User login
For MD-IQ use only
Targeted Osteoporosis Program May Benefit At-Risk Older Men
Efforts to identify older men at risk for osteoporosis and treat those who are eligible received a boost from results reported from a Veterans Affairs (VA) study that showed a significant increase in screening, treatment, and medication adherence.
The cluster randomized trial used a centralized nurse-led intervention to assess men for traditional osteoporosis risk factors, offer bone density testing, and recommend treatment for eligible men. Over 2 years, the intervention group had a higher average femoral neck bone density than patients who underwent usual care.
“We designed this study to see if a risk factor-based approach, which is what most of the guidelines use, made sense and was feasible — that men would be accepting of screening and [the approach] would yield a similar proportion of people who need osteoporosis treatment as screening in women, which is widely recommended and implemented. And sure enough, we found that about 85% of the men in the VA primary care practices in our target age range of between 65 and 85 actually met criteria for screening, and over half of them had low bone mass. They were very accepting of screening, very accepting of treatment, and had excellent compliance rates. So, our study, we believe, supports the idea of identifying men with at least one risk factor for fracture and offering them osteoporosis screening starting at age 65, similar to what we do for women,” Cathleen S. Colón-Emeric, MD, MHS, said in an interview. She is the lead author of the study, a physician in the Durham VA Health Care System, and professor of medicine at Duke University School of Medicine, Durham, North Carolina.
“We were able to see a positive effect on bone density in the bone health group, compared with the usual care group, which suggests that if we followed these folks longer and had enough of them, we would be able to show a fracture reduction benefit,” Colón-Emeric said.
There have been few randomized trials of screening interventions in men, leading to inconsistencies in guidelines, according to the authors of the new study, published online in JAMA Internal Medicine . Both the US Preventive Services Task Force and the Veterans Health Administration National Center for Health Promotion and Disease Prevention consider there to be insufficient evidence to recommend for or against screening in men who have not experienced a fracture. Some professional societies recommend such screening, but there are inconsistencies in the recommended criteria, such as age range or risk factors.
Beyond the age of 50 years, one in five men will experience an osteoporosis-related fracture at some point in their life, according to a 2009 study. Treatment is inexpensive and effective in both men and women, and economic models suggest that screening using dual-energy x-ray absorptiometry (DXA) would be cost-effective. Still, screening is rare among men, with fewer than 10% of men getting screened before having an osteoporosis-related fracture.
“It’s important to screen men at risk for osteoporosis due to the dramatically increased mortality men suffer after a fragility fracture compared with women. Within 1 year of a hip fracture, mortality is as high as 36%. Studies have also shown that osteoporosis in men is undertreated, with only 10%-50% being prescribed antifracture treatment within 1 year of a hip fracture. Most individuals do not regain their prior level of function after a hip fracture,” said Joe C. Huang, MD, who was asked for comment. He is a clinical assistant professor of gerontology and geriatric medicine at Harborview Medical Center Senior Care Clinic and Healthy Bones Clinic in Seattle.
Details of the Intervention
The bone health service (BHS) intervention employed an electronic health record case-finding tool and a nurse care manager who undertook screening and treatment monitoring. They identified potential risk factors that included hyperthyroidism, hyperparathyroidism, rheumatoid arthritis, alcohol dependence, chronic lung disease, chronic liver disease, stroke, parkinsonism, prostate cancer, smoking, diabetes, pernicious anemia, gastrectomy, or high-risk medication use in at least 3 months of the prior 2 years. These medications included traditional antiepileptics, glucocorticoids, and androgen deprivation therapy.
The BHS nurse invited eligible men to be screened using an initial letter, followed by up to three phone calls. After DXA screening, the nurse scheduled an electronic consult with an osteoporosis expert, and patients with a T-score between -1 and -2.4 and an elevated 10-year fracture risk as measured by the Fracture Risk Assessment Tool were recommended for osteoporosis medication, vitamin D, and dietary or supplemental calcium. Following the prescription, the nurse provided patient education over the phone and mailed out written instructions. The nurse also made phone calls at 1 month, 6 months, and 12 months to encourage adherence and address common treatment barriers such as forgetting to take medication or dealing with gastrointestinal effects. The researchers recruited 38 primary care physicians from two VA health systems. The study included 3112 male veterans between the ages of 65 and 85 years (40.4% Black and 56% White). Nearly all participants (85.5%) had at least one indication for screening according to VA undersecretary guidelines, and almost a third (32.1%) had been prescribed androgen deprivation therapy, traditional antiepileptic drugs, or glucocorticoids.
Over a mean follow-up of 1.5 years, there was a much higher screening rate in the BHS group (49.2% vs 2.3%; P < .001), with a similar overall yield of DXA results recommending osteoporosis treatment (22.4% vs 27.2%). In the BHS group, 84.4% of patients who had treatment recommended followed through with treatment initiation. The mean persistence over follow-up was 657 days (SD, 366 days), and adherence was high with a mean proportion of days covered of 91.7%.
It was not possible to statistically compare adherence with the usual-care group because there were too few screened patients found to be eligible for treatment in that group, but the historic mean proportion of days covered at the two participating facilities was 52%.
After 2 years, the mean femoral neck T-score tested randomly in a subset of patients was better in the BHS arm, although it did not meet statistical significance according to the Bonferroni corrected criterion of P < .025 (-0.55 vs -0.70; P = .04). Fracture rates were similar between the two groups (1.8% vs 2.0%; P = .69).
Can the Findings Be Translated Across Clinics?
It remains to be seen how well the model could translate to other healthcare settings, according to Kenny Lin, MD, MPH, who was asked for comment on the study. “Outside of the VA health system and perhaps integrated HMOs [health maintenance organizations] such as Kaiser, Geisinger, etc., it seems unlikely that most primary care docs will have access to a centralized bone health service. Who’s going to pay for it? It leaves unanswered the question of whether it’s more efficient to address [osteoporosis] screening on a practice or population level. I suspect the latter is probably superior, but this study doesn’t provide any empiric evidence that this is so,” said Lin, associate director of the Penn Medicine Lancaster General Hospital’s Family Medicine Residency Program, Lancaster, Pennsylvania. The findings could help sway recommendations to screen men for osteoporosis, according to Susan Ott, MD, who was also asked for comment. Guideline committees “have been trying to be very scientific [about it]. I think they overdo it because they only look at one or two kinds of studies, and there are more kinds of science than just a randomized clinical trial. But they’re kind of stuck on that. The fact that this study was a randomized trial maybe they will finally change their recommendation, because there really shouldn’t be any difference in screening for men and for women. The men are actually discriminated against,” said Ott, emeritus professor of medicine at the University of Washington, Seattle.
In fact, she noted that the risks for men are similar to those for women, except that men tend to develop issues 5-10 years later in life. To screen and treat men, healthcare systems can “do the same thing they do with women. Just change the age range,” Ott said.
Lin sounded a different note, suggesting that the focus should remain on improvement of screening and treatment adherence in women. “We know that up to two thirds of women discontinue osteoporosis drugs within a year, and if we can’t figure out how to improve abysmal adherence in women, it’s unlikely we will persuade enough men to take these drugs to make a difference,” he said.
The study was funded by a grant from the VA Health Systems Research. Colón-Emeric, Lin, Ott, and Huang reported having no relevant financial disclosures.
A version of this article first appeared on Medscape.com.
Efforts to identify older men at risk for osteoporosis and treat those who are eligible received a boost from results reported from a Veterans Affairs (VA) study that showed a significant increase in screening, treatment, and medication adherence.
The cluster randomized trial used a centralized nurse-led intervention to assess men for traditional osteoporosis risk factors, offer bone density testing, and recommend treatment for eligible men. Over 2 years, the intervention group had a higher average femoral neck bone density than patients who underwent usual care.
“We designed this study to see if a risk factor-based approach, which is what most of the guidelines use, made sense and was feasible — that men would be accepting of screening and [the approach] would yield a similar proportion of people who need osteoporosis treatment as screening in women, which is widely recommended and implemented. And sure enough, we found that about 85% of the men in the VA primary care practices in our target age range of between 65 and 85 actually met criteria for screening, and over half of them had low bone mass. They were very accepting of screening, very accepting of treatment, and had excellent compliance rates. So, our study, we believe, supports the idea of identifying men with at least one risk factor for fracture and offering them osteoporosis screening starting at age 65, similar to what we do for women,” Cathleen S. Colón-Emeric, MD, MHS, said in an interview. She is the lead author of the study, a physician in the Durham VA Health Care System, and professor of medicine at Duke University School of Medicine, Durham, North Carolina.
“We were able to see a positive effect on bone density in the bone health group, compared with the usual care group, which suggests that if we followed these folks longer and had enough of them, we would be able to show a fracture reduction benefit,” Colón-Emeric said.
There have been few randomized trials of screening interventions in men, leading to inconsistencies in guidelines, according to the authors of the new study, published online in JAMA Internal Medicine . Both the US Preventive Services Task Force and the Veterans Health Administration National Center for Health Promotion and Disease Prevention consider there to be insufficient evidence to recommend for or against screening in men who have not experienced a fracture. Some professional societies recommend such screening, but there are inconsistencies in the recommended criteria, such as age range or risk factors.
Beyond the age of 50 years, one in five men will experience an osteoporosis-related fracture at some point in their life, according to a 2009 study. Treatment is inexpensive and effective in both men and women, and economic models suggest that screening using dual-energy x-ray absorptiometry (DXA) would be cost-effective. Still, screening is rare among men, with fewer than 10% of men getting screened before having an osteoporosis-related fracture.
“It’s important to screen men at risk for osteoporosis due to the dramatically increased mortality men suffer after a fragility fracture compared with women. Within 1 year of a hip fracture, mortality is as high as 36%. Studies have also shown that osteoporosis in men is undertreated, with only 10%-50% being prescribed antifracture treatment within 1 year of a hip fracture. Most individuals do not regain their prior level of function after a hip fracture,” said Joe C. Huang, MD, who was asked for comment. He is a clinical assistant professor of gerontology and geriatric medicine at Harborview Medical Center Senior Care Clinic and Healthy Bones Clinic in Seattle.
Details of the Intervention
The bone health service (BHS) intervention employed an electronic health record case-finding tool and a nurse care manager who undertook screening and treatment monitoring. They identified potential risk factors that included hyperthyroidism, hyperparathyroidism, rheumatoid arthritis, alcohol dependence, chronic lung disease, chronic liver disease, stroke, parkinsonism, prostate cancer, smoking, diabetes, pernicious anemia, gastrectomy, or high-risk medication use in at least 3 months of the prior 2 years. These medications included traditional antiepileptics, glucocorticoids, and androgen deprivation therapy.
The BHS nurse invited eligible men to be screened using an initial letter, followed by up to three phone calls. After DXA screening, the nurse scheduled an electronic consult with an osteoporosis expert, and patients with a T-score between -1 and -2.4 and an elevated 10-year fracture risk as measured by the Fracture Risk Assessment Tool were recommended for osteoporosis medication, vitamin D, and dietary or supplemental calcium. Following the prescription, the nurse provided patient education over the phone and mailed out written instructions. The nurse also made phone calls at 1 month, 6 months, and 12 months to encourage adherence and address common treatment barriers such as forgetting to take medication or dealing with gastrointestinal effects. The researchers recruited 38 primary care physicians from two VA health systems. The study included 3112 male veterans between the ages of 65 and 85 years (40.4% Black and 56% White). Nearly all participants (85.5%) had at least one indication for screening according to VA undersecretary guidelines, and almost a third (32.1%) had been prescribed androgen deprivation therapy, traditional antiepileptic drugs, or glucocorticoids.
Over a mean follow-up of 1.5 years, there was a much higher screening rate in the BHS group (49.2% vs 2.3%; P < .001), with a similar overall yield of DXA results recommending osteoporosis treatment (22.4% vs 27.2%). In the BHS group, 84.4% of patients who had treatment recommended followed through with treatment initiation. The mean persistence over follow-up was 657 days (SD, 366 days), and adherence was high with a mean proportion of days covered of 91.7%.
It was not possible to statistically compare adherence with the usual-care group because there were too few screened patients found to be eligible for treatment in that group, but the historic mean proportion of days covered at the two participating facilities was 52%.
