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Racial morphing: A conundrum in cosmetic dermatology
HONOLULU – In the opinion of Nazanin A. Saedi, MD, social media-induced dissatisfaction with appearance is getting out of hand in the field of cosmetic dermatology, with the emergence of apps to filter and edit images to the patient’s liking.
This, coupled with
“Overexposure of celebrity images and altered faces on social media have led to a trend of overarching brows, sculpted noses, enlarged cheeks, and sharply defined jawlines,” Dr. Saedi, cochair of the laser and aesthetics surgery center at Dermatology Associates of Plymouth Meeting, Pa., said at the Hawaii Dermatology Seminar provided by MedscapeLIVE! “These trends have made people of different ethnicities morph into a similar appearance.”
At the meeting, she showed early career images of celebrities from different ethnic backgrounds, “and they all have unique features that make them look great,” said Dr. Saedi, clinical associate professor of dermatology at Thomas Jefferson University, Philadelphia. She then showed images of the same celebrities after they had undergone cosmetic procedures, “and they look so much more similar,” with overarched brows, sculpted noses, enlarged cheeks, and sharply defined jawlines. “Whereas they were all beautiful before individually, now they look very similar,” she said. “This is what we see on social media.”
Referring to the Kardashians as an example of celebrities who have had a lot of aesthetic treatments, look different than they did years ago, and are seen “more and more,” she added, “it’s this repeated overexposure to people on social media, to celebrities, that’s created this different trend of attractiveness.”
This trend also affects patients seeking cosmetic treatments, she noted. Individuals can use an app to alter their appearance, “changing the way they look to create the best version of themselves, they might say, or a filtered version of themselves,” said Dr. Saedi, one of the authors of a commentary on patient perception of beauty on social media published several years ago.
“I tell people, ‘Don’t use filters in your photos. Embrace your beauty.’ I have patients coming in who want to look like the social media photos they’ve curated, maybe larger lips or more definition in their jawline. What they don’t understand is that it takes a long time for that to happen. It’s a process.” In other cases, their desired outcome is not possible due to limits of their individual facial anatomy.
In a study published almost 20 years ago in the journal Perception, Irish researchers manipulated the familiarity of typical and distinctive faces to measure the effect on attractiveness. They found that episodic familiarity affects attractiveness ratings independently of general or structural familiarity.
“So, the more you saw a face, the more familiar that face was to you,” said Dr. Saedi, who was not involved with the study. “Over time, you felt that to be more attractive. I think that’s a lot of what’s going on in the trends that we’re seeing – both in real life and on social media. I do think we need to be more mindful of maintaining features that make an individual unique, while also maintaining their ethnic beauty.”
In an interview at the meeting, Jacqueline D. Watchmaker, MD, a board-certified cosmetic and medical dermatologist who practices in Scottsdale, Ariz., said that she identifies with the notion of racial morphing in her own clinical experience. “Patients come in and specifically ask for chiseled jawlines, high cheekbones, and bigger lips,” Dr. Watchmaker said. “It’s a tricky situation when they ask for [a treatment] you don’t think they need. I prefer a more staged approach to maintain their individuality while giving them a little bit of the aesthetic benefit that they’re looking for.”
Dr. Saedi disclosed ties with AbbVie, Aerolase, Allergan, Alma, Cartessa, Cynosure, Galderma Laboratories, LP, Grand Cosmetics, Revelle Aesthetics, and Revision Skincare. Dr. Watchmaker reported having no financial disclosures.
Medscape and this news organization are owned by the same parent company.
HONOLULU – In the opinion of Nazanin A. Saedi, MD, social media-induced dissatisfaction with appearance is getting out of hand in the field of cosmetic dermatology, with the emergence of apps to filter and edit images to the patient’s liking.
This, coupled with
“Overexposure of celebrity images and altered faces on social media have led to a trend of overarching brows, sculpted noses, enlarged cheeks, and sharply defined jawlines,” Dr. Saedi, cochair of the laser and aesthetics surgery center at Dermatology Associates of Plymouth Meeting, Pa., said at the Hawaii Dermatology Seminar provided by MedscapeLIVE! “These trends have made people of different ethnicities morph into a similar appearance.”
At the meeting, she showed early career images of celebrities from different ethnic backgrounds, “and they all have unique features that make them look great,” said Dr. Saedi, clinical associate professor of dermatology at Thomas Jefferson University, Philadelphia. She then showed images of the same celebrities after they had undergone cosmetic procedures, “and they look so much more similar,” with overarched brows, sculpted noses, enlarged cheeks, and sharply defined jawlines. “Whereas they were all beautiful before individually, now they look very similar,” she said. “This is what we see on social media.”
Referring to the Kardashians as an example of celebrities who have had a lot of aesthetic treatments, look different than they did years ago, and are seen “more and more,” she added, “it’s this repeated overexposure to people on social media, to celebrities, that’s created this different trend of attractiveness.”
This trend also affects patients seeking cosmetic treatments, she noted. Individuals can use an app to alter their appearance, “changing the way they look to create the best version of themselves, they might say, or a filtered version of themselves,” said Dr. Saedi, one of the authors of a commentary on patient perception of beauty on social media published several years ago.
“I tell people, ‘Don’t use filters in your photos. Embrace your beauty.’ I have patients coming in who want to look like the social media photos they’ve curated, maybe larger lips or more definition in their jawline. What they don’t understand is that it takes a long time for that to happen. It’s a process.” In other cases, their desired outcome is not possible due to limits of their individual facial anatomy.
In a study published almost 20 years ago in the journal Perception, Irish researchers manipulated the familiarity of typical and distinctive faces to measure the effect on attractiveness. They found that episodic familiarity affects attractiveness ratings independently of general or structural familiarity.
“So, the more you saw a face, the more familiar that face was to you,” said Dr. Saedi, who was not involved with the study. “Over time, you felt that to be more attractive. I think that’s a lot of what’s going on in the trends that we’re seeing – both in real life and on social media. I do think we need to be more mindful of maintaining features that make an individual unique, while also maintaining their ethnic beauty.”
In an interview at the meeting, Jacqueline D. Watchmaker, MD, a board-certified cosmetic and medical dermatologist who practices in Scottsdale, Ariz., said that she identifies with the notion of racial morphing in her own clinical experience. “Patients come in and specifically ask for chiseled jawlines, high cheekbones, and bigger lips,” Dr. Watchmaker said. “It’s a tricky situation when they ask for [a treatment] you don’t think they need. I prefer a more staged approach to maintain their individuality while giving them a little bit of the aesthetic benefit that they’re looking for.”
Dr. Saedi disclosed ties with AbbVie, Aerolase, Allergan, Alma, Cartessa, Cynosure, Galderma Laboratories, LP, Grand Cosmetics, Revelle Aesthetics, and Revision Skincare. Dr. Watchmaker reported having no financial disclosures.
Medscape and this news organization are owned by the same parent company.
HONOLULU – In the opinion of Nazanin A. Saedi, MD, social media-induced dissatisfaction with appearance is getting out of hand in the field of cosmetic dermatology, with the emergence of apps to filter and edit images to the patient’s liking.
This, coupled with
“Overexposure of celebrity images and altered faces on social media have led to a trend of overarching brows, sculpted noses, enlarged cheeks, and sharply defined jawlines,” Dr. Saedi, cochair of the laser and aesthetics surgery center at Dermatology Associates of Plymouth Meeting, Pa., said at the Hawaii Dermatology Seminar provided by MedscapeLIVE! “These trends have made people of different ethnicities morph into a similar appearance.”
At the meeting, she showed early career images of celebrities from different ethnic backgrounds, “and they all have unique features that make them look great,” said Dr. Saedi, clinical associate professor of dermatology at Thomas Jefferson University, Philadelphia. She then showed images of the same celebrities after they had undergone cosmetic procedures, “and they look so much more similar,” with overarched brows, sculpted noses, enlarged cheeks, and sharply defined jawlines. “Whereas they were all beautiful before individually, now they look very similar,” she said. “This is what we see on social media.”
Referring to the Kardashians as an example of celebrities who have had a lot of aesthetic treatments, look different than they did years ago, and are seen “more and more,” she added, “it’s this repeated overexposure to people on social media, to celebrities, that’s created this different trend of attractiveness.”
This trend also affects patients seeking cosmetic treatments, she noted. Individuals can use an app to alter their appearance, “changing the way they look to create the best version of themselves, they might say, or a filtered version of themselves,” said Dr. Saedi, one of the authors of a commentary on patient perception of beauty on social media published several years ago.
“I tell people, ‘Don’t use filters in your photos. Embrace your beauty.’ I have patients coming in who want to look like the social media photos they’ve curated, maybe larger lips or more definition in their jawline. What they don’t understand is that it takes a long time for that to happen. It’s a process.” In other cases, their desired outcome is not possible due to limits of their individual facial anatomy.
In a study published almost 20 years ago in the journal Perception, Irish researchers manipulated the familiarity of typical and distinctive faces to measure the effect on attractiveness. They found that episodic familiarity affects attractiveness ratings independently of general or structural familiarity.
“So, the more you saw a face, the more familiar that face was to you,” said Dr. Saedi, who was not involved with the study. “Over time, you felt that to be more attractive. I think that’s a lot of what’s going on in the trends that we’re seeing – both in real life and on social media. I do think we need to be more mindful of maintaining features that make an individual unique, while also maintaining their ethnic beauty.”
In an interview at the meeting, Jacqueline D. Watchmaker, MD, a board-certified cosmetic and medical dermatologist who practices in Scottsdale, Ariz., said that she identifies with the notion of racial morphing in her own clinical experience. “Patients come in and specifically ask for chiseled jawlines, high cheekbones, and bigger lips,” Dr. Watchmaker said. “It’s a tricky situation when they ask for [a treatment] you don’t think they need. I prefer a more staged approach to maintain their individuality while giving them a little bit of the aesthetic benefit that they’re looking for.”
Dr. Saedi disclosed ties with AbbVie, Aerolase, Allergan, Alma, Cartessa, Cynosure, Galderma Laboratories, LP, Grand Cosmetics, Revelle Aesthetics, and Revision Skincare. Dr. Watchmaker reported having no financial disclosures.
Medscape and this news organization are owned by the same parent company.
AT THE MEDSCAPELIVE! HAWAII DERMATOLOGY SEMINAR
White male presents with pruritic, scaly, erythematous patches on his feet and left hand
Two feet–one hand syndrome
This condition, also known as ringworm, is a fungal infection caused by a dermatophyte, and presents as a superficial annular or circular rash with a raised, scaly border.
Symptoms include dryness and itchiness, and the lesions may appear red-pink on lighter skin and gray-brown on darker skin types. Although these infections can arise in a variety of combinations, two feet–one hand syndrome occurs in about 60% of cases. Trichophyton rubrum is the most common agent.
Diagnosis is made by patient history, dermoscopic visualization, and staining of skin scraping with KOH or fungal culture. Dermatophytes prefer moist, warm environments, so this disease is prevalent in tropical conditions and associated with moist public areas such as locker rooms and showers. As a result, tinea pedis is also nicknamed “athlete’s foot” for its common presentation in athletes. The fungus spreads easily through contact and can survive on infected surfaces, so patients often self-inoculate by touching/scratching the affected area then touching another body part. Cautions that should be taken to avoid transmission include not sharing personal care products, washing the area and keeping it dry, and avoiding close, humid environments.
The syndrome is highly associated with onychomycosis, which can be more difficult to treat and often requires oral antifungals. Tinea manuum is commonly misdiagnosed as hand dermatitis or eczema and treated with topical steroids, which will exacerbate or flare the tinea.
Two feet–one hand syndrome can typically be treated with over-the-counter topical antifungal medications such as miconazole or clotrimazole. Topical ketoconazole may be prescribed, and oral terbinafine or itraconazole are used in more severe cases when a larger body surface area is affected or in immunocompromised patients.
This case and photo were submitted by Lucas Shapiro, BS, Nova Southeastern University, Davie, Fla.; Kiran C. Patel, Tampa Bay Regional Campus; and Dr. Bilu Martin.
Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.
References
Cleveland Clinic. Tinea manuum: Symptoms, causes & treatment. 2022. https://my.clevelandclinic.org/health/diseases/24063-tinea-manuum.
Ugalde-Trejo NX et al. Curr Fungal Infect Rep. 2022 Nov 17. doi: 10.1007/s12281-022-00447-9.
Mizumoto J. Cureus. 2021 Dec 27;13(12):e20758.
Two feet–one hand syndrome
This condition, also known as ringworm, is a fungal infection caused by a dermatophyte, and presents as a superficial annular or circular rash with a raised, scaly border.
Symptoms include dryness and itchiness, and the lesions may appear red-pink on lighter skin and gray-brown on darker skin types. Although these infections can arise in a variety of combinations, two feet–one hand syndrome occurs in about 60% of cases. Trichophyton rubrum is the most common agent.
Diagnosis is made by patient history, dermoscopic visualization, and staining of skin scraping with KOH or fungal culture. Dermatophytes prefer moist, warm environments, so this disease is prevalent in tropical conditions and associated with moist public areas such as locker rooms and showers. As a result, tinea pedis is also nicknamed “athlete’s foot” for its common presentation in athletes. The fungus spreads easily through contact and can survive on infected surfaces, so patients often self-inoculate by touching/scratching the affected area then touching another body part. Cautions that should be taken to avoid transmission include not sharing personal care products, washing the area and keeping it dry, and avoiding close, humid environments.
The syndrome is highly associated with onychomycosis, which can be more difficult to treat and often requires oral antifungals. Tinea manuum is commonly misdiagnosed as hand dermatitis or eczema and treated with topical steroids, which will exacerbate or flare the tinea.
Two feet–one hand syndrome can typically be treated with over-the-counter topical antifungal medications such as miconazole or clotrimazole. Topical ketoconazole may be prescribed, and oral terbinafine or itraconazole are used in more severe cases when a larger body surface area is affected or in immunocompromised patients.
This case and photo were submitted by Lucas Shapiro, BS, Nova Southeastern University, Davie, Fla.; Kiran C. Patel, Tampa Bay Regional Campus; and Dr. Bilu Martin.
Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.
References
Cleveland Clinic. Tinea manuum: Symptoms, causes & treatment. 2022. https://my.clevelandclinic.org/health/diseases/24063-tinea-manuum.
Ugalde-Trejo NX et al. Curr Fungal Infect Rep. 2022 Nov 17. doi: 10.1007/s12281-022-00447-9.
Mizumoto J. Cureus. 2021 Dec 27;13(12):e20758.
Two feet–one hand syndrome
This condition, also known as ringworm, is a fungal infection caused by a dermatophyte, and presents as a superficial annular or circular rash with a raised, scaly border.
Symptoms include dryness and itchiness, and the lesions may appear red-pink on lighter skin and gray-brown on darker skin types. Although these infections can arise in a variety of combinations, two feet–one hand syndrome occurs in about 60% of cases. Trichophyton rubrum is the most common agent.
Diagnosis is made by patient history, dermoscopic visualization, and staining of skin scraping with KOH or fungal culture. Dermatophytes prefer moist, warm environments, so this disease is prevalent in tropical conditions and associated with moist public areas such as locker rooms and showers. As a result, tinea pedis is also nicknamed “athlete’s foot” for its common presentation in athletes. The fungus spreads easily through contact and can survive on infected surfaces, so patients often self-inoculate by touching/scratching the affected area then touching another body part. Cautions that should be taken to avoid transmission include not sharing personal care products, washing the area and keeping it dry, and avoiding close, humid environments.
The syndrome is highly associated with onychomycosis, which can be more difficult to treat and often requires oral antifungals. Tinea manuum is commonly misdiagnosed as hand dermatitis or eczema and treated with topical steroids, which will exacerbate or flare the tinea.
Two feet–one hand syndrome can typically be treated with over-the-counter topical antifungal medications such as miconazole or clotrimazole. Topical ketoconazole may be prescribed, and oral terbinafine or itraconazole are used in more severe cases when a larger body surface area is affected or in immunocompromised patients.
This case and photo were submitted by Lucas Shapiro, BS, Nova Southeastern University, Davie, Fla.; Kiran C. Patel, Tampa Bay Regional Campus; and Dr. Bilu Martin.
Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.
References
Cleveland Clinic. Tinea manuum: Symptoms, causes & treatment. 2022. https://my.clevelandclinic.org/health/diseases/24063-tinea-manuum.
Ugalde-Trejo NX et al. Curr Fungal Infect Rep. 2022 Nov 17. doi: 10.1007/s12281-022-00447-9.
Mizumoto J. Cureus. 2021 Dec 27;13(12):e20758.
Telehealth doctor indicted on health care fraud, opioid distribution charges
Sangita Patel, MD, 50, practiced at Advance Medical Home Physicians in Troy.
According to court documents, between July 2020 and June 2022 Patel was responsible for submitting Medicare claims for improper telehealth visits she didn’t conduct herself.
Dr. Patel, who accepted patients who paid in cash as well as those with Medicare and Medicaid coverage, billed approximately $3.4 million to Medicare between 2018 and 2022, according to court documents. An unusual number of these visits were billed using complex codes, an indication of health care fraud. The investigation also found that on many days, Dr. Patel billed for more than 24 hours of services. During this period, according to the document, 76% of Dr. Patel’s Medicare reimbursements were for telehealth.
Prosecutors say that Dr. Patel prescribed Schedule II controlled substances to more than 90% of the patients in these telehealth visits. She delegated her prescription authority to an unlicensed medical assistant. Through undercover visits and cell site search warrant data, the investigation found that Dr. Patel directed patients to contact, via cell phone, this assistant, who then entered electronic prescriptions into the electronic medical records system. Dr. Patel then signed the prescriptions and sent them to the pharmacies without ever interacting with the patients. Prosecutors also used text messages, obtained by search warrant, between Dr. Patel and her assistant and between the assistant and undercover informers to build their case.
Dr. Patel is also accused of referring patients to other providers, who in turn billed Medicare for claims associated with those patients. Advance Medical received $143,000 from these providers, potentially in violation of anti-kickback laws, according to bank records obtained by subpoena.
If convicted, Dr. Patel could be sentenced to up to 10 years in federal prison.
A version of this article first appeared on Medscape.com.
Sangita Patel, MD, 50, practiced at Advance Medical Home Physicians in Troy.
According to court documents, between July 2020 and June 2022 Patel was responsible for submitting Medicare claims for improper telehealth visits she didn’t conduct herself.
Dr. Patel, who accepted patients who paid in cash as well as those with Medicare and Medicaid coverage, billed approximately $3.4 million to Medicare between 2018 and 2022, according to court documents. An unusual number of these visits were billed using complex codes, an indication of health care fraud. The investigation also found that on many days, Dr. Patel billed for more than 24 hours of services. During this period, according to the document, 76% of Dr. Patel’s Medicare reimbursements were for telehealth.
Prosecutors say that Dr. Patel prescribed Schedule II controlled substances to more than 90% of the patients in these telehealth visits. She delegated her prescription authority to an unlicensed medical assistant. Through undercover visits and cell site search warrant data, the investigation found that Dr. Patel directed patients to contact, via cell phone, this assistant, who then entered electronic prescriptions into the electronic medical records system. Dr. Patel then signed the prescriptions and sent them to the pharmacies without ever interacting with the patients. Prosecutors also used text messages, obtained by search warrant, between Dr. Patel and her assistant and between the assistant and undercover informers to build their case.
Dr. Patel is also accused of referring patients to other providers, who in turn billed Medicare for claims associated with those patients. Advance Medical received $143,000 from these providers, potentially in violation of anti-kickback laws, according to bank records obtained by subpoena.
If convicted, Dr. Patel could be sentenced to up to 10 years in federal prison.
A version of this article first appeared on Medscape.com.
Sangita Patel, MD, 50, practiced at Advance Medical Home Physicians in Troy.
According to court documents, between July 2020 and June 2022 Patel was responsible for submitting Medicare claims for improper telehealth visits she didn’t conduct herself.
Dr. Patel, who accepted patients who paid in cash as well as those with Medicare and Medicaid coverage, billed approximately $3.4 million to Medicare between 2018 and 2022, according to court documents. An unusual number of these visits were billed using complex codes, an indication of health care fraud. The investigation also found that on many days, Dr. Patel billed for more than 24 hours of services. During this period, according to the document, 76% of Dr. Patel’s Medicare reimbursements were for telehealth.
Prosecutors say that Dr. Patel prescribed Schedule II controlled substances to more than 90% of the patients in these telehealth visits. She delegated her prescription authority to an unlicensed medical assistant. Through undercover visits and cell site search warrant data, the investigation found that Dr. Patel directed patients to contact, via cell phone, this assistant, who then entered electronic prescriptions into the electronic medical records system. Dr. Patel then signed the prescriptions and sent them to the pharmacies without ever interacting with the patients. Prosecutors also used text messages, obtained by search warrant, between Dr. Patel and her assistant and between the assistant and undercover informers to build their case.
Dr. Patel is also accused of referring patients to other providers, who in turn billed Medicare for claims associated with those patients. Advance Medical received $143,000 from these providers, potentially in violation of anti-kickback laws, according to bank records obtained by subpoena.
If convicted, Dr. Patel could be sentenced to up to 10 years in federal prison.
A version of this article first appeared on Medscape.com.
Biologics show signs of delaying arthritis in psoriasis patients
Patients with psoriasis treated with interleukin-12/23 inhibitors or IL-23 inhibitors were less likely to develop inflammatory arthritis, compared with those treated with tumor necrosis factor (TNF) inhibitors, according to findings from a large retrospective study.
While previous retrospective cohort studies have found biologic therapies for psoriasis can reduce the risk of developing psoriatic arthritis when compared with other treatments such as phototherapy and oral nonbiologic disease-modifying antirheumatic drugs, this analysis is the first to compare classes of biologics, Shikha Singla, MD, of the Medical College of Wisconsin, Milwaukee, and colleagues wrote in The Lancet Rheumatology.
In the analysis, researchers used the TriNetX database, which contains deidentified data from electronic medical health records from health care organizations across the United States. The study included adults diagnosed with psoriasis who were newly prescribed a biologic approved by the Food and Drug Administration for the treatment of psoriasis. Biologics were defined by drug class: anti-TNF, anti-IL-17, anti-IL-23, and anti–IL-12/23. Any patient with a diagnosis of psoriatic arthritis or other inflammatory arthritis prior to receiving a biologic prescription or within 2 weeks of receiving the prescription were excluded.
The researchers identified 15,501 eligible patients diagnosed with psoriasis during Jan. 1, 2014, to June 1, 2022, with an average follow-up time of 2.4 years. The researchers chose to start the study period in 2014 because the first non–anti-TNF drug for psoriatic arthritis was approved by the FDA in 2013 – the anti–IL-12/23 drug ustekinumab. During the study period, 976 patients developed inflammatory arthritis and were diagnosed on average 528 days after their biologic prescription.
In a multivariable analysis, the researchers found that patients prescribed IL-23 inhibitors (guselkumab [Tremfya], risankizumab [Skyrizi], tildrakizumab [Ilumya]) were nearly 60% less likely (adjusted hazard ratio, 0.41; 95% confidence interval, 0.17–0.95) to develop inflammatory arthritis than were patients taking TNF inhibitors (infliximab [Remicade], adalimumab [Humira], etanercept [Enbrel], golimumab [Simponi], certolizumab pegol [Cimzia]). The risk of developing arthritis was 42% lower (aHR, 0.58; 95% CI, 0.43-0.76) with the IL-12/23 inhibitor ustekinumab (Stelara), but there was no difference in outcomes among patients taking with IL-17 inhibitors (secukinumab [Cosentyx], ixekizumab [Taltz], or brodalumab [Siliq]), compared with TNF inhibitors. For the IL-12/23 inhibitor ustekinumab, all sensitivity analyses did not change this association. For IL-23 inhibitors, the results persisted when excluding patients who developed arthritis within 3 or 6 months after first biologic prescription and when using a higher diagnostic threshold for incident arthritis.
“There is a lot of interest in understanding if treatment of psoriasis will prevent onset of psoriatic arthritis,” said Joel M. Gelfand, MD, MSCE, director of the Psoriasis and Phototherapy Treatment Center at the University of Pennsylvania, Philadelphia, who was asked to comment on the results.
“To date, the literature is inconclusive with some studies suggesting biologics reduce risk of PsA, whereas others suggest biologic use is associated with an increased risk of PsA,” he said. “The current study is unique in that it compares biologic classes to one another and suggests that IL-12/23 and IL-23 biologics are associated with a reduced risk of PsA compared to psoriasis patients treated with TNF inhibitors and no difference was found between TNF inhibitors and IL-17 inhibitors.”
While the study posed an interesting research question, “I wouldn’t use these results to actually change treatment patterns,” Alexis R. Ogdie-Beatty, MD, an associate professor of medicine at the University of Pennsylvania, Philadelphia, said in an interview. She coauthored a commentary on the analysis. Dr. Gelfand also emphasized that this bias may have influenced the results and that these findings “should not impact clinical practice at this time.”
Although the analyses were strong, Dr. Ogdie-Beatty noted, there are inherent biases in this type of observational data that cannot be overcome. For example, if a patient comes into a dermatologist’s office with psoriasis and also has joint pain, the dermatologist may suspect that a patient could also have psoriatic arthritis and would be more likely to choose a drug that will work well for both of these conditions.
“The drugs that are known to work best for psoriatic arthritis are the TNF inhibitors and the IL-17 inhibitors,” she said. So, while the analysis found these medications were associated with higher incidence of PsA, the dermatologist was possibly treating presumptive arthritis and the patient had yet to be referred to a rheumatologist to confirm the diagnosis.
The researchers noted that they attempted to mitigate these issues by requiring that patients have at least 1 year of follow-up before receiving biologic prescription “to capture only the patients with no previous codes for any type of arthritis,” as well as conducting six sensitivity analyses.
The authors, and Dr. Ogdie-Beatty and Dr. Gelfand agreed that more research is necessary to confirm these findings. A large randomized trial may be “prohibitively expensive,” the authors noted, but pooled analyses from previous clinical trials may help with this issue. “We identified 14 published randomized trials that did head-to-head comparisons of different biologic classes with regard to effect on psoriasis, and these trials collectively contained data on more than 13,000 patients. Pooled analyses of these data could confirm the findings of the present study and would be adequately powered.”
But that approach also has limitations, as psoriatic arthritis was not assessed an outcome in these studies, Dr. Ogdie-Beatty noted. Randomizing patients who are already at a higher risk of developing PsA to different biologics could be one approach to address these questions without needing such a large patient population.
The study was conducted without outside funding or industry involvement. Dr. Singla reported no relevant financial relationships with industry, but several coauthors reported financial relationships with pharmaceutical companies that market biologics for psoriasis and psoriatic arthritis. Dr. Ogdie-Beatty reported financial relationships with AbbVie, Amgen, Bristol-Myers Squibb, Celgene, CorEvitas, Gilead, Happify Health, Janssen, Lilly, Novartis, Pfizer, and UCB. Dr. Gelfand reported financial relationships with Abbvie, Amgen, BMS, Boehringer Ingelheim, FIDE, Lilly, Leo, Janssen Biologics, Novartis, Pfizer, and UCB. Dr. Gelfand is a deputy editor for the Journal of Investigative Dermatology.
This article was updated 3/15/23.
