyst. Baylor Univ Med Cent Proc. 2022;35:688-690. doi:10.1080/08998280.2022.207760
  15. Nanes BA, Laknezhad S, Chamseddin B, et al. Verrucous pilar cysts infected with beta human papillomavirus. J Cutan Pathol. 2020;47:381-386. doi:10.1111/cup.13599
References
  1. Ye J, Nappi O, Swanson PE, et al. Proliferating pilar tumors: a clinicopathologic study of 76 cases with a proposal for definition of benign and malignant variants. Am J Clin Pathol. 2004;122:566-574. doi:10.1309/0XLEGFQ64XYJU4G6
  2. Saida T, Oohara K, Hori Y, et al. Development of a malignant proliferating trichilemmal cyst in a patient with multiple trichilemmal cysts. Dermatologica. 1983;166:203-208. doi:10.1159/000249868
  3. Rao S, Ramakrishnan R, Kamakshi D, et al. Malignant proliferating trichilemmal tumour presenting early in life: an uncommon feature. J Cutan Aesthet Surg. 2011;4:51-55. doi:10.4103/0974-2077.79196
  4. Kearns-Turcotte S, Thériault M, Blouin MM. Malignant proliferating trichilemmal tumors arising in patients with multiple trichilemmal cysts: a case series. JAAD Case Rep. 2022;22:42-46. doi:10.1016
  5. Karamese M, Akatekin A, Abaci M, et al. Unusual invasion of trichilemmal tumors: two case reports. Modern Plastic Surg. 2012; 2:54-57. doi:10.4236/MPS.2012.23014 /j.jdcr.2022.01.033
  6. Lobo L, Amonkar AD, Dontamsetty VV. Malignant proliferating trichilemmal tumour of the scalp with intra-cranial extension and lung metastasis-a case report. Indian J Surg. 2016;78:493-495. doi:10.1007/s12262-015-1427-0
  7. Jones CD, Ho W, Robertson BF, et al. Pilomatrixoma: a comprehensive review of the literature. Am J Dermatopathol. 2018;40:631-641. doi:10.1097/DAD.0000000000001118
  8. Sharma D, Agarwal S, Jain LS, et al. Pilomatrixoma masquerading as metastatic adenocarcinoma. A diagnostic pitfall on cytology. J Clin Diagn Res. 2014;8:FD13-FD14. doi:10.7860/JCDR/2014/9696.5064
  9. Valerio E, Parro FHS, Macedo MP, et al. Proliferating trichilemmal cyst with clinical, radiological, macroscopic, and microscopic orrelation. An Bras Dermatol. 2019;94:452-454. doi:10.1590 /abd1806-4841.20198199
  10. Joshi TP, Marchand S, Tschen J. Malignant proliferating trichilemmal tumor: a subtle presentation in an African American woman and review of immunohistochemical markers for this rare condition. Cureus. 2021;13:E17289. doi:10.7759/cureus.17289
  11. Gulati HK, Deshmukh SD, Anand M, et al. Low-grade malignant proliferating pilar tumor simulating a squamous-cell carcinoma in an elderly female: a case report and immunohistochemical study. Int J Trichology. 2011;3:98-101. doi:10.4103/0974-7753.90818
  12. Rangel-Gamboa L, Reyes-Castro M, Dominguez-Cherit J, et al. Proliferating trichilemmal cyst: the value of ki67 immunostaining. Int J Trichology. 2013;5:115-117. doi:10.4103/0974-7753.125599
  13. Asad U, Alkul S, Shimizu I, et al. Squamous cell carcinoma with unusual benign-appearing cystic features on histology. Cureus. 2023;15:E33610. doi:10.7759/cureus.33610
  14. Alkul S, Nguyen CN, Ramani NS, et al. Squamous cell carcinoma arising in an epidermal inclusion cyst. Baylor Univ Med Cent Proc. 2022;35:688-690. doi:10.1080/08998280.2022.207760
  15. Nanes BA, Laknezhad S, Chamseddin B, et al. Verrucous pilar cysts infected with beta human papillomavirus. J Cutan Pathol. 2020;47:381-386. doi:10.1111/cup.13599
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Growing Nodule on the Parietal Scalp

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Growing Nodule on the Parietal Scalp

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A 38-year-old woman with no notable medical history presented to the dermatology department with a firm enlarging nodule on the scalp of many years’ duration. The patient noted there was no drainage or bleeding. Physical examination revealed a mobile, 2.5-cm, subcutaneous nodule on the right parietal medial scalp. An excisional biopsy was performed.

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