After 2 years, the mean femoral neck T-score tested randomly in a subset of patients was better in the BHS arm, although it did not meet statistical significance according to the Bonferroni corrected criterion of P < .025 (-0.55 vs -0.70; P = .04). Fracture rates were similar between the two groups (1.8% vs 2.0%; P = .69).
Can the Findings Be Translated Across Clinics?
It remains to be seen how well the model could translate to other healthcare settings, according to Kenny Lin, MD, MPH, who was asked for comment on the study. “Outside of the VA health system and perhaps integrated HMOs [health maintenance organizations] such as Kaiser, Geisinger, etc., it seems unlikely that most primary care docs will have access to a centralized bone health service. Who’s going to pay for it? It leaves unanswered the question of whether it’s more efficient to address [osteoporosis] screening on a practice or population level. I suspect the latter is probably superior, but this study doesn’t provide any empiric evidence that this is so,” said Lin, associate director of the Penn Medicine Lancaster General Hospital’s Family Medicine Residency Program, Lancaster, Pennsylvania. The findings could help sway recommendations to screen men for osteoporosis, according to Susan Ott, MD, who was also asked for comment. Guideline committees “have been trying to be very scientific [about it]. I think they overdo it because they only look at one or two kinds of studies, and there are more kinds of science than just a randomized clinical trial. But they’re kind of stuck on that. The fact that this study was a randomized trial maybe they will finally change their recommendation, because there really shouldn’t be any difference in screening for men and for women. The men are actually discriminated against,” said Ott, emeritus professor of medicine at the University of Washington, Seattle.
In fact, she noted that the risks for men are similar to those for women, except that men tend to develop issues 5-10 years later in life. To screen and treat men, healthcare systems can “do the same thing they do with women. Just change the age range,” Ott said.
Lin sounded a different note, suggesting that the focus should remain on improvement of screening and treatment adherence in women. “We know that up to two thirds of women discontinue osteoporosis drugs within a year, and if we can’t figure out how to improve abysmal adherence in women, it’s unlikely we will persuade enough men to take these drugs to make a difference,” he said.
The study was funded by a grant from the VA Health Systems Research. Colón-Emeric, Lin, Ott, and Huang reported having no relevant financial disclosures.
A version of this article first appeared on Medscape.com.
Efforts to identify older men at risk for osteoporosis and treat those who are eligible received a boost from results reported from a Veterans Affairs (VA) study that showed a significant increase in screening, treatment, and medication adherence.
The cluster randomized trial used a centralized nurse-led intervention to assess men for traditional osteoporosis risk factors, offer bone density testing, and recommend treatment for eligible men. Over 2 years, the intervention group had a higher average femoral neck bone density than patients who underwent usual care.
“We designed this study to see if a risk factor-based approach, which is what most of the guidelines use, made sense and was feasible — that men would be accepting of screening and [the approach] would yield a similar proportion of people who need osteoporosis treatment as screening in women, which is widely recommended and implemented. And sure enough, we found that about 85% of the men in the VA primary care practices in our target age range of between 65 and 85 actually met criteria for screening, and over half of them had low bone mass. They were very accepting of screening, very accepting of treatment, and had excellent compliance rates. So, our study, we believe, supports the idea of identifying men with at least one risk factor for fracture and offering them osteoporosis screening starting at age 65, similar to what we do for women,” Cathleen S. Colón-Emeric, MD, MHS, said in an interview. She is the lead author of the study, a physician in the Durham VA Health Care System, and professor of medicine at Duke University School of Medicine, Durham, North Carolina.
“We were able to see a positive effect on bone density in the bone health group, compared with the usual care group, which suggests that if we followed these folks longer and had enough of them, we would be able to show a fracture reduction benefit,” Colón-Emeric said.
There have been few randomized trials of screening interventions in men, leading to inconsistencies in guidelines, according to the authors of the new study, published online in JAMA Internal Medicine . Both the US Preventive Services Task Force and the Veterans Health Administration National Center for Health Promotion and Disease Prevention consider there to be insufficient evidence to recommend for or against screening in men who have not experienced a fracture. Some professional societies recommend such screening, but there are inconsistencies in the recommended criteria, such as age range or risk factors.
Beyond the age of 50 years, one in five men will experience an osteoporosis-related fracture at some point in their life, according to a 2009 study. Treatment is inexpensive and effective in both men and women, and economic models suggest that screening using dual-energy x-ray absorptiometry (DXA) would be cost-effective. Still, screening is rare among men, with fewer than 10% of men getting screened before having an osteoporosis-related fracture.
“It’s important to screen men at risk for osteoporosis due to the dramatically increased mortality men suffer after a fragility fracture compared with women. Within 1 year of a hip fracture, mortality is as high as 36%. Studies have also shown that osteoporosis in men is undertreated, with only 10%-50% being prescribed antifracture treatment within 1 year of a hip fracture. Most individuals do not regain their prior level of function after a hip fracture,” said Joe C. Huang, MD, who was asked for comment. He is a clinical assistant professor of gerontology and geriatric medicine at Harborview Medical Center Senior Care Clinic and Healthy Bones Clinic in Seattle.
Details of the Intervention
The bone health service (BHS) intervention employed an electronic health record case-finding tool and a nurse care manager who undertook screening and treatment monitoring. They identified potential risk factors that included hyperthyroidism, hyperparathyroidism, rheumatoid arthritis, alcohol dependence, chronic lung disease, chronic liver disease, stroke, parkinsonism, prostate cancer, smoking, diabetes, pernicious anemia, gastrectomy, or high-risk medication use in at least 3 months of the prior 2 years. These medications included traditional antiepileptics, glucocorticoids, and androgen deprivation therapy.
The BHS nurse invited eligible men to be screened using an initial letter, followed by up to three phone calls. After DXA screening, the nurse scheduled an electronic consult with an osteoporosis expert, and patients with a T-score between -1 and -2.4 and an elevated 10-year fracture risk as measured by the Fracture Risk Assessment Tool were recommended for osteoporosis medication, vitamin D, and dietary or supplemental calcium. Following the prescription, the nurse provided patient education over the phone and mailed out written instructions. The nurse also made phone calls at 1 month, 6 months, and 12 months to encourage adherence and address common treatment barriers such as forgetting to take medication or dealing with gastrointestinal effects. The researchers recruited 38 primary care physicians from two VA health systems. The study included 3112 male veterans between the ages of 65 and 85 years (40.4% Black and 56% White). Nearly all participants (85.5%) had at least one indication for screening according to VA undersecretary guidelines, and almost a third (32.1%) had been prescribed androgen deprivation therapy, traditional antiepileptic drugs, or glucocorticoids.
Over a mean follow-up of 1.5 years, there was a much higher screening rate in the BHS group (49.2% vs 2.3%; P < .001), with a similar overall yield of DXA results recommending osteoporosis treatment (22.4% vs 27.2%). In the BHS group, 84.4% of patients who had treatment recommended followed through with treatment initiation. The mean persistence over follow-up was 657 days (SD, 366 days), and adherence was high with a mean proportion of days covered of 91.7%.
It was not possible to statistically compare adherence with the usual-care group because there were too few screened patients found to be eligible for treatment in that group, but the historic mean proportion of days covered at the two participating facilities was 52%.
After 2 years, the mean femoral neck T-score tested randomly in a subset of patients was better in the BHS arm, although it did not meet statistical significance according to the Bonferroni corrected criterion of P < .025 (-0.55 vs -0.70; P = .04). Fracture rates were similar between the two groups (1.8% vs 2.0%; P = .69).
Can the Findings Be Translated Across Clinics?
It remains to be seen how well the model could translate to other healthcare settings, according to Kenny Lin, MD, MPH, who was asked for comment on the study. “Outside of the VA health system and perhaps integrated HMOs [health maintenance organizations] such as Kaiser, Geisinger, etc., it seems unlikely that most primary care docs will have access to a centralized bone health service. Who’s going to pay for it? It leaves unanswered the question of whether it’s more efficient to address [osteoporosis] screening on a practice or population level. I suspect the latter is probably superior, but this study doesn’t provide any empiric evidence that this is so,” said Lin, associate director of the Penn Medicine Lancaster General Hospital’s Family Medicine Residency Program, Lancaster, Pennsylvania. The findings could help sway recommendations to screen men for osteoporosis, according to Susan Ott, MD, who was also asked for comment. Guideline committees “have been trying to be very scientific [about it]. I think they overdo it because they only look at one or two kinds of studies, and there are more kinds of science than just a randomized clinical trial. But they’re kind of stuck on that. The fact that this study was a randomized trial maybe they will finally change their recommendation, because there really shouldn’t be any difference in screening for men and for women. The men are actually discriminated against,” said Ott, emeritus professor of medicine at the University of Washington, Seattle.
In fact, she noted that the risks for men are similar to those for women, except that men tend to develop issues 5-10 years later in life. To screen and treat men, healthcare systems can “do the same thing they do with women. Just change the age range,” Ott said.
Lin sounded a different note, suggesting that the focus should remain on improvement of screening and treatment adherence in women. “We know that up to two thirds of women discontinue osteoporosis drugs within a year, and if we can’t figure out how to improve abysmal adherence in women, it’s unlikely we will persuade enough men to take these drugs to make a difference,” he said.
The study was funded by a grant from the VA Health Systems Research. Colón-Emeric, Lin, Ott, and Huang reported having no relevant financial disclosures.
A version of this article first appeared on Medscape.com.
U.S. Health Chief Kennedy Targets Vaccine Injury Compensation Program
WASHINGTON (Reuters) - U.S. Health Secretary Robert F. Kennedy Jr. said on July 28 that he will work to “fix” the program that compensates victims of vaccine injuries, the National Vaccine Injury Compensation Program.
Kennedy, a long-time vaccine skeptic and former vaccine injury plaintiff lawyer, accused the program and its so-called “Vaccine Court” of corruption and inefficiency in a post on X. He has long been an outspoken critic of the program.
“I will not allow the VICP to continue to ignore its mandate and fail its mission of quickly and fairly compensating vaccine-injured individuals,” he wrote, adding he was working with Attorney General Pam Bondi. “Together, we will steer the Vaccine Court back to its original congressional intent.”
He said the structure disadvantaged claimants because the Department of Health & Human Services – which he now leads – is the defendant, as opposed to vaccine makers.
Changing the VICP would be the latest in a series of far-reaching actions by Kennedy to reshape U.S. regulation of vaccines, food and medicine.
In June, he fired all 17 members of the Centers for Disease Control and Prevention’s Advisory Committee on Immunization Practices, a panel of vaccine experts, replacing them with 7 handpicked members, including known vaccine skeptics.
One of them earned thousands of dollars as an expert witness in litigation against Merck’s, Gardasil vaccine, court records show. Kennedy himself played an instrumental role in organizing mass litigation over the vaccine.
He also is planning to remove all the members of another advisory panel that determines what preventive health measures insurers must cover, the Wall Street Journal reported on July 25. An HHS spokesperson said Kennedy had not yet made a decision regarding the 16-member U.S. Preventive Services Task Force.
Kennedy has for years sown doubt about the safety and efficacy of vaccines. He has a history of clashing with the medical establishment and spreading misinformation about vaccines, including promoting a debunked link between vaccines and autism despite scientific evidence to the contrary.
He has also said the measles vaccine contains cells from aborted fetuses and that the mumps vaccination does not work, comments he made as the U.S. battles one of its worst outbreaks of measles in 25 years.
Kennedy made millions over the years from advocating against vaccines through case referrals, book sales, and consulting fees paid by a nonprofit he founded, according to ethics disclosures.
(Reporting by Ahmed Aboulenein; Additional reporting by Ryan Patrick Jones in Toronto; Editing by Doina Chiacu and Nia Williams)
A version of this article appeared on Medscape.com.
WASHINGTON (Reuters) - U.S. Health Secretary Robert F. Kennedy Jr. said on July 28 that he will work to “fix” the program that compensates victims of vaccine injuries, the National Vaccine Injury Compensation Program.
Kennedy, a long-time vaccine skeptic and former vaccine injury plaintiff lawyer, accused the program and its so-called “Vaccine Court” of corruption and inefficiency in a post on X. He has long been an outspoken critic of the program.