Patients with psoriasis treated with interleukin-12/23 inhibitors or IL-23 inhibitors were less likely to develop inflammatory arthritis, compared with those treated with tumor necrosis factor (TNF) inhibitors, according to findings from a large retrospective study.
While previous retrospective cohort studies have found biologic therapies for psoriasis can reduce the risk of developing psoriatic arthritis when compared with other treatments such as phototherapy and oral nonbiologic disease-modifying antirheumatic drugs, this analysis is the first to compare classes of biologics, Shikha Singla, MD, of the Medical College of Wisconsin, Milwaukee, and colleagues wrote in The Lancet Rheumatology.
In the analysis, researchers used the TriNetX database, which contains deidentified data from electronic medical health records from health care organizations across the United States. The study included adults diagnosed with psoriasis who were newly prescribed a biologic approved by the Food and Drug Administration for the treatment of psoriasis. Biologics were defined by drug class: anti-TNF, anti-IL-17, anti-IL-23, and anti–IL-12/23. Any patient with a diagnosis of psoriatic arthritis or other inflammatory arthritis prior to receiving a biologic prescription or within 2 weeks of receiving the prescription were excluded.
The researchers identified 15,501 eligible patients diagnosed with psoriasis during Jan. 1, 2014, to June 1, 2022, with an average follow-up time of 2.4 years. The researchers chose to start the study period in 2014 because the first non–anti-TNF drug for psoriatic arthritis was approved by the FDA in 2013 – the anti–IL-12/23 drug ustekinumab. During the study period, 976 patients developed inflammatory arthritis and were diagnosed on average 528 days after their biologic prescription.
In a multivariable analysis, the researchers found that patients prescribed IL-23 inhibitors (guselkumab [Tremfya], risankizumab [Skyrizi], tildrakizumab [Ilumya]) were nearly 60% less likely (adjusted hazard ratio, 0.41; 95% confidence interval, 0.17–0.95) to develop inflammatory arthritis than were patients taking TNF inhibitors (infliximab [Remicade], adalimumab [Humira], etanercept [Enbrel], golimumab [Simponi], certolizumab pegol [Cimzia]). The risk of developing arthritis was 42% lower (aHR, 0.58; 95% CI, 0.43-0.76) with the IL-12/23 inhibitor ustekinumab (Stelara), but there was no difference in outcomes among patients taking with IL-17 inhibitors (secukinumab [Cosentyx], ixekizumab [Taltz], or brodalumab [Siliq]), compared with TNF inhibitors. For the IL-12/23 inhibitor ustekinumab, all sensitivity analyses did not change this association. For IL-23 inhibitors, the results persisted when excluding patients who developed arthritis within 3 or 6 months after first biologic prescription and when using a higher diagnostic threshold for incident arthritis.
“There is a lot of interest in understanding if treatment of psoriasis will prevent onset of psoriatic arthritis,” said Joel M. Gelfand, MD, MSCE, director of the Psoriasis and Phototherapy Treatment Center at the University of Pennsylvania, Philadelphia, who was asked to comment on the results.
“To date, the literature is inconclusive with some studies suggesting biologics reduce risk of PsA, whereas others suggest biologic use is associated with an increased risk of PsA,” he said. “The current study is unique in that it compares biologic classes to one another and suggests that IL-12/23 and IL-23 biologics are associated with a reduced risk of PsA compared to psoriasis patients treated with TNF inhibitors and no difference was found between TNF inhibitors and IL-17 inhibitors.”
While the study posed an interesting research question, “I wouldn’t use these results to actually change treatment patterns,” Alexis R. Ogdie-Beatty, MD, an associate professor of medicine at the University of Pennsylvania, Philadelphia, said in an interview. She coauthored a commentary on the analysis. Dr. Gelfand also emphasized that this bias may have influenced the results and that these findings “should not impact clinical practice at this time.”
Although the analyses were strong, Dr. Ogdie-Beatty noted, there are inherent biases in this type of observational data that cannot be overcome. For example, if a patient comes into a dermatologist’s office with psoriasis and also has joint pain, the dermatologist may suspect that a patient could also have psoriatic arthritis and would be more likely to choose a drug that will work well for both of these conditions.
“The drugs that are known to work best for psoriatic arthritis are the TNF inhibitors and the IL-17 inhibitors,” she said. So, while the analysis found these medications were associated with higher incidence of PsA, the dermatologist was possibly treating presumptive arthritis and the patient had yet to be referred to a rheumatologist to confirm the diagnosis.
The researchers noted that they attempted to mitigate these issues by requiring that patients have at least 1 year of follow-up before receiving biologic prescription “to capture only the patients with no previous codes for any type of arthritis,” as well as conducting six sensitivity analyses.
The authors, and Dr. Ogdie-Beatty and Dr. Gelfand agreed that more research is necessary to confirm these findings. A large randomized trial may be “prohibitively expensive,” the authors noted, but pooled analyses from previous clinical trials may help with this issue. “We identified 14 published randomized trials that did head-to-head comparisons of different biologic classes with regard to effect on psoriasis, and these trials collectively contained data on more than 13,000 patients. Pooled analyses of these data could confirm the findings of the present study and would be adequately powered.”
But that approach also has limitations, as psoriatic arthritis was not assessed an outcome in these studies, Dr. Ogdie-Beatty noted. Randomizing patients who are already at a higher risk of developing PsA to different biologics could be one approach to address these questions without needing such a large patient population.
The study was conducted without outside funding or industry involvement. Dr. Singla reported no relevant financial relationships with industry, but several coauthors reported financial relationships with pharmaceutical companies that market biologics for psoriasis and psoriatic arthritis. Dr. Ogdie-Beatty reported financial relationships with AbbVie, Amgen, Bristol-Myers Squibb, Celgene, CorEvitas, Gilead, Happify Health, Janssen, Lilly, Novartis, Pfizer, and UCB. Dr. Gelfand reported financial relationships with Abbvie, Amgen, BMS, Boehringer Ingelheim, FIDE, Lilly, Leo, Janssen Biologics, Novartis, Pfizer, and UCB. Dr. Gelfand is a deputy editor for the Journal of Investigative Dermatology.
This article was updated 3/15/23.
Patients with psoriasis treated with interleukin-12/23 inhibitors or IL-23 inhibitors were less likely to develop inflammatory arthritis, compared with those treated with tumor necrosis factor (TNF) inhibitors, according to findings from a large retrospective study.
While previous retrospective cohort studies have found biologic therapies for psoriasis can reduce the risk of developing psoriatic arthritis when compared with other treatments such as phototherapy and oral nonbiologic disease-modifying antirheumatic drugs, this analysis is the first to compare classes of biologics, Shikha Singla, MD, of the Medical College of Wisconsin, Milwaukee, and colleagues wrote in The Lancet Rheumatology.
In the analysis, researchers used the TriNetX database, which contains deidentified data from electronic medical health records from health care organizations across the United States. The study included adults diagnosed with psoriasis who were newly prescribed a biologic approved by the Food and Drug Administration for the treatment of psoriasis. Biologics were defined by drug class: anti-TNF, anti-IL-17, anti-IL-23, and anti–IL-12/23. Any patient with a diagnosis of psoriatic arthritis or other inflammatory arthritis prior to receiving a biologic prescription or within 2 weeks of receiving the prescription were excluded.
The researchers identified 15,501 eligible patients diagnosed with psoriasis during Jan. 1, 2014, to June 1, 2022, with an average follow-up time of 2.4 years. The researchers chose to start the study period in 2014 because the first non–anti-TNF drug for psoriatic arthritis was approved by the FDA in 2013 – the anti–IL-12/23 drug ustekinumab. During the study period, 976 patients developed inflammatory arthritis and were diagnosed on average 528 days after their biologic prescription.
In a multivariable analysis, the researchers found that patients prescribed IL-23 inhibitors (guselkumab [Tremfya], risankizumab [Skyrizi], tildrakizumab [Ilumya]) were nearly 60% less likely (adjusted hazard ratio, 0.41; 95% confidence interval, 0.17–0.95) to develop inflammatory arthritis than were patients taking TNF inhibitors (infliximab [Remicade], adalimumab [Humira], etanercept [Enbrel], golimumab [Simponi], certolizumab pegol [Cimzia]). The risk of developing arthritis was 42% lower (aHR, 0.58; 95% CI, 0.43-0.76) with the IL-12/23 inhibitor ustekinumab (Stelara), but there was no difference in outcomes among patients taking with IL-17 inhibitors (secukinumab [Cosentyx], ixekizumab [Taltz], or brodalumab [Siliq]), compared with TNF inhibitors. For the IL-12/23 inhibitor ustekinumab, all sensitivity analyses did not change this association. For IL-23 inhibitors, the results persisted when excluding patients who developed arthritis within 3 or 6 months after first biologic prescription and when using a higher diagnostic threshold for incident arthritis.
“There is a lot of interest in understanding if treatment of psoriasis will prevent onset of psoriatic arthritis,” said Joel M. Gelfand, MD, MSCE, director of the Psoriasis and Phototherapy Treatment Center at the University of Pennsylvania, Philadelphia, who was asked to comment on the results.
“To date, the literature is inconclusive with some studies suggesting biologics reduce risk of PsA, whereas others suggest biologic use is associated with an increased risk of PsA,” he said. “The current study is unique in that it compares biologic classes to one another and suggests that IL-12/23 and IL-23 biologics are associated with a reduced risk of PsA compared to psoriasis patients treated with TNF inhibitors and no difference was found between TNF inhibitors and IL-17 inhibitors.”
While the study posed an interesting research question, “I wouldn’t use these results to actually change treatment patterns,” Alexis R. Ogdie-Beatty, MD, an associate professor of medicine at the University of Pennsylvania, Philadelphia, said in an interview. She coauthored a commentary on the analysis. Dr. Gelfand also emphasized that this bias may have influenced the results and that these findings “should not impact clinical practice at this time.”
Although the analyses were strong, Dr. Ogdie-Beatty noted, there are inherent biases in this type of observational data that cannot be overcome. For example, if a patient comes into a dermatologist’s office with psoriasis and also has joint pain, the dermatologist may suspect that a patient could also have psoriatic arthritis and would be more likely to choose a drug that will work well for both of these conditions.
“The drugs that are known to work best for psoriatic arthritis are the TNF inhibitors and the IL-17 inhibitors,” she said. So, while the analysis found these medications were associated with higher incidence of PsA, the dermatologist was possibly treating presumptive arthritis and the patient had yet to be referred to a rheumatologist to confirm the diagnosis.
The researchers noted that they attempted to mitigate these issues by requiring that patients have at least 1 year of follow-up before receiving biologic prescription “to capture only the patients with no previous codes for any type of arthritis,” as well as conducting six sensitivity analyses.
The authors, and Dr. Ogdie-Beatty and Dr. Gelfand agreed that more research is necessary to confirm these findings. A large randomized trial may be “prohibitively expensive,” the authors noted, but pooled analyses from previous clinical trials may help with this issue. “We identified 14 published randomized trials that did head-to-head comparisons of different biologic classes with regard to effect on psoriasis, and these trials collectively contained data on more than 13,000 patients. Pooled analyses of these data could confirm the findings of the present study and would be adequately powered.”
But that approach also has limitations, as psoriatic arthritis was not assessed an outcome in these studies, Dr. Ogdie-Beatty noted. Randomizing patients who are already at a higher risk of developing PsA to different biologics could be one approach to address these questions without needing such a large patient population.
The study was conducted without outside funding or industry involvement. Dr. Singla reported no relevant financial relationships with industry, but several coauthors reported financial relationships with pharmaceutical companies that market biologics for psoriasis and psoriatic arthritis. Dr. Ogdie-Beatty reported financial relationships with AbbVie, Amgen, Bristol-Myers Squibb, Celgene, CorEvitas, Gilead, Happify Health, Janssen, Lilly, Novartis, Pfizer, and UCB. Dr. Gelfand reported financial relationships with Abbvie, Amgen, BMS, Boehringer Ingelheim, FIDE, Lilly, Leo, Janssen Biologics, Novartis, Pfizer, and UCB. Dr. Gelfand is a deputy editor for the Journal of Investigative Dermatology.
This article was updated 3/15/23.
FROM LANCET RHEUMATOLOGY
We have seen the future of healthy muffins, and its name is Roselle
Get ‘em while they’re hot … for your health
Today on the Eating Channel, it’s a very special episode of “Much Ado About Muffin.”
The muffin. For some of us, it’s a good way to pretend we’re not having dessert for breakfast. A bran muffin can be loaded with calcium and fiber, and our beloved blueberry is full of yummy antioxidants and vitamins. Definitely not dessert.
Well, the muffin denial can stop there because there’s a new flavor on the scene, and research suggests it may actually be healthy. (Disclaimer: Muffin may not be considered healthy in Norway.) This new muffin has a name, Roselle, that comes from the calyx extract used in it, which is found in the Hibiscus sabdariffa plant of the same name.
Now, when it comes to new foods, especially ones that are supposed to be healthy, the No. 1 criteria is the same: It has to taste good. Researchers at the Norwegian University of Science and Technology and Amity University in India agreed, but they also set out to make it nutritionally valuable and give it a long shelf life without the addition of preservatives.
Sounds like a tall order, but they figured it out.
Not only is it tasty, but the properties of it could rival your morning multivitamin. Hibiscus extract has huge amounts of antioxidants, like phenolics, which are believed to help prevent cell membrane damage. Foods like vegetables, flax seed, and whole grains also have these antioxidants, but why not just have a Roselle muffin instead? You also get a dose of ascorbic acid without the glass of OJ in the morning.
The ascorbic acid, however, is not there just to help you. It also helps to check the researcher’s third box, shelf life. These naturally rosy-colored pastries will stay mold-free for 6 days without refrigeration at room temperature and without added preservatives.
Our guess, though, is they won’t be on the kitchen counter long enough to find out.
A sobering proposition
If Hollywood is to be believed, there’s no amount of drunkenness that can’t be cured with a cup of coffee or a stern slap in the face. Unfortunately, here in the real world the only thing that can make you less drunk is time. Maybe next time you’ll stop after that seventh Manhattan.
But what if we could beat time? What if there’s an actual sobriety drug out there?
Say hello to fibroblast growth factor 21. Although the liver already does good work filtering out what is essentially poison, it then goes the extra mile and produces fibroblast growth factor 21 (or, as her friends call her, FGF21), a hormone that suppresses the desire to drink, makes you desire water, and protects the liver all at the same time.
Now, FGF21 in its current role is great, but if you’ve ever seen or been a drunk person before, you’ve experienced the lack of interest in listening to reason, especially when it comes from within our own bodies. Who are you to tell us what to do, body? You’re not the boss of us! So a group of scientists decided to push the limits of FGF21. Could it do more than it already does?
First off, they genetically altered a group of mice so that they didn’t produce FGF21 on their own. Then they got them drunk. We’re going to assume they built a scale model of the bar from Cheers and had the mice filter in through the front door as they served their subjects beer out of tiny little glasses.
Once the mice were nice and liquored up, some were given a treatment of FGF21 while others were given a placebo. Lo and behold, the mice given FGF21 recovered about 50% faster than those that received the control treatment. Not exactly instant, but 50% is nothing to sniff at.
Before you bring your FGF21 supplement to the bar, though, this research only applies to mice. We don’t know if it works in people. And make sure you stick to booze. If your choice of intoxication is a bit more exotic, FGF21 isn’t going to do anything for you. Yes, the scientists tried. Yes, those mice are living a very interesting life. And yes, we are jealous of drugged-up lab mice.
Supersize your imagination, shrink your snacks
Have you ever heard of the meal-recall effect? Did you know that, in England, a biscuit is really a cookie? Did you also know that the magazine Bon Appétit is not the same as the peer-reviewed journal Appetite? We do … now.
The meal-recall effect is the subsequent reduction in snacking that comes from remembering a recent meal. It was used to great effect in a recent study conducted at the University of Cambridge, which is in England, where they feed their experimental humans cookies but, for some reason, call them biscuits.
For the first part of the study, the participants were invited to dine at Che Laboratory, where they “were given a microwave ready meal of rice and sauce and a cup of water,” according to a statement from the university. As our Uncle Ernie would say, “Gourmet all the way.”
The test subjects were instructed not to eat anything for 3 hours and “then invited back to the lab to perform imagination tasks.” Those who did come back were randomly divided into five different groups, each with a different task:
- Imagine moving their recent lunch at the lab around a plate.
- Recall eating their recent lunch in detail.
- Imagine that the lunch was twice as big and filling as it really was.
- Look at a photograph of spaghetti hoops in tomato sauce and write a description of it before imagining moving the food around a plate.
- Look at a photo of paper clips and rubber bands and imagine moving them around.
Now, at last, we get to the biscuits/cookies, which were the subject of a taste test that “was simply a rouse for covertly assessing snacking,” the investigators explained. As part of that test, participants were told they could eat as many biscuits as they wanted.
When the tables were cleared and the leftovers examined, the group that imagined spaghetti hoops had eaten the most biscuits (75.9 g), followed by the group that imagined paper clips (75.5 g), the moving-their-lunch-around-the-plate group (72.0 g), and the group that relived eating their lunch (70.0 g).
In a victory for the meal-recall effect, the people who imagined their meal being twice as big ate the fewest biscuits (51.1 g). “Your mind can be more powerful than your stomach in dictating how much you eat,” lead author Joanna Szypula, PhD, said in the university statement.
Oh! One more thing. The study appeared in Appetite, which is a peer-reviewed journal, not in Bon Appétit, which is not a peer-reviewed journal. Thanks to the fine folks at both publications for pointing that out to us.
Get ‘em while they’re hot … for your health
Today on the Eating Channel, it’s a very special episode of “Much Ado About Muffin.”
The muffin. For some of us, it’s a good way to pretend we’re not having dessert for breakfast. A bran muffin can be loaded with calcium and fiber, and our beloved blueberry is full of yummy antioxidants and vitamins. Definitely not dessert.
Well, the muffin denial can stop there because there’s a new flavor on the scene, and research suggests it may actually be healthy. (Disclaimer: Muffin may not be considered healthy in Norway.) This new muffin has a name, Roselle, that comes from the calyx extract used in it, which is found in the Hibiscus sabdariffa plant of the same name.
Now, when it comes to new foods, especially ones that are supposed to be healthy, the No. 1 criteria is the same: It has to taste good. Researchers at the Norwegian University of Science and Technology and Amity University in India agreed, but they also set out to make it nutritionally valuable and give it a long shelf life without the addition of preservatives.
Sounds like a tall order, but they figured it out.
Not only is it tasty, but the properties of it could rival your morning multivitamin. Hibiscus extract has huge amounts of antioxidants, like phenolics, which are believed to help prevent cell membrane damage. Foods like vegetables, flax seed, and whole grains also have these antioxidants, but why not just have a Roselle muffin instead? You also get a dose of ascorbic acid without the glass of OJ in the morning.
The ascorbic acid, however, is not there just to help you. It also helps to check the researcher’s third box, shelf life. These naturally rosy-colored pastries will stay mold-free for 6 days without refrigeration at room temperature and without added preservatives.
Our guess, though, is they won’t be on the kitchen counter long enough to find out.
A sobering proposition
If Hollywood is to be believed, there’s no amount of drunkenness that can’t be cured with a cup of coffee or a stern slap in the face. Unfortunately, here in the real world the only thing that can make you less drunk is time. Maybe next time you’ll stop after that seventh Manhattan.
But what if we could beat time? What if there’s an actual sobriety drug out there?
Say hello to fibroblast growth factor 21. Although the liver already does good work filtering out what is essentially poison, it then goes the extra mile and produces fibroblast growth factor 21 (or, as her friends call her, FGF21), a hormone that suppresses the desire to drink, makes you desire water, and protects the liver all at the same time.
Now, FGF21 in its current role is great, but if you’ve ever seen or been a drunk person before, you’ve experienced the lack of interest in listening to reason, especially when it comes from within our own bodies. Who are you to tell us what to do, body? You’re not the boss of us! So a group of scientists decided to push the limits of FGF21. Could it do more than it already does?
First off, they genetically altered a group of mice so that they didn’t produce FGF21 on their own. Then they got them drunk. We’re going to assume they built a scale model of the bar from Cheers and had the mice filter in through the front door as they served their subjects beer out of tiny little glasses.
Once the mice were nice and liquored up, some were given a treatment of FGF21 while others were given a placebo. Lo and behold, the mice given FGF21 recovered about 50% faster than those that received the control treatment. Not exactly instant, but 50% is nothing to sniff at.
Before you bring your FGF21 supplement to the bar, though, this research only applies to mice. We don’t know if it works in people. And make sure you stick to booze. If your choice of intoxication is a bit more exotic, FGF21 isn’t going to do anything for you. Yes, the scientists tried. Yes, those mice are living a very interesting life. And yes, we are jealous of drugged-up lab mice.
Supersize your imagination, shrink your snacks
Have you ever heard of the meal-recall effect? Did you know that, in England, a biscuit is really a cookie? Did you also know that the magazine Bon Appétit is not the same as the peer-reviewed journal Appetite? We do … now.
The meal-recall effect is the subsequent reduction in snacking that comes from remembering a recent meal. It was used to great effect in a recent study conducted at the University of Cambridge, which is in England, where they feed their experimental humans cookies but, for some reason, call them biscuits.
For the first part of the study, the participants were invited to dine at Che Laboratory, where they “were given a microwave ready meal of rice and sauce and a cup of water,” according to a statement from the university. As our Uncle Ernie would say, “Gourmet all the way.”
The test subjects were instructed not to eat anything for 3 hours and “then invited back to the lab to perform imagination tasks.” Those who did come back were randomly divided into five different groups, each with a different task:
- Imagine moving their recent lunch at the lab around a plate.
- Recall eating their recent lunch in detail.
- Imagine that the lunch was twice as big and filling as it really was.
- Look at a photograph of spaghetti hoops in tomato sauce and write a description of it before imagining moving the food around a plate.
- Look at a photo of paper clips and rubber bands and imagine moving them around.
Now, at last, we get to the biscuits/cookies, which were the subject of a taste test that “was simply a rouse for covertly assessing snacking,” the investigators explained. As part of that test, participants were told they could eat as many biscuits as they wanted.
When the tables were cleared and the leftovers examined, the group that imagined spaghetti hoops had eaten the most biscuits (75.9 g), followed by the group that imagined paper clips (75.5 g), the moving-their-lunch-around-the-plate group (72.0 g), and the group that relived eating their lunch (70.0 g).
In a victory for the meal-recall effect, the people who imagined their meal being twice as big ate the fewest biscuits (51.1 g). “Your mind can be more powerful than your stomach in dictating how much you eat,” lead author Joanna Szypula, PhD, said in the university statement.
Oh! One more thing. The study appeared in Appetite, which is a peer-reviewed journal, not in Bon Appétit, which is not a peer-reviewed journal. Thanks to the fine folks at both publications for pointing that out to us.
Get ‘em while they’re hot … for your health
Today on the Eating Channel, it’s a very special episode of “Much Ado About Muffin.”
The muffin. For some of us, it’s a good way to pretend we’re not having dessert for breakfast. A bran muffin can be loaded with calcium and fiber, and our beloved blueberry is full of yummy antioxidants and vitamins. Definitely not dessert.
Well, the muffin denial can stop there because there’s a new flavor on the scene, and research suggests it may actually be healthy. (Disclaimer: Muffin may not be considered healthy in Norway.) This new muffin has a name, Roselle, that comes from the calyx extract used in it, which is found in the Hibiscus sabdariffa plant of the same name.
Now, when it comes to new foods, especially ones that are supposed to be healthy, the No. 1 criteria is the same: It has to taste good. Researchers at the Norwegian University of Science and Technology and Amity University in India agreed, but they also set out to make it nutritionally valuable and give it a long shelf life without the addition of preservatives.
Sounds like a tall order, but they figured it out.
Not only is it tasty, but the properties of it could rival your morning multivitamin. Hibiscus extract has huge amounts of antioxidants, like phenolics, which are believed to help prevent cell membrane damage. Foods like vegetables, flax seed, and whole grains also have these antioxidants, but why not just have a Roselle muffin instead? You also get a dose of ascorbic acid without the glass of OJ in the morning.
The ascorbic acid, however, is not there just to help you. It also helps to check the researcher’s third box, shelf life. These naturally rosy-colored pastries will stay mold-free for 6 days without refrigeration at room temperature and without added preservatives.
Our guess, though, is they won’t be on the kitchen counter long enough to find out.
A sobering proposition
If Hollywood is to be believed, there’s no amount of drunkenness that can’t be cured with a cup of coffee or a stern slap in the face. Unfortunately, here in the real world the only thing that can make you less drunk is time. Maybe next time you’ll stop after that seventh Manhattan.
But what if we could beat time? What if there’s an actual sobriety drug out there?
Say hello to fibroblast growth factor 21. Although the liver already does good work filtering out what is essentially poison, it then goes the extra mile and produces fibroblast growth factor 21 (or, as her friends call her, FGF21), a hormone that suppresses the desire to drink, makes you desire water, and protects the liver all at the same time.
Now, FGF21 in its current role is great, but if you’ve ever seen or been a drunk person before, you’ve experienced the lack of interest in listening to reason, especially when it comes from within our own bodies. Who are you to tell us what to do, body? You’re not the boss of us! So a group of scientists decided to push the limits of FGF21. Could it do more than it already does?
First off, they genetically altered a group of mice so that they didn’t produce FGF21 on their own. Then they got them drunk. We’re going to assume they built a scale model of the bar from Cheers and had the mice filter in through the front door as they served their subjects beer out of tiny little glasses.
Once the mice were nice and liquored up, some were given a treatment of FGF21 while others were given a placebo. Lo and behold, the mice given FGF21 recovered about 50% faster than those that received the control treatment. Not exactly instant, but 50% is nothing to sniff at.
Before you bring your FGF21 supplement to the bar, though, this research only applies to mice. We don’t know if it works in people. And make sure you stick to booze. If your choice of intoxication is a bit more exotic, FGF21 isn’t going to do anything for you. Yes, the scientists tried. Yes, those mice are living a very interesting life. And yes, we are jealous of drugged-up lab mice.
Supersize your imagination, shrink your snacks
Have you ever heard of the meal-recall effect? Did you know that, in England, a biscuit is really a cookie? Did you also know that the magazine Bon Appétit is not the same as the peer-reviewed journal Appetite? We do … now.
The meal-recall effect is the subsequent reduction in snacking that comes from remembering a recent meal. It was used to great effect in a recent study conducted at the University of Cambridge, which is in England, where they feed their experimental humans cookies but, for some reason, call them biscuits.
For the first part of the study, the participants were invited to dine at Che Laboratory, where they “were given a microwave ready meal of rice and sauce and a cup of water,” according to a statement from the university. As our Uncle Ernie would say, “Gourmet all the way.”
The test subjects were instructed not to eat anything for 3 hours and “then invited back to the lab to perform imagination tasks.” Those who did come back were randomly divided into five different groups, each with a different task:
- Imagine moving their recent lunch at the lab around a plate.
- Recall eating their recent lunch in detail.
- Imagine that the lunch was twice as big and filling as it really was.
- Look at a photograph of spaghetti hoops in tomato sauce and write a description of it before imagining moving the food around a plate.
- Look at a photo of paper clips and rubber bands and imagine moving them around.