“I will not allow the VICP to continue to ignore its mandate and fail its mission of quickly and fairly compensating vaccine-injured individuals,” he wrote, adding he was working with Attorney General Pam Bondi. “Together, we will steer the Vaccine Court back to its original congressional intent.”
He said the structure disadvantaged claimants because the Department of Health & Human Services – which he now leads – is the defendant, as opposed to vaccine makers.
Changing the VICP would be the latest in a series of far-reaching actions by Kennedy to reshape U.S. regulation of vaccines, food and medicine.
In June, he fired all 17 members of the Centers for Disease Control and Prevention’s Advisory Committee on Immunization Practices, a panel of vaccine experts, replacing them with 7 handpicked members, including known vaccine skeptics.
One of them earned thousands of dollars as an expert witness in litigation against Merck’s, Gardasil vaccine, court records show. Kennedy himself played an instrumental role in organizing mass litigation over the vaccine.
He also is planning to remove all the members of another advisory panel that determines what preventive health measures insurers must cover, the Wall Street Journal reported on July 25. An HHS spokesperson said Kennedy had not yet made a decision regarding the 16-member U.S. Preventive Services Task Force.
Kennedy has for years sown doubt about the safety and efficacy of vaccines. He has a history of clashing with the medical establishment and spreading misinformation about vaccines, including promoting a debunked link between vaccines and autism despite scientific evidence to the contrary.
He has also said the measles vaccine contains cells from aborted fetuses and that the mumps vaccination does not work, comments he made as the U.S. battles one of its worst outbreaks of measles in 25 years.
Kennedy made millions over the years from advocating against vaccines through case referrals, book sales, and consulting fees paid by a nonprofit he founded, according to ethics disclosures.
(Reporting by Ahmed Aboulenein; Additional reporting by Ryan Patrick Jones in Toronto; Editing by Doina Chiacu and Nia Williams)
A version of this article appeared on Medscape.com.
WASHINGTON (Reuters) - U.S. Health Secretary Robert F. Kennedy Jr. said on July 28 that he will work to “fix” the program that compensates victims of vaccine injuries, the National Vaccine Injury Compensation Program.
Kennedy, a long-time vaccine skeptic and former vaccine injury plaintiff lawyer, accused the program and its so-called “Vaccine Court” of corruption and inefficiency in a post on X. He has long been an outspoken critic of the program.
“I will not allow the VICP to continue to ignore its mandate and fail its mission of quickly and fairly compensating vaccine-injured individuals,” he wrote, adding he was working with Attorney General Pam Bondi. “Together, we will steer the Vaccine Court back to its original congressional intent.”
He said the structure disadvantaged claimants because the Department of Health & Human Services – which he now leads – is the defendant, as opposed to vaccine makers.
Changing the VICP would be the latest in a series of far-reaching actions by Kennedy to reshape U.S. regulation of vaccines, food and medicine.
In June, he fired all 17 members of the Centers for Disease Control and Prevention’s Advisory Committee on Immunization Practices, a panel of vaccine experts, replacing them with 7 handpicked members, including known vaccine skeptics.
One of them earned thousands of dollars as an expert witness in litigation against Merck’s, Gardasil vaccine, court records show. Kennedy himself played an instrumental role in organizing mass litigation over the vaccine.
He also is planning to remove all the members of another advisory panel that determines what preventive health measures insurers must cover, the Wall Street Journal reported on July 25. An HHS spokesperson said Kennedy had not yet made a decision regarding the 16-member U.S. Preventive Services Task Force.
Kennedy has for years sown doubt about the safety and efficacy of vaccines. He has a history of clashing with the medical establishment and spreading misinformation about vaccines, including promoting a debunked link between vaccines and autism despite scientific evidence to the contrary.
He has also said the measles vaccine contains cells from aborted fetuses and that the mumps vaccination does not work, comments he made as the U.S. battles one of its worst outbreaks of measles in 25 years.
Kennedy made millions over the years from advocating against vaccines through case referrals, book sales, and consulting fees paid by a nonprofit he founded, according to ethics disclosures.
(Reporting by Ahmed Aboulenein; Additional reporting by Ryan Patrick Jones in Toronto; Editing by Doina Chiacu and Nia Williams)
A version of this article appeared on Medscape.com.
Rurality and Age May Shape Phone-Only Mental Health Care Access Among Veterans
TOPLINE:
Patients living in rural areas and those aged ≥ 65 y had increased odds of receiving mental health care exclusively by phone.
METHODOLOGY:
- Researchers explored factors linked to receiving phone-only mental health care among patients within the Department of Veterans Affairs.
- They included data for 1,156,146 veteran patients with at least one mental health-specific outpatient encounter between October 2021 and September 2022 and at least one between October 2022 and September 2023.
- Patients were categorized as those who received care through phone only (n = 49,125) and those who received care through other methods (n = 1,107,021. Care was received exclusively through video (6.39%), in-person (6.63%), or a combination of in-person, video, and/or phone (86.98%).
- Demographic and clinical predictors, including rurality, age, sex, race, ethnicity, and the number of mental health diagnoses (< 3 vs ≥ 3), were evaluated.
TAKEAWAY:
- The phone-only group had a mean of 6.27 phone visits, whereas those who received care through other methods had a mean of 4.79 phone visits.
- Highly rural patients had 1.50 times higher odds of receiving phone-only mental health care than their urban counterparts (adjusted odds ratio [aOR], 1.50; P < .0001).
- Patients aged 65 years or older were more than twice as likely to receive phone-only care than those younger than 30 years (aOR, ≥ 2.17; P < .0001).
- Having fewer than three mental health diagnoses and more than 50% of mental health visits conducted by medical providers was associated with higher odds of receiving mental health care exclusively by phone (aORs, 2.03 and 1.87, respectively; P < .0001).
IN PRACTICE:
“The results of this work help to characterize the phone-only patient population and can serve to inform future implementation efforts to ensure that patients are receiving care via the modality that best meets their needs,” the authors wrote.
SOURCE:
This study was led by Samantha L. Connolly, PhD, at the VA Boston Healthcare System in Boston. It was published online in The Journal of Rural Health.
LIMITATIONS:
This study focused on a veteran population which may limit the generalizability of the findings to other groups. Additionally, its cross-sectional design restricted the ability to determine cause-and-effect relationships between factors and phone-only care.
DISCLOSURES:
This study was supported by the US Department of Veterans Affairs. The authors declared having no conflicts of interest.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
A version of this article first appeared on Medscape.com.
TOPLINE:
Patients living in rural areas and those aged ≥ 65 y had increased odds of receiving mental health care exclusively by phone.
METHODOLOGY:
- Researchers explored factors linked to receiving phone-only mental health care among patients within the Department of Veterans Affairs.
- They included data for 1,156,146 veteran patients with at least one mental health-specific outpatient encounter between October 2021 and September 2022 and at least one between October 2022 and September 2023.
- Patients were categorized as those who received care through phone only (n = 49,125) and those who received care through other methods (n = 1,107,021. Care was received exclusively through video (6.39%), in-person (6.63%), or a combination of in-person, video, and/or phone (86.98%).
- Demographic and clinical predictors, including rurality, age, sex, race, ethnicity, and the number of mental health diagnoses (< 3 vs ≥ 3), were evaluated.
TAKEAWAY:
- The phone-only group had a mean of 6.27 phone visits, whereas those who received care through other methods had a mean of 4.79 phone visits.
- Highly rural patients had 1.50 times higher odds of receiving phone-only mental health care than their urban counterparts (adjusted odds ratio [aOR], 1.50; P < .0001).
- Patients aged 65 years or older were more than twice as likely to receive phone-only care than those younger than 30 years (aOR, ≥ 2.17; P < .0001).
- Having fewer than three mental health diagnoses and more than 50% of mental health visits conducted by medical providers was associated with higher odds of receiving mental health care exclusively by phone (aORs, 2.03 and 1.87, respectively; P < .0001).
IN PRACTICE:
“The results of this work help to characterize the phone-only patient population and can serve to inform future implementation efforts to ensure that patients are receiving care via the modality that best meets their needs,” the authors wrote.
SOURCE:
This study was led by Samantha L. Connolly, PhD, at the VA Boston Healthcare System in Boston. It was published online in The Journal of Rural Health.
LIMITATIONS:
This study focused on a veteran population which may limit the generalizability of the findings to other groups. Additionally, its cross-sectional design restricted the ability to determine cause-and-effect relationships between factors and phone-only care.
DISCLOSURES:
This study was supported by the US Department of Veterans Affairs. The authors declared having no conflicts of interest.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
A version of this article first appeared on Medscape.com.
TOPLINE:
Patients living in rural areas and those aged ≥ 65 y had increased odds of receiving mental health care exclusively by phone.
METHODOLOGY:
- Researchers explored factors linked to receiving phone-only mental health care among patients within the Department of Veterans Affairs.
- They included data for 1,156,146 veteran patients with at least one mental health-specific outpatient encounter between October 2021 and September 2022 and at least one between October 2022 and September 2023.
- Patients were categorized as those who received care through phone only (n = 49,125) and those who received care through other methods (n = 1,107,021. Care was received exclusively through video (6.39%), in-person (6.63%), or a combination of in-person, video, and/or phone (86.98%).
- Demographic and clinical predictors, including rurality, age, sex, race, ethnicity, and the number of mental health diagnoses (< 3 vs ≥ 3), were evaluated.
TAKEAWAY:
- The phone-only group had a mean of 6.27 phone visits, whereas those who received care through other methods had a mean of 4.79 phone visits.
- Highly rural patients had 1.50 times higher odds of receiving phone-only mental health care than their urban counterparts (adjusted odds ratio [aOR], 1.50; P < .0001).
- Patients aged 65 years or older were more than twice as likely to receive phone-only care than those younger than 30 years (aOR, ≥ 2.17; P < .0001).
- Having fewer than three mental health diagnoses and more than 50% of mental health visits conducted by medical providers was associated with higher odds of receiving mental health care exclusively by phone (aORs, 2.03 and 1.87, respectively; P < .0001).
IN PRACTICE:
“The results of this work help to characterize the phone-only patient population and can serve to inform future implementation efforts to ensure that patients are receiving care via the modality that best meets their needs,” the authors wrote.
SOURCE:
This study was led by Samantha L. Connolly, PhD, at the VA Boston Healthcare System in Boston. It was published online in The Journal of Rural Health.
LIMITATIONS:
This study focused on a veteran population which may limit the generalizability of the findings to other groups. Additionally, its cross-sectional design restricted the ability to determine cause-and-effect relationships between factors and phone-only care.
DISCLOSURES:
This study was supported by the US Department of Veterans Affairs. The authors declared having no conflicts of interest.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
A version of this article first appeared on Medscape.com.
Searching for the Optimal CRC Surveillance Test
About a third of the US population are eligible for colorectal cancer screening but aren’t up to date on screening.
Many patients are reluctant to test for colon cancer for a variety of reasons, said Jeffrey K. Lee, MD, MPH, a research scientist at the Kaiser Permanente Northern California Division of Research and an attending gastroenterologist at Kaiser Permanente San Francisco Medical Center.
“As a gastroenterologist, I strongly believe we should emphasize the importance of colorectal cancer screening. And there’s many tests available, not just a colonoscopy, to help reduce your chances of developing colorectal cancer and even dying from colorectal cancer,” said Dr. Lee.
Many patients prefer a test that’s more convenient, that doesn’t require them to take time out of their busy schedules. “We must educate our patients that there are some noninvasive screening options that are helpful, and to be able to share with them some of the benefits, but also some of the drawbacks compared to colonoscopy and allow them to have a choice,” he advised.
He is a recipient of the AGA Research Scholar Award, and has in turn supported other researchers by contributing to the AGA Research Foundation. In 2012, Dr. Lee received a grant from the Sylvia Allison Kaplan Clinical Research Fund to fund a study on long-term colorectal cancer risk in patients with normal colonoscopy results.
The findings, published in JAMA Internal Medicine, determined that 10 years after a negative colonoscopy, Kaiser Permanente members had a 46% lower risk of being diagnosed with CRC and were 88% less likely to die from disease compared with patients who didn’t undergo screening.
“Furthermore, the reduced risk of developing colorectal cancer, even dying from it, persisted for more than 12 years after the examination compared with an unscreened population,” said Dr. Lee. “I firmly believe our study really supports the ten-year screening interval after a normal colonoscopy, as currently recommended by our guidelines.”
In an interview, he discussed his research efforts to find the best detection regimens for CRC, and the mentors who guided his career path as a GI scientist.
Q: Why did you choose GI?
During medical school I was fortunate to work in the lab of Dr. John M. Carethers at UC San Diego. He introduced me to GI and inspired me to choose GI as a career. His mentorship was invaluable because he not only solidified my interest in GI, but also inspired me to become a physician scientist, focusing on colorectal cancer prevention and control. His amazing mentorship drew me to this field.
Q: One of your clinical focus areas is hereditary gastrointestinal cancer syndromes. How did you become interested in this area of GI medicine?
My interest in hereditary GI cancer syndromes stemmed from my work as a medical student in Dr. Carethers’ lab. One of my research projects was looking at certain gene mutations among patients with hereditary GI cancer syndromes, specifically, familial hamartomatous polyposis syndrome. It was through these research projects and seeing how these genetic mutations impacted their risk of developing colorectal cancer, inspired me to care for patients with hereditary GI cancer syndromes.
Q: Have you been doing any research on the reasons why more young people are getting colon cancer?
We recently published work looking at the potential factors that may be driving the rising rates of early onset colorectal cancer. One hypothesis that’s been floating around is antibiotic exposure in early adulthood or childhood because of its effect on the microbiome. Using our large database at Kaiser Permanente Northern California, we did not find an association between oral antibiotic use during early adulthood and the risk of early-onset colorectal cancer.
You have the usual suspects like obesity and diabetes, but it’s not explaining all that risk. While familial colorectal cancer syndromes contribute to a small proportion of early-onset colorectal, these syndromes are not increasing across generations. I really do feel it’s something in the diet or how foods are processed and environmental factors that’s driving some of the risk of early onset colorectal cancer and this should be explored further.
Q: In 2018, you issued a landmark study which found an association between a 10-year follow-up after negative colonoscopy and reduced risk of disease and mortality. Has there been any updates to these findings over the last 6 years?
We recently saw a study in JAMA Oncology of a Swedish cohort that showed a negative colonoscopy result was associated with a reduced risk of developing and even dying from colorectal cancer 15 years from that examination, compared to the general population of Sweden. I think there’s some things that we need to be cautious about regarding that study. We have to think about the comparison group that they used and the lack of information regarding the indication of the colonoscopy and the quality of the examination. So, it remains uncertain whether future guidelines are going to stretch out that 10-year interval to 15 years.
Q: What other CRC studies are you working on now?
We have several studies that we are working on right now. One is called the PREVENT CRC study, which is looking at whether a polygenic risk score can improve risk stratification following adenoma removal for colorectal cancer prevention and tailoring post-polypectomy surveillance. This is a large observational cohort study that we have teamed up with the Fred Hutchinson Cancer Center, Erasmus University, and Kaiser Permanente Northwest to answer this important question that may have implications for personalized medicine.
Then there’s the COOP study, funded by the Patient-Centered Outcomes Research Institute. This is looking at the best surveillance test to use among older adults 65 years and older with a history of polyps. The trial is randomizing them to either getting a colonoscopy for surveillance or annual fecal immunochemical test (FIT) for surveillance. This is to see which test is best for detecting colorectal cancer among older adults with a history of polyps.
Q: Do you think FIT tests could eventually replace colonoscopy, given that it’s less invasive?
Although FIT and other stool-based tests are less invasive and have been shown to have high accuracy for detecting colorectal cancer, I personally do not think they are going to replace colonoscopy as the most popular screening modality in the United States. Colonoscopy remains the gold standard for detecting and removing precancerous polyps and has the highest accuracy for detecting colorectal cancer.
Q: Besides Dr. Carethers, what teacher or mentor had the greatest impact on you?
Clinically it’s been Dr. Jonathan Terdiman from UCSF, who taught me everything I know about clinical GI, and the art of colonoscopy. In addition, Douglas A. Corley, MD, PhD, the Permanente Medical Group’s chief research officer, has made the greatest impact on my research career. He’s really taught me how to rigorously design a research study to answer important clinically relevant questions, and has given me the skill set to write NIH grants. I would not be here without these mentors who are truly giants in the field of GI.
Q: When you’re not being a GI, how do you spend your free weekend afternoons? Are you still a “Cal Bears” fan at your alma mater, UC Berkeley?
I spend a lot of time taking my kids to their activities on the weekends. I just took my son to a Cal Bears Game Day, which was hosted by ESPN at Berkeley.
It was an incredible experience hearing sports analyst Pat McAfee lead all the Cal chants, seeing Nick Saban from the University of Alabama take off his red tie and replace it with a Cal Bears tie, and watching a Cal student win a hundred thousand dollars by kicking a football through the goal posts wearing checkered vans.
Lightning Round
Texting or talking?
Text
Favorite breakfast?
Taiwanese breakfast
Place you most want to travel to?
Japan
Favorite junk food?
Trader Joe’s chili lime chips
Favorite season?
Springtime, baseball season
Favorite ice cream flavor?
Mint chocolate chip
How many cups of coffee do you drink per day?
2-3
Last movie you watched?
Oppenheimer
Best place you ever went on vacation?
Hawaii
If you weren’t a gastroenterologist, what would you be?
Barber
Best Halloween costume you ever wore?
SpongeBob SquarePants
Favorite sport?
Tennis
What song do you have to sing along with when you hear it?
Any classic 80s song
Introvert or extrovert?
Introvert
About a third of the US population are eligible for colorectal cancer screening but aren’t up to date on screening.
Many patients are reluctant to test for colon cancer for a variety of reasons, said Jeffrey K. Lee, MD, MPH, a research scientist at the Kaiser Permanente Northern California Division of Research and an attending gastroenterologist at Kaiser Permanente San Francisco Medical Center.
“As a gastroenterologist, I strongly believe we should emphasize the importance of colorectal cancer screening. And there’s many tests available, not just a colonoscopy, to help reduce your chances of developing colorectal cancer and even dying from colorectal cancer,” said Dr. Lee.
Many patients prefer a test that’s more convenient, that doesn’t require them to take time out of their busy schedules. “We must educate our patients that there are some noninvasive screening options that are helpful, and to be able to share with them some of the benefits, but also some of the drawbacks compared to colonoscopy and allow them to have a choice,” he advised.
He is a recipient of the AGA Research Scholar Award, and has in turn supported other researchers by contributing to the AGA Research Foundation. In 2012, Dr. Lee received a grant from the Sylvia Allison Kaplan Clinical Research Fund to fund a study on long-term colorectal cancer risk in patients with normal colonoscopy results.
The findings, published in JAMA Internal Medicine, determined that 10 years after a negative colonoscopy, Kaiser Permanente members had a 46% lower risk of being diagnosed with CRC and were 88% less likely to die from disease compared with patients who didn’t undergo screening.
“Furthermore, the reduced risk of developing colorectal cancer, even dying from it, persisted for more than 12 years after the examination compared with an unscreened population,” said Dr. Lee. “I firmly believe our study really supports the ten-year screening interval after a normal colonoscopy, as currently recommended by our guidelines.”
In an interview, he discussed his research efforts to find the best detection regimens for CRC, and the mentors who guided his career path as a GI scientist.
Q: Why did you choose GI?
During medical school I was fortunate to work in the lab of Dr. John M. Carethers at UC San Diego. He introduced me to GI and inspired me to choose GI as a career. His mentorship was invaluable because he not only solidified my interest in GI, but also inspired me to become a physician scientist, focusing on colorectal cancer prevention and control. His amazing mentorship drew me to this field.
Q: One of your clinical focus areas is hereditary gastrointestinal cancer syndromes. How did you become interested in this area of GI medicine?
My interest in hereditary GI cancer syndromes stemmed from my work as a medical student in Dr. Carethers’ lab. One of my research projects was looking at certain gene mutations among patients with hereditary GI cancer syndromes, specifically, familial hamartomatous polyposis syndrome. It was through these research projects and seeing how these genetic mutations impacted their risk of developing colorectal cancer, inspired me to care for patients with hereditary GI cancer syndromes.
Q: Have you been doing any research on the reasons why more young people are getting colon cancer?
We recently published work looking at the potential factors that may be driving the rising rates of early onset colorectal cancer. One hypothesis that’s been floating around is antibiotic exposure in early adulthood or childhood because of its effect on the microbiome. Using our large database at Kaiser Permanente Northern California, we did not find an association between oral antibiotic use during early adulthood and the risk of early-onset colorectal cancer.
You have the usual suspects like obesity and diabetes, but it’s not explaining all that risk. While familial colorectal cancer syndromes contribute to a small proportion of early-onset colorectal, these syndromes are not increasing across generations. I really do feel it’s something in the diet or how foods are processed and environmental factors that’s driving some of the risk of early onset colorectal cancer and this should be explored further.
Q: In 2018, you issued a landmark study which found an association between a 10-year follow-up after negative colonoscopy and reduced risk of disease and mortality. Has there been any updates to these findings over the last 6 years?
We recently saw a study in JAMA Oncology of a Swedish cohort that showed a negative colonoscopy result was associated with a reduced risk of developing and even dying from colorectal cancer 15 years from that examination, compared to the general population of Sweden. I think there’s some things that we need to be cautious about regarding that study. We have to think about the comparison group that they used and the lack of information regarding the indication of the colonoscopy and the quality of the examination. So, it remains uncertain whether future guidelines are going to stretch out that 10-year interval to 15 years.
Q: What other CRC studies are you working on now?
We have several studies that we are working on right now. One is called the PREVENT CRC study, which is looking at whether a polygenic risk score can improve risk stratification following adenoma removal for colorectal cancer prevention and tailoring post-polypectomy surveillance. This is a large observational cohort study that we have teamed up with the Fred Hutchinson Cancer Center, Erasmus University, and Kaiser Permanente Northwest to answer this important question that may have implications for personalized medicine.
Then there’s the COOP study, funded by the Patient-Centered Outcomes Research Institute. This is looking at the best surveillance test to use among older adults 65 years and older with a history of polyps. The trial is randomizing them to either getting a colonoscopy for surveillance or annual fecal immunochemical test (FIT) for surveillance. This is to see which test is best for detecting colorectal cancer among older adults with a history of polyps.
Q: Do you think FIT tests could eventually replace colonoscopy, given that it’s less invasive?
Although FIT and other stool-based tests are less invasive and have been shown to have high accuracy for detecting colorectal cancer, I personally do not think they are going to replace colonoscopy as the most popular screening modality in the United States. Colonoscopy remains the gold standard for detecting and removing precancerous polyps and has the highest accuracy for detecting colorectal cancer.
Q: Besides Dr. Carethers, what teacher or mentor had the greatest impact on you?
Clinically it’s been Dr. Jonathan Terdiman from UCSF, who taught me everything I know about clinical GI, and the art of colonoscopy. In addition, Douglas A. Corley, MD, PhD, the Permanente Medical Group’s chief research officer, has made the greatest impact on my research career. He’s really taught me how to rigorously design a research study to answer important clinically relevant questions, and has given me the skill set to write NIH grants. I would not be here without these mentors who are truly giants in the field of GI.
Q: When you’re not being a GI, how do you spend your free weekend afternoons? Are you still a “Cal Bears” fan at your alma mater, UC Berkeley?
I spend a lot of time taking my kids to their activities on the weekends. I just took my son to a Cal Bears Game Day, which was hosted by ESPN at Berkeley.
It was an incredible experience hearing sports analyst Pat McAfee lead all the Cal chants, seeing Nick Saban from the University of Alabama take off his red tie and replace it with a Cal Bears tie, and watching a Cal student win a hundred thousand dollars by kicking a football through the goal posts wearing checkered vans.
Lightning Round
Texting or talking?
Text
Favorite breakfast?
Taiwanese breakfast
Place you most want to travel to?
Japan
Favorite junk food?