Now, at last, we get to the biscuits/cookies, which were the subject of a taste test that “was simply a rouse for covertly assessing snacking,” the investigators explained. As part of that test, participants were told they could eat as many biscuits as they wanted.
When the tables were cleared and the leftovers examined, the group that imagined spaghetti hoops had eaten the most biscuits (75.9 g), followed by the group that imagined paper clips (75.5 g), the moving-their-lunch-around-the-plate group (72.0 g), and the group that relived eating their lunch (70.0 g).
In a victory for the meal-recall effect, the people who imagined their meal being twice as big ate the fewest biscuits (51.1 g). “Your mind can be more powerful than your stomach in dictating how much you eat,” lead author Joanna Szypula, PhD, said in the university statement.
Oh! One more thing. The study appeared in Appetite, which is a peer-reviewed journal, not in Bon Appétit, which is not a peer-reviewed journal. Thanks to the fine folks at both publications for pointing that out to us.
Protuberant, Pink, Irritated Growth on the Buttocks
The Diagnosis: Superficial Angiomyxoma
Superficial angiomyxoma is a rare, benign, cutaneous tumor of a myxoid matrix and blood vessels that was first described in association with Carney complex.1 Tumors may be solitary or multiple. A recent review of cases in the literature revealed a roughly equal distribution of superficial angiomyxomas in males and females occurring most frequently on the head and neck, extremities, and trunk or back. The peak incidence is between the fourth and fifth decades of life.2 Superficial angiomyxomas can occur sporadically or in association with Carney complex, an autosomal-dominant condition with germline inactivating mutations in protein kinase A, PRKAR1A. Interestingly, sporadic cases of superficial angiomyxoma also have shown loss of PRKAR1A expression on immunohistochemistry (IHC).3
Common histologic mimics of superficial angiomyxoma include aggressive angiomyxoma and angiomyofibroblastoma.4 It is thought that these 3 distinct tumor entities may arise from a common pluripotent cell of origin located near connective tissue vasculature, which may contribute to the similarities observed between them.5 For example, aggressive angiomyxomas and angiomyofibroblastomas also demonstrate a similar myxoid background and vascular proliferation that can closely mimic superficial angiomyxomas clinically. However, the vessels of superficial angiomyxomas tend to be long and thin walled, while aggressive angiomyxomas are characterized by large and thick-walled vessels and angiomyofibroblastomas by abundant smaller vessels. Additionally, unlike superficial angiomyxomas, both aggressive angiomyxomas and angiomyofibroblastomas typically occur in the genital tract of young to middle-aged women.6
Histopathologic examination is imperative for differentiating between superficial angiomyxoma and more aggressive histologic mimics. Superficial angiomyxomas typically consist of a rich myxoid stroma, thin-walled or arborizing blood vessels, and spindled to stellate fibroblastlike cells (quiz image 2).3 Although not prominent in our case, superficial angiomyxomas also frequently present with stromal neutrophils and epithelial components, including keratinous cysts, basaloid buds, and strands of squamous epithelium.7 Minimal cellular atypia, mitotic activity, and nuclear pleomorphism often are seen, with IHC negative for desmin, estrogen receptor, and progesterone receptor; positive for CD34 and smooth muscle actin; and variable for S-100 and muscle-specific actin. Although IHC has limited utility in the diagnosis of superficial angiomyxomas, it may be useful to rule out other differential diagnoses.2,3 Superficial angiomyxomas usually show fibroblastic stromal cells, proteoglycan matrix, and collagen fibers on electron microscopy.8 Importantly, histopathologic examination of aggressive angiomyxoma will comparatively present with more invasive, infiltrative, and less well-circumscribed tumors.9 Other differential diagnoses on histology may include neurofibroma, focal cutaneous mucinosis, spindle cell lipoma, and myxofibrosarcoma. Additional considerations include fibroepithelial polyp, nevus lipomatosis, angiomyxolipoma, and anetoderma.
An important differential diagnosis in the evaluation of superficial angiomyxoma is neurofibroma, a benign peripheral nerve sheath tumor that presents as a smooth, flesh-colored, and painless papule or nodule commonly associated with the buttonhole sign. Histopathology of neurofibroma features elongated spindle cells with comma-shaped or buckled wavy nuclei and variably sized collagen bundles described as “shredded carrots” (Figure 1).10 Occasional mast cells also can be seen. Immunohistochemistry targeting elements of peripheral nerve sheaths may assist in the diagnosis of neurofibromas, including positive S-100 and SOX10 in Schwann cells, epithelial membrane antigen in perineural cells, and fingerprint positivity for CD34 in fibroblasts.10
Cutaneous mucinoses encompass a diverse group of connective tissue disorders characterized by accumulation of mucin in the skin. Solitary focal cutaneous mucinoses (FCMs) are individual isolated lesions of mucin deposits that are unassociated with systemic conditions.11 Conversely, multiple FCMs presenting with multiple cutaneous lesions also have been described in association with systemic diseases such as scleroderma, systemic lupus erythematosus, and thyroid disease.12 Solitary FCM typically presents as an asymptomatic, flesh-colored papule or nodule on the extremities. It often arises in mid to late adulthood with a slightly increased frequency among males.12 Histopathology of solitary FCM commonly demonstrates a dome-shaped pool of basophilic mucin in the upper dermis sparing involvement of the underlying subcutaneous tissue (Figure 2).13 Notably, FCM often lacks the vascularity as well as stromal neutrophils and epithelial elements that are seen in superficial angiomyxomas. Although hematoxylin and eosin stains can be sufficient for diagnosis of solitary FCM, additional stains for mucin such as Alcian blue, colloidal iron, or toluidine blue also may be considered to support the diagnosis.12
Spindle cell lipomas (SCLs) are rare, benign, subcutaneous, adipocytic tumors that arise on the upper back, posterior neck, or shoulders of middle-aged or elderly adult males.14 The clinical presentation often is an asymptomatic, well-circumscribed, mobile subcutaneous mass that is firmer than a common lipoma. Histologically, SCLs are characterized by mature adipocytes, spindle cells, and wire or ropelike collagen fibers in a myxoid background (Figure 3). The spindle cells usually are bland with a notable bipolar shape and blunted ends. Infiltrative growth patterns or mitotic figures are uncommon. Diagnosis can be supported by IHC, as SCLs stain diffusely positive for CD34 with loss of the retinoblastoma protein.7
Another important differential diagnosis to consider is myxofibrosarcoma, a rare and malignant myxoid cutaneous tumor. Clinically, it presents asymptomatically as an indolent, slow-growing nodule on the limbs and limb girdles.7 Histopathologic features demonstrate a multilobular tumor composed of a mixture of hypocellular and hypercellular regions with incomplete fibrous septae (Figure 4). The presence of curvilinear vasculature is characteristic. Multinucleated giant cells and cellular atypia with nuclear pleomorphism also can be seen. Although IHC findings generally are not specific, they can be used to rule out other potential diagnoses. Myxofibrosarcomas stain positive for vimentin and occasionally smooth muscle actin, muscle-specific actin, and CD34.7
Superficial angiomyxomas are benign; however, excision is recommended to distinguish between mimics. Local recurrence after excision is common in 30% to 40% of patients.15 Mohs micrographic surgery has been considered, especially if the following are present: tumor characteristics (eg, poorly circumscribed), location (eg, head and neck or other cosmetically or functionally sensitive areas), and likelihood of recurrence (high for superficial angiomyxomas). 16 This case otherwise highlights a rare example of superficial angiomyxomas involving the buttocks.
- Allen PW, Dymock RB, MacCormac LB. Superficial angiomyxomas with and without epithelial components. report of 30 tumors in 28 patients. Am J Surg Pathol. 1988;12:519-530. doi:10.1097 /00000478-198807000-00003
- Sharma A, Khaitan N, Ko JS, et al. A clinicopathologic analysis of 54 cases of cutaneous myxoma. Hum Pathol. 2021:S0046-8177(21) 00201-X. doi:10.1016/j.humpath.2021.12.003
- Hafeez F, Krakowski AC, Lian CG, et al. Sporadic superficial angiomyxomas demonstrate loss of PRKAR1A expression [published online March 17, 2022]. Histopathology. 2022;80:1001-1003. doi:10.1111/his.14568
- Mehrotra K, Bhandari M, Khullar G, et al. Large superficial angiomyxoma of the vulva: report of two cases with varied clinical presentation. Indian Dermatol Online J. 2021;12:605-607. doi:10.4103/idoj.IDOJ_489_20
- Alameda F, Munné A, Baró T, et al. Vulvar angiomyxoma, aggressive angiomyxoma, and angiomyofibroblastoma: an immunohistochemical and ultrastructural study. Ultrastruct Pathol. 2006;30:193-205. doi:10.1080/01913120500520911
- Haroon S, Irshad L, Zia S, et al. Aggressive angiomyxoma, angiomyofibroblastoma, and cellular angiofibroma of the lower female genital tract: related entities with different outcomes. Cureus. 2022;14:E29250. doi:10.7759/cureus.29250
- Zou Y, Billings SD. Myxoid cutaneous tumors: a review. J Cutan Pathol. 2016;43:903-918. doi:10.1111/cup.12749
- Allen PW. Myxoma is not a single entity: a review of the concept of myxoma. Ann Diagn Pathol. 2000;4:99-123. doi:10.1016 /s1092-9134(00)90019-4
- Lee C-C, Chen Y-L, Liau J-Y, et al. Superficial angiomyxoma on the vulva of an adolescent. Taiwan J Obstet Gynecol. 2014;53:104-106. doi:10.1016/j.tjog.2013.08.001
- Magro G, Amico P, Vecchio GM, et al. Multinucleated floret-like giant cells in sporadic and NF1-associated neurofibromas: a clinicopathologic study of 94 cases. Virchows Arch. 2010;456:71-76. doi:10.1007/s00428-009-0859-y
- Kuo KL, Lee LY, Kuo TT. Solitary cutaneous focal mucinosis: a clinicopathological study of 11 cases of soft fibroma-like cutaneous mucinous lesions. J Dermatol. 2017;44:335-338. doi:10.1111/1346-8138.13523
- Gutierrez N, Erickson C, Calame A, et al. Solitary cutaneous focal mucinosis. Cureus. 2021;13:E18618. doi:10.7759/cureus.18618
- Biondo G, Sola S, Pastorino C, et al. Clinical, dermoscopic, and histologic aspects of two cases of cutaneous focal mucinosis. An Bras Dermatol. 2019;94:334-336. doi:10.1590/abd1806-4841.20198381
- Chen S, Huang H, He S, et al. Spindle cell lipoma: clinicopathologic characterization of 40 cases. Int J Clin Exp Pathol. 2019;12:2613-2621.
- Bembem K, Jaiswal A, Singh M, et al. Cyto-histo correlation of a very rare tumor: superficial angiomyxoma. J Cytol. 2017;34:230-232. doi:10.4103/0970-9371.216119
- Aberdein G, Veitch D, Perrett C. Mohs micrographic surgery for the treatment of superficial angiomyxoma. Dermatol Surg. 2016;42: 1014-1016. doi:10.1097/DSS.0000000000000782
The Diagnosis: Superficial Angiomyxoma
Superficial angiomyxoma is a rare, benign, cutaneous tumor of a myxoid matrix and blood vessels that was first described in association with Carney complex.1 Tumors may be solitary or multiple. A recent review of cases in the literature revealed a roughly equal distribution of superficial angiomyxomas in males and females occurring most frequently on the head and neck, extremities, and trunk or back. The peak incidence is between the fourth and fifth decades of life.2 Superficial angiomyxomas can occur sporadically or in association with Carney complex, an autosomal-dominant condition with germline inactivating mutations in protein kinase A, PRKAR1A. Interestingly, sporadic cases of superficial angiomyxoma also have shown loss of PRKAR1A expression on immunohistochemistry (IHC).3
Common histologic mimics of superficial angiomyxoma include aggressive angiomyxoma and angiomyofibroblastoma.4 It is thought that these 3 distinct tumor entities may arise from a common pluripotent cell of origin located near connective tissue vasculature, which may contribute to the similarities observed between them.5 For example, aggressive angiomyxomas and angiomyofibroblastomas also demonstrate a similar myxoid background and vascular proliferation that can closely mimic superficial angiomyxomas clinically. However, the vessels of superficial angiomyxomas tend to be long and thin walled, while aggressive angiomyxomas are characterized by large and thick-walled vessels and angiomyofibroblastomas by abundant smaller vessels. Additionally, unlike superficial angiomyxomas, both aggressive angiomyxomas and angiomyofibroblastomas typically occur in the genital tract of young to middle-aged women.6
Histopathologic examination is imperative for differentiating between superficial angiomyxoma and more aggressive histologic mimics. Superficial angiomyxomas typically consist of a rich myxoid stroma, thin-walled or arborizing blood vessels, and spindled to stellate fibroblastlike cells (quiz image 2).3 Although not prominent in our case, superficial angiomyxomas also frequently present with stromal neutrophils and epithelial components, including keratinous cysts, basaloid buds, and strands of squamous epithelium.7 Minimal cellular atypia, mitotic activity, and nuclear pleomorphism often are seen, with IHC negative for desmin, estrogen receptor, and progesterone receptor; positive for CD34 and smooth muscle actin; and variable for S-100 and muscle-specific actin. Although IHC has limited utility in the diagnosis of superficial angiomyxomas, it may be useful to rule out other differential diagnoses.2,3 Superficial angiomyxomas usually show fibroblastic stromal cells, proteoglycan matrix, and collagen fibers on electron microscopy.8 Importantly, histopathologic examination of aggressive angiomyxoma will comparatively present with more invasive, infiltrative, and less well-circumscribed tumors.9 Other differential diagnoses on histology may include neurofibroma, focal cutaneous mucinosis, spindle cell lipoma, and myxofibrosarcoma. Additional considerations include fibroepithelial polyp, nevus lipomatosis, angiomyxolipoma, and anetoderma.
An important differential diagnosis in the evaluation of superficial angiomyxoma is neurofibroma, a benign peripheral nerve sheath tumor that presents as a smooth, flesh-colored, and painless papule or nodule commonly associated with the buttonhole sign. Histopathology of neurofibroma features elongated spindle cells with comma-shaped or buckled wavy nuclei and variably sized collagen bundles described as “shredded carrots” (Figure 1).10 Occasional mast cells also can be seen. Immunohistochemistry targeting elements of peripheral nerve sheaths may assist in the diagnosis of neurofibromas, including positive S-100 and SOX10 in Schwann cells, epithelial membrane antigen in perineural cells, and fingerprint positivity for CD34 in fibroblasts.10
Cutaneous mucinoses encompass a diverse group of connective tissue disorders characterized by accumulation of mucin in the skin. Solitary focal cutaneous mucinoses (FCMs) are individual isolated lesions of mucin deposits that are unassociated with systemic conditions.11 Conversely, multiple FCMs presenting with multiple cutaneous lesions also have been described in association with systemic diseases such as scleroderma, systemic lupus erythematosus, and thyroid disease.12 Solitary FCM typically presents as an asymptomatic, flesh-colored papule or nodule on the extremities. It often arises in mid to late adulthood with a slightly increased frequency among males.12 Histopathology of solitary FCM commonly demonstrates a dome-shaped pool of basophilic mucin in the upper dermis sparing involvement of the underlying subcutaneous tissue (Figure 2).13 Notably, FCM often lacks the vascularity as well as stromal neutrophils and epithelial elements that are seen in superficial angiomyxomas. Although hematoxylin and eosin stains can be sufficient for diagnosis of solitary FCM, additional stains for mucin such as Alcian blue, colloidal iron, or toluidine blue also may be considered to support the diagnosis.12
Spindle cell lipomas (SCLs) are rare, benign, subcutaneous, adipocytic tumors that arise on the upper back, posterior neck, or shoulders of middle-aged or elderly adult males.14 The clinical presentation often is an asymptomatic, well-circumscribed, mobile subcutaneous mass that is firmer than a common lipoma. Histologically, SCLs are characterized by mature adipocytes, spindle cells, and wire or ropelike collagen fibers in a myxoid background (Figure 3). The spindle cells usually are bland with a notable bipolar shape and blunted ends. Infiltrative growth patterns or mitotic figures are uncommon. Diagnosis can be supported by IHC, as SCLs stain diffusely positive for CD34 with loss of the retinoblastoma protein.7
Another important differential diagnosis to consider is myxofibrosarcoma, a rare and malignant myxoid cutaneous tumor. Clinically, it presents asymptomatically as an indolent, slow-growing nodule on the limbs and limb girdles.7 Histopathologic features demonstrate a multilobular tumor composed of a mixture of hypocellular and hypercellular regions with incomplete fibrous septae (Figure 4). The presence of curvilinear vasculature is characteristic. Multinucleated giant cells and cellular atypia with nuclear pleomorphism also can be seen. Although IHC findings generally are not specific, they can be used to rule out other potential diagnoses. Myxofibrosarcomas stain positive for vimentin and occasionally smooth muscle actin, muscle-specific actin, and CD34.7
Superficial angiomyxomas are benign; however, excision is recommended to distinguish between mimics. Local recurrence after excision is common in 30% to 40% of patients.15 Mohs micrographic surgery has been considered, especially if the following are present: tumor characteristics (eg, poorly circumscribed), location (eg, head and neck or other cosmetically or functionally sensitive areas), and likelihood of recurrence (high for superficial angiomyxomas). 16 This case otherwise highlights a rare example of superficial angiomyxomas involving the buttocks.
The Diagnosis: Superficial Angiomyxoma
Superficial angiomyxoma is a rare, benign, cutaneous tumor of a myxoid matrix and blood vessels that was first described in association with Carney complex.1 Tumors may be solitary or multiple. A recent review of cases in the literature revealed a roughly equal distribution of superficial angiomyxomas in males and females occurring most frequently on the head and neck, extremities, and trunk or back. The peak incidence is between the fourth and fifth decades of life.2 Superficial angiomyxomas can occur sporadically or in association with Carney complex, an autosomal-dominant condition with germline inactivating mutations in protein kinase A, PRKAR1A. Interestingly, sporadic cases of superficial angiomyxoma also have shown loss of PRKAR1A expression on immunohistochemistry (IHC).3
Common histologic mimics of superficial angiomyxoma include aggressive angiomyxoma and angiomyofibroblastoma.4 It is thought that these 3 distinct tumor entities may arise from a common pluripotent cell of origin located near connective tissue vasculature, which may contribute to the similarities observed between them.5 For example, aggressive angiomyxomas and angiomyofibroblastomas also demonstrate a similar myxoid background and vascular proliferation that can closely mimic superficial angiomyxomas clinically. However, the vessels of superficial angiomyxomas tend to be long and thin walled, while aggressive angiomyxomas are characterized by large and thick-walled vessels and angiomyofibroblastomas by abundant smaller vessels. Additionally, unlike superficial angiomyxomas, both aggressive angiomyxomas and angiomyofibroblastomas typically occur in the genital tract of young to middle-aged women.6
Histopathologic examination is imperative for differentiating between superficial angiomyxoma and more aggressive histologic mimics. Superficial angiomyxomas typically consist of a rich myxoid stroma, thin-walled or arborizing blood vessels, and spindled to stellate fibroblastlike cells (quiz image 2).3 Although not prominent in our case, superficial angiomyxomas also frequently present with stromal neutrophils and epithelial components, including keratinous cysts, basaloid buds, and strands of squamous epithelium.7 Minimal cellular atypia, mitotic activity, and nuclear pleomorphism often are seen, with IHC negative for desmin, estrogen receptor, and progesterone receptor; positive for CD34 and smooth muscle actin; and variable for S-100 and muscle-specific actin. Although IHC has limited utility in the diagnosis of superficial angiomyxomas, it may be useful to rule out other differential diagnoses.2,3 Superficial angiomyxomas usually show fibroblastic stromal cells, proteoglycan matrix, and collagen fibers on electron microscopy.8 Importantly, histopathologic examination of aggressive angiomyxoma will comparatively present with more invasive, infiltrative, and less well-circumscribed tumors.9 Other differential diagnoses on histology may include neurofibroma, focal cutaneous mucinosis, spindle cell lipoma, and myxofibrosarcoma. Additional considerations include fibroepithelial polyp, nevus lipomatosis, angiomyxolipoma, and anetoderma.
An important differential diagnosis in the evaluation of superficial angiomyxoma is neurofibroma, a benign peripheral nerve sheath tumor that presents as a smooth, flesh-colored, and painless papule or nodule commonly associated with the buttonhole sign. Histopathology of neurofibroma features elongated spindle cells with comma-shaped or buckled wavy nuclei and variably sized collagen bundles described as “shredded carrots” (Figure 1).10 Occasional mast cells also can be seen. Immunohistochemistry targeting elements of peripheral nerve sheaths may assist in the diagnosis of neurofibromas, including positive S-100 and SOX10 in Schwann cells, epithelial membrane antigen in perineural cells, and fingerprint positivity for CD34 in fibroblasts.10
Cutaneous mucinoses encompass a diverse group of connective tissue disorders characterized by accumulation of mucin in the skin. Solitary focal cutaneous mucinoses (FCMs) are individual isolated lesions of mucin deposits that are unassociated with systemic conditions.11 Conversely, multiple FCMs presenting with multiple cutaneous lesions also have been described in association with systemic diseases such as scleroderma, systemic lupus erythematosus, and thyroid disease.12 Solitary FCM typically presents as an asymptomatic, flesh-colored papule or nodule on the extremities. It often arises in mid to late adulthood with a slightly increased frequency among males.12 Histopathology of solitary FCM commonly demonstrates a dome-shaped pool of basophilic mucin in the upper dermis sparing involvement of the underlying subcutaneous tissue (Figure 2).13 Notably, FCM often lacks the vascularity as well as stromal neutrophils and epithelial elements that are seen in superficial angiomyxomas. Although hematoxylin and eosin stains can be sufficient for diagnosis of solitary FCM, additional stains for mucin such as Alcian blue, colloidal iron, or toluidine blue also may be considered to support the diagnosis.12
Spindle cell lipomas (SCLs) are rare, benign, subcutaneous, adipocytic tumors that arise on the upper back, posterior neck, or shoulders of middle-aged or elderly adult males.14 The clinical presentation often is an asymptomatic, well-circumscribed, mobile subcutaneous mass that is firmer than a common lipoma. Histologically, SCLs are characterized by mature adipocytes, spindle cells, and wire or ropelike collagen fibers in a myxoid background (Figure 3). The spindle cells usually are bland with a notable bipolar shape and blunted ends. Infiltrative growth patterns or mitotic figures are uncommon. Diagnosis can be supported by IHC, as SCLs stain diffusely positive for CD34 with loss of the retinoblastoma protein.7
Another important differential diagnosis to consider is myxofibrosarcoma, a rare and malignant myxoid cutaneous tumor. Clinically, it presents asymptomatically as an indolent, slow-growing nodule on the limbs and limb girdles.7 Histopathologic features demonstrate a multilobular tumor composed of a mixture of hypocellular and hypercellular regions with incomplete fibrous septae (Figure 4). The presence of curvilinear vasculature is characteristic. Multinucleated giant cells and cellular atypia with nuclear pleomorphism also can be seen. Although IHC findings generally are not specific, they can be used to rule out other potential diagnoses. Myxofibrosarcomas stain positive for vimentin and occasionally smooth muscle actin, muscle-specific actin, and CD34.7
Superficial angiomyxomas are benign; however, excision is recommended to distinguish between mimics. Local recurrence after excision is common in 30% to 40% of patients.15 Mohs micrographic surgery has been considered, especially if the following are present: tumor characteristics (eg, poorly circumscribed), location (eg, head and neck or other cosmetically or functionally sensitive areas), and likelihood of recurrence (high for superficial angiomyxomas). 16 This case otherwise highlights a rare example of superficial angiomyxomas involving the buttocks.
- Allen PW, Dymock RB, MacCormac LB. Superficial angiomyxomas with and without epithelial components. report of 30 tumors in 28 patients. Am J Surg Pathol. 1988;12:519-530. doi:10.1097 /00000478-198807000-00003
- Sharma A, Khaitan N, Ko JS, et al. A clinicopathologic analysis of 54 cases of cutaneous myxoma. Hum Pathol. 2021:S0046-8177(21) 00201-X. doi:10.1016/j.humpath.2021.12.003
- Hafeez F, Krakowski AC, Lian CG, et al. Sporadic superficial angiomyxomas demonstrate loss of PRKAR1A expression [published online March 17, 2022]. Histopathology. 2022;80:1001-1003. doi:10.1111/his.14568
- Mehrotra K, Bhandari M, Khullar G, et al. Large superficial angiomyxoma of the vulva: report of two cases with varied clinical presentation. Indian Dermatol Online J. 2021;12:605-607. doi:10.4103/idoj.IDOJ_489_20
- Alameda F, Munné A, Baró T, et al. Vulvar angiomyxoma, aggressive angiomyxoma, and angiomyofibroblastoma: an immunohistochemical and ultrastructural study. Ultrastruct Pathol. 2006;30:193-205. doi:10.1080/01913120500520911
- Haroon S, Irshad L, Zia S, et al. Aggressive angiomyxoma, angiomyofibroblastoma, and cellular angiofibroma of the lower female genital tract: related entities with different outcomes. Cureus. 2022;14:E29250. doi:10.7759/cureus.29250
- Zou Y, Billings SD. Myxoid cutaneous tumors: a review. J Cutan Pathol. 2016;43:903-918. doi:10.1111/cup.12749
- Allen PW. Myxoma is not a single entity: a review of the concept of myxoma. Ann Diagn Pathol. 2000;4:99-123. doi:10.1016 /s1092-9134(00)90019-4
- Lee C-C, Chen Y-L, Liau J-Y, et al. Superficial angiomyxoma on the vulva of an adolescent. Taiwan J Obstet Gynecol. 2014;53:104-106. doi:10.1016/j.tjog.2013.08.001
- Magro G, Amico P, Vecchio GM, et al. Multinucleated floret-like giant cells in sporadic and NF1-associated neurofibromas: a clinicopathologic study of 94 cases. Virchows Arch. 2010;456:71-76. doi:10.1007/s00428-009-0859-y
- Kuo KL, Lee LY, Kuo TT. Solitary cutaneous focal mucinosis: a clinicopathological study of 11 cases of soft fibroma-like cutaneous mucinous lesions. J Dermatol. 2017;44:335-338. doi:10.1111/1346-8138.13523
- Gutierrez N, Erickson C, Calame A, et al. Solitary cutaneous focal mucinosis. Cureus. 2021;13:E18618. doi:10.7759/cureus.18618
- Biondo G, Sola S, Pastorino C, et al. Clinical, dermoscopic, and histologic aspects of two cases of cutaneous focal mucinosis. An Bras Dermatol. 2019;94:334-336. doi:10.1590/abd1806-4841.20198381
- Chen S, Huang H, He S, et al. Spindle cell lipoma: clinicopathologic characterization of 40 cases. Int J Clin Exp Pathol. 2019;12:2613-2621.
- Bembem K, Jaiswal A, Singh M, et al. Cyto-histo correlation of a very rare tumor: superficial angiomyxoma. J Cytol. 2017;34:230-232. doi:10.4103/0970-9371.216119
- Aberdein G, Veitch D, Perrett C. Mohs micrographic surgery for the treatment of superficial angiomyxoma. Dermatol Surg. 2016;42: 1014-1016. doi:10.1097/DSS.0000000000000782
- Allen PW, Dymock RB, MacCormac LB. Superficial angiomyxomas with and without epithelial components. report of 30 tumors in 28 patients. Am J Surg Pathol. 1988;12:519-530. doi:10.1097 /00000478-198807000-00003
- Sharma A, Khaitan N, Ko JS, et al. A clinicopathologic analysis of 54 cases of cutaneous myxoma. Hum Pathol. 2021:S0046-8177(21) 00201-X. doi:10.1016/j.humpath.2021.12.003
- Hafeez F, Krakowski AC, Lian CG, et al. Sporadic superficial angiomyxomas demonstrate loss of PRKAR1A expression [published online March 17, 2022]. Histopathology. 2022;80:1001-1003. doi:10.1111/his.14568
- Mehrotra K, Bhandari M, Khullar G, et al. Large superficial angiomyxoma of the vulva: report of two cases with varied clinical presentation. Indian Dermatol Online J. 2021;12:605-607. doi:10.4103/idoj.IDOJ_489_20
- Alameda F, Munné A, Baró T, et al. Vulvar angiomyxoma, aggressive angiomyxoma, and angiomyofibroblastoma: an immunohistochemical and ultrastructural study. Ultrastruct Pathol. 2006;30:193-205. doi:10.1080/01913120500520911
- Haroon S, Irshad L, Zia S, et al. Aggressive angiomyxoma, angiomyofibroblastoma, and cellular angiofibroma of the lower female genital tract: related entities with different outcomes. Cureus. 2022;14:E29250. doi:10.7759/cureus.29250
- Zou Y, Billings SD. Myxoid cutaneous tumors: a review. J Cutan Pathol. 2016;43:903-918. doi:10.1111/cup.12749
- Allen PW. Myxoma is not a single entity: a review of the concept of myxoma. Ann Diagn Pathol. 2000;4:99-123. doi:10.1016 /s1092-9134(00)90019-4
- Lee C-C, Chen Y-L, Liau J-Y, et al. Superficial angiomyxoma on the vulva of an adolescent. Taiwan J Obstet Gynecol. 2014;53:104-106. doi:10.1016/j.tjog.2013.08.001
- Magro G, Amico P, Vecchio GM, et al. Multinucleated floret-like giant cells in sporadic and NF1-associated neurofibromas: a clinicopathologic study of 94 cases. Virchows Arch. 2010;456:71-76. doi:10.1007/s00428-009-0859-y
- Kuo KL, Lee LY, Kuo TT. Solitary cutaneous focal mucinosis: a clinicopathological study of 11 cases of soft fibroma-like cutaneous mucinous lesions. J Dermatol. 2017;44:335-338. doi:10.1111/1346-8138.13523
- Gutierrez N, Erickson C, Calame A, et al. Solitary cutaneous focal mucinosis. Cureus. 2021;13:E18618. doi:10.7759/cureus.18618
- Biondo G, Sola S, Pastorino C, et al. Clinical, dermoscopic, and histologic aspects of two cases of cutaneous focal mucinosis. An Bras Dermatol. 2019;94:334-336. doi:10.1590/abd1806-4841.20198381
- Chen S, Huang H, He S, et al. Spindle cell lipoma: clinicopathologic characterization of 40 cases. Int J Clin Exp Pathol. 2019;12:2613-2621.
- Bembem K, Jaiswal A, Singh M, et al. Cyto-histo correlation of a very rare tumor: superficial angiomyxoma. J Cytol. 2017;34:230-232. doi:10.4103/0970-9371.216119
- Aberdein G, Veitch D, Perrett C. Mohs micrographic surgery for the treatment of superficial angiomyxoma. Dermatol Surg. 2016;42: 1014-1016. doi:10.1097/DSS.0000000000000782
A 25-year-old woman presented with an irritated growth on the left buttock of 6 months’ duration. The lesion had grown slowly over time and became irritated because of the constant rubbing on her clothing due to its location. Physical examination revealed a 1-cm, pink, protuberant, soft, dome-shaped nodule on the left upper medial buttock (inset). A biopsy was performed for diagnostic purposes.
Dermatologic Implications of Sleep Deprivation in the US Military
Sleep deprivation can increase emotional distress and mood disorders; reduce quality of life; and lead to cognitive, memory, and performance deficits.1 Military service predisposes members to disordered sleep due to the rigors of deployments and field training, such as long shifts, shift changes, stressful work environments, and time zone changes. Evidence shows that sleep deprivation is associated with cardiovascular disease, gastrointestinal disease, and some cancers.2 We explore multiple mechanisms by which sleep deprivation may affect the skin. We also review the potential impacts of sleep deprivation on specific topics in dermatology, including atopic dermatitis (AD), psoriasis, alopecia areata, physical attractiveness, wound healing, and skin cancer.
Sleep and Military Service
Approximately 35.2% of Americans experience short sleep duration, which the Centers for Disease Control and Prevention defines as sleeping fewer than 7 hours per 24-hour period.3 Short sleep duration is even more common among individuals working in protective services and the military (50.4%).4 United States military service members experience multiple contributors to disordered sleep, including combat operations, shift work, psychiatric disorders such as posttraumatic stress disorder, and traumatic brain injury.5 Bramoweth and Germain6 described the case of a 27-year-old man who served 2 combat tours as an infantryman in Afghanistan, during which time he routinely remained awake for more than 24 hours at a time due to night missions and extended operations. Even when he was not directly involved in combat operations, he was rarely able to keep a regular sleep schedule.6 Service members returning from deployment also report decreased sleep. In one study (N=2717), 43% of respondents reported short sleep duration (<7 hours of sleep per night) and 29% reported very short sleep duration (<6 hours of sleep per night).7 Even stateside, service members experience acute sleep deprivation during training.8
Sleep and Skin
The idea that skin conditions can affect quality of sleep is not controversial. Pruritus, pain, and emotional distress associated with different dermatologic conditions have all been implicated in adversely affecting sleep.9 Given the effects of sleep deprivation on other organ systems, it also can affect the skin. Possible mechanisms of action include negative effects of sleep deprivation on the hypothalamic-pituitary-adrenal (HPA) axis, cutaneous barrier function, and immune function. First, the HPA axis activity follows a circadian rhythm.10 Activation outside of the bounds of this normal rhythm can have adverse effects on sleep. Alternatively, sleep deprivation and decreased sleep quality can negatively affect the HPA axis.10 These changes can adversely affect cutaneous barrier and immune function.11 Cutaneous barrier function is vitally important in the context of inflammatory dermatologic conditions. Transepidermal water loss, a measurement used to estimate cutaneous barrier function, is increased by sleep deprivation.12 Finally, the cutaneous immune system is an important component of inflammatory dermatologic conditions, cancer immune surveillance, and wound healing, and it also is negatively impacted by sleep deprivation.13 This framework of sleep deprivation affecting the HPA axis, cutaneous barrier function, and cutaneous immune function will help to guide the following discussion on the effects of decreased sleep on specific dermatologic conditions.
Atopic Dermatitis—Individuals with AD are at higher odds of having insomnia, fatigue, and overall poorer health status, including more sick days and increased visits to a physician.14 Additionally, it is possible that the relationship between AD and sleep is not unidirectional. Chang and Chiang15 discussed the possibility of sleep disturbances contributing to AD flares and listed 3 possible mechanisms by which sleep disturbance could potentially flare AD: exacerbation of the itch-scratch cycle; changes in the immune system, including a possible shift to helper T cell (TH2) dominance; and worsening of chronic stress in patients with AD. These changes may lead to a vicious cycle of impaired sleep and AD exacerbations. It may be helpful to view sleep impairment and AD as comorbid conditions requiring co-management for optimal outcomes. This perspective has military relevance because even without considering sleep deprivation, deployment and field conditions are known to increase the risk for AD flares.16
Psoriasis—Psoriasis also may have a bidirectional relationship with sleep. A study utilizing data from the Nurses’ Health Study showed that working a night shift increased the risk for psoriasis.17 Importantly, this connection is associative and not causative. It is possible that other factors in those who worked night shifts such as probable decreased UV exposure or reported increased body mass index played a role. Studies using psoriasis mice models have shown increased inflammation with sleep deprivation.18 Another possible connection is the effect of sleep deprivation on the gut microbiome. Sleep dysfunction is associated with altered gut bacteria ratios, and similar gut bacteria ratios were found in patients with psoriasis, which may indicate an association between sleep deprivation and psoriasis disease progression.19 There also is an increased association of obstructive sleep apnea in patients with psoriasis compared to the general population.20 Fortunately, the rate of consultations for psoriasis in deployed soldiers in the last several conflicts has been quite low, making up only 2.1% of diagnosed dermatologic conditions,21 which is because service members with moderate to severe psoriasis likely will not be deployed.
Alopecia Areata—Alopecia areata also may be associated with sleep deprivation. A large retrospective cohort study looking at the risk for alopecia in patients with sleep disorders showed that a sleep disorder was an independent risk factor for alopecia areata.22 The impact of sleep on the HPA axis portrays a possible mechanism for the negative effects of sleep deprivation on the immune system. Interestingly, in this study, the association was strongest for the 0- to 24-year-old age group. According to the 2020 demographics profile of the military community, 45% of active-duty personnel are 25 years or younger.23 Fortunately, although alopecia areata can be a distressing condition, it should not have much effect on military readiness, as most individuals with this diagnosis are still deployable.
Physical Appearance—
Wound Healing—Wound healing is of particular importance to the health of military members. Research is suggestive but not definitive of the relationship between sleep and wound healing. One intriguing study looked at the healing of blisters induced via suction in well-rested and sleep-deprived individuals. The results showed a difference, with the sleep-deprived individuals taking approximately 1 day longer to heal.13 This has some specific relevance to the military, as friction blisters can be common.30 A cross-sectional survey looking at a group of service members deployed in Iraq showed a prevalence of foot friction blisters of 33%, with 11% of individuals requiring medical care.31 Although this is an interesting example, it is not necessarily applicable to full-thickness wounds. A study utilizing rat models did not identify any differences between sleep-deprived and well-rested models in the healing of punch biopsy sites.32
Skin Cancer—Altered circadian rhythms resulting in changes in melatonin levels, changes in circadian rhythm–related gene pathways, and immunologic changes have been proposed as possible contributing mechanisms for the observed increased risk for skin cancers in military and civilian pilots.33,34 One study showed that UV-related erythema resolved quicker in well-rested individuals compared with those with short sleep duration, which could represent more efficient DNA repair given the relationship between UV-associated erythema and DNA damage and repair.35 Another study looking at circadian changes in the repair of UV-related DNA damage showed that mice exposed to UV radiation in the early morning had higher rates of squamous cell carcinoma than those exposed in the afternoon.36 However, a large cohort study using data from the Nurses’ Health Study II did not support a positive connection between short sleep duration and skin cancer; rather, it showed that a short sleep duration was associated with a decreased risk for melanoma and basal cell carcinoma, with no effect noted for squamous cell carcinoma.37 This does not support a positive association between short sleep duration and skin cancer and in some cases actually suggests a negative association.
Final Thoughts
Although more research is needed, there is evidence that sleep deprivation can negatively affect the skin. Randomized controlled trials looking at groups of individuals with specific dermatologic conditions with a very short sleep duration group (<6 hours of sleep per night), short sleep duration group (<7 hours of sleep per night), and a well-rested group (>7 hours of sleep per night) could be very helpful in this endeavor. Possible mechanisms include the HPA axis, immune system, and skin barrier function that are associated with sleep deprivation. Specific dermatologic conditions that may be affected by sleep deprivation include AD, psoriasis, alopecia areata, physical appearance, wound healing, and skin cancer. The impact of sleep deprivation on dermatologic conditions is particularly relevant to the military, as service members are at an increased risk for short sleep duration. It is possible that improving sleep may lead to better disease control for many dermatologic conditions.
- Carskadon M, Dement WC. Cumulative effects of sleep restriction on daytime sleepiness. Psychophysiology. 1981;18:107-113.
- Medic G, Wille M, Hemels ME. Short- and long-term health consequences of sleep disruption. Nat Sci Sleep. 2017;19;9:151-161.
- Sleep and sleep disorders. Centers for Disease Control and Prevention website. Reviewed September 12, 2022. Accessed February 17, 2023. https://www.cdc.gov/sleep/data_statistics.html
- Khubchandani J, Price JH. Short sleep duration in working American adults, 2010-2018. J Community Health. 2020;45:219-227.
- Good CH, Brager AJ, Capaldi VF, et al. Sleep in the United States military. Neuropsychopharmacology. 2020;45:176-191.
- Bramoweth AD, Germain A. Deployment-related insomnia in military personnel and veterans. Curr Psychiatry Rep. 2013;15:401.
- Luxton DD, Greenburg D, Ryan J, et al. Prevalence and impact of short sleep duration in redeployed OIF soldiers. Sleep. 2011;34:1189-1195.
- Crowley SK, Wilkinson LL, Burroughs EL, et al. Sleep during basic combat training: a qualitative study. Mil Med. 2012;177:823-828.
- Spindler M, Przybyłowicz K, Hawro M, et al. Sleep disturbance in adult dermatologic patients: a cross-sectional study on prevalence, burden, and associated factors. J Am Acad Dermatol. 2021;85:910-922.
- Guyon A, Balbo M, Morselli LL, et al. Adverse effects of two nights of sleep restriction on the hypothalamic-pituitary-adrenal axis in healthy men. J Clin Endocrinol Metab. 2014;99:2861-2868.
- Lin TK, Zhong L, Santiago JL. Association between stress and the HPA axis in the atopic dermatitis. Int J Mol Sci. 2017;18:2131.
- Pinnagoda J, Tupker RA, Agner T, et al. Guidelines for transepidermal water loss (TEWL) measurement. a report from theStandardization Group of the European Society of Contact Dermatitis. Contact Dermatitis. 1990;22:164-178.
- Smith TJ, Wilson MA, Karl JP, et al. Impact of sleep restriction on local immune response and skin barrier restoration with and without “multinutrient” nutrition intervention. J Appl Physiol (1985). 2018;124:190-200.
- Silverberg JI, Garg NK, Paller AS, et al. Sleep disturbances in adults with eczema are associated with impaired overall health: a US population-based study. J Invest Dermatol. 2015;135:56-66.
- Chang YS, Chiang BL. Sleep disorders and atopic dermatitis: a 2-way street? J Allergy Clin Immunol. 2018;142:1033-1040.
- Riegleman KL, Farnsworth GS, Wong EB. Atopic dermatitis in the US military. Cutis. 2019;104:144-147.
- Li WQ, Qureshi AA, Schernhammer ES, et al. Rotating night-shift work and risk of psoriasis in US women. J Invest Dermatol. 2013;133:565-567.
- Hirotsu C, Rydlewski M, Araújo MS, et al. Sleep loss and cytokines levels in an experimental model of psoriasis. PLoS One. 2012;7:E51183.
- Myers B, Vidhatha R, Nicholas B, et al. Sleep and the gut microbiome in psoriasis: clinical implications for disease progression and the development of cardiometabolic comorbidities. J Psoriasis Psoriatic Arthritis. 2021;6:27-37.
- Gupta MA, Simpson FC, Gupta AK. Psoriasis and sleep disorders: a systematic review. Sleep Med Rev. 2016;29:63-75.
- Gelman AB, Norton SA, Valdes-Rodriguez R, et al. A review of skin conditions in modern warfare and peacekeeping operations. Mil Med. 2015;180:32-37.
- Seo HM, Kim TL, Kim JS. The risk of alopecia areata and other related autoimmune diseases in patients with sleep disorders: a Korean population-based retrospective cohort study. Sleep. 2018;41:10.1093/sleep/zsy111.
- Department of Defense. 2020 Demographics: Profile of the Military Community. Military One Source website. Accessed February 17, 2023. https://download.militaryonesource.mil/12038/MOS/Reports/2020-demographics-report.pdf
- Sundelin T, Lekander M, Kecklund G, et al. Cues of fatigue: effects of sleep deprivation on facial appearance. Sleep. 2013;36:1355-1360.
- Sundelin T, Lekander M, Sorjonen K, et a. Negative effects of restricted sleep on facial appearance and social appeal. R Soc Open Sci. 2017;4:160918.
- Holding BC, Sundelin T, Cairns P, et al. The effect of sleep deprivation on objective and subjective measures of facial appearance. J Sleep Res. 2019;28:E12860.
- Léger D, Gauriau C, Etzi C, et al. “You look sleepy…” the impact of sleep restriction on skin parameters and facial appearance of 24 women. Sleep Med. 2022;89:97-103.
- Talamas SN, Mavor KI, Perrett DI. Blinded by beauty: attractiveness bias and accurate perceptions of academic performance. PLoS One. 2016;11:E0148284.
- Department of the Army. Enlisted Promotions and Reductions. Army Publishing Directorate website. Published May 16, 2019. Accessed February 17, 2023. https://armypubs.army.mil/epubs/DR_pubs/DR_a/pdf/web/ARN17424_R600_8_19_Admin_FINAL.pdf
- Levy PD, Hile DC, Hile LM, et al. A prospective analysis of the treatment of friction blisters with 2-octylcyanoacrylate. J Am Podiatr Med Assoc. 2006;96:232-237.
- Brennan FH Jr, Jackson CR, Olsen C, et al. Blisters on the battlefield: the prevalence of and factors associated with foot friction blisters during Operation Iraqi Freedom I. Mil Med. 2012;177:157-162.
- Mostaghimi L, Obermeyer WH, Ballamudi B, et al. Effects of sleep deprivation on wound healing. J Sleep Res. 2005;14:213-219.
- Wilkison BD, Wong EB. Skin cancer in military pilots: a special population with special risk factors. Cutis. 2017;100:218-220.
- IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Painting, Firefighting, and Shiftwork. World Health Organization International Agency for Research on Cancer; 2010. Accessed February 20, 2023. https://www.ncbi.nlm.nih.gov/books/NBK326814/
- Oyetakin-White P, Suggs A, Koo B, et al. Does poor sleep quality affect skin ageing? Clin Exp Dermatol. 2015;40:17-22.
- Gaddameedhi S, Selby CP, Kaufmann WK, et al. Control of skin cancer by the circadian rhythm. Proc Natl Acad Sci USA. 2011;108:18790-18795.
- Heckman CJ, Kloss JD, Feskanich D, et al. Associations among rotating night shift work, sleep and skin cancer in Nurses’ Health Study II participants. Occup Environ Med. 2017;74:169-175.
Sleep deprivation can increase emotional distress and mood disorders; reduce quality of life; and lead to cognitive, memory, and performance deficits.1 Military service predisposes members to disordered sleep due to the rigors of deployments and field training, such as long shifts, shift changes, stressful work environments, and time zone changes. Evidence shows that sleep deprivation is associated with cardiovascular disease, gastrointestinal disease, and some cancers.2 We explore multiple mechanisms by which sleep deprivation may affect the skin. We also review the potential impacts of sleep deprivation on specific topics in dermatology, including atopic dermatitis (AD), psoriasis, alopecia areata, physical attractiveness, wound healing, and skin cancer.
Sleep and Military Service
Approximately 35.2% of Americans experience short sleep duration, which the Centers for Disease Control and Prevention defines as sleeping fewer than 7 hours per 24-hour period.3 Short sleep duration is even more common among individuals working in protective services and the military (50.4%).4 United States military service members experience multiple contributors to disordered sleep, including combat operations, shift work, psychiatric disorders such as posttraumatic stress disorder, and traumatic brain injury.5 Bramoweth and Germain6 described the case of a 27-year-old man who served 2 combat tours as an infantryman in Afghanistan, during which time he routinely remained awake for more than 24 hours at a time due to night missions and extended operations. Even when he was not directly involved in combat operations, he was rarely able to keep a regular sleep schedule.6 Service members returning from deployment also report decreased sleep. In one study (N=2717), 43% of respondents reported short sleep duration (<7 hours of sleep per night) and 29% reported very short sleep duration (<6 hours of sleep per night).7 Even stateside, service members experience acute sleep deprivation during training.8
Sleep and Skin
The idea that skin conditions can affect quality of sleep is not controversial. Pruritus, pain, and emotional distress associated with different dermatologic conditions have all been implicated in adversely affecting sleep.9 Given the effects of sleep deprivation on other organ systems, it also can affect the skin. Possible mechanisms of action include negative effects of sleep deprivation on the hypothalamic-pituitary-adrenal (HPA) axis, cutaneous barrier function, and immune function. First, the HPA axis activity follows a circadian rhythm.10 Activation outside of the bounds of this normal rhythm can have adverse effects on sleep. Alternatively, sleep deprivation and decreased sleep quality can negatively affect the HPA axis.10 These changes can adversely affect cutaneous barrier and immune function.11 Cutaneous barrier function is vitally important in the context of inflammatory dermatologic conditions. Transepidermal water loss, a measurement used to estimate cutaneous barrier function, is increased by sleep deprivation.12 Finally, the cutaneous immune system is an important component of inflammatory dermatologic conditions, cancer immune surveillance, and wound healing, and it also is negatively impacted by sleep deprivation.13 This framework of sleep deprivation affecting the HPA axis, cutaneous barrier function, and cutaneous immune function will help to guide the following discussion on the effects of decreased sleep on specific dermatologic conditions.
Atopic Dermatitis—Individuals with AD are at higher odds of having insomnia, fatigue, and overall poorer health status, including more sick days and increased visits to a physician.14 Additionally, it is possible that the relationship between AD and sleep is not unidirectional. Chang and Chiang15 discussed the possibility of sleep disturbances contributing to AD flares and listed 3 possible mechanisms by which sleep disturbance could potentially flare AD: exacerbation of the itch-scratch cycle; changes in the immune system, including a possible shift to helper T cell (TH2) dominance; and worsening of chronic stress in patients with AD. These changes may lead to a vicious cycle of impaired sleep and AD exacerbations. It may be helpful to view sleep impairment and AD as comorbid conditions requiring co-management for optimal outcomes. This perspective has military relevance because even without considering sleep deprivation, deployment and field conditions are known to increase the risk for AD flares.16
Psoriasis—Psoriasis also may have a bidirectional relationship with sleep. A study utilizing data from the Nurses’ Health Study showed that working a night shift increased the risk for psoriasis.17 Importantly, this connection is associative and not causative. It is possible that other factors in those who worked night shifts such as probable decreased UV exposure or reported increased body mass index played a role. Studies using psoriasis mice models have shown increased inflammation with sleep deprivation.18 Another possible connection is the effect of sleep deprivation on the gut microbiome. Sleep dysfunction is associated with altered gut bacteria ratios, and similar gut bacteria ratios were found in patients with psoriasis, which may indicate an association between sleep deprivation and psoriasis disease progression.19 There also is an increased association of obstructive sleep apnea in patients with psoriasis compared to the general population.20 Fortunately, the rate of consultations for psoriasis in deployed soldiers in the last several conflicts has been quite low, making up only 2.1% of diagnosed dermatologic conditions,21 which is because service members with moderate to severe psoriasis likely will not be deployed.
Alopecia Areata—Alopecia areata also may be associated with sleep deprivation. A large retrospective cohort study looking at the risk for alopecia in patients with sleep disorders showed that a sleep disorder was an independent risk factor for alopecia areata.22 The impact of sleep on the HPA axis portrays a possible mechanism for the negative effects of sleep deprivation on the immune system. Interestingly, in this study, the association was strongest for the 0- to 24-year-old age group. According to the 2020 demographics profile of the military community, 45% of active-duty personnel are 25 years or younger.23 Fortunately, although alopecia areata can be a distressing condition, it should not have much effect on military readiness, as most individuals with this diagnosis are still deployable.
Physical Appearance—
Wound Healing—Wound healing is of particular importance to the health of military members. Research is suggestive but not definitive of the relationship between sleep and wound healing. One intriguing study looked at the healing of blisters induced via suction in well-rested and sleep-deprived individuals. The results showed a difference, with the sleep-deprived individuals taking approximately 1 day longer to heal.13 This has some specific relevance to the military, as friction blisters can be common.30 A cross-sectional survey looking at a group of service members deployed in Iraq showed a prevalence of foot friction blisters of 33%, with 11% of individuals requiring medical care.31 Although this is an interesting example, it is not necessarily applicable to full-thickness wounds. A study utilizing rat models did not identify any differences between sleep-deprived and well-rested models in the healing of punch biopsy sites.32
Skin Cancer—Altered circadian rhythms resulting in changes in melatonin levels, changes in circadian rhythm–related gene pathways, and immunologic changes have been proposed as possible contributing mechanisms for the observed increased risk for skin cancers in military and civilian pilots.33,34 One study showed that UV-related erythema resolved quicker in well-rested individuals compared with those with short sleep duration, which could represent more efficient DNA repair given the relationship between UV-associated erythema and DNA damage and repair.35 Another study looking at circadian changes in the repair of UV-related DNA damage showed that mice exposed to UV radiation in the early morning had higher rates of squamous cell carcinoma than those exposed in the afternoon.36 However, a large cohort study using data from the Nurses’ Health Study II did not support a positive connection between short sleep duration and skin cancer; rather, it showed that a short sleep duration was associated with a decreased risk for melanoma and basal cell carcinoma, with no effect noted for squamous cell carcinoma.37 This does not support a positive association between short sleep duration and skin cancer and in some cases actually suggests a negative association.
Final Thoughts
Although more research is needed, there is evidence that sleep deprivation can negatively affect the skin. Randomized controlled trials looking at groups of individuals with specific dermatologic conditions with a very short sleep duration group (<6 hours of sleep per night), short sleep duration group (<7 hours of sleep per night), and a well-rested group (>7 hours of sleep per night) could be very helpful in this endeavor. Possible mechanisms include the HPA axis, immune system, and skin barrier function that are associated with sleep deprivation. Specific dermatologic conditions that may be affected by sleep deprivation include AD, psoriasis, alopecia areata, physical appearance, wound healing, and skin cancer. The impact of sleep deprivation on dermatologic conditions is particularly relevant to the military, as service members are at an increased risk for short sleep duration. It is possible that improving sleep may lead to better disease control for many dermatologic conditions.
Sleep deprivation can increase emotional distress and mood disorders; reduce quality of life; and lead to cognitive, memory, and performance deficits.1 Military service predisposes members to disordered sleep due to the rigors of deployments and field training, such as long shifts, shift changes, stressful work environments, and time zone changes. Evidence shows that sleep deprivation is associated with cardiovascular disease, gastrointestinal disease, and some cancers.2 We explore multiple mechanisms by which sleep deprivation may affect the skin. We also review the potential impacts of sleep deprivation on specific topics in dermatology, including atopic dermatitis (AD), psoriasis, alopecia areata, physical attractiveness, wound healing, and skin cancer.