Trader Joe’s chili lime chips
Favorite season?
Springtime, baseball season
Favorite ice cream flavor?
Mint chocolate chip
How many cups of coffee do you drink per day?
2-3
Last movie you watched?
Oppenheimer
Best place you ever went on vacation?
Hawaii
If you weren’t a gastroenterologist, what would you be?
Barber
Best Halloween costume you ever wore?
SpongeBob SquarePants
Favorite sport?
Tennis
What song do you have to sing along with when you hear it?
Any classic 80s song
Introvert or extrovert?
Introvert
About a third of the US population are eligible for colorectal cancer screening but aren’t up to date on screening.
Many patients are reluctant to test for colon cancer for a variety of reasons, said Jeffrey K. Lee, MD, MPH, a research scientist at the Kaiser Permanente Northern California Division of Research and an attending gastroenterologist at Kaiser Permanente San Francisco Medical Center.
“As a gastroenterologist, I strongly believe we should emphasize the importance of colorectal cancer screening. And there’s many tests available, not just a colonoscopy, to help reduce your chances of developing colorectal cancer and even dying from colorectal cancer,” said Dr. Lee.
Many patients prefer a test that’s more convenient, that doesn’t require them to take time out of their busy schedules. “We must educate our patients that there are some noninvasive screening options that are helpful, and to be able to share with them some of the benefits, but also some of the drawbacks compared to colonoscopy and allow them to have a choice,” he advised.
He is a recipient of the AGA Research Scholar Award, and has in turn supported other researchers by contributing to the AGA Research Foundation. In 2012, Dr. Lee received a grant from the Sylvia Allison Kaplan Clinical Research Fund to fund a study on long-term colorectal cancer risk in patients with normal colonoscopy results.
The findings, published in JAMA Internal Medicine, determined that 10 years after a negative colonoscopy, Kaiser Permanente members had a 46% lower risk of being diagnosed with CRC and were 88% less likely to die from disease compared with patients who didn’t undergo screening.
“Furthermore, the reduced risk of developing colorectal cancer, even dying from it, persisted for more than 12 years after the examination compared with an unscreened population,” said Dr. Lee. “I firmly believe our study really supports the ten-year screening interval after a normal colonoscopy, as currently recommended by our guidelines.”
In an interview, he discussed his research efforts to find the best detection regimens for CRC, and the mentors who guided his career path as a GI scientist.
Q: Why did you choose GI?
During medical school I was fortunate to work in the lab of Dr. John M. Carethers at UC San Diego. He introduced me to GI and inspired me to choose GI as a career. His mentorship was invaluable because he not only solidified my interest in GI, but also inspired me to become a physician scientist, focusing on colorectal cancer prevention and control. His amazing mentorship drew me to this field.
Q: One of your clinical focus areas is hereditary gastrointestinal cancer syndromes. How did you become interested in this area of GI medicine?
My interest in hereditary GI cancer syndromes stemmed from my work as a medical student in Dr. Carethers’ lab. One of my research projects was looking at certain gene mutations among patients with hereditary GI cancer syndromes, specifically, familial hamartomatous polyposis syndrome. It was through these research projects and seeing how these genetic mutations impacted their risk of developing colorectal cancer, inspired me to care for patients with hereditary GI cancer syndromes.
Q: Have you been doing any research on the reasons why more young people are getting colon cancer?
We recently published work looking at the potential factors that may be driving the rising rates of early onset colorectal cancer. One hypothesis that’s been floating around is antibiotic exposure in early adulthood or childhood because of its effect on the microbiome. Using our large database at Kaiser Permanente Northern California, we did not find an association between oral antibiotic use during early adulthood and the risk of early-onset colorectal cancer.
You have the usual suspects like obesity and diabetes, but it’s not explaining all that risk. While familial colorectal cancer syndromes contribute to a small proportion of early-onset colorectal, these syndromes are not increasing across generations. I really do feel it’s something in the diet or how foods are processed and environmental factors that’s driving some of the risk of early onset colorectal cancer and this should be explored further.
Q: In 2018, you issued a landmark study which found an association between a 10-year follow-up after negative colonoscopy and reduced risk of disease and mortality. Has there been any updates to these findings over the last 6 years?
We recently saw a study in JAMA Oncology of a Swedish cohort that showed a negative colonoscopy result was associated with a reduced risk of developing and even dying from colorectal cancer 15 years from that examination, compared to the general population of Sweden. I think there’s some things that we need to be cautious about regarding that study. We have to think about the comparison group that they used and the lack of information regarding the indication of the colonoscopy and the quality of the examination. So, it remains uncertain whether future guidelines are going to stretch out that 10-year interval to 15 years.
Q: What other CRC studies are you working on now?
We have several studies that we are working on right now. One is called the PREVENT CRC study, which is looking at whether a polygenic risk score can improve risk stratification following adenoma removal for colorectal cancer prevention and tailoring post-polypectomy surveillance. This is a large observational cohort study that we have teamed up with the Fred Hutchinson Cancer Center, Erasmus University, and Kaiser Permanente Northwest to answer this important question that may have implications for personalized medicine.
Then there’s the COOP study, funded by the Patient-Centered Outcomes Research Institute. This is looking at the best surveillance test to use among older adults 65 years and older with a history of polyps. The trial is randomizing them to either getting a colonoscopy for surveillance or annual fecal immunochemical test (FIT) for surveillance. This is to see which test is best for detecting colorectal cancer among older adults with a history of polyps.
Q: Do you think FIT tests could eventually replace colonoscopy, given that it’s less invasive?
Although FIT and other stool-based tests are less invasive and have been shown to have high accuracy for detecting colorectal cancer, I personally do not think they are going to replace colonoscopy as the most popular screening modality in the United States. Colonoscopy remains the gold standard for detecting and removing precancerous polyps and has the highest accuracy for detecting colorectal cancer.
Q: Besides Dr. Carethers, what teacher or mentor had the greatest impact on you?
Clinically it’s been Dr. Jonathan Terdiman from UCSF, who taught me everything I know about clinical GI, and the art of colonoscopy. In addition, Douglas A. Corley, MD, PhD, the Permanente Medical Group’s chief research officer, has made the greatest impact on my research career. He’s really taught me how to rigorously design a research study to answer important clinically relevant questions, and has given me the skill set to write NIH grants. I would not be here without these mentors who are truly giants in the field of GI.
Q: When you’re not being a GI, how do you spend your free weekend afternoons? Are you still a “Cal Bears” fan at your alma mater, UC Berkeley?
I spend a lot of time taking my kids to their activities on the weekends. I just took my son to a Cal Bears Game Day, which was hosted by ESPN at Berkeley.
It was an incredible experience hearing sports analyst Pat McAfee lead all the Cal chants, seeing Nick Saban from the University of Alabama take off his red tie and replace it with a Cal Bears tie, and watching a Cal student win a hundred thousand dollars by kicking a football through the goal posts wearing checkered vans.
Lightning Round
Texting or talking?
Text
Favorite breakfast?
Taiwanese breakfast
Place you most want to travel to?
Japan
Favorite junk food?
Trader Joe’s chili lime chips
Favorite season?
Springtime, baseball season
Favorite ice cream flavor?
Mint chocolate chip
How many cups of coffee do you drink per day?
2-3
Last movie you watched?
Oppenheimer
Best place you ever went on vacation?
Hawaii
If you weren’t a gastroenterologist, what would you be?
Barber
Best Halloween costume you ever wore?
SpongeBob SquarePants
Favorite sport?
Tennis
What song do you have to sing along with when you hear it?
Any classic 80s song
Introvert or extrovert?
Introvert
Racial, Ethnic Discrimination Tied to Psychosis Risk
TOPLINE:
Racial and ethnic discrimination was consistently associated with increased risk for psychosis in studies included in a new umbrella review, with odds nearly doubled for both psychotic symptoms and experiences.
METHODOLOGY:
- Researchers searched 5 databases and then conducted an umbrella review of 7 systematic reviews, 4 of which included meta-analyses, published between 2003 and 2023.
- The systematic reviews included 23 primary studies representing more than 40,000 participants from Europe and the US.
- Investigators assessed the potential association between perceived racial or ethnic discrimination (mostly measured using self-reported questionnaires) and risk for psychosis (measured using established questionnaires).
- They assessed the risk for bias using the 16-item A MeaSurement Tool to Assess systematic Reviews, version 2 (AMSTAR-2) checklist.
TAKEAWAY:
- All reviews that included meta-analyses showed significant associations between perceived ethnic discrimination and psychotic symptoms (adjusted odds ratio [aOR], 1.78; 95% CI, 1.3-2.5) and psychotic experiences (pooled OR, 1.9; 95% CI, 1.4-2.7).
- Perceived racial or ethnic discrimination was also strongly linked to delusional symptoms (OR, 2.5; 95% CI, 1.6-4.0) and hallucinatory symptoms (OR, 1.65; 95% CI, 1.3-2.1).
- The largest of the included studies showed a dose-response relationship between higher levels of lifetime perceived racial or ethnic discrimination and greater likelihood of psychotic experiences.
- More robust associations were found in nonclinical populations compared to clinical ones, but there were significant associations in both.
IN PRACTICE:
“Our review was only looking at the impact of a person directly perceiving racism or interpersonal racial or ethnic discrimination; it may be that systemic racism, which can go unseen but still have profound impacts, could further contribute to mental health disparities,” lead investigator India Francis-Crossley, University College London, London, UK, said in a press release.
SOURCE:
The study was published online in PLOS Mental Health.
LIMITATIONS:
The evidence was primarily based on cross-sectional studies and was limited by high heterogeneity. The reviews included showed low or critically low AMSTAR-2 quality scores, which may have affected the robustness of the findings. More robust evidence was observed for psychotic outcomes in nonclinical populations compared to clinical samples. Additionally, the study potentially exacerbated errors or misreporting in the original reviews and did not include relevant structural factors such as income, education, housing, and poverty.
DISCLOSURES:
The study was funded by the University College London-Windsor Fellowship Research Opportunities scholarship, Wellcome Trust PhD Fellowship in Mental Health Science, Mental Health Mission Early Psychosis Workstream, and UK Research and Innovation funding for the Population Mental Health Consortium. The investigators reported having no relevant conflicts of interest.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
A version of this article first appeared on Medscape.com.
TOPLINE:
Racial and ethnic discrimination was consistently associated with increased risk for psychosis in studies included in a new umbrella review, with odds nearly doubled for both psychotic symptoms and experiences.
METHODOLOGY:
- Researchers searched 5 databases and then conducted an umbrella review of 7 systematic reviews, 4 of which included meta-analyses, published between 2003 and 2023.
- The systematic reviews included 23 primary studies representing more than 40,000 participants from Europe and the US.
- Investigators assessed the potential association between perceived racial or ethnic discrimination (mostly measured using self-reported questionnaires) and risk for psychosis (measured using established questionnaires).
- They assessed the risk for bias using the 16-item A MeaSurement Tool to Assess systematic Reviews, version 2 (AMSTAR-2) checklist.
TAKEAWAY:
- All reviews that included meta-analyses showed significant associations between perceived ethnic discrimination and psychotic symptoms (adjusted odds ratio [aOR], 1.78; 95% CI, 1.3-2.5) and psychotic experiences (pooled OR, 1.9; 95% CI, 1.4-2.7).
- Perceived racial or ethnic discrimination was also strongly linked to delusional symptoms (OR, 2.5; 95% CI, 1.6-4.0) and hallucinatory symptoms (OR, 1.65; 95% CI, 1.3-2.1).
- The largest of the included studies showed a dose-response relationship between higher levels of lifetime perceived racial or ethnic discrimination and greater likelihood of psychotic experiences.
- More robust associations were found in nonclinical populations compared to clinical ones, but there were significant associations in both.
IN PRACTICE:
“Our review was only looking at the impact of a person directly perceiving racism or interpersonal racial or ethnic discrimination; it may be that systemic racism, which can go unseen but still have profound impacts, could further contribute to mental health disparities,” lead investigator India Francis-Crossley, University College London, London, UK, said in a press release.
SOURCE:
The study was published online in PLOS Mental Health.