Sleep and Military Service
Approximately 35.2% of Americans experience short sleep duration, which the Centers for Disease Control and Prevention defines as sleeping fewer than 7 hours per 24-hour period.3 Short sleep duration is even more common among individuals working in protective services and the military (50.4%).4 United States military service members experience multiple contributors to disordered sleep, including combat operations, shift work, psychiatric disorders such as posttraumatic stress disorder, and traumatic brain injury.5 Bramoweth and Germain6 described the case of a 27-year-old man who served 2 combat tours as an infantryman in Afghanistan, during which time he routinely remained awake for more than 24 hours at a time due to night missions and extended operations. Even when he was not directly involved in combat operations, he was rarely able to keep a regular sleep schedule.6 Service members returning from deployment also report decreased sleep. In one study (N=2717), 43% of respondents reported short sleep duration (<7 hours of sleep per night) and 29% reported very short sleep duration (<6 hours of sleep per night).7 Even stateside, service members experience acute sleep deprivation during training.8
Sleep and Skin
The idea that skin conditions can affect quality of sleep is not controversial. Pruritus, pain, and emotional distress associated with different dermatologic conditions have all been implicated in adversely affecting sleep.9 Given the effects of sleep deprivation on other organ systems, it also can affect the skin. Possible mechanisms of action include negative effects of sleep deprivation on the hypothalamic-pituitary-adrenal (HPA) axis, cutaneous barrier function, and immune function. First, the HPA axis activity follows a circadian rhythm.10 Activation outside of the bounds of this normal rhythm can have adverse effects on sleep. Alternatively, sleep deprivation and decreased sleep quality can negatively affect the HPA axis.10 These changes can adversely affect cutaneous barrier and immune function.11 Cutaneous barrier function is vitally important in the context of inflammatory dermatologic conditions. Transepidermal water loss, a measurement used to estimate cutaneous barrier function, is increased by sleep deprivation.12 Finally, the cutaneous immune system is an important component of inflammatory dermatologic conditions, cancer immune surveillance, and wound healing, and it also is negatively impacted by sleep deprivation.13 This framework of sleep deprivation affecting the HPA axis, cutaneous barrier function, and cutaneous immune function will help to guide the following discussion on the effects of decreased sleep on specific dermatologic conditions.
Atopic Dermatitis—Individuals with AD are at higher odds of having insomnia, fatigue, and overall poorer health status, including more sick days and increased visits to a physician.14 Additionally, it is possible that the relationship between AD and sleep is not unidirectional. Chang and Chiang15 discussed the possibility of sleep disturbances contributing to AD flares and listed 3 possible mechanisms by which sleep disturbance could potentially flare AD: exacerbation of the itch-scratch cycle; changes in the immune system, including a possible shift to helper T cell (TH2) dominance; and worsening of chronic stress in patients with AD. These changes may lead to a vicious cycle of impaired sleep and AD exacerbations. It may be helpful to view sleep impairment and AD as comorbid conditions requiring co-management for optimal outcomes. This perspective has military relevance because even without considering sleep deprivation, deployment and field conditions are known to increase the risk for AD flares.16
Psoriasis—Psoriasis also may have a bidirectional relationship with sleep. A study utilizing data from the Nurses’ Health Study showed that working a night shift increased the risk for psoriasis.17 Importantly, this connection is associative and not causative. It is possible that other factors in those who worked night shifts such as probable decreased UV exposure or reported increased body mass index played a role. Studies using psoriasis mice models have shown increased inflammation with sleep deprivation.18 Another possible connection is the effect of sleep deprivation on the gut microbiome. Sleep dysfunction is associated with altered gut bacteria ratios, and similar gut bacteria ratios were found in patients with psoriasis, which may indicate an association between sleep deprivation and psoriasis disease progression.19 There also is an increased association of obstructive sleep apnea in patients with psoriasis compared to the general population.20 Fortunately, the rate of consultations for psoriasis in deployed soldiers in the last several conflicts has been quite low, making up only 2.1% of diagnosed dermatologic conditions,21 which is because service members with moderate to severe psoriasis likely will not be deployed.
Alopecia Areata—Alopecia areata also may be associated with sleep deprivation. A large retrospective cohort study looking at the risk for alopecia in patients with sleep disorders showed that a sleep disorder was an independent risk factor for alopecia areata.22 The impact of sleep on the HPA axis portrays a possible mechanism for the negative effects of sleep deprivation on the immune system. Interestingly, in this study, the association was strongest for the 0- to 24-year-old age group. According to the 2020 demographics profile of the military community, 45% of active-duty personnel are 25 years or younger.23 Fortunately, although alopecia areata can be a distressing condition, it should not have much effect on military readiness, as most individuals with this diagnosis are still deployable.
Physical Appearance—
Wound Healing—Wound healing is of particular importance to the health of military members. Research is suggestive but not definitive of the relationship between sleep and wound healing. One intriguing study looked at the healing of blisters induced via suction in well-rested and sleep-deprived individuals. The results showed a difference, with the sleep-deprived individuals taking approximately 1 day longer to heal.13 This has some specific relevance to the military, as friction blisters can be common.30 A cross-sectional survey looking at a group of service members deployed in Iraq showed a prevalence of foot friction blisters of 33%, with 11% of individuals requiring medical care.31 Although this is an interesting example, it is not necessarily applicable to full-thickness wounds. A study utilizing rat models did not identify any differences between sleep-deprived and well-rested models in the healing of punch biopsy sites.32
Skin Cancer—Altered circadian rhythms resulting in changes in melatonin levels, changes in circadian rhythm–related gene pathways, and immunologic changes have been proposed as possible contributing mechanisms for the observed increased risk for skin cancers in military and civilian pilots.33,34 One study showed that UV-related erythema resolved quicker in well-rested individuals compared with those with short sleep duration, which could represent more efficient DNA repair given the relationship between UV-associated erythema and DNA damage and repair.35 Another study looking at circadian changes in the repair of UV-related DNA damage showed that mice exposed to UV radiation in the early morning had higher rates of squamous cell carcinoma than those exposed in the afternoon.36 However, a large cohort study using data from the Nurses’ Health Study II did not support a positive connection between short sleep duration and skin cancer; rather, it showed that a short sleep duration was associated with a decreased risk for melanoma and basal cell carcinoma, with no effect noted for squamous cell carcinoma.37 This does not support a positive association between short sleep duration and skin cancer and in some cases actually suggests a negative association.
Final Thoughts
Although more research is needed, there is evidence that sleep deprivation can negatively affect the skin. Randomized controlled trials looking at groups of individuals with specific dermatologic conditions with a very short sleep duration group (<6 hours of sleep per night), short sleep duration group (<7 hours of sleep per night), and a well-rested group (>7 hours of sleep per night) could be very helpful in this endeavor. Possible mechanisms include the HPA axis, immune system, and skin barrier function that are associated with sleep deprivation. Specific dermatologic conditions that may be affected by sleep deprivation include AD, psoriasis, alopecia areata, physical appearance, wound healing, and skin cancer. The impact of sleep deprivation on dermatologic conditions is particularly relevant to the military, as service members are at an increased risk for short sleep duration. It is possible that improving sleep may lead to better disease control for many dermatologic conditions.
- Carskadon M, Dement WC. Cumulative effects of sleep restriction on daytime sleepiness. Psychophysiology. 1981;18:107-113.
- Medic G, Wille M, Hemels ME. Short- and long-term health consequences of sleep disruption. Nat Sci Sleep. 2017;19;9:151-161.
- Sleep and sleep disorders. Centers for Disease Control and Prevention website. Reviewed September 12, 2022. Accessed February 17, 2023. https://www.cdc.gov/sleep/data_statistics.html
- Khubchandani J, Price JH. Short sleep duration in working American adults, 2010-2018. J Community Health. 2020;45:219-227.
- Good CH, Brager AJ, Capaldi VF, et al. Sleep in the United States military. Neuropsychopharmacology. 2020;45:176-191.
- Bramoweth AD, Germain A. Deployment-related insomnia in military personnel and veterans. Curr Psychiatry Rep. 2013;15:401.
- Luxton DD, Greenburg D, Ryan J, et al. Prevalence and impact of short sleep duration in redeployed OIF soldiers. Sleep. 2011;34:1189-1195.
- Crowley SK, Wilkinson LL, Burroughs EL, et al. Sleep during basic combat training: a qualitative study. Mil Med. 2012;177:823-828.
- Spindler M, Przybyłowicz K, Hawro M, et al. Sleep disturbance in adult dermatologic patients: a cross-sectional study on prevalence, burden, and associated factors. J Am Acad Dermatol. 2021;85:910-922.
- Guyon A, Balbo M, Morselli LL, et al. Adverse effects of two nights of sleep restriction on the hypothalamic-pituitary-adrenal axis in healthy men. J Clin Endocrinol Metab. 2014;99:2861-2868.
- Lin TK, Zhong L, Santiago JL. Association between stress and the HPA axis in the atopic dermatitis. Int J Mol Sci. 2017;18:2131.
- Pinnagoda J, Tupker RA, Agner T, et al. Guidelines for transepidermal water loss (TEWL) measurement. a report from theStandardization Group of the European Society of Contact Dermatitis. Contact Dermatitis. 1990;22:164-178.
- Smith TJ, Wilson MA, Karl JP, et al. Impact of sleep restriction on local immune response and skin barrier restoration with and without “multinutrient” nutrition intervention. J Appl Physiol (1985). 2018;124:190-200.
- Silverberg JI, Garg NK, Paller AS, et al. Sleep disturbances in adults with eczema are associated with impaired overall health: a US population-based study. J Invest Dermatol. 2015;135:56-66.
- Chang YS, Chiang BL. Sleep disorders and atopic dermatitis: a 2-way street? J Allergy Clin Immunol. 2018;142:1033-1040.
- Riegleman KL, Farnsworth GS, Wong EB. Atopic dermatitis in the US military. Cutis. 2019;104:144-147.
- Li WQ, Qureshi AA, Schernhammer ES, et al. Rotating night-shift work and risk of psoriasis in US women. J Invest Dermatol. 2013;133:565-567.
- Hirotsu C, Rydlewski M, Araújo MS, et al. Sleep loss and cytokines levels in an experimental model of psoriasis. PLoS One. 2012;7:E51183.
- Myers B, Vidhatha R, Nicholas B, et al. Sleep and the gut microbiome in psoriasis: clinical implications for disease progression and the development of cardiometabolic comorbidities. J Psoriasis Psoriatic Arthritis. 2021;6:27-37.
- Gupta MA, Simpson FC, Gupta AK. Psoriasis and sleep disorders: a systematic review. Sleep Med Rev. 2016;29:63-75.
- Gelman AB, Norton SA, Valdes-Rodriguez R, et al. A review of skin conditions in modern warfare and peacekeeping operations. Mil Med. 2015;180:32-37.
- Seo HM, Kim TL, Kim JS. The risk of alopecia areata and other related autoimmune diseases in patients with sleep disorders: a Korean population-based retrospective cohort study. Sleep. 2018;41:10.1093/sleep/zsy111.
- Department of Defense. 2020 Demographics: Profile of the Military Community. Military One Source website. Accessed February 17, 2023. https://download.militaryonesource.mil/12038/MOS/Reports/2020-demographics-report.pdf
- Sundelin T, Lekander M, Kecklund G, et al. Cues of fatigue: effects of sleep deprivation on facial appearance. Sleep. 2013;36:1355-1360.
- Sundelin T, Lekander M, Sorjonen K, et a. Negative effects of restricted sleep on facial appearance and social appeal. R Soc Open Sci. 2017;4:160918.
- Holding BC, Sundelin T, Cairns P, et al. The effect of sleep deprivation on objective and subjective measures of facial appearance. J Sleep Res. 2019;28:E12860.
- Léger D, Gauriau C, Etzi C, et al. “You look sleepy…” the impact of sleep restriction on skin parameters and facial appearance of 24 women. Sleep Med. 2022;89:97-103.
- Talamas SN, Mavor KI, Perrett DI. Blinded by beauty: attractiveness bias and accurate perceptions of academic performance. PLoS One. 2016;11:E0148284.
- Department of the Army. Enlisted Promotions and Reductions. Army Publishing Directorate website. Published May 16, 2019. Accessed February 17, 2023. https://armypubs.army.mil/epubs/DR_pubs/DR_a/pdf/web/ARN17424_R600_8_19_Admin_FINAL.pdf
- Levy PD, Hile DC, Hile LM, et al. A prospective analysis of the treatment of friction blisters with 2-octylcyanoacrylate. J Am Podiatr Med Assoc. 2006;96:232-237.
- Brennan FH Jr, Jackson CR, Olsen C, et al. Blisters on the battlefield: the prevalence of and factors associated with foot friction blisters during Operation Iraqi Freedom I. Mil Med. 2012;177:157-162.
- Mostaghimi L, Obermeyer WH, Ballamudi B, et al. Effects of sleep deprivation on wound healing. J Sleep Res. 2005;14:213-219.
- Wilkison BD, Wong EB. Skin cancer in military pilots: a special population with special risk factors. Cutis. 2017;100:218-220.
- IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Painting, Firefighting, and Shiftwork. World Health Organization International Agency for Research on Cancer; 2010. Accessed February 20, 2023. https://www.ncbi.nlm.nih.gov/books/NBK326814/
- Oyetakin-White P, Suggs A, Koo B, et al. Does poor sleep quality affect skin ageing? Clin Exp Dermatol. 2015;40:17-22.
- Gaddameedhi S, Selby CP, Kaufmann WK, et al. Control of skin cancer by the circadian rhythm. Proc Natl Acad Sci USA. 2011;108:18790-18795.
- Heckman CJ, Kloss JD, Feskanich D, et al. Associations among rotating night shift work, sleep and skin cancer in Nurses’ Health Study II participants. Occup Environ Med. 2017;74:169-175.
- Carskadon M, Dement WC. Cumulative effects of sleep restriction on daytime sleepiness. Psychophysiology. 1981;18:107-113.
- Medic G, Wille M, Hemels ME. Short- and long-term health consequences of sleep disruption. Nat Sci Sleep. 2017;19;9:151-161.
- Sleep and sleep disorders. Centers for Disease Control and Prevention website. Reviewed September 12, 2022. Accessed February 17, 2023. https://www.cdc.gov/sleep/data_statistics.html
- Khubchandani J, Price JH. Short sleep duration in working American adults, 2010-2018. J Community Health. 2020;45:219-227.
- Good CH, Brager AJ, Capaldi VF, et al. Sleep in the United States military. Neuropsychopharmacology. 2020;45:176-191.
- Bramoweth AD, Germain A. Deployment-related insomnia in military personnel and veterans. Curr Psychiatry Rep. 2013;15:401.
- Luxton DD, Greenburg D, Ryan J, et al. Prevalence and impact of short sleep duration in redeployed OIF soldiers. Sleep. 2011;34:1189-1195.
- Crowley SK, Wilkinson LL, Burroughs EL, et al. Sleep during basic combat training: a qualitative study. Mil Med. 2012;177:823-828.
- Spindler M, Przybyłowicz K, Hawro M, et al. Sleep disturbance in adult dermatologic patients: a cross-sectional study on prevalence, burden, and associated factors. J Am Acad Dermatol. 2021;85:910-922.
- Guyon A, Balbo M, Morselli LL, et al. Adverse effects of two nights of sleep restriction on the hypothalamic-pituitary-adrenal axis in healthy men. J Clin Endocrinol Metab. 2014;99:2861-2868.
- Lin TK, Zhong L, Santiago JL. Association between stress and the HPA axis in the atopic dermatitis. Int J Mol Sci. 2017;18:2131.
- Pinnagoda J, Tupker RA, Agner T, et al. Guidelines for transepidermal water loss (TEWL) measurement. a report from theStandardization Group of the European Society of Contact Dermatitis. Contact Dermatitis. 1990;22:164-178.
- Smith TJ, Wilson MA, Karl JP, et al. Impact of sleep restriction on local immune response and skin barrier restoration with and without “multinutrient” nutrition intervention. J Appl Physiol (1985). 2018;124:190-200.
- Silverberg JI, Garg NK, Paller AS, et al. Sleep disturbances in adults with eczema are associated with impaired overall health: a US population-based study. J Invest Dermatol. 2015;135:56-66.
- Chang YS, Chiang BL. Sleep disorders and atopic dermatitis: a 2-way street? J Allergy Clin Immunol. 2018;142:1033-1040.
- Riegleman KL, Farnsworth GS, Wong EB. Atopic dermatitis in the US military. Cutis. 2019;104:144-147.
- Li WQ, Qureshi AA, Schernhammer ES, et al. Rotating night-shift work and risk of psoriasis in US women. J Invest Dermatol. 2013;133:565-567.
- Hirotsu C, Rydlewski M, Araújo MS, et al. Sleep loss and cytokines levels in an experimental model of psoriasis. PLoS One. 2012;7:E51183.
- Myers B, Vidhatha R, Nicholas B, et al. Sleep and the gut microbiome in psoriasis: clinical implications for disease progression and the development of cardiometabolic comorbidities. J Psoriasis Psoriatic Arthritis. 2021;6:27-37.
- Gupta MA, Simpson FC, Gupta AK. Psoriasis and sleep disorders: a systematic review. Sleep Med Rev. 2016;29:63-75.
- Gelman AB, Norton SA, Valdes-Rodriguez R, et al. A review of skin conditions in modern warfare and peacekeeping operations. Mil Med. 2015;180:32-37.
- Seo HM, Kim TL, Kim JS. The risk of alopecia areata and other related autoimmune diseases in patients with sleep disorders: a Korean population-based retrospective cohort study. Sleep. 2018;41:10.1093/sleep/zsy111.
- Department of Defense. 2020 Demographics: Profile of the Military Community. Military One Source website. Accessed February 17, 2023. https://download.militaryonesource.mil/12038/MOS/Reports/2020-demographics-report.pdf
- Sundelin T, Lekander M, Kecklund G, et al. Cues of fatigue: effects of sleep deprivation on facial appearance. Sleep. 2013;36:1355-1360.
- Sundelin T, Lekander M, Sorjonen K, et a. Negative effects of restricted sleep on facial appearance and social appeal. R Soc Open Sci. 2017;4:160918.
- Holding BC, Sundelin T, Cairns P, et al. The effect of sleep deprivation on objective and subjective measures of facial appearance. J Sleep Res. 2019;28:E12860.
- Léger D, Gauriau C, Etzi C, et al. “You look sleepy…” the impact of sleep restriction on skin parameters and facial appearance of 24 women. Sleep Med. 2022;89:97-103.
- Talamas SN, Mavor KI, Perrett DI. Blinded by beauty: attractiveness bias and accurate perceptions of academic performance. PLoS One. 2016;11:E0148284.
- Department of the Army. Enlisted Promotions and Reductions. Army Publishing Directorate website. Published May 16, 2019. Accessed February 17, 2023. https://armypubs.army.mil/epubs/DR_pubs/DR_a/pdf/web/ARN17424_R600_8_19_Admin_FINAL.pdf
- Levy PD, Hile DC, Hile LM, et al. A prospective analysis of the treatment of friction blisters with 2-octylcyanoacrylate. J Am Podiatr Med Assoc. 2006;96:232-237.
- Brennan FH Jr, Jackson CR, Olsen C, et al. Blisters on the battlefield: the prevalence of and factors associated with foot friction blisters during Operation Iraqi Freedom I. Mil Med. 2012;177:157-162.
- Mostaghimi L, Obermeyer WH, Ballamudi B, et al. Effects of sleep deprivation on wound healing. J Sleep Res. 2005;14:213-219.
- Wilkison BD, Wong EB. Skin cancer in military pilots: a special population with special risk factors. Cutis. 2017;100:218-220.
- IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Painting, Firefighting, and Shiftwork. World Health Organization International Agency for Research on Cancer; 2010. Accessed February 20, 2023. https://www.ncbi.nlm.nih.gov/books/NBK326814/
- Oyetakin-White P, Suggs A, Koo B, et al. Does poor sleep quality affect skin ageing? Clin Exp Dermatol. 2015;40:17-22.
- Gaddameedhi S, Selby CP, Kaufmann WK, et al. Control of skin cancer by the circadian rhythm. Proc Natl Acad Sci USA. 2011;108:18790-18795.
- Heckman CJ, Kloss JD, Feskanich D, et al. Associations among rotating night shift work, sleep and skin cancer in Nurses’ Health Study II participants. Occup Environ Med. 2017;74:169-175.
Practice Points
- Sleep deprivation may have negative effects on skin function and worsen dermatologic conditions.
- Proposed mechanisms of action for these negative effects include dysregulation of the hypothalamic-pituitary-adrenal axis, impairment of cutaneous barrier function, and alteration of cutaneous immune function.
- Members of the US Military are at an increased risk for sleep deprivation, especially during training and overseas deployments.
Severe Esophageal Lichen Planus Treated With Tofacitinib
To reach early diagnoses and improve outcomes in cases of mucosal and esophageal lichen planus (ELP), patient education along with a multidisciplinary approach centered on collaboration among dermatologists, gastroenterologists, gynecologists, and dental practitioners should be a priority. Tofacitinib therapy should be considered in the treatment of patients presenting with cutaneous lichen planus (CLP), mucosal lichen planus, and ELP.
Lichen planus is a papulosquamous disease of the skin and mucous membranes that is most common on the skin and oral mucosa. Typical lesions of CLP present as purple, pruritic, polygonal papules and plaques on the flexural surfaces of the wrists and ankles as well as areas of friction or trauma due to scratching such as the shins and lower back. Various subtypes of lichen planus can present simultaneously, resulting in extensive involvement that worsens through koebnerization and affects the oral cavity, esophagus, larynx, sclera, genitalia, scalp, and nails.1,2
Esophageal lichen planus can develop with or without the presence of CLP, oral lichen planus (OLP), or genital lichen planus.3 It typically affects women older than 50 years and is linked to OLP and vulvar lichen planus, with 1 study reporting that 87% (63/72) of ELP patients were women with a median age of 61.9 years at the time of diagnosis (range, 22–85 years). Almost all ELP patients in the study had lichen planus symptoms in other locations; 89% (64/72) had OLP, and 42% (30/72) had vulvar lichen planus.4 Consequently, a diagnosis of ELP should be followed by a thorough full-body examination to check for lichen planus at other sites. Studies that examined lichen planus patients for ELP found that 25% to 50% of patients diagnosed with orocutaneous lichen planus also had ELP, with ELP frequently presenting without symptoms.3,5 These findings indicate that ELP likely is underdiagnosed and often misdiagnosed, resulting in an underestimation of its prevalence.
Our case highlights a frequently misdiagnosed condition and underscores the importance of close examination of patients presenting with CLP and OLP for signs and symptoms of ELP. Furthermore, we discuss the importance of patient education and collaboration among different specialties in attaining an early diagnosis to improve patient outcomes. Finally, we review the clinical presentation, diagnosis, and treatment of CLP, OLP, and ELP, as well as the utility of tofacitinib for ELP.
Case Report
An emaciated 89-year-old woman with an 11-year history of CLP, OLP, and genital lichen planus that had been successfully treated with topicals presented with an OLP recurrence alongside difficulties eating and swallowing. Her symptoms lasted 1 year and would recur when treatment was paused. Her medical history included rheumatoid arthritis, hypothyroidism, and hypertension, and she was taking levothyroxine, olmesartan, and vitamin D supplements. Dentures and olmesartan previously were ruled out as potential triggers following a 2-month elimination. None of her remaining natural teeth had fillings. She also reported that neither she nor her partner had ever smoked or chewed tobacco.
The patient’s lichen planus involvement first manifested as red, itchy, polygonal, lichenoid papules on the superior and inferior mid back 11 years prior to the current presentation (Figure 1). Further examination noted erosions on the genitalia, and a subsequent biopsy of the vulva confirmed a diagnosis of lichen planus (Figure 2). Treatment with halobetasol propionate ointment and tacrolimus ointment 0.1% twice daily (BID) resulted in remission of the CLP and vulvar lichen planus. She presented a year later with oral involvement revealing Wickham striae on the buccal mucosa and erosions on the upper palate that resolved after 2 months of treatment with cyclosporine oral solution mixed with a 5-times-daily nystatin swish-and-spit (Figure 3). The CLP did not recur but OLP was punctuated by remissions and recurrences on a yearly basis, often related to the cessation of mouthwash and topical creams. The OLP and vulvar lichen planus were successfully treated with as-needed use of a cyclosporine mouthwash swish-and-spit 3 times daily as well as halobetasol ointment 0.05% 3 times daily, respectively. Six years later, the patient was hospitalized for unrelated causes and was lost to follow-up for 2 years.
The patient experienced worsening dysphagia and odynophagia over a period of 2 years (mild dysphagia was first recorded 7 years prior to the initial presentation) and reported an unintentional weight loss of 20 pounds. An endoscopy was performed 3 years after the initial report of dysphagia and noted esophageal erosions (Figure 4A) and a stricture (Figure 4B), but all abnormal involvement was attributed to active gastroesophageal reflux disease. She underwent 8 esophageal dilations to treat the stricture but noted that the duration of symptomatic relief decreased with every subsequent dilation. An esophageal stent was placed 4 years after the initial concern of dysphagia, but it was not well tolerated and had to be removed soon thereafter. A year later, the patient underwent an esophageal bypass with a substernal gastric conduit that provided relief for 2 months but failed to permanently resolve the condition. In fact, her condition worsened over the next 1.5 years when she presented with extreme emaciation attributed to a low appetite and pain while eating. A review of the slides from a prior hospital esophageal biopsy revealed lichen planus (Figure 5). She was prescribed tofacitinib 5 mg BID as a dual-purpose treatment for the rheumatoid arthritis and OLP/ELP. At 1-month follow-up she noted that she had only taken one 5-mg pill daily without notable improvement, and after the visit she started the initial recommendation of 5 mg BID. Over the next several months, her condition continued to consistently improve; the odynophagia resolved, and she regained the majority of her lost weight. Tofacitinib was well tolerated across the course of treatment, and no adverse side effects were noted. Furthermore, the patient regained a full range of motion in the previously immobile arthritic right shoulder. She has experienced no recurrence of the genital lichen planus, OLP, or CLP since starting tofacitinib. To date, the patient is still taking only tofacitinib 5 mg BID with no recurrence of the cutaneous, mucosal, or esophageal lichen planus and has experienced no adverse events from the medication.
Comment
Clinical Presentation—Lichen planus—CLP and OLP—most frequently presents between the ages of 40 and 60 years, with a slight female predilection.1,2 The lesions typically present with the 5 P’s—purple, pruritic, polygonal papules and plaques—with some lesions revealing white lacy lines overlying them called Wickham striae.6 The lesions may be red at first before turning purple. They often present on the flexural surfaces of the wrists and ankles as well as the shins and back but rarely affect the face, perhaps because of increased chronic sun exposure.2,6 Less common locations include the scalp, nails, and mucosal areas (eg, oral, vulvar, conjunctival, laryngeal, esophageal, anal).1
If CLP is diagnosed, the patient likely will also have oral lesions, which occur in 50% of patients.2 Once any form of lichen planus is found, it is important to examine all of the most frequently involved locations—mucocutaneous and cutaneous as well as the nails and scalp. Special care should be taken when examining OLP and genital lichen planus, as long-standing lesions have a 2% to 5% chance of transforming into squamous cell carcinoma.2
Although cases of traditional OLP and CLP are ubiquitous in the literature, ELP rarely is documented because of frequent misdiagnoses. Esophageal lichen planus has a closer histopathologic resemblance to OLP compared to CLP, and its highly variable presentation often results in an inconclusive diagnosis.3 A review of 27 patients with lichen planus highlighted the difficult nature of diagnosing ELP; ELP manifested up to 20 years after initial lichen planus diagnosis, and patients underwent an average of 2.5 dilations prior to the successful diagnosis of ELP. Interestingly, 2 patients in the study presented with ELP in isolation, which emphasizes the importance of secondary examination for lichen planus in the presence of esophageal strictures.7 The eTable provides common patient demographics and symptoms to more effectively identify ELP.Differential Diagnosis—Because lichen planus can present anywhere on the body, it may be difficult to differentiate it from other skin conditions. Clinical appearance alone often is insufficient for diagnosing lichen planus, and a punch biopsy often is needed.2,20 Cutaneous lichen planus may resemble eczema, lichen simplex chronicus, pityriasis rosea, prurigo nodularis, and psoriasis, while OLP may resemble bite trauma, leukoplakia, pemphigus, and thrush.20 Dermoscopy of the tissue makes Wickham striae easier to visualize and assists in the diagnosis of lichen planus. Furthermore, thickening of the stratum granulosum, a prevalence of lymphocytes in the dermoepidermal junction, and vacuolar alteration of the stratum basale help to distinguish between lichen planus and other inflammatory dermatoses.20 A diagnosis of lichen planus merits a full-body skin examination—hair, nails, eyes, oral mucosa, and genitalia—to rule out additional involvement.
Esophageal lichen planus most frequently presents as dysphagia, odynophagia, and weight loss, but other symptoms including heartburn, hoarseness, choking, and epigastric pain may suggest esophageal involvement.4 Typically, ELP presents in the proximal and/or central esophagus, assisting in the differentiation between ELP and other esophageal conditions.3 Special consideration should be taken when both ELP and gastroesophageal reflux disease are considered in a differential diagnosis, and it is recommended to pair an upper endoscopy with pH monitoring to avoid misdiagnosis.8 Screening endoscopies also are helpful, as they assist in identifying the characteristic white webs, skin peeling, skin surface erosion, and strictures of ELP.4 Taken together, dermatologists should encourage patients with cutaneous or mucocutaneous lichen planus to undergo an esophagogastroduodenoscopy, especially in the presence of any of ELP’s common symptoms (eTable).
Etiology—Although the exact etiology of lichen planus is not well established, there are several known correlative factors, including hepatitis C; increased stress; dental materials; oral medications, most frequently antihypertensives and nonsteroidal anti-inflammatory drugs; systemic diseases; and tobacco usage.6,21
Dental materials used in oral treatments such as silver amalgam, gold, cobalt, palladium, chromium, epoxy resins, and dentures can trigger or exacerbate OLP, and patch testing of a patient’s dental materials can help determine if the reaction was caused by the materials.6,22 The removal of material contributing to lesions often will cause OLP to resolve.22
It also has been suggested that the presence of thyroid disorders, autoimmune disease, various cancers, hypertension, type 2 diabetes mellitus, hyperlipidemia, oral sedative usage, and/or vitamin D deficiency may be associated with OLP.21,23 Although OLP patients who were initially deficient in vitamin D demonstrated marked improvement with supplementation, it is unlikely that vitamin D supplements impacted our patient’s presentation of OLP, as she had been consistently taking them for more than 5 years with no change in OLP presentation.24
Pathogenesis—Lichen planus is thought to be a cytotoxic CD8+ T cell–mediated autoimmune disease to a virally modified epidermal self-antigen on keratinocytes. The cytotoxic T cells target the modified self-antigens on basal keratinocytes and induce apoptosis.25 The cytokine-mediated lymphocyte homing mechanism is human leukocyte antigen dependent and involves tumor necrosis factor α as well as IFN-γ and IL-1. The latter cytokines lead to upregulation of vascular adhesion molecules on endothelial vessels of subepithelial vascular plexus as well as a cascade of nonspecific mechanisms such as mast cell degranulation and matrix metalloproteinase activation, resulting in increased basement membrane disruption.6
Shao et al19 underscored the role of IFN-γ in CD8+ T cell–mediated cytotoxic cellular responses, noting that the Janus kinase (JAK)–signal transducer and activator of transcription pathway may play a key role in the pathogenesis of lichen planus. They proposed using JAK inhibitors for the treatment of lichen planus, specifically tofacitinib, a JAK1/JAK3 inhibitor, and baricitinib, a JAK1/JAK2 inhibitor, as top therapeutic agents for lichen planus (eTable).19 Tofacitinib has been reported to successfully treat conditions such as psoriasis, psoriatic arthritis, alopecia areata, vitiligo, atopic dermatitis, sarcoidosis, pyoderma gangrenosum, and lichen planopilaris.26 Additionally, the efficacy of tofacitinib has been established in patients with erosive lichen planus; tofacitinib resulted in marked improvement while prednisone, acitretin, methotrexate, mycophenolate mofetil, and cyclosporine treatment failed.27 Although more studies on tofacitinib’s long-term efficacy, cost, and safety are necessary, tofacitinib may soon play an integral role in the battle against inflammatory dermatoses.
Conclusion
Esophageal lichen planus is an underreported form of lichen planus that often is misdiagnosed. It frequently causes dysphagia and odynophagia, resulting in a major decrease in a patient’s quality of life. We present the case of an 89-year-old woman who underwent procedures to dilate her esophagus that worsened her condition. We emphasize the importance of considering ELP in the differential diagnosis of patients presenting with lichen planus in another region. In our patient, tofacitinib 5 mg BID resolved her condition without any adverse effects.
- Le Cleach L, Chosidow O. Lichen planus. N Engl J Med. 2012;366:723-732. doi:10.1056/nejmcp1103641
- Heath L, Matin R. Lichen planus. InnovAiT. 2017;10:133-138. doi:10.1177/1755738016686804
- Oliveira JP, Uribe NC, Abulafia LA, et al. Esophageal lichenplanus. An Bras Dermatol. 2015;90:394-396. doi:10.1590/abd1806-4841.20153255
- Fox LP, Lightdale CJ, Grossman ME. Lichen planus of the esophagus: what dermatologists need to know. J Am Acad Dermatol. 2011;65:175-183. doi:10.1016/j.jaad.2010.03.029
- Quispel R, van Boxel O, Schipper M, et al. High prevalence of esophageal involvement in lichen planus: a study using magnification chromoendoscopy. Endoscopy. 2009;41:187-193. doi:10.1055/s-0028-1119590
- Gupta S, Jawanda MK. Oral lichen planus: an update on etiology, pathogenesis, clinical presentation, diagnosis and management. Indian J Dermatol. 2015;60:222-229. doi:10.4103/0019-5154.156315
- Katzka DA, Smyrk TC, Bruce AJ, et al. Variations in presentations of esophageal involvement in lichen planus. Clin Gastroenterol Hepatol. 2010;8:777-782. doi:10.1016/j.cgh.2010.04.024
- Abraham SC, Ravich WJ, Anhalt GJ, et al. Esophageal lichen planus. Am J Surg Pathol. 2000;24:1678-1682. doi:10.1097/00000478-200012000-00014
- Murro D, Jakate S. Radiation esophagitis. Arch Pathol Lab Med. 2015;139:827-830. doi:10.5858/arpa.2014-0111-RS
- Wilcox CM. Infectious esophagitis. Gastroenterol Hepatol (N Y). 2006;2:567-568.
- Cancio A, Cruz C. A case of Kaposi’s sarcoma of the esophagus presenting with odynophagia. Am J Gastroenterol. 2018;113:S995-S996.
- Kokturk A. Clinical and pathological manifestations with differential diagnosis in Behçet’s disease. Patholog Res Int. 2012;2012:690390. doi:10.1155/2012/690390
- Madhusudhan KS, Sharma R. Esophageal lichen planus: a case report and review of literature. Indian J Dermatol. 2008;53:26-27. doi:10.4103/0019-5154.39738
- Bottomley WW, Dakkak M, Walton S, et al. Esophageal involvement in Behçet’s disease. is endoscopy necessary? Dig Dis Sci. 1992;37:594-597. doi:10.1007/BF01307585
- McDonald GB, Sullivan KM, Schuffler MD, et al. Esophageal abnormalities in chronic graft-versus-host disease in humans. Gastroenterology. 1981;80:914-921.
- Trabulo D, Ferreira S, Lage P, et al. Esophageal stenosis with sloughing esophagitis: a curious manifestation of graft-vs-host disease. World J Gastroenterol. 2015;21:9217-9222. doi:10.3748/wjg.v21.i30.9217
- Abbas H, Ghazanfar H, Ul Hussain AN, et al. Atypical presentation of esophageal squamous cell carcinoma masquerading as diffuse severe esophagitis. Case Rep Gastroenterol. 2021;15:533-538. doi:10.1159/000517129
- Ellis A, Risk JM, Maruthappu T, et al. Tylosis with oesophageal cancer: diagnosis, management and molecular mechanisms. Orphanet J Rare Dis. 2015;10:126. doi:10.1186/s13023-015-0346-2
- Shao S, Tsoi LC, Sarkar MK, et al. IFN-γ enhances cell-mediated cytotoxicity against keratinocytes via JAK2/STAT1 in lichen planus. Sci Transl Med. 2019;11:eaav7561. doi:10.1126/scitranslmed.aav7561
- Usatine RP, Tinitigan M. Diagnosis and treatment of lichen planus. Am Fam Physician. 2011;84:53-60.
- Dave A, Shariff J, Philipone E. Association between oral lichen planus and systemic conditions and medications: case-control study. Oral Dis. 2020;27:515-524. doi:10.1111/odi.13572
- Krupaa RJ, Sankari SL, Masthan KM, et al. Oral lichen planus: an overview. J Pharm Bioallied Sci. 2015;7(suppl 1):S158-S161. doi:10.4103/0975-7406.155873
- Tak MM, Chalkoo AH. Vitamin D deficiency—a possible contributing factor in the aetiopathogenesis of oral lichen planus. J Evolution Med Dent Sci. 2017;6:4769-4772. doi:10.14260/jemds/2017/1033
- Gupta J, Aggarwal A, Asadullah M, et al. Vitamin D in thetreatment of oral lichen planus: a pilot clinical study. J Indian Acad Oral Med Radiol. 2019;31:222-227. doi:10.4103/jiaomr.jiaomr_97_19
- Shiohara T, Moriya N, Mochizuki T, et al. Lichenoid tissue reaction (LTR) induced by local transfer of Ia-reactive T-cell clones. II. LTR by epidermal invasion of cytotoxic lymphokine-producing autoreactive T cells. J Invest Dermatol. 1987;89:8-14.
- Sonthalia S, Aggarwal P. Oral tofacitinib: contemporary appraisal of its role in dermatology. Indian Dermatol Online J. 2019;10:503-518. doi:10.4103/idoj.idoj_474_18
- Damsky W, Wang A, Olamiju B, et al. Treatment of severe lichen planus with the JAK inhibitor tofacitinib. J Allergy Clin Immunol. 2020;145:1708-1710.e2. doi:10.1016/j.jaci.2020.01.031
To reach early diagnoses and improve outcomes in cases of mucosal and esophageal lichen planus (ELP), patient education along with a multidisciplinary approach centered on collaboration among dermatologists, gastroenterologists, gynecologists, and dental practitioners should be a priority. Tofacitinib therapy should be considered in the treatment of patients presenting with cutaneous lichen planus (CLP), mucosal lichen planus, and ELP.
Lichen planus is a papulosquamous disease of the skin and mucous membranes that is most common on the skin and oral mucosa. Typical lesions of CLP present as purple, pruritic, polygonal papules and plaques on the flexural surfaces of the wrists and ankles as well as areas of friction or trauma due to scratching such as the shins and lower back. Various subtypes of lichen planus can present simultaneously, resulting in extensive involvement that worsens through koebnerization and affects the oral cavity, esophagus, larynx, sclera, genitalia, scalp, and nails.1,2
Esophageal lichen planus can develop with or without the presence of CLP, oral lichen planus (OLP), or genital lichen planus.3 It typically affects women older than 50 years and is linked to OLP and vulvar lichen planus, with 1 study reporting that 87% (63/72) of ELP patients were women with a median age of 61.9 years at the time of diagnosis (range, 22–85 years). Almost all ELP patients in the study had lichen planus symptoms in other locations; 89% (64/72) had OLP, and 42% (30/72) had vulvar lichen planus.4 Consequently, a diagnosis of ELP should be followed by a thorough full-body examination to check for lichen planus at other sites. Studies that examined lichen planus patients for ELP found that 25% to 50% of patients diagnosed with orocutaneous lichen planus also had ELP, with ELP frequently presenting without symptoms.3,5 These findings indicate that ELP likely is underdiagnosed and often misdiagnosed, resulting in an underestimation of its prevalence.
Our case highlights a frequently misdiagnosed condition and underscores the importance of close examination of patients presenting with CLP and OLP for signs and symptoms of ELP. Furthermore, we discuss the importance of patient education and collaboration among different specialties in attaining an early diagnosis to improve patient outcomes. Finally, we review the clinical presentation, diagnosis, and treatment of CLP, OLP, and ELP, as well as the utility of tofacitinib for ELP.
Case Report
An emaciated 89-year-old woman with an 11-year history of CLP, OLP, and genital lichen planus that had been successfully treated with topicals presented with an OLP recurrence alongside difficulties eating and swallowing. Her symptoms lasted 1 year and would recur when treatment was paused. Her medical history included rheumatoid arthritis, hypothyroidism, and hypertension, and she was taking levothyroxine, olmesartan, and vitamin D supplements. Dentures and olmesartan previously were ruled out as potential triggers following a 2-month elimination. None of her remaining natural teeth had fillings. She also reported that neither she nor her partner had ever smoked or chewed tobacco.
The patient’s lichen planus involvement first manifested as red, itchy, polygonal, lichenoid papules on the superior and inferior mid back 11 years prior to the current presentation (Figure 1). Further examination noted erosions on the genitalia, and a subsequent biopsy of the vulva confirmed a diagnosis of lichen planus (Figure 2). Treatment with halobetasol propionate ointment and tacrolimus ointment 0.1% twice daily (BID) resulted in remission of the CLP and vulvar lichen planus. She presented a year later with oral involvement revealing Wickham striae on the buccal mucosa and erosions on the upper palate that resolved after 2 months of treatment with cyclosporine oral solution mixed with a 5-times-daily nystatin swish-and-spit (Figure 3). The CLP did not recur but OLP was punctuated by remissions and recurrences on a yearly basis, often related to the cessation of mouthwash and topical creams. The OLP and vulvar lichen planus were successfully treated with as-needed use of a cyclosporine mouthwash swish-and-spit 3 times daily as well as halobetasol ointment 0.05% 3 times daily, respectively. Six years later, the patient was hospitalized for unrelated causes and was lost to follow-up for 2 years.
The patient experienced worsening dysphagia and odynophagia over a period of 2 years (mild dysphagia was first recorded 7 years prior to the initial presentation) and reported an unintentional weight loss of 20 pounds. An endoscopy was performed 3 years after the initial report of dysphagia and noted esophageal erosions (Figure 4A) and a stricture (Figure 4B), but all abnormal involvement was attributed to active gastroesophageal reflux disease. She underwent 8 esophageal dilations to treat the stricture but noted that the duration of symptomatic relief decreased with every subsequent dilation. An esophageal stent was placed 4 years after the initial concern of dysphagia, but it was not well tolerated and had to be removed soon thereafter. A year later, the patient underwent an esophageal bypass with a substernal gastric conduit that provided relief for 2 months but failed to permanently resolve the condition. In fact, her condition worsened over the next 1.5 years when she presented with extreme emaciation attributed to a low appetite and pain while eating. A review of the slides from a prior hospital esophageal biopsy revealed lichen planus (Figure 5). She was prescribed tofacitinib 5 mg BID as a dual-purpose treatment for the rheumatoid arthritis and OLP/ELP. At 1-month follow-up she noted that she had only taken one 5-mg pill daily without notable improvement, and after the visit she started the initial recommendation of 5 mg BID. Over the next several months, her condition continued to consistently improve; the odynophagia resolved, and she regained the majority of her lost weight. Tofacitinib was well tolerated across the course of treatment, and no adverse side effects were noted. Furthermore, the patient regained a full range of motion in the previously immobile arthritic right shoulder. She has experienced no recurrence of the genital lichen planus, OLP, or CLP since starting tofacitinib. To date, the patient is still taking only tofacitinib 5 mg BID with no recurrence of the cutaneous, mucosal, or esophageal lichen planus and has experienced no adverse events from the medication.
Comment
Clinical Presentation—Lichen planus—CLP and OLP—most frequently presents between the ages of 40 and 60 years, with a slight female predilection.1,2 The lesions typically present with the 5 P’s—purple, pruritic, polygonal papules and plaques—with some lesions revealing white lacy lines overlying them called Wickham striae.6 The lesions may be red at first before turning purple. They often present on the flexural surfaces of the wrists and ankles as well as the shins and back but rarely affect the face, perhaps because of increased chronic sun exposure.2,6 Less common locations include the scalp, nails, and mucosal areas (eg, oral, vulvar, conjunctival, laryngeal, esophageal, anal).1
If CLP is diagnosed, the patient likely will also have oral lesions, which occur in 50% of patients.2 Once any form of lichen planus is found, it is important to examine all of the most frequently involved locations—mucocutaneous and cutaneous as well as the nails and scalp. Special care should be taken when examining OLP and genital lichen planus, as long-standing lesions have a 2% to 5% chance of transforming into squamous cell carcinoma.2
Although cases of traditional OLP and CLP are ubiquitous in the literature, ELP rarely is documented because of frequent misdiagnoses. Esophageal lichen planus has a closer histopathologic resemblance to OLP compared to CLP, and its highly variable presentation often results in an inconclusive diagnosis.3 A review of 27 patients with lichen planus highlighted the difficult nature of diagnosing ELP; ELP manifested up to 20 years after initial lichen planus diagnosis, and patients underwent an average of 2.5 dilations prior to the successful diagnosis of ELP. Interestingly, 2 patients in the study presented with ELP in isolation, which emphasizes the importance of secondary examination for lichen planus in the presence of esophageal strictures.7 The eTable provides common patient demographics and symptoms to more effectively identify ELP.Differential Diagnosis—Because lichen planus can present anywhere on the body, it may be difficult to differentiate it from other skin conditions. Clinical appearance alone often is insufficient for diagnosing lichen planus, and a punch biopsy often is needed.2,20 Cutaneous lichen planus may resemble eczema, lichen simplex chronicus, pityriasis rosea, prurigo nodularis, and psoriasis, while OLP may resemble bite trauma, leukoplakia, pemphigus, and thrush.20 Dermoscopy of the tissue makes Wickham striae easier to visualize and assists in the diagnosis of lichen planus. Furthermore, thickening of the stratum granulosum, a prevalence of lymphocytes in the dermoepidermal junction, and vacuolar alteration of the stratum basale help to distinguish between lichen planus and other inflammatory dermatoses.20 A diagnosis of lichen planus merits a full-body skin examination—hair, nails, eyes, oral mucosa, and genitalia—to rule out additional involvement.
Esophageal lichen planus most frequently presents as dysphagia, odynophagia, and weight loss, but other symptoms including heartburn, hoarseness, choking, and epigastric pain may suggest esophageal involvement.4 Typically, ELP presents in the proximal and/or central esophagus, assisting in the differentiation between ELP and other esophageal conditions.3 Special consideration should be taken when both ELP and gastroesophageal reflux disease are considered in a differential diagnosis, and it is recommended to pair an upper endoscopy with pH monitoring to avoid misdiagnosis.8 Screening endoscopies also are helpful, as they assist in identifying the characteristic white webs, skin peeling, skin surface erosion, and strictures of ELP.4 Taken together, dermatologists should encourage patients with cutaneous or mucocutaneous lichen planus to undergo an esophagogastroduodenoscopy, especially in the presence of any of ELP’s common symptoms (eTable).
Etiology—Although the exact etiology of lichen planus is not well established, there are several known correlative factors, including hepatitis C; increased stress; dental materials; oral medications, most frequently antihypertensives and nonsteroidal anti-inflammatory drugs; systemic diseases; and tobacco usage.6,21
Dental materials used in oral treatments such as silver amalgam, gold, cobalt, palladium, chromium, epoxy resins, and dentures can trigger or exacerbate OLP, and patch testing of a patient’s dental materials can help determine if the reaction was caused by the materials.6,22 The removal of material contributing to lesions often will cause OLP to resolve.22
It also has been suggested that the presence of thyroid disorders, autoimmune disease, various cancers, hypertension, type 2 diabetes mellitus, hyperlipidemia, oral sedative usage, and/or vitamin D deficiency may be associated with OLP.21,23 Although OLP patients who were initially deficient in vitamin D demonstrated marked improvement with supplementation, it is unlikely that vitamin D supplements impacted our patient’s presentation of OLP, as she had been consistently taking them for more than 5 years with no change in OLP presentation.24
Pathogenesis—Lichen planus is thought to be a cytotoxic CD8+ T cell–mediated autoimmune disease to a virally modified epidermal self-antigen on keratinocytes. The cytotoxic T cells target the modified self-antigens on basal keratinocytes and induce apoptosis.25 The cytokine-mediated lymphocyte homing mechanism is human leukocyte antigen dependent and involves tumor necrosis factor α as well as IFN-γ and IL-1. The latter cytokines lead to upregulation of vascular adhesion molecules on endothelial vessels of subepithelial vascular plexus as well as a cascade of nonspecific mechanisms such as mast cell degranulation and matrix metalloproteinase activation, resulting in increased basement membrane disruption.6
Shao et al19 underscored the role of IFN-γ in CD8+ T cell–mediated cytotoxic cellular responses, noting that the Janus kinase (JAK)–signal transducer and activator of transcription pathway may play a key role in the pathogenesis of lichen planus. They proposed using JAK inhibitors for the treatment of lichen planus, specifically tofacitinib, a JAK1/JAK3 inhibitor, and baricitinib, a JAK1/JAK2 inhibitor, as top therapeutic agents for lichen planus (eTable).19 Tofacitinib has been reported to successfully treat conditions such as psoriasis, psoriatic arthritis, alopecia areata, vitiligo, atopic dermatitis, sarcoidosis, pyoderma gangrenosum, and lichen planopilaris.26 Additionally, the efficacy of tofacitinib has been established in patients with erosive lichen planus; tofacitinib resulted in marked improvement while prednisone, acitretin, methotrexate, mycophenolate mofetil, and cyclosporine treatment failed.27 Although more studies on tofacitinib’s long-term efficacy, cost, and safety are necessary, tofacitinib may soon play an integral role in the battle against inflammatory dermatoses.
Conclusion
Esophageal lichen planus is an underreported form of lichen planus that often is misdiagnosed. It frequently causes dysphagia and odynophagia, resulting in a major decrease in a patient’s quality of life. We present the case of an 89-year-old woman who underwent procedures to dilate her esophagus that worsened her condition. We emphasize the importance of considering ELP in the differential diagnosis of patients presenting with lichen planus in another region. In our patient, tofacitinib 5 mg BID resolved her condition without any adverse effects.
To reach early diagnoses and improve outcomes in cases of mucosal and esophageal lichen planus (ELP), patient education along with a multidisciplinary approach centered on collaboration among dermatologists, gastroenterologists, gynecologists, and dental practitioners should be a priority. Tofacitinib therapy should be considered in the treatment of patients presenting with cutaneous lichen planus (CLP), mucosal lichen planus, and ELP.
Lichen planus is a papulosquamous disease of the skin and mucous membranes that is most common on the skin and oral mucosa. Typical lesions of CLP present as purple, pruritic, polygonal papules and plaques on the flexural surfaces of the wrists and ankles as well as areas of friction or trauma due to scratching such as the shins and lower back. Various subtypes of lichen planus can present simultaneously, resulting in extensive involvement that worsens through koebnerization and affects the oral cavity, esophagus, larynx, sclera, genitalia, scalp, and nails.1,2
Esophageal lichen planus can develop with or without the presence of CLP, oral lichen planus (OLP), or genital lichen planus.3 It typically affects women older than 50 years and is linked to OLP and vulvar lichen planus, with 1 study reporting that 87% (63/72) of ELP patients were women with a median age of 61.9 years at the time of diagnosis (range, 22–85 years). Almost all ELP patients in the study had lichen planus symptoms in other locations; 89% (64/72) had OLP, and 42% (30/72) had vulvar lichen planus.4 Consequently, a diagnosis of ELP should be followed by a thorough full-body examination to check for lichen planus at other sites. Studies that examined lichen planus patients for ELP found that 25% to 50% of patients diagnosed with orocutaneous lichen planus also had ELP, with ELP frequently presenting without symptoms.3,5 These findings indicate that ELP likely is underdiagnosed and often misdiagnosed, resulting in an underestimation of its prevalence.
Our case highlights a frequently misdiagnosed condition and underscores the importance of close examination of patients presenting with CLP and OLP for signs and symptoms of ELP. Furthermore, we discuss the importance of patient education and collaboration among different specialties in attaining an early diagnosis to improve patient outcomes. Finally, we review the clinical presentation, diagnosis, and treatment of CLP, OLP, and ELP, as well as the utility of tofacitinib for ELP.
Case Report
An emaciated 89-year-old woman with an 11-year history of CLP, OLP, and genital lichen planus that had been successfully treated with topicals presented with an OLP recurrence alongside difficulties eating and swallowing. Her symptoms lasted 1 year and would recur when treatment was paused. Her medical history included rheumatoid arthritis, hypothyroidism, and hypertension, and she was taking levothyroxine, olmesartan, and vitamin D supplements. Dentures and olmesartan previously were ruled out as potential triggers following a 2-month elimination. None of her remaining natural teeth had fillings. She also reported that neither she nor her partner had ever smoked or chewed tobacco.
The patient’s lichen planus involvement first manifested as red, itchy, polygonal, lichenoid papules on the superior and inferior mid back 11 years prior to the current presentation (Figure 1). Further examination noted erosions on the genitalia, and a subsequent biopsy of the vulva confirmed a diagnosis of lichen planus (Figure 2). Treatment with halobetasol propionate ointment and tacrolimus ointment 0.1% twice daily (BID) resulted in remission of the CLP and vulvar lichen planus. She presented a year later with oral involvement revealing Wickham striae on the buccal mucosa and erosions on the upper palate that resolved after 2 months of treatment with cyclosporine oral solution mixed with a 5-times-daily nystatin swish-and-spit (Figure 3). The CLP did not recur but OLP was punctuated by remissions and recurrences on a yearly basis, often related to the cessation of mouthwash and topical creams. The OLP and vulvar lichen planus were successfully treated with as-needed use of a cyclosporine mouthwash swish-and-spit 3 times daily as well as halobetasol ointment 0.05% 3 times daily, respectively. Six years later, the patient was hospitalized for unrelated causes and was lost to follow-up for 2 years.
The patient experienced worsening dysphagia and odynophagia over a period of 2 years (mild dysphagia was first recorded 7 years prior to the initial presentation) and reported an unintentional weight loss of 20 pounds. An endoscopy was performed 3 years after the initial report of dysphagia and noted esophageal erosions (Figure 4A) and a stricture (Figure 4B), but all abnormal involvement was attributed to active gastroesophageal reflux disease. She underwent 8 esophageal dilations to treat the stricture but noted that the duration of symptomatic relief decreased with every subsequent dilation. An esophageal stent was placed 4 years after the initial concern of dysphagia, but it was not well tolerated and had to be removed soon thereafter. A year later, the patient underwent an esophageal bypass with a substernal gastric conduit that provided relief for 2 months but failed to permanently resolve the condition. In fact, her condition worsened over the next 1.5 years when she presented with extreme emaciation attributed to a low appetite and pain while eating. A review of the slides from a prior hospital esophageal biopsy revealed lichen planus (Figure 5). She was prescribed tofacitinib 5 mg BID as a dual-purpose treatment for the rheumatoid arthritis and OLP/ELP. At 1-month follow-up she noted that she had only taken one 5-mg pill daily without notable improvement, and after the visit she started the initial recommendation of 5 mg BID. Over the next several months, her condition continued to consistently improve; the odynophagia resolved, and she regained the majority of her lost weight. Tofacitinib was well tolerated across the course of treatment, and no adverse side effects were noted. Furthermore, the patient regained a full range of motion in the previously immobile arthritic right shoulder. She has experienced no recurrence of the genital lichen planus, OLP, or CLP since starting tofacitinib. To date, the patient is still taking only tofacitinib 5 mg BID with no recurrence of the cutaneous, mucosal, or esophageal lichen planus and has experienced no adverse events from the medication.