LIMITATIONS:
The evidence was primarily based on cross-sectional studies and was limited by high heterogeneity. The reviews included showed low or critically low AMSTAR-2 quality scores, which may have affected the robustness of the findings. More robust evidence was observed for psychotic outcomes in nonclinical populations compared to clinical samples. Additionally, the study potentially exacerbated errors or misreporting in the original reviews and did not include relevant structural factors such as income, education, housing, and poverty.
DISCLOSURES:
The study was funded by the University College London-Windsor Fellowship Research Opportunities scholarship, Wellcome Trust PhD Fellowship in Mental Health Science, Mental Health Mission Early Psychosis Workstream, and UK Research and Innovation funding for the Population Mental Health Consortium. The investigators reported having no relevant conflicts of interest.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
A version of this article first appeared on Medscape.com.
TOPLINE:
Racial and ethnic discrimination was consistently associated with increased risk for psychosis in studies included in a new umbrella review, with odds nearly doubled for both psychotic symptoms and experiences.
METHODOLOGY:
- Researchers searched 5 databases and then conducted an umbrella review of 7 systematic reviews, 4 of which included meta-analyses, published between 2003 and 2023.
- The systematic reviews included 23 primary studies representing more than 40,000 participants from Europe and the US.
- Investigators assessed the potential association between perceived racial or ethnic discrimination (mostly measured using self-reported questionnaires) and risk for psychosis (measured using established questionnaires).
- They assessed the risk for bias using the 16-item A MeaSurement Tool to Assess systematic Reviews, version 2 (AMSTAR-2) checklist.
TAKEAWAY:
- All reviews that included meta-analyses showed significant associations between perceived ethnic discrimination and psychotic symptoms (adjusted odds ratio [aOR], 1.78; 95% CI, 1.3-2.5) and psychotic experiences (pooled OR, 1.9; 95% CI, 1.4-2.7).
- Perceived racial or ethnic discrimination was also strongly linked to delusional symptoms (OR, 2.5; 95% CI, 1.6-4.0) and hallucinatory symptoms (OR, 1.65; 95% CI, 1.3-2.1).
- The largest of the included studies showed a dose-response relationship between higher levels of lifetime perceived racial or ethnic discrimination and greater likelihood of psychotic experiences.
- More robust associations were found in nonclinical populations compared to clinical ones, but there were significant associations in both.
IN PRACTICE:
“Our review was only looking at the impact of a person directly perceiving racism or interpersonal racial or ethnic discrimination; it may be that systemic racism, which can go unseen but still have profound impacts, could further contribute to mental health disparities,” lead investigator India Francis-Crossley, University College London, London, UK, said in a press release.
SOURCE:
The study was published online in PLOS Mental Health.
LIMITATIONS:
The evidence was primarily based on cross-sectional studies and was limited by high heterogeneity. The reviews included showed low or critically low AMSTAR-2 quality scores, which may have affected the robustness of the findings. More robust evidence was observed for psychotic outcomes in nonclinical populations compared to clinical samples. Additionally, the study potentially exacerbated errors or misreporting in the original reviews and did not include relevant structural factors such as income, education, housing, and poverty.
DISCLOSURES:
The study was funded by the University College London-Windsor Fellowship Research Opportunities scholarship, Wellcome Trust PhD Fellowship in Mental Health Science, Mental Health Mission Early Psychosis Workstream, and UK Research and Innovation funding for the Population Mental Health Consortium. The investigators reported having no relevant conflicts of interest.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
A version of this article first appeared on Medscape.com.
Parental Mental Disorders May Double Offspring Mortality Risk
TOPLINE:
Offspring of parents with mental disorders had nearly double the risk for mortality, especially from unnatural causes, compared to those with parents did not have a mental disorder, a new Swedish cohort study showed. Additionally, mortality risk was highest when both parents had mental disorders but was not affected by the sex of the affected parent.
METHODOLOGY:
- A nationwide register-based cohort study in Sweden included more than 3.5 million individuals born between 1973 and 2014 (51% men); 35% had a parent with a mental disorder (13% paternal, 16% maternal, and 6% both parents).
- Mental disorder categories included alcohol or substance use, psychotic, mood, anxiety or stress-related, eating, and personality disorders and intellectual disability. Exposure timing was classified by offspring age (mean age, 15.8 years) at parental diagnosis.
- Participants were followed up from birth until death, the death of either parent, emigration (up to 2014), either parent’s emigration, or the end of 2023, whichever came first (median follow-up duration, 20.1 years).
- The main outcome was all-cause mortality; secondary outcomes were deaths from natural and unnatural causes, as well as deaths from cardiovascular disease, cancer, suicide, and unintentional injuries. Cousin comparison analyses were also conducted to account for confounding.
TAKEAWAY:
- During the follow-up, offspring exposed to parental psychiatric disorders had higher overall mortality rates than unexposed offspring (7.9 vs 3.55 per 10,000 person-years). Mortality rates due to natural causes were 4.0 vs 2.4 per 10,000 person-years and were 3.95 vs 1.1 per 10,000 person-years for mortality due to unnatural causes.
- Exposed offspring had an increased risk for mortality due to any cause (adjusted hazard ratio [aHR], 2.1), natural causes (aHR, 1.9), and unnatural causes (aHR, 2.45). Exposure was also associated with an increased risk for cardiovascular and cancer-related death, suicide, and death due to unintentional injuries. The associations remained significant, although slightly attenuated, in cousin comparison analyses.
- The highest risks for mortality were in offspring exposed at ages 1-2 years to both parents having mental disorders (HR for natural causes, 4.5; HR for unnatural causes, 5.3).
- The risk varied by the type of parental mental disorder, with HRs ranging from 1.6 for eating disorders to 2.2 for intellectual disability.
IN PRACTICE:
“Our findings highlight the need for improved surveillance, prevention, and early detection strategies to reduce the risk of premature mortality among offspring exposed to parental mental disorders. Whether additional support for families affected by mental disorders could mitigate the risk warrants further investigation,” the investigators wrote.
SOURCE:
This study was led by Hui Wang, PhD, Karolinska Institutet, Stockholm, Sweden. It was published online in JAMA Psychiatry.
LIMITATIONS:
Reliance on registry data may have led to the misclassification of parental mental disorders. The study lacked data on genetic factors, parenting quality, cohabitation, and social support, and its generalizability may have been limited. Immigration data after 2014 were unavailable, potentially leading to misclassifications of exposure and outcomes. The Patient Register did not distinguish between diagnoses made in general vs psychiatric hospital settings, and cousin comparisons remained susceptible to bias from unmeasured confounding and may have been limited in capturing temporal and familial heterogeneity.
DISCLOSURES:
This study was funded by the Swedish Research Council for Health, Working Life and Welfare and the Heart and Lung Foundation. Wang reported having no relevant financial relationships. The other investigator reported receiving grants from Forte and the Heart and Lung Foundation.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
A version of this article first appeared on Medscape.com.
TOPLINE:
Offspring of parents with mental disorders had nearly double the risk for mortality, especially from unnatural causes, compared to those with parents did not have a mental disorder, a new Swedish cohort study showed. Additionally, mortality risk was highest when both parents had mental disorders but was not affected by the sex of the affected parent.
METHODOLOGY:
- A nationwide register-based cohort study in Sweden included more than 3.5 million individuals born between 1973 and 2014 (51% men); 35% had a parent with a mental disorder (13% paternal, 16% maternal, and 6% both parents).
- Mental disorder categories included alcohol or substance use, psychotic, mood, anxiety or stress-related, eating, and personality disorders and intellectual disability. Exposure timing was classified by offspring age (mean age, 15.8 years) at parental diagnosis.
- Participants were followed up from birth until death, the death of either parent, emigration (up to 2014), either parent’s emigration, or the end of 2023, whichever came first (median follow-up duration, 20.1 years).
- The main outcome was all-cause mortality; secondary outcomes were deaths from natural and unnatural causes, as well as deaths from cardiovascular disease, cancer, suicide, and unintentional injuries. Cousin comparison analyses were also conducted to account for confounding.
TAKEAWAY:
- During the follow-up, offspring exposed to parental psychiatric disorders had higher overall mortality rates than unexposed offspring (7.9 vs 3.55 per 10,000 person-years). Mortality rates due to natural causes were 4.0 vs 2.4 per 10,000 person-years and were 3.95 vs 1.1 per 10,000 person-years for mortality due to unnatural causes.
- Exposed offspring had an increased risk for mortality due to any cause (adjusted hazard ratio [aHR], 2.1), natural causes (aHR, 1.9), and unnatural causes (aHR, 2.45). Exposure was also associated with an increased risk for cardiovascular and cancer-related death, suicide, and death due to unintentional injuries. The associations remained significant, although slightly attenuated, in cousin comparison analyses.
- The highest risks for mortality were in offspring exposed at ages 1-2 years to both parents having mental disorders (HR for natural causes, 4.5; HR for unnatural causes, 5.3).
- The risk varied by the type of parental mental disorder, with HRs ranging from 1.6 for eating disorders to 2.2 for intellectual disability.
IN PRACTICE:
“Our findings highlight the need for improved surveillance, prevention, and early detection strategies to reduce the risk of premature mortality among offspring exposed to parental mental disorders. Whether additional support for families affected by mental disorders could mitigate the risk warrants further investigation,” the investigators wrote.
SOURCE:
This study was led by Hui Wang, PhD, Karolinska Institutet, Stockholm, Sweden. It was published online in JAMA Psychiatry.
LIMITATIONS:
Reliance on registry data may have led to the misclassification of parental mental disorders. The study lacked data on genetic factors, parenting quality, cohabitation, and social support, and its generalizability may have been limited. Immigration data after 2014 were unavailable, potentially leading to misclassifications of exposure and outcomes. The Patient Register did not distinguish between diagnoses made in general vs psychiatric hospital settings, and cousin comparisons remained susceptible to bias from unmeasured confounding and may have been limited in capturing temporal and familial heterogeneity.
DISCLOSURES:
This study was funded by the Swedish Research Council for Health, Working Life and Welfare and the Heart and Lung Foundation. Wang reported having no relevant financial relationships. The other investigator reported receiving grants from Forte and the Heart and Lung Foundation.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
A version of this article first appeared on Medscape.com.
TOPLINE:
Offspring of parents with mental disorders had nearly double the risk for mortality, especially from unnatural causes, compared to those with parents did not have a mental disorder, a new Swedish cohort study showed. Additionally, mortality risk was highest when both parents had mental disorders but was not affected by the sex of the affected parent.
METHODOLOGY:
- A nationwide register-based cohort study in Sweden included more than 3.5 million individuals born between 1973 and 2014 (51% men); 35% had a parent with a mental disorder (13% paternal, 16% maternal, and 6% both parents).
- Mental disorder categories included alcohol or substance use, psychotic, mood, anxiety or stress-related, eating, and personality disorders and intellectual disability. Exposure timing was classified by offspring age (mean age, 15.8 years) at parental diagnosis.
- Participants were followed up from birth until death, the death of either parent, emigration (up to 2014), either parent’s emigration, or the end of 2023, whichever came first (median follow-up duration, 20.1 years).
- The main outcome was all-cause mortality; secondary outcomes were deaths from natural and unnatural causes, as well as deaths from cardiovascular disease, cancer, suicide, and unintentional injuries. Cousin comparison analyses were also conducted to account for confounding.
TAKEAWAY:
- During the follow-up, offspring exposed to parental psychiatric disorders had higher overall mortality rates than unexposed offspring (7.9 vs 3.55 per 10,000 person-years). Mortality rates due to natural causes were 4.0 vs 2.4 per 10,000 person-years and were 3.95 vs 1.1 per 10,000 person-years for mortality due to unnatural causes.
- Exposed offspring had an increased risk for mortality due to any cause (adjusted hazard ratio [aHR], 2.1), natural causes (aHR, 1.9), and unnatural causes (aHR, 2.45). Exposure was also associated with an increased risk for cardiovascular and cancer-related death, suicide, and death due to unintentional injuries. The associations remained significant, although slightly attenuated, in cousin comparison analyses.
- The highest risks for mortality were in offspring exposed at ages 1-2 years to both parents having mental disorders (HR for natural causes, 4.5; HR for unnatural causes, 5.3).