Comment
Clinical Presentation—Lichen planus—CLP and OLP—most frequently presents between the ages of 40 and 60 years, with a slight female predilection.1,2 The lesions typically present with the 5 P’s—purple, pruritic, polygonal papules and plaques—with some lesions revealing white lacy lines overlying them called Wickham striae.6 The lesions may be red at first before turning purple. They often present on the flexural surfaces of the wrists and ankles as well as the shins and back but rarely affect the face, perhaps because of increased chronic sun exposure.2,6 Less common locations include the scalp, nails, and mucosal areas (eg, oral, vulvar, conjunctival, laryngeal, esophageal, anal).1
If CLP is diagnosed, the patient likely will also have oral lesions, which occur in 50% of patients.2 Once any form of lichen planus is found, it is important to examine all of the most frequently involved locations—mucocutaneous and cutaneous as well as the nails and scalp. Special care should be taken when examining OLP and genital lichen planus, as long-standing lesions have a 2% to 5% chance of transforming into squamous cell carcinoma.2
Although cases of traditional OLP and CLP are ubiquitous in the literature, ELP rarely is documented because of frequent misdiagnoses. Esophageal lichen planus has a closer histopathologic resemblance to OLP compared to CLP, and its highly variable presentation often results in an inconclusive diagnosis.3 A review of 27 patients with lichen planus highlighted the difficult nature of diagnosing ELP; ELP manifested up to 20 years after initial lichen planus diagnosis, and patients underwent an average of 2.5 dilations prior to the successful diagnosis of ELP. Interestingly, 2 patients in the study presented with ELP in isolation, which emphasizes the importance of secondary examination for lichen planus in the presence of esophageal strictures.7 The eTable provides common patient demographics and symptoms to more effectively identify ELP.Differential Diagnosis—Because lichen planus can present anywhere on the body, it may be difficult to differentiate it from other skin conditions. Clinical appearance alone often is insufficient for diagnosing lichen planus, and a punch biopsy often is needed.2,20 Cutaneous lichen planus may resemble eczema, lichen simplex chronicus, pityriasis rosea, prurigo nodularis, and psoriasis, while OLP may resemble bite trauma, leukoplakia, pemphigus, and thrush.20 Dermoscopy of the tissue makes Wickham striae easier to visualize and assists in the diagnosis of lichen planus. Furthermore, thickening of the stratum granulosum, a prevalence of lymphocytes in the dermoepidermal junction, and vacuolar alteration of the stratum basale help to distinguish between lichen planus and other inflammatory dermatoses.20 A diagnosis of lichen planus merits a full-body skin examination—hair, nails, eyes, oral mucosa, and genitalia—to rule out additional involvement.
Esophageal lichen planus most frequently presents as dysphagia, odynophagia, and weight loss, but other symptoms including heartburn, hoarseness, choking, and epigastric pain may suggest esophageal involvement.4 Typically, ELP presents in the proximal and/or central esophagus, assisting in the differentiation between ELP and other esophageal conditions.3 Special consideration should be taken when both ELP and gastroesophageal reflux disease are considered in a differential diagnosis, and it is recommended to pair an upper endoscopy with pH monitoring to avoid misdiagnosis.8 Screening endoscopies also are helpful, as they assist in identifying the characteristic white webs, skin peeling, skin surface erosion, and strictures of ELP.4 Taken together, dermatologists should encourage patients with cutaneous or mucocutaneous lichen planus to undergo an esophagogastroduodenoscopy, especially in the presence of any of ELP’s common symptoms (eTable).
Etiology—Although the exact etiology of lichen planus is not well established, there are several known correlative factors, including hepatitis C; increased stress; dental materials; oral medications, most frequently antihypertensives and nonsteroidal anti-inflammatory drugs; systemic diseases; and tobacco usage.6,21
Dental materials used in oral treatments such as silver amalgam, gold, cobalt, palladium, chromium, epoxy resins, and dentures can trigger or exacerbate OLP, and patch testing of a patient’s dental materials can help determine if the reaction was caused by the materials.6,22 The removal of material contributing to lesions often will cause OLP to resolve.22
It also has been suggested that the presence of thyroid disorders, autoimmune disease, various cancers, hypertension, type 2 diabetes mellitus, hyperlipidemia, oral sedative usage, and/or vitamin D deficiency may be associated with OLP.21,23 Although OLP patients who were initially deficient in vitamin D demonstrated marked improvement with supplementation, it is unlikely that vitamin D supplements impacted our patient’s presentation of OLP, as she had been consistently taking them for more than 5 years with no change in OLP presentation.24
Pathogenesis—Lichen planus is thought to be a cytotoxic CD8+ T cell–mediated autoimmune disease to a virally modified epidermal self-antigen on keratinocytes. The cytotoxic T cells target the modified self-antigens on basal keratinocytes and induce apoptosis.25 The cytokine-mediated lymphocyte homing mechanism is human leukocyte antigen dependent and involves tumor necrosis factor α as well as IFN-γ and IL-1. The latter cytokines lead to upregulation of vascular adhesion molecules on endothelial vessels of subepithelial vascular plexus as well as a cascade of nonspecific mechanisms such as mast cell degranulation and matrix metalloproteinase activation, resulting in increased basement membrane disruption.6
Shao et al19 underscored the role of IFN-γ in CD8+ T cell–mediated cytotoxic cellular responses, noting that the Janus kinase (JAK)–signal transducer and activator of transcription pathway may play a key role in the pathogenesis of lichen planus. They proposed using JAK inhibitors for the treatment of lichen planus, specifically tofacitinib, a JAK1/JAK3 inhibitor, and baricitinib, a JAK1/JAK2 inhibitor, as top therapeutic agents for lichen planus (eTable).19 Tofacitinib has been reported to successfully treat conditions such as psoriasis, psoriatic arthritis, alopecia areata, vitiligo, atopic dermatitis, sarcoidosis, pyoderma gangrenosum, and lichen planopilaris.26 Additionally, the efficacy of tofacitinib has been established in patients with erosive lichen planus; tofacitinib resulted in marked improvement while prednisone, acitretin, methotrexate, mycophenolate mofetil, and cyclosporine treatment failed.27 Although more studies on tofacitinib’s long-term efficacy, cost, and safety are necessary, tofacitinib may soon play an integral role in the battle against inflammatory dermatoses.
Conclusion
Esophageal lichen planus is an underreported form of lichen planus that often is misdiagnosed. It frequently causes dysphagia and odynophagia, resulting in a major decrease in a patient’s quality of life. We present the case of an 89-year-old woman who underwent procedures to dilate her esophagus that worsened her condition. We emphasize the importance of considering ELP in the differential diagnosis of patients presenting with lichen planus in another region. In our patient, tofacitinib 5 mg BID resolved her condition without any adverse effects.
- Le Cleach L, Chosidow O. Lichen planus. N Engl J Med. 2012;366:723-732. doi:10.1056/nejmcp1103641
- Heath L, Matin R. Lichen planus. InnovAiT. 2017;10:133-138. doi:10.1177/1755738016686804
- Oliveira JP, Uribe NC, Abulafia LA, et al. Esophageal lichenplanus. An Bras Dermatol. 2015;90:394-396. doi:10.1590/abd1806-4841.20153255
- Fox LP, Lightdale CJ, Grossman ME. Lichen planus of the esophagus: what dermatologists need to know. J Am Acad Dermatol. 2011;65:175-183. doi:10.1016/j.jaad.2010.03.029
- Quispel R, van Boxel O, Schipper M, et al. High prevalence of esophageal involvement in lichen planus: a study using magnification chromoendoscopy. Endoscopy. 2009;41:187-193. doi:10.1055/s-0028-1119590
- Gupta S, Jawanda MK. Oral lichen planus: an update on etiology, pathogenesis, clinical presentation, diagnosis and management. Indian J Dermatol. 2015;60:222-229. doi:10.4103/0019-5154.156315
- Katzka DA, Smyrk TC, Bruce AJ, et al. Variations in presentations of esophageal involvement in lichen planus. Clin Gastroenterol Hepatol. 2010;8:777-782. doi:10.1016/j.cgh.2010.04.024
- Abraham SC, Ravich WJ, Anhalt GJ, et al. Esophageal lichen planus. Am J Surg Pathol. 2000;24:1678-1682. doi:10.1097/00000478-200012000-00014
- Murro D, Jakate S. Radiation esophagitis. Arch Pathol Lab Med. 2015;139:827-830. doi:10.5858/arpa.2014-0111-RS
- Wilcox CM. Infectious esophagitis. Gastroenterol Hepatol (N Y). 2006;2:567-568.
- Cancio A, Cruz C. A case of Kaposi’s sarcoma of the esophagus presenting with odynophagia. Am J Gastroenterol. 2018;113:S995-S996.
- Kokturk A. Clinical and pathological manifestations with differential diagnosis in Behçet’s disease. Patholog Res Int. 2012;2012:690390. doi:10.1155/2012/690390
- Madhusudhan KS, Sharma R. Esophageal lichen planus: a case report and review of literature. Indian J Dermatol. 2008;53:26-27. doi:10.4103/0019-5154.39738
- Bottomley WW, Dakkak M, Walton S, et al. Esophageal involvement in Behçet’s disease. is endoscopy necessary? Dig Dis Sci. 1992;37:594-597. doi:10.1007/BF01307585
- McDonald GB, Sullivan KM, Schuffler MD, et al. Esophageal abnormalities in chronic graft-versus-host disease in humans. Gastroenterology. 1981;80:914-921.
- Trabulo D, Ferreira S, Lage P, et al. Esophageal stenosis with sloughing esophagitis: a curious manifestation of graft-vs-host disease. World J Gastroenterol. 2015;21:9217-9222. doi:10.3748/wjg.v21.i30.9217
- Abbas H, Ghazanfar H, Ul Hussain AN, et al. Atypical presentation of esophageal squamous cell carcinoma masquerading as diffuse severe esophagitis. Case Rep Gastroenterol. 2021;15:533-538. doi:10.1159/000517129
- Ellis A, Risk JM, Maruthappu T, et al. Tylosis with oesophageal cancer: diagnosis, management and molecular mechanisms. Orphanet J Rare Dis. 2015;10:126. doi:10.1186/s13023-015-0346-2
- Shao S, Tsoi LC, Sarkar MK, et al. IFN-γ enhances cell-mediated cytotoxicity against keratinocytes via JAK2/STAT1 in lichen planus. Sci Transl Med. 2019;11:eaav7561. doi:10.1126/scitranslmed.aav7561
- Usatine RP, Tinitigan M. Diagnosis and treatment of lichen planus. Am Fam Physician. 2011;84:53-60.
- Dave A, Shariff J, Philipone E. Association between oral lichen planus and systemic conditions and medications: case-control study. Oral Dis. 2020;27:515-524. doi:10.1111/odi.13572
- Krupaa RJ, Sankari SL, Masthan KM, et al. Oral lichen planus: an overview. J Pharm Bioallied Sci. 2015;7(suppl 1):S158-S161. doi:10.4103/0975-7406.155873
- Tak MM, Chalkoo AH. Vitamin D deficiency—a possible contributing factor in the aetiopathogenesis of oral lichen planus. J Evolution Med Dent Sci. 2017;6:4769-4772. doi:10.14260/jemds/2017/1033
- Gupta J, Aggarwal A, Asadullah M, et al. Vitamin D in thetreatment of oral lichen planus: a pilot clinical study. J Indian Acad Oral Med Radiol. 2019;31:222-227. doi:10.4103/jiaomr.jiaomr_97_19
- Shiohara T, Moriya N, Mochizuki T, et al. Lichenoid tissue reaction (LTR) induced by local transfer of Ia-reactive T-cell clones. II. LTR by epidermal invasion of cytotoxic lymphokine-producing autoreactive T cells. J Invest Dermatol. 1987;89:8-14.
- Sonthalia S, Aggarwal P. Oral tofacitinib: contemporary appraisal of its role in dermatology. Indian Dermatol Online J. 2019;10:503-518. doi:10.4103/idoj.idoj_474_18
- Damsky W, Wang A, Olamiju B, et al. Treatment of severe lichen planus with the JAK inhibitor tofacitinib. J Allergy Clin Immunol. 2020;145:1708-1710.e2. doi:10.1016/j.jaci.2020.01.031
- Le Cleach L, Chosidow O. Lichen planus. N Engl J Med. 2012;366:723-732. doi:10.1056/nejmcp1103641
- Heath L, Matin R. Lichen planus. InnovAiT. 2017;10:133-138. doi:10.1177/1755738016686804
- Oliveira JP, Uribe NC, Abulafia LA, et al. Esophageal lichenplanus. An Bras Dermatol. 2015;90:394-396. doi:10.1590/abd1806-4841.20153255
- Fox LP, Lightdale CJ, Grossman ME. Lichen planus of the esophagus: what dermatologists need to know. J Am Acad Dermatol. 2011;65:175-183. doi:10.1016/j.jaad.2010.03.029
- Quispel R, van Boxel O, Schipper M, et al. High prevalence of esophageal involvement in lichen planus: a study using magnification chromoendoscopy. Endoscopy. 2009;41:187-193. doi:10.1055/s-0028-1119590
- Gupta S, Jawanda MK. Oral lichen planus: an update on etiology, pathogenesis, clinical presentation, diagnosis and management. Indian J Dermatol. 2015;60:222-229. doi:10.4103/0019-5154.156315
- Katzka DA, Smyrk TC, Bruce AJ, et al. Variations in presentations of esophageal involvement in lichen planus. Clin Gastroenterol Hepatol. 2010;8:777-782. doi:10.1016/j.cgh.2010.04.024
- Abraham SC, Ravich WJ, Anhalt GJ, et al. Esophageal lichen planus. Am J Surg Pathol. 2000;24:1678-1682. doi:10.1097/00000478-200012000-00014
- Murro D, Jakate S. Radiation esophagitis. Arch Pathol Lab Med. 2015;139:827-830. doi:10.5858/arpa.2014-0111-RS
- Wilcox CM. Infectious esophagitis. Gastroenterol Hepatol (N Y). 2006;2:567-568.
- Cancio A, Cruz C. A case of Kaposi’s sarcoma of the esophagus presenting with odynophagia. Am J Gastroenterol. 2018;113:S995-S996.
- Kokturk A. Clinical and pathological manifestations with differential diagnosis in Behçet’s disease. Patholog Res Int. 2012;2012:690390. doi:10.1155/2012/690390
- Madhusudhan KS, Sharma R. Esophageal lichen planus: a case report and review of literature. Indian J Dermatol. 2008;53:26-27. doi:10.4103/0019-5154.39738
- Bottomley WW, Dakkak M, Walton S, et al. Esophageal involvement in Behçet’s disease. is endoscopy necessary? Dig Dis Sci. 1992;37:594-597. doi:10.1007/BF01307585
- McDonald GB, Sullivan KM, Schuffler MD, et al. Esophageal abnormalities in chronic graft-versus-host disease in humans. Gastroenterology. 1981;80:914-921.
- Trabulo D, Ferreira S, Lage P, et al. Esophageal stenosis with sloughing esophagitis: a curious manifestation of graft-vs-host disease. World J Gastroenterol. 2015;21:9217-9222. doi:10.3748/wjg.v21.i30.9217
- Abbas H, Ghazanfar H, Ul Hussain AN, et al. Atypical presentation of esophageal squamous cell carcinoma masquerading as diffuse severe esophagitis. Case Rep Gastroenterol. 2021;15:533-538. doi:10.1159/000517129
- Ellis A, Risk JM, Maruthappu T, et al. Tylosis with oesophageal cancer: diagnosis, management and molecular mechanisms. Orphanet J Rare Dis. 2015;10:126. doi:10.1186/s13023-015-0346-2
- Shao S, Tsoi LC, Sarkar MK, et al. IFN-γ enhances cell-mediated cytotoxicity against keratinocytes via JAK2/STAT1 in lichen planus. Sci Transl Med. 2019;11:eaav7561. doi:10.1126/scitranslmed.aav7561
- Usatine RP, Tinitigan M. Diagnosis and treatment of lichen planus. Am Fam Physician. 2011;84:53-60.
- Dave A, Shariff J, Philipone E. Association between oral lichen planus and systemic conditions and medications: case-control study. Oral Dis. 2020;27:515-524. doi:10.1111/odi.13572
- Krupaa RJ, Sankari SL, Masthan KM, et al. Oral lichen planus: an overview. J Pharm Bioallied Sci. 2015;7(suppl 1):S158-S161. doi:10.4103/0975-7406.155873
- Tak MM, Chalkoo AH. Vitamin D deficiency—a possible contributing factor in the aetiopathogenesis of oral lichen planus. J Evolution Med Dent Sci. 2017;6:4769-4772. doi:10.14260/jemds/2017/1033
- Gupta J, Aggarwal A, Asadullah M, et al. Vitamin D in thetreatment of oral lichen planus: a pilot clinical study. J Indian Acad Oral Med Radiol. 2019;31:222-227. doi:10.4103/jiaomr.jiaomr_97_19
- Shiohara T, Moriya N, Mochizuki T, et al. Lichenoid tissue reaction (LTR) induced by local transfer of Ia-reactive T-cell clones. II. LTR by epidermal invasion of cytotoxic lymphokine-producing autoreactive T cells. J Invest Dermatol. 1987;89:8-14.
- Sonthalia S, Aggarwal P. Oral tofacitinib: contemporary appraisal of its role in dermatology. Indian Dermatol Online J. 2019;10:503-518. doi:10.4103/idoj.idoj_474_18
- Damsky W, Wang A, Olamiju B, et al. Treatment of severe lichen planus with the JAK inhibitor tofacitinib. J Allergy Clin Immunol. 2020;145:1708-1710.e2. doi:10.1016/j.jaci.2020.01.031
Practice Points
- Patients diagnosed with lichen planus should be informed about the signs of esophageal lichen planus (ELP).
- Twenty-five percent to 50% of patients with oral lichen planus (OLP) have been shown to have concomitant ELP.
- Esophageal lichen planus may be asymptomatic and often is misdiagnosed.
- Tofacitinib should be considered for the treatment of ELP, OLP, and cutaneous lichen planus.
Characterization of Blood-borne Pathogen Exposures During Dermatologic Procedures: The Mayo Clinic Experience
Dermatology providers are at an increased risk for blood-borne pathogen (BBP) exposures during procedures in clinical practice.1-3 Current data regarding the characterization of these exposures are limited. Prior studies are based on surveys that result in low response rates and potential for selection bias. Donnelly et al1 reported a 26% response rate in a national survey-based study evaluating BBP exposures in resident physicians, fellows, and practicing dermatologists, with 85% of respondents reporting at least 1 injury. Similarly, Goulart et al2 reported a 35% response rate in a survey evaluating sharps injuries in residents and medical students, with 85% reporting a sharps injury. In addition, there are conflicting data regarding characteristics of these exposures, including common implicated instruments and procedures.1-3 Prior studies also have not evaluated exposures in all members of dermatologic staff, including resident physicians, practicing dermatologists, and ancillary staff.
To make appropriate quality improvements in dermatologic procedures, a more comprehensive understanding of BBP exposures is needed. We conducted a retrospective review of BBP incidence reports to identify the incidence of BBP events among all dermatologic staff, including resident physicians, practicing dermatologists, and ancillary staff. We further investigated the type of exposure, the type of procedure associated with each exposure, anatomic locations of exposures, and instruments involved in each exposure.
Methods
Data on BBP exposures in the dermatology departments were obtained from the occupational health departments at each of 3 Mayo Clinic sites—Scottsdale, Arizona; Jacksonville, Florida; and Rochester, Minnesota—from March 2010 through January 2021. The institutional review board at Mayo Clinic, Scottsdale, Arizona, granted approval of this study (IRB #20-012625). A retrospective review of each exposure was conducted to identify the incidence of BBP exposures. Occupational BBP exposure was defined as
Statistical Analysis—Variables were summarized using counts and percentages. The 3 most common categories for each variable were then compared among occupational groups using the Fisher exact test. All other categories were grouped for analysis purposes. Medical staff were categorized into 3 occupational groups: practicing dermatologists; resident physicians; and ancillary staff, including nurse/medical assistants, physician assistants, and clinical laboratory technologists. All analyses were 2 sided and considered statistically significant at P<.05. Analyses were performed using SAS 9.4 (SAS Institute Inc).
Results
Type of Exposure—A total of 222 BBP exposures were identified through the trisite retrospective review from March 2010 through January 2021. One hundred ninety-nine (89.6%) of 222 exposures were attributed to needlesticks and medical sharps, while 23 (10.4%) of 222 exposures were attributed to splash incidents (Table).
Anatomic Sites Affected—The anatomic location most frequently involved was the thumb (130/217 events [59.9%]), followed by the hand (39/217 events [18.0%]) and finger (22/217 events [10.1%]). The arm, face, and knee were affected with the lowest frequency, with only 1 event reported at each anatomic site (0.5%)(eTable). Five incidents were excluded from the analysis of anatomic location because of insufficient details of events.
Incident Tasks and Tools—Most BBP exposures occurred during suturing or assisting with suturing (64/210 events [30.5%]), followed by handling of sharps, wires, or instruments (40/210 events [19.0%]) and medication administration (37/210 events [17.6%])(eTable). Twelve incidents were excluded from the analysis of implicated tasks because of insufficient details of events.
The tools involved in exposure events with the greatest prevalence included the suture needle (76/201 events [37.8%]), injection syringe/needle (43/201 events [21.4%]), and shave biopsy razor (24/201 events [11.9%])(eTable). Twenty-one incidents were excluded from the analysis of implicated instruments because of insufficient details of events.
Providers Affected by BBP Exposures—Resident physicians experienced the greatest number of BBP exposures (105/222 events [47.3%]), followed by ancillary providers (84/222 events [37.8%]) and practicing dermatologists (33/222 events [14.9%]). All occupational groups experienced more BBP exposures through needlesticks/medical sharps compared with splash incidents (resident physicians, 88.6%; ancillary staff, 91.7%; practicing dermatologists, 87.9%; P=.725)(Table).
Among resident physicians, practicing dermatologists, and ancillary staff, the most frequent site of injury was the thumb. Suturing/assisting with suturing was the most common task leading to injury, and the suture needle was the most common instrument of injury for both resident physicians and practicing dermatologists. Handling of sharps, wires, or instruments was the most common task leading to injury for ancillary staff, and the injection syringe/needle was the most common instrument of injury in this cohort.
Resident physicians experienced the lowest rate of BBP exposures during administration of medications (12.7%; P=.003). Ancillary staff experienced the highest rate of BBP exposures with an injection needle (35.5%; P=.001). There were no statistically significant differences among occupational groups for the anatomic location of injury (P=.074)(eTable).
Comment
In the year 2000, the annual global incidence of occupational BBP exposures among health care workers worldwide for hepatitis B virus, hepatitis C virus, and HIV was estimated at 2.1 million, 926,000, and 327,000, respectively. Most of these exposures were due to sharps injuries.4 Dermatologists are particularly at risk for BBP exposures given their reliance on frequent procedures in practice. During an 11-year period, 222 BBP exposures were documented in the dermatology departments at 3 Mayo Clinic institutions. Most exposures were due to needlestick/sharps across all occupational groups compared with splash injuries. Prior survey studies confirm that sharps injuries are frequently implicated, with 75% to 94% of residents and practicing dermatologists reporting at least 1 sharps injury.1
Among occupational groups, resident physicians had the highest rate of BBP exposures, followed by nurse/medical assistants and practicing dermatologists, which may be secondary to lack of training or experience. Data from other surgical fields, including general surgery, support that resident physicians have the highest rate of sharps injuries.5 In a survey study (N=452), 51% of residents reported that extra training in safe techniques would be beneficial.2 Safety training may be beneficial in reducing the incidence of BBP exposures in residency programs.
The most common implicated task in resident physicians and practicing dermatologists was suturing or assisting with suturing, and the most common implicated instrument was the suture needle. Prior studies showed conflicting data regarding common implicated tasks and instruments in this cohort.1,2 The task of suturing and the suture needle also were the most implicated means of injury among other surgical specialties.6 Ancillary staff experienced most BBP exposures during handling of sharps, wires, or instruments, as well as the use of an injection needle. The designation of tasks among dermatologic staff likely explains the difference among occupational groups. This new information may provide the opportunity to improve safety measures among all members of the dermatologic team.
Limitations—There are several limitations to this study. This retrospective review was conducted at a single health system at 3 institutions. Hence, similar safety protocols likely were in place across all sites, which may reduce the generalizability of the results. In addition, there is risk of nonreporting bias among staff, as only documented incidence reports were evaluated. Prior studies demonstrated a nonreporting prevalence of 33% to 64% among dermatology staff.1-3 We also did not evaluate whether injuries resulted in BBP exposure or transmission. The rates of postexposure prophylaxis also were not studied. This information was not available for review because of concerns for privacy. Demographic features, such as gender or years of training, also were not evaluated.
Conclusion
This study provides additional insight on the incidence of BBP exposures in dermatology, as well as the implicated tasks, instruments, and anatomic locations of injury. Studies show that implementing formal education regarding the risks of BBP exposure may result in reduction of sharps injuries.7 Formal education in residency programs may be needed in the field of dermatology to reduce BBP exposures. Quality improvement measures should focus on identified risk factors among occupational groups to reduce BBP exposures in the workplace.
- Donnelly AF, Chang Y-HH, Nemeth-Ochoa SA. Sharps injuries and reporting practices of U.S. dermatologists [published online November 14, 2013]. Dermatol Surg. 2013;39:1813-1821.
- Goulart J, Oliveria S, Levitt J. Safety during dermatologic procedures and surgeries: a survey of resident injuries and prevention strategies. J Am Acad Dermatol. 2011;65:648-650.
- Ken K, Golda N. Contaminated sharps injuries: a survey among dermatology residents. J Am Acad Dermatol. 2019;80:1786-1788.
- Pruss-Ustun A, Rapiti E, Hutin Y. Estimation of global burden of disease attributable to contaminated sharps injuries among health-care workers. Am J Ind Med. 2005;48:482-490.
- Choi L, Torres R, Syed S, et al. Sharps and needlestick injuries among medical students, surgical residents, faculty, and operating room staff at a single academic institution. J Surg Educ. 2017;74:131-136.
- Bakaeen F, Awad S, Albo D, et al. Epidemiology of exposure to blood borne pathogens on a surgical service. Am J Surg. 2006;192:E18-E21.
- Li WJ, Zhang M, Shi CL, et al. Study on intervention of bloodborne pathogen exposure in a general hospital [in Chinese]. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2017;35:34-41.