- The risk varied by the type of parental mental disorder, with HRs ranging from 1.6 for eating disorders to 2.2 for intellectual disability.
IN PRACTICE:
“Our findings highlight the need for improved surveillance, prevention, and early detection strategies to reduce the risk of premature mortality among offspring exposed to parental mental disorders. Whether additional support for families affected by mental disorders could mitigate the risk warrants further investigation,” the investigators wrote.
SOURCE:
This study was led by Hui Wang, PhD, Karolinska Institutet, Stockholm, Sweden. It was published online in JAMA Psychiatry.
LIMITATIONS:
Reliance on registry data may have led to the misclassification of parental mental disorders. The study lacked data on genetic factors, parenting quality, cohabitation, and social support, and its generalizability may have been limited. Immigration data after 2014 were unavailable, potentially leading to misclassifications of exposure and outcomes. The Patient Register did not distinguish between diagnoses made in general vs psychiatric hospital settings, and cousin comparisons remained susceptible to bias from unmeasured confounding and may have been limited in capturing temporal and familial heterogeneity.
DISCLOSURES:
This study was funded by the Swedish Research Council for Health, Working Life and Welfare and the Heart and Lung Foundation. Wang reported having no relevant financial relationships. The other investigator reported receiving grants from Forte and the Heart and Lung Foundation.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
A version of this article first appeared on Medscape.com.
Steatocystomas: Update on Clinical Manifestations, Diagnosis, and Management
Steatocystomas: Update on Clinical Manifestations, Diagnosis, and Management
Steatocystomas are small sebum-filled cysts that typically manifest in the dermis and originate from sebaceous follicles. Although commonly asymptomatic, these lesions can manifest with pruritus or become infected, predisposing patients to further complications.1 Steatocystomas can manifest as single (steatocystoma simplex [SS]) or numerous (steatocystoma multiplex [SM]) lesions; the lesions also can spontaneously rupture with characteristics that resemble hidradenitis suppurativa (HS)(steatocystoma multiplex suppurativa [SMS]).1,2
Steatocystomas are relatively rare, and there is limited consensus in the published literature on the etiology and management of this condition. In this article, we present a comprehensive review of steatocystomas in the current literature. We highlight important features to consider when making the diagnosis and also offer recommendations for best-practice treatment.
Historical Background
Although not explicitly identified by name, the first documentation of steatocystomas is a case report published in 1873. In this account, the author described a patient who presented with approximately 250 flesh-colored dermal cysts across the body that varied in size.3 In 1899, the term steatocystoma multiple—derived from Greek roots meaning “fatty bag”—was first used.4
In 1982, almost a century later, Brownstein5 reported some of the earliest cases of SS. This solitary subtype is identical to SM on a microscopic level; however, unlike SM, this variant occurs as a single lesion that typically forms in adulthood and in the absence of family history. Other benign adnexal tumors (eg, pilomatricomas, pilar cysts, and sebaceous hyperplasias) also can manifest as either solitary or multiple lesions.
In 1976, McDonald and Reed6 reported the first known cases of patients with both SM and HS. At the time, the co-occurrence of these conditions was viewed as coincidental, but there were postulations of a shared inflammatory process and hereditary link6; it was not until 1982 that the term steatocystoma multiplex suppurativum was coined to describe this variant.7 Although rare, there have been multiple documented instances of SMS since. It has been suggested that the convergence of these conditions may indicate a shared follicular proliferation defect.8 Ongoing investigation is warranted to explain the underlying pathogenesis of this unique variant.
Epidemiology
The available epidemiologic data primarily relate to SM, the most common steatocystoma variant. Nevertheless, SM is a relatively rare condition, and the exact incidence and prevalence remain unknown.8,9 Steatocystomas typically manifest in the first and second decades of life and have been observed in patients of both sexes, with studies demonstrating no notable sex bias.4,9
Etiology and Pathophysiology
Steatocystomas can occur sporadically or may be inherited as an autosomal-dominant condition.4 Typically, SS tends to manifest as an isolated occurrence without any inherent genetic predisposition.5 Alternatively, SM may develop sporadically or be associated with a mutation in the keratin 17 gene (KRT17).4 Steatocystoma multiplex also has been associated with at least 4 different missense mutations, including N92H, R94H, and R94C, located on the long (q) arm of chromosome 17.4,10-12
The keratin 17 gene is responsible for encoding the keratin 17 protein, a type I intermediate filament predominantly synthesized in the basal cells of epithelial tissue. This fibrous structural protein can regulate many processes, including inflammation and cell proliferation, and is found in regions such as the sebaceous glands, hair follicles, and eccrine sweat glands. Overexpression of KRT17 has been suggested in other cutaneous conditions, most notably psoriasis.12 Despite KRT17’s many roles, it remains unclear why SM typically manifests with a myriad of sebum-containing cysts as the primary symptom.12 Continued investigation into the genetic underpinnings of SM and the keratin 17 protein is necessary to further elucidate a more comprehensive understanding of this condition.
Hormonal influences have been suggested as a potential trigger for steatocystoma growth.4,13 This condition is associated with dysfunction of the sebaceous glands, and, correspondingly, the incidence of disease is highest in pubertal patients, in whom androgen levels and sebum production are elevated.4,13,14 Two cases of transgender men taking testosterone therapy presenting with steatocystomas provide additional clinical support for this association.15
Additionally, the use of immunomodulatory agents, such as ustekinumab (anti–interleukin 12/interleukin 23), has been shown to trigger SM. It is predicted that the reduced expression of certain interferons and interleukins may lead to downstream consequences in the keratin 17 pathway and lead to SM lesion formation in genetically susceptible individuals.16 Targeting these potential causes in the future may prove efficacious in the secondary prevention of familial SM manifestation or exacerbations.
Mutations in the KRT17 gene also have been implicated in pachyonychia congenita type 2 (PC-2).4 Marked by extensive systemic hyperkeratosis, PC-2 has been observed to coincide with SM in certain patients.4,5 Interestingly, the location of the KRT17 mutations are identical in both PC-2 and SM.4 Although most individuals with hereditary SM do not exhibit the characteristic features of PC-2, mild nail and dental abnormalities have been observed in some SM cases.4,10 This relationship suggests that SM may be a less severe variant of PC-2 or part of a complex polygenetic spectrum of disease.10 Further research is imperative to determine the exact nature and extent of the relationship between these conditions.
Clinical Manifestations
Steatocystomas are flesh-colored subcutaneous cysts that range in size from less than 3 mm to larger than 3 cm in diameter (Figure). They form within a single pilosebaceous unit and typically display firm attachment due to their origination in the dermis.2,7,17 Steatocystomas generally contain lipid material, and less frequently, keratin and hair shafts, distinguishing them as the only “true” sebaceous cysts.18 Their color can range from flesh-toned to yellow, with reports of occasional dark-blue shades and calcifications.19,20 Steatocystomas can persist indefinitely, and they usually are asymptomatic.
Diagnosis of steatocystoma is confirmed by biopsy.4 Steatocystomas are characterized by a dermal cyst lined by stratified squamous cell epithelium (eFigures 1 and 2).21 Classically they feature flattened sebaceous lobules, multinucleated giant cells, and abortive hair follicles. The lining of these cysts is marked by lymphocytic infiltrate and a dense, wrinkled, eosinophilic keratin cuticle that replaces the granular layer.22 The cyst maintains an epidermal connection through a follicular infundibulum characterized by clumps of keratinocytes, sebocytes, corneocytes, and/or hair follicles.7 Aspirated contents reveal crystalline structures and anucleate squamous cells upon microscopic analysis. That being said, variable histologic findings of steatocystomas have been described.23
Steatocystoma simplex, as the name implies, classifies a single isolated steatocystoma. This subtype exhibits similar histopathologic and clinical features to the other subtypes of steatocystomas. Notably, SS is not associated with a genetic mutation and is not an inherited condition within families.5 Steatocystoma multiplex manifests with many steatocystomas, often distributed widely across the body.3,4 The chest, axillae, and groin are the most common locations; however, these cysts can manifest on the face, back, abdomen, and extremities.4,18-22 Rare occurrences of SM limited to the face, scalp, and distal extremities have been documented.18,21,24,25 Due to the possibility of an autosomal-dominant inheritance, it is advisable to take a comprehensive family history in patients for whom SM is in the differential.17
Steatocystoma multiplex—especially familial variants—has been shown to develop in conjunction with other dermatologic conditions, including eruptive vellus hair (EVH) cysts, persistent infantile milia, and epidermoid/dermoid cysts.26 While some investigators regard these as separate entities due to their varied genetic etiology, it has been suggested that these conditions may be related and that the diagnosis is determined by the location of cyst origin along the sebaceous ducts.26,27 Other dermatologic conditions and lesions that frequently manifest comorbidly with SM include hidrocystomas, syringomas, pilonidal cysts, lichen planus, nodulocystic acne, trichotillomania, trichoblastomas, trichoepithelioma, HS, keratoacanthomas, acrokeratosis verruciformis of Hopf, and embryonal hair formation. Steatocystoma multiplex, manifesting comorbidly with dental and orofacial malformations (eg, partial noneruption of secondary teeth, natal and defective teeth, and bilateral preauricular sinuses) has been classified as SM natal teeth syndrome.6
Steatocystoma multiplex suppurativa is a rare and serious variant of SM characterized by inflammation, cyst rupture, sinus tract formation, and scarring.24 Patients with SMS typically have multiple intact SM cysts, which can aid in differentiation from HS.2,24 Steatocystoma multiplex suppurativa is associated with more complications than SS and SM, including cyst perforation, development of purulent and/or foul-smelling discharge, infection, scarring, pain, and overall discomfort.2
Given its rarity and the potential manifestations that overlap with other conditions, steatocystomas easily can be misdiagnosed. In some clinical instances, EVHs may share similar characteristics with SM; however, certain distinguishing features exist, including a central tuft of protruding hairs and different expressed contents, such as the vellus hair shafts, from the cyst’s lumen.28 Furthermore, histologic examination of EVHs reveals epidermoid keratinization of the lining as well as a lack of sebaceous glands within the wall.28,29 Other similar conditions include epidermoid cysts, pilar cysts, lipomas, epidermal inclusion cysts, dermoid cysts, sebaceous hyperplasia, folliculitis, xanthomas, neurofibromatosis, and syringomas.30 Occasionally, SMS can be mistaken for HS or acne conglobata, and SM lesions with a facial distribution can mimic acne vulgaris.1,31 These conditions should be excluded before a diagnosis of SS, SM, or SMS is made.
Importantly, SM is visually indistinguishable from subcutaneous metastasis on physical examination, and there are reports of oncologic conditions (eg, pulmonary adenocarcinoma metastasized to the skin) being mistaken for SS or SM.32 Therefore, a thorough clinical examination, histopathologic analysis, and potential use of other imaging modalities such as ultrasonography (US) are needed to ensure an accurate diagnosis.
Ultrasonography has demonstrated utility in diagnosing steatocystomas.33-35 Steatocystomas have incidentally been found on routine mammograms and can demonstrate well-defined circular nodules with radiolucent characteristics and a thin radiodense outline.33,36 Homogeneous hypoechoic nodules within the dermis without posterior acoustic features generally are observed (eFigure 3).33,37 In patients declining biopsy, US may be useful in further characterization of an unknown lesion. Color Doppler US can be used to distinguish SMS from HS. Specifically, SM typically exhibits an absence of Doppler signaling due to a lack of vascularity, providing a helpful diagnostic clue for the SMS variant.33
Management and Treatment Options
There is no established standard treatment for steatocystomas; therefore, the approach to management is contingent on clinical presentation and patient preferences. Various medical, surgical, and laser management options are available, each with its own advantages and limitations. Treatment of SM is difficult due to the large number of lesions.38 In many cases, continued observation is a viable treatment option, as most SS and SM lesions are asymptomatic; however, cosmetic concerns can be debilitating for patients with SM and may warrant intervention.39 More extensive medical and surgical management often are necessary in SMS due to associated morbidity. Discussing options and goals as well as setting realistic expectations with the patient are essential in determining the optimal approach.
Medical Management—In medical literature, oral isotretinoin (13-cis-retinoic acid) has been the mainstay of therapy for steatocystoma, as its effect on the size and activity of sebaceous glands is hypothesized to decrease disease activity.38,40 Interventional studies and case reports have exhibited varying degrees of effectiveness.1,38-41 Some reports depict a reduction in the formation of new lesions and a decrease in the size of pre-existing lesions, some show mild delayed therapeutic efficacy, and others suggest exacerbation of the condition.1,38-41 This outcome variability is attributed to isotretinoin’s preferential efficacy in treating inflammatory lesions.40,42
Tetracycline derivatives and intralesional steroid injections also have been employed with some efficacy in patients with focal inflammatory SM and SMS.43 There is limited evidence on the long-term outcomes of these interventions, and intralesional injections often are not recommended in conditions such as SM, in which there are many lesions present.
Surgical Management—Minimally invasive surgical procedures including drainage and resections have been used with varying efficacy in SS and SM. Typically, a 2- to 3-mm incision or sharp-tipped cautery is employed to puncture the cyst. Alternatively, radiofrequency probes with a 2.4-MHz frequency setting have been used to minimize incision size.44 The contents then are expressed with manual pressure or forceps, and the cyst sac is extracted using forceps and/or a vein hook (eFigure 4).44,45 The specific surgical techniques and their respective advantages and limitations are summarized in the eTable. Reported advantages and limitations of surgical techniques are derived from information provided by the authors of steatocystoma case reports, which are based on observations of a very limited sample size.
Laser Treatment—Various laser modalities have been used in the management of steatocystomas, including carbon dioxide lasers, erbium-doped yttrium aluminum garnet lasers, 1450-nm diode plus 1550-nm fractionated erbium-doped fiber lasers, and 1927-nm diode lasers.54,55-57 These lasers are used to perforate the cyst before extirpation and have displayed advantages in minimizing scar length.58 The super-pulse mode of carbon dioxide lasers demonstrates efficacy with minimal scarring and recurrence, and this mode is preferred to minimize thermal damage.54,59 Furthermore, this modality can be especially useful in patients whose condition is refractory to other noninvasive options.59 Similarly, the erbium-doped yttrium aluminum garnet laser was well tolerated with no complications noted.55 The 1927-nm diode laser also displayed good outcomes as well as no recurrence.57 With laser use, it is important to note that multiple treatments are needed to see optimal outcomes.54 Moreover, laser settings must be carefully considered, especially in patients with Fitzpatrick skin type III or higher, and topical anti-inflammatory agents should be considered posttreatment to minimize complications.54,59,60
Recommendations
For management of SS, we recommend conservative therapy of watchful observation, as scarring or postinflammatory pigment change may be brought on by medical or surgical therapy; however, if SS is cosmetically bothersome, laser or surgical excision can be done (eFigure 4).4,43-53 It is important to counsel the patient on risks/benefits. For SM, watchful observation also is indicated; however, systemic therapies aimed at prevention may be the most efficacious by limiting disease progression, and oral tetracycline or isotretinoin may be tried.4 Tetracyclines have the risk for photosensitivity and are teratogenic, while isotretinoin is extremely teratogenic, requires laboratory monitoring and regular pregnancy tests in women, and often causes substantial mucosal dryness. If lesions are bothersome or refractory to these therapies, intralesional steroids or surgical/laser procedures can be tried throughout multiple visits.43-53 For SMS, systemic therapies frequently are recommended. The risks of systemic tetracycline and isotretinoin therapies must be discussed. Patients with treatment-refractory SMS may require surgical excision or deroofing of sinus tracts.43-53 This management is similar to that of HS and must be tailored to the patient.
Conclusion
Overall, steatocystomas are a relatively rare pathology, with a limited consensus on their etiology and management. This review summarizes the current knowledge on the condition to support clinicians in diagnosis and management, ranging from watchful waiting to surgical removal. By individualizing treatment plans, clinicians ultimately can optimize outcomes in patients with steatocystomas.
- Santana CN, Pereira DD, Lisboa AP, et al. Steatocystoma multiplex suppurativa: case report of a rare condition. An Bras Dermatol. 2016;91(5 suppl 1):51-53.
- Atzori L, Zanniello R, Pilloni L, et al. Steatocystoma multiplex suppurativa associated with hidradenitis suppurativa successfully treated with adalimumab. J Eur Acad Dermatol Venereol. 2019;33(Suppl 6):42-44.
- Jamieson WA. Case of numerous cutaneous cysts scattered over the body. Edinb Med J. 1873;19:223-225.
- Kamra HT, Gadgil PA, Ovhal AG, et al. Steatocystoma multiplex-a rare genetic disorder: a case report and review of the literature. J Clin Diagn Res. 2013;7:166-168.
- Brownstein MH. Steatocystoma simplex. A solitary steatocystoma. Arch Dermatol. 1982;118:409-411.
- McDonald RM, Reed WB. Natal teeth and steatocystoma multiplex complicated by hidradenitis suppurativa. A new syndrome. Arch Dermatol. 1976;112:1132-1134.
- Plewig G, Wolff HH, Braun-Falco O. Steatocystoma multiplex: anatomic reevaluation, electron microscopy, and autoradiography. Arch Dermatol. 1982;272:363-380.
- Fletcher J, Posso-De Los Rios C, Jambrosic J, A, et al. Coexistence of hidradenitis suppurativa and steatocystoma multiplex: is it a new variant of hidradenitis suppurativa? J Cutan Med Surg. 2021;25:586-590.
- Cho S, Chang SE, Choi JH, et al. Clinical and histologic features of 64 cases of steatocystoma multiplex. J Dermatol. 2002;29:152-156.
- Covello SP, Smith FJ, Sillevis Smitt JH, et al. Keratin 17 mutations cause either steatocystoma multiplex or pachyonychia congenita type 2. Br J Dermatol. 1998;139:475-480.
- Liu Q, Wu W, Lu J, et al. Steatocystoma multiplex is associated with the R94C mutation in the KRTl7 gene. Mol Med Rep. 2015;12:5072-5076.
- Yang L, Zhang S, Wang G. Keratin 17 in disease pathogenesis: from cancer to dermatoses. J Pathol. 2019;247:158-165.
- Shamloul G, Khachemoune A. An updated review of the sebaceous gland and its role in health and diseases Part 1: embryology, evolution, structure, and function of sebaceous glands. Dermatol Ther. 2021;34:e14695.
- Del Rosso JQ, Kircik LH, Stein Gold L, et al. Androgens, androgen receptors, and the skin: from the laboratory to the clinic with emphasis on clinical and therapeutic implications. J Drugs Dermatol. 2020;19:30-35.
- Porras Fimbres DC, Wolfe SA, Kelley CE. Proliferation of steatocystomas in 2 transgender men. JAAD Case Rep. 2022;26:70-72.
- Marasca C, Megna M, Donnarumma M, et al. A case of steatocystoma multiplex in a psoriatic patient during treatment with anti-IL-12/23. Skin Appendage Disord. 2020;6:309-311.
- Gordon Spratt EA, Kaplan J, Patel RR, et al. Steatocystoma. Dermatol Online J. 2013;19:20721.
- Sharma A, Agrawal S, Dhurat R, et al. An unusual case of facial steatocystoma multiplex: a clinicopathologic and dermoscopic report. Dermatopathology (Basel). 2018;5:58-63.
- Rahman MH, Islam MS, Ansari NP. Atypical steatocystoma multiplex with calcification. ISRN Dermatol. 2011;2011:381901.
- Beyer AV, Vossmann D. Steatocystoma multiplex. Article in German. Hautarzt. 1996;47:469-471.
- Yanagi T, Matsumura T. Steatocystoma multiplex presenting as acral subcutaneous nodules. Acta Derm Venereol. 2006;86:374-375.
- Marzano AV, Tavecchio S, Balice Y, et al. Acral subcutaneous steatocystoma multiplex: a distinct subtype of the disease? Australas J Dermatol. 2012;53:198-201.
- Ferrandiz C, Peyri J. Steatocystoma multiplex. Article in Spanish. Med Cutan Ibero Lat Am. 1984;12:173-176.
- Alotaibi L, Alsaif M, Alhumidi A, et al. Steatocystoma multiplex suppurativa: a case with unusual giant cysts over the scalp and neck. Case Rep Dermatol. 2019;11:71-76.
- Kim SJ, Park HJ, Oh ST, et al. A case of steatocystoma multiplex limited to scalp. Ann Dermatol. 2009;21:106-109.
- Patrizi A, Neri I, Guerrini V, et al. Persistent milia, steatocystoma multiplex and eruptive vellus hair cysts: variable expression of multiple pilosebaceous cysts within an affected family. Dermatology. 1998;196:392-396.
- Tomková H, Fujimoto W, Arata J. Expression of keratins (K10 and K17) in steatocystoma multiplex, eruptive vellus hair cysts, and epidermoid and trichilemmal cysts. Am J Dermatopathol. 1997;19:250-253.
- Patokar AS, Holani AR, Khandait GH, et al. Eruptive vellus hair cysts: an underdiagnosed entity. Int J Trichology. 2022;14:31-33.
- Ohtake N, Kubota Y, Takayama O, et al. Relationship between steatocystoma multiplex and eruptive vellus hair cysts. J Am Acad Dermatol. 1992;26(5 Pt 2):876-878.
- Yoon H, Kang Y, Park H, et al. Sonographic appearance of steatocystoma: an analysis of 14 pathologically confirmed lesions. Taehan Yongsang Uihakhoe Chi. 2021;82:382-392.
- Varshney M, Aziz M, Maheshwari V, et al. Steatocystoma multiplex. BMJ Case Rep. 2011;2011:bcr0420114165.
- Tsai MH, Hsiao YP, Lin WL, et al. Steatocystoma multiplex as initial impression of non-small cell lung cancer with complete response to gefitinib. Chin J Cancer Res. 2014;26:E5-E9.
- Zussino M, Nazzaro G, Moltrasio C, et al. Coexistence of steatocystoma multiplex and hidradenitis suppurativa: assessment of this unique association by means of ultrasonography and color Doppler. Skin Res Technol. 2019;25:877-880.
- Whittle C, Silva-Hirschberg C, Loyola K, et al. Ultrasonographic spectrum of cutaneous cysts with stratified squamous epithelium in pediatric dermatology: pictorial essay. J Ultrasound Med. 2023;42:923-930.
- Arceu M, Martinez G, Alfaro D, et al. Ultrasound morphologic features of steatocystoma multiplex with clinical correlation. J Ultrasound Med. 2020;39:2255-2260.
- Reick-Mitrisin V, Reddy A, Shah BA. A breast imaging case of steatocystoma multiplex: a rare condition involving multiple anatomic regions. Cureus. 2022;14:E27756.
- Yoon H, Kang Y, Park H, et al. Sonographic appearance of steatocystoma: an analysis of 14 pathologically confirmed lesions. Taehan Yongsang Uihakhoe Chi. 2021;82:382-392.
- Apaydin R, Bilen N, Bayramgurler D, et al. Steatocystoma multiplex suppurativum: oral isotretinoin treatment combined with cryotherapy. Australas J Dermatol. 2000;41:98-100.
- Sharma A, Agrawal S, Dhurat R, et al. An unusual case of facial steatocystoma multiplex: a clinicopathologic and dermoscopic report. Dermatopathology (Basel). 2018;5:58-63.
- Moritz DL, Silverman RA. Steatocystoma multiplex treated with isotretinoin: a delayed response. Cutis. 1988;42:437-439.
- Schwartz JL, Goldsmith LA. Steatocystoma multiplex suppurativum: treatment with isotretinoin. Cutis. 1984;34:149-153.
- Kim SJ, Park HJ, Oh ST, et al. A case of steatocystoma multiplex limited to the scalp. Ann Dermatol. 2009;21:106-109.
- Fekete GL, Fekete JE. Steatocystoma multiplex generalisata partially suppurativa--case report. Acta Dermatovenerol Croat. 2010;18:114-119.
- Choudhary S, Koley S, Salodkar A. A modified surgical technique for steatocystoma multiplex. J Cutan Aesthet Surg. 2010;3:25-28.
- Kaya TI, Ikizoglu G, Kokturk A