Dermatology providers are at an increased risk for blood-borne pathogen (BBP) exposures during procedures in clinical practice.1-3 Current data regarding the characterization of these exposures are limited. Prior studies are based on surveys that result in low response rates and potential for selection bias. Donnelly et al1 reported a 26% response rate in a national survey-based study evaluating BBP exposures in resident physicians, fellows, and practicing dermatologists, with 85% of respondents reporting at least 1 injury. Similarly, Goulart et al2 reported a 35% response rate in a survey evaluating sharps injuries in residents and medical students, with 85% reporting a sharps injury. In addition, there are conflicting data regarding characteristics of these exposures, including common implicated instruments and procedures.1-3 Prior studies also have not evaluated exposures in all members of dermatologic staff, including resident physicians, practicing dermatologists, and ancillary staff.
To make appropriate quality improvements in dermatologic procedures, a more comprehensive understanding of BBP exposures is needed. We conducted a retrospective review of BBP incidence reports to identify the incidence of BBP events among all dermatologic staff, including resident physicians, practicing dermatologists, and ancillary staff. We further investigated the type of exposure, the type of procedure associated with each exposure, anatomic locations of exposures, and instruments involved in each exposure.
Methods
Data on BBP exposures in the dermatology departments were obtained from the occupational health departments at each of 3 Mayo Clinic sites—Scottsdale, Arizona; Jacksonville, Florida; and Rochester, Minnesota—from March 2010 through January 2021. The institutional review board at Mayo Clinic, Scottsdale, Arizona, granted approval of this study (IRB #20-012625). A retrospective review of each exposure was conducted to identify the incidence of BBP exposures. Occupational BBP exposure was defined as
Statistical Analysis—Variables were summarized using counts and percentages. The 3 most common categories for each variable were then compared among occupational groups using the Fisher exact test. All other categories were grouped for analysis purposes. Medical staff were categorized into 3 occupational groups: practicing dermatologists; resident physicians; and ancillary staff, including nurse/medical assistants, physician assistants, and clinical laboratory technologists. All analyses were 2 sided and considered statistically significant at P<.05. Analyses were performed using SAS 9.4 (SAS Institute Inc).
Results
Type of Exposure—A total of 222 BBP exposures were identified through the trisite retrospective review from March 2010 through January 2021. One hundred ninety-nine (89.6%) of 222 exposures were attributed to needlesticks and medical sharps, while 23 (10.4%) of 222 exposures were attributed to splash incidents (Table).
Anatomic Sites Affected—The anatomic location most frequently involved was the thumb (130/217 events [59.9%]), followed by the hand (39/217 events [18.0%]) and finger (22/217 events [10.1%]). The arm, face, and knee were affected with the lowest frequency, with only 1 event reported at each anatomic site (0.5%)(eTable). Five incidents were excluded from the analysis of anatomic location because of insufficient details of events.
Incident Tasks and Tools—Most BBP exposures occurred during suturing or assisting with suturing (64/210 events [30.5%]), followed by handling of sharps, wires, or instruments (40/210 events [19.0%]) and medication administration (37/210 events [17.6%])(eTable). Twelve incidents were excluded from the analysis of implicated tasks because of insufficient details of events.
The tools involved in exposure events with the greatest prevalence included the suture needle (76/201 events [37.8%]), injection syringe/needle (43/201 events [21.4%]), and shave biopsy razor (24/201 events [11.9%])(eTable). Twenty-one incidents were excluded from the analysis of implicated instruments because of insufficient details of events.
Providers Affected by BBP Exposures—Resident physicians experienced the greatest number of BBP exposures (105/222 events [47.3%]), followed by ancillary providers (84/222 events [37.8%]) and practicing dermatologists (33/222 events [14.9%]). All occupational groups experienced more BBP exposures through needlesticks/medical sharps compared with splash incidents (resident physicians, 88.6%; ancillary staff, 91.7%; practicing dermatologists, 87.9%; P=.725)(Table).
Among resident physicians, practicing dermatologists, and ancillary staff, the most frequent site of injury was the thumb. Suturing/assisting with suturing was the most common task leading to injury, and the suture needle was the most common instrument of injury for both resident physicians and practicing dermatologists. Handling of sharps, wires, or instruments was the most common task leading to injury for ancillary staff, and the injection syringe/needle was the most common instrument of injury in this cohort.
Resident physicians experienced the lowest rate of BBP exposures during administration of medications (12.7%; P=.003). Ancillary staff experienced the highest rate of BBP exposures with an injection needle (35.5%; P=.001). There were no statistically significant differences among occupational groups for the anatomic location of injury (P=.074)(eTable).
Comment
In the year 2000, the annual global incidence of occupational BBP exposures among health care workers worldwide for hepatitis B virus, hepatitis C virus, and HIV was estimated at 2.1 million, 926,000, and 327,000, respectively. Most of these exposures were due to sharps injuries.4 Dermatologists are particularly at risk for BBP exposures given their reliance on frequent procedures in practice. During an 11-year period, 222 BBP exposures were documented in the dermatology departments at 3 Mayo Clinic institutions. Most exposures were due to needlestick/sharps across all occupational groups compared with splash injuries. Prior survey studies confirm that sharps injuries are frequently implicated, with 75% to 94% of residents and practicing dermatologists reporting at least 1 sharps injury.1
Among occupational groups, resident physicians had the highest rate of BBP exposures, followed by nurse/medical assistants and practicing dermatologists, which may be secondary to lack of training or experience. Data from other surgical fields, including general surgery, support that resident physicians have the highest rate of sharps injuries.5 In a survey study (N=452), 51% of residents reported that extra training in safe techniques would be beneficial.2 Safety training may be beneficial in reducing the incidence of BBP exposures in residency programs.
The most common implicated task in resident physicians and practicing dermatologists was suturing or assisting with suturing, and the most common implicated instrument was the suture needle. Prior studies showed conflicting data regarding common implicated tasks and instruments in this cohort.1,2 The task of suturing and the suture needle also were the most implicated means of injury among other surgical specialties.6 Ancillary staff experienced most BBP exposures during handling of sharps, wires, or instruments, as well as the use of an injection needle. The designation of tasks among dermatologic staff likely explains the difference among occupational groups. This new information may provide the opportunity to improve safety measures among all members of the dermatologic team.
Limitations—There are several limitations to this study. This retrospective review was conducted at a single health system at 3 institutions. Hence, similar safety protocols likely were in place across all sites, which may reduce the generalizability of the results. In addition, there is risk of nonreporting bias among staff, as only documented incidence reports were evaluated. Prior studies demonstrated a nonreporting prevalence of 33% to 64% among dermatology staff.1-3 We also did not evaluate whether injuries resulted in BBP exposure or transmission. The rates of postexposure prophylaxis also were not studied. This information was not available for review because of concerns for privacy. Demographic features, such as gender or years of training, also were not evaluated.
Conclusion
This study provides additional insight on the incidence of BBP exposures in dermatology, as well as the implicated tasks, instruments, and anatomic locations of injury. Studies show that implementing formal education regarding the risks of BBP exposure may result in reduction of sharps injuries.7 Formal education in residency programs may be needed in the field of dermatology to reduce BBP exposures. Quality improvement measures should focus on identified risk factors among occupational groups to reduce BBP exposures in the workplace.
Dermatology providers are at an increased risk for blood-borne pathogen (BBP) exposures during procedures in clinical practice.1-3 Current data regarding the characterization of these exposures are limited. Prior studies are based on surveys that result in low response rates and potential for selection bias. Donnelly et al1 reported a 26% response rate in a national survey-based study evaluating BBP exposures in resident physicians, fellows, and practicing dermatologists, with 85% of respondents reporting at least 1 injury. Similarly, Goulart et al2 reported a 35% response rate in a survey evaluating sharps injuries in residents and medical students, with 85% reporting a sharps injury. In addition, there are conflicting data regarding characteristics of these exposures, including common implicated instruments and procedures.1-3 Prior studies also have not evaluated exposures in all members of dermatologic staff, including resident physicians, practicing dermatologists, and ancillary staff.
To make appropriate quality improvements in dermatologic procedures, a more comprehensive understanding of BBP exposures is needed. We conducted a retrospective review of BBP incidence reports to identify the incidence of BBP events among all dermatologic staff, including resident physicians, practicing dermatologists, and ancillary staff. We further investigated the type of exposure, the type of procedure associated with each exposure, anatomic locations of exposures, and instruments involved in each exposure.
Methods
Data on BBP exposures in the dermatology departments were obtained from the occupational health departments at each of 3 Mayo Clinic sites—Scottsdale, Arizona; Jacksonville, Florida; and Rochester, Minnesota—from March 2010 through January 2021. The institutional review board at Mayo Clinic, Scottsdale, Arizona, granted approval of this study (IRB #20-012625). A retrospective review of each exposure was conducted to identify the incidence of BBP exposures. Occupational BBP exposure was defined as
Statistical Analysis—Variables were summarized using counts and percentages. The 3 most common categories for each variable were then compared among occupational groups using the Fisher exact test. All other categories were grouped for analysis purposes. Medical staff were categorized into 3 occupational groups: practicing dermatologists; resident physicians; and ancillary staff, including nurse/medical assistants, physician assistants, and clinical laboratory technologists. All analyses were 2 sided and considered statistically significant at P<.05. Analyses were performed using SAS 9.4 (SAS Institute Inc).
Results
Type of Exposure—A total of 222 BBP exposures were identified through the trisite retrospective review from March 2010 through January 2021. One hundred ninety-nine (89.6%) of 222 exposures were attributed to needlesticks and medical sharps, while 23 (10.4%) of 222 exposures were attributed to splash incidents (Table).
Anatomic Sites Affected—The anatomic location most frequently involved was the thumb (130/217 events [59.9%]), followed by the hand (39/217 events [18.0%]) and finger (22/217 events [10.1%]). The arm, face, and knee were affected with the lowest frequency, with only 1 event reported at each anatomic site (0.5%)(eTable). Five incidents were excluded from the analysis of anatomic location because of insufficient details of events.
Incident Tasks and Tools—Most BBP exposures occurred during suturing or assisting with suturing (64/210 events [30.5%]), followed by handling of sharps, wires, or instruments (40/210 events [19.0%]) and medication administration (37/210 events [17.6%])(eTable). Twelve incidents were excluded from the analysis of implicated tasks because of insufficient details of events.
The tools involved in exposure events with the greatest prevalence included the suture needle (76/201 events [37.8%]), injection syringe/needle (43/201 events [21.4%]), and shave biopsy razor (24/201 events [11.9%])(eTable). Twenty-one incidents were excluded from the analysis of implicated instruments because of insufficient details of events.
Providers Affected by BBP Exposures—Resident physicians experienced the greatest number of BBP exposures (105/222 events [47.3%]), followed by ancillary providers (84/222 events [37.8%]) and practicing dermatologists (33/222 events [14.9%]). All occupational groups experienced more BBP exposures through needlesticks/medical sharps compared with splash incidents (resident physicians, 88.6%; ancillary staff, 91.7%; practicing dermatologists, 87.9%; P=.725)(Table).
Among resident physicians, practicing dermatologists, and ancillary staff, the most frequent site of injury was the thumb. Suturing/assisting with suturing was the most common task leading to injury, and the suture needle was the most common instrument of injury for both resident physicians and practicing dermatologists. Handling of sharps, wires, or instruments was the most common task leading to injury for ancillary staff, and the injection syringe/needle was the most common instrument of injury in this cohort.
Resident physicians experienced the lowest rate of BBP exposures during administration of medications (12.7%; P=.003). Ancillary staff experienced the highest rate of BBP exposures with an injection needle (35.5%; P=.001). There were no statistically significant differences among occupational groups for the anatomic location of injury (P=.074)(eTable).
Comment
In the year 2000, the annual global incidence of occupational BBP exposures among health care workers worldwide for hepatitis B virus, hepatitis C virus, and HIV was estimated at 2.1 million, 926,000, and 327,000, respectively. Most of these exposures were due to sharps injuries.4 Dermatologists are particularly at risk for BBP exposures given their reliance on frequent procedures in practice. During an 11-year period, 222 BBP exposures were documented in the dermatology departments at 3 Mayo Clinic institutions. Most exposures were due to needlestick/sharps across all occupational groups compared with splash injuries. Prior survey studies confirm that sharps injuries are frequently implicated, with 75% to 94% of residents and practicing dermatologists reporting at least 1 sharps injury.1
Among occupational groups, resident physicians had the highest rate of BBP exposures, followed by nurse/medical assistants and practicing dermatologists, which may be secondary to lack of training or experience. Data from other surgical fields, including general surgery, support that resident physicians have the highest rate of sharps injuries.5 In a survey study (N=452), 51% of residents reported that extra training in safe techniques would be beneficial.2 Safety training may be beneficial in reducing the incidence of BBP exposures in residency programs.
The most common implicated task in resident physicians and practicing dermatologists was suturing or assisting with suturing, and the most common implicated instrument was the suture needle. Prior studies showed conflicting data regarding common implicated tasks and instruments in this cohort.1,2 The task of suturing and the suture needle also were the most implicated means of injury among other surgical specialties.6 Ancillary staff experienced most BBP exposures during handling of sharps, wires, or instruments, as well as the use of an injection needle. The designation of tasks among dermatologic staff likely explains the difference among occupational groups. This new information may provide the opportunity to improve safety measures among all members of the dermatologic team.
Limitations—There are several limitations to this study. This retrospective review was conducted at a single health system at 3 institutions. Hence, similar safety protocols likely were in place across all sites, which may reduce the generalizability of the results. In addition, there is risk of nonreporting bias among staff, as only documented incidence reports were evaluated. Prior studies demonstrated a nonreporting prevalence of 33% to 64% among dermatology staff.1-3 We also did not evaluate whether injuries resulted in BBP exposure or transmission. The rates of postexposure prophylaxis also were not studied. This information was not available for review because of concerns for privacy. Demographic features, such as gender or years of training, also were not evaluated.
Conclusion
This study provides additional insight on the incidence of BBP exposures in dermatology, as well as the implicated tasks, instruments, and anatomic locations of injury. Studies show that implementing formal education regarding the risks of BBP exposure may result in reduction of sharps injuries.7 Formal education in residency programs may be needed in the field of dermatology to reduce BBP exposures. Quality improvement measures should focus on identified risk factors among occupational groups to reduce BBP exposures in the workplace.
- Donnelly AF, Chang Y-HH, Nemeth-Ochoa SA. Sharps injuries and reporting practices of U.S. dermatologists [published online November 14, 2013]. Dermatol Surg. 2013;39:1813-1821.
- Goulart J, Oliveria S, Levitt J. Safety during dermatologic procedures and surgeries: a survey of resident injuries and prevention strategies. J Am Acad Dermatol. 2011;65:648-650.
- Ken K, Golda N. Contaminated sharps injuries: a survey among dermatology residents. J Am Acad Dermatol. 2019;80:1786-1788.
- Pruss-Ustun A, Rapiti E, Hutin Y. Estimation of global burden of disease attributable to contaminated sharps injuries among health-care workers. Am J Ind Med. 2005;48:482-490.
- Choi L, Torres R, Syed S, et al. Sharps and needlestick injuries among medical students, surgical residents, faculty, and operating room staff at a single academic institution. J Surg Educ. 2017;74:131-136.
- Bakaeen F, Awad S, Albo D, et al. Epidemiology of exposure to blood borne pathogens on a surgical service. Am J Surg. 2006;192:E18-E21.
- Li WJ, Zhang M, Shi CL, et al. Study on intervention of bloodborne pathogen exposure in a general hospital [in Chinese]. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2017;35:34-41.
- Donnelly AF, Chang Y-HH, Nemeth-Ochoa SA. Sharps injuries and reporting practices of U.S. dermatologists [published online November 14, 2013]. Dermatol Surg. 2013;39:1813-1821.
- Goulart J, Oliveria S, Levitt J. Safety during dermatologic procedures and surgeries: a survey of resident injuries and prevention strategies. J Am Acad Dermatol. 2011;65:648-650.
- Ken K, Golda N. Contaminated sharps injuries: a survey among dermatology residents. J Am Acad Dermatol. 2019;80:1786-1788.
- Pruss-Ustun A, Rapiti E, Hutin Y. Estimation of global burden of disease attributable to contaminated sharps injuries among health-care workers. Am J Ind Med. 2005;48:482-490.
- Choi L, Torres R, Syed S, et al. Sharps and needlestick injuries among medical students, surgical residents, faculty, and operating room staff at a single academic institution. J Surg Educ. 2017;74:131-136.
- Bakaeen F, Awad S, Albo D, et al. Epidemiology of exposure to blood borne pathogens on a surgical service. Am J Surg. 2006;192:E18-E21.
- Li WJ, Zhang M, Shi CL, et al. Study on intervention of bloodborne pathogen exposure in a general hospital [in Chinese]. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2017;35:34-41.
Practice Points
- Most blood-borne pathogen (BBP) exposures in dermatologic staff occur due to medical sharps as opposed to splash incidents.
- The most common implicated task in resident physicians and practicing dermatologists is suturing or assisting with suturing, and the most commonly associated instrument is the suture needle. In contrast, ancillary staff experience most BBP exposures during handling of sharps, wires, or instruments, and the injection syringe/needle is the most common instrument of injury.
- Quality improvement measures are needed in prevention of BBP exposures and should focus on identified risk factors among occupational groups in the workplace.
Specialty and age may contribute to suicidal thoughts among physicians
A physician’s specialty can make a difference when it comes to having suicidal thoughts. Doctors who specialize in family medicine, obstetrics-gynecology, and psychiatry reported double the rates of suicidal thoughts than doctors in oncology, rheumatology, and pulmonary medicine, according to Doctors’ Burden: Medscape Physician Suicide Report 2023.
“The specialties with the highest reporting of physician suicidal thoughts are also those with the greatest physician shortages, based on the number of job openings posted by recruiting sites,” said Peter Yellowlees, MD, professor of psychiatry and chief wellness officer at UC Davis Health.
Doctors in those specialties are overworked, which can lead to burnout, he said.
There’s also a generational divide among physicians who reported suicidal thoughts. Millennials (age 27-41) and Gen-X physicians (age 42-56) were more likely to report these thoughts than were Baby Boomers (age 57-75) and the Silent Generation (age 76-95).
“Younger physicians are more burned out – they may have less control over their lives and less meaning than some older doctors who can do what they want,” said Dr. Yellowlees.
One millennial respondent commented that being on call and being required to chart detailed notes in the EHR has contributed to her burnout. “I’m more impatient and make less time and effort to see my friends and family.”
One Silent Generation respondent commented, “I am semi-retired, I take no call, I work no weekends, I provide anesthesia care in my area of special expertise, I work clinically about 46 days a year. Life is good, particularly compared to my younger colleagues who are working 60-plus hours a week with evening work, weekend work, and call. I feel really sorry for them.”
When young people enter medical school, they’re quite healthy, with low rates of depression and burnout, said Dr. Yellowlees. Yet, studies have shown that rates of burnout and suicidal thoughts increased within 2 years. “That reflects what happens when a group of idealistic young people hit a horrible system,” he said.
Who’s responsible?
Millennials were three times as likely as baby boomers to say that a medical school or health care organization should be responsible when a student or physician commits suicide.
“Young physicians may expect more of their employers than my generation did, which we see in residency programs that have unionized,” said Dr. Yellowlees, a Baby Boomer.
“As more young doctors are employed by health care organizations, they also may expect more resources to be available to them, such as wellness programs,” he added.
Younger doctors also focus more on work-life balance than older doctors, including time off and having hobbies, he said. “They are much more rational in terms of their overall beliefs and expectations than the older generation.”
Whom doctors confide in
Nearly 60% of physician-respondents with suicidal thoughts said they confided in a professional or someone they knew. Men were just as likely as women to reach out to a therapist (38%), whereas men were slightly more likely to confide in a family member and women were slightly more likely to confide in a colleague.
“It’s interesting that women are more active in seeking support at work – they often have developed a network of colleagues to support each other’s careers and whom they can confide in,” said Dr. Yellowlees.
He emphasized that 40% of physicians said they didn’t confide in anyone when they had suicidal thoughts. Of those, just over half said they could cope without professional help.
One respondent commented, “It’s just a thought; nothing I would actually do.” Another commented, “Mental health professionals can’t fix the underlying reason for the problem.”
Many doctors were concerned about risking disclosure to their medical boards (42%); that it would show up on their insurance records (33%); and that their colleagues would find out (25%), according to the report.
One respondent commented, “I don’t trust doctors to keep it to themselves.”
Another barrier doctors mentioned was a lack of time to seek help. One commented, “Time. I have none, when am I supposed to find an hour for counseling?”
A version of this article originally appeared on Medscape.com.
A physician’s specialty can make a difference when it comes to having suicidal thoughts. Doctors who specialize in family medicine, obstetrics-gynecology, and psychiatry reported double the rates of suicidal thoughts than doctors in oncology, rheumatology, and pulmonary medicine, according to Doctors’ Burden: Medscape Physician Suicide Report 2023.
“The specialties with the highest reporting of physician suicidal thoughts are also those with the greatest physician shortages, based on the number of job openings posted by recruiting sites,” said Peter Yellowlees, MD, professor of psychiatry and chief wellness officer at UC Davis Health.
Doctors in those specialties are overworked, which can lead to burnout, he said.
There’s also a generational divide among physicians who reported suicidal thoughts. Millennials (age 27-41) and Gen-X physicians (age 42-56) were more likely to report these thoughts than were Baby Boomers (age 57-75) and the Silent Generation (age 76-95).
“Younger physicians are more burned out – they may have less control over their lives and less meaning than some older doctors who can do what they want,” said Dr. Yellowlees.
One millennial respondent commented that being on call and being required to chart detailed notes in the EHR has contributed to her burnout. “I’m more impatient and make less time and effort to see my friends and family.”
One Silent Generation respondent commented, “I am semi-retired, I take no call, I work no weekends, I provide anesthesia care in my area of special expertise, I work clinically about 46 days a year. Life is good, particularly compared to my younger colleagues who are working 60-plus hours a week with evening work, weekend work, and call. I feel really sorry for them.”
When young people enter medical school, they’re quite healthy, with low rates of depression and burnout, said Dr. Yellowlees. Yet, studies have shown that rates of burnout and suicidal thoughts increased within 2 years. “That reflects what happens when a group of idealistic young people hit a horrible system,” he said.
Who’s responsible?
Millennials were three times as likely as baby boomers to say that a medical school or health care organization should be responsible when a student or physician commits suicide.
“Young physicians may expect more of their employers than my generation did, which we see in residency programs that have unionized,” said Dr. Yellowlees, a Baby Boomer.
“As more young doctors are employed by health care organizations, they also may expect more resources to be available to them, such as wellness programs,” he added.
Younger doctors also focus more on work-life balance than older doctors, including time off and having hobbies, he said. “They are much more rational in terms of their overall beliefs and expectations than the older generation.”
Whom doctors confide in
Nearly 60% of physician-respondents with suicidal thoughts said they confided in a professional or someone they knew. Men were just as likely as women to reach out to a therapist (38%), whereas men were slightly more likely to confide in a family member and women were slightly more likely to confide in a colleague.
“It’s interesting that women are more active in seeking support at work – they often have developed a network of colleagues to support each other’s careers and whom they can confide in,” said Dr. Yellowlees.
He emphasized that 40% of physicians said they didn’t confide in anyone when they had suicidal thoughts. Of those, just over half said they could cope without professional help.
One respondent commented, “It’s just a thought; nothing I would actually do.” Another commented, “Mental health professionals can’t fix the underlying reason for the problem.”
Many doctors were concerned about risking disclosure to their medical boards (42%); that it would show up on their insurance records (33%); and that their colleagues would find out (25%), according to the report.
One respondent commented, “I don’t trust doctors to keep it to themselves.”
Another barrier doctors mentioned was a lack of time to seek help. One commented, “Time. I have none, when am I supposed to find an hour for counseling?”
A version of this article originally appeared on Medscape.com.
A physician’s specialty can make a difference when it comes to having suicidal thoughts. Doctors who specialize in family medicine, obstetrics-gynecology, and psychiatry reported double the rates of suicidal thoughts than doctors in oncology, rheumatology, and pulmonary medicine, according to Doctors’ Burden: Medscape Physician Suicide Report 2023.
“The specialties with the highest reporting of physician suicidal thoughts are also those with the greatest physician shortages, based on the number of job openings posted by recruiting sites,” said Peter Yellowlees, MD, professor of psychiatry and chief wellness officer at UC Davis Health.
Doctors in those specialties are overworked, which can lead to burnout, he said.
There’s also a generational divide among physicians who reported suicidal thoughts. Millennials (age 27-41) and Gen-X physicians (age 42-56) were more likely to report these thoughts than were Baby Boomers (age 57-75) and the Silent Generation (age 76-95).
“Younger physicians are more burned out – they may have less control over their lives and less meaning than some older doctors who can do what they want,” said Dr. Yellowlees.
One millennial respondent commented that being on call and being required to chart detailed notes in the EHR has contributed to her burnout. “I’m more impatient and make less time and effort to see my friends and family.”
One Silent Generation respondent commented, “I am semi-retired, I take no call, I work no weekends, I provide anesthesia care in my area of special expertise, I work clinically about 46 days a year. Life is good, particularly compared to my younger colleagues who are working 60-plus hours a week with evening work, weekend work, and call. I feel really sorry for them.”
When young people enter medical school, they’re quite healthy, with low rates of depression and burnout, said Dr. Yellowlees. Yet, studies have shown that rates of burnout and suicidal thoughts increased within 2 years. “That reflects what happens when a group of idealistic young people hit a horrible system,” he said.
Who’s responsible?
Millennials were three times as likely as baby boomers to say that a medical school or health care organization should be responsible when a student or physician commits suicide.
“Young physicians may expect more of their employers than my generation did, which we see in residency programs that have unionized,” said Dr. Yellowlees, a Baby Boomer.
“As more young doctors are employed by health care organizations, they also may expect more resources to be available to them, such as wellness programs,” he added.
Younger doctors also focus more on work-life balance than older doctors, including time off and having hobbies, he said. “They are much more rational in terms of their overall beliefs and expectations than the older generation.”
Whom doctors confide in
Nearly 60% of physician-respondents with suicidal thoughts said they confided in a professional or someone they knew. Men were just as likely as women to reach out to a therapist (38%), whereas men were slightly more likely to confide in a family member and women were slightly more likely to confide in a colleague.
“It’s interesting that women are more active in seeking support at work – they often have developed a network of colleagues to support each other’s careers and whom they can confide in,” said Dr. Yellowlees.
He emphasized that 40% of physicians said they didn’t confide in anyone when they had suicidal thoughts. Of those, just over half said they could cope without professional help.
One respondent commented, “It’s just a thought; nothing I would actually do.” Another commented, “Mental health professionals can’t fix the underlying reason for the problem.”
Many doctors were concerned about risking disclosure to their medical boards (42%); that it would show up on their insurance records (33%); and that their colleagues would find out (25%), according to the report.
One respondent commented, “I don’t trust doctors to keep it to themselves.”
Another barrier doctors mentioned was a lack of time to seek help. One commented, “Time. I have none, when am I supposed to find an hour for counseling?”
A version of this article originally appeared on Medscape.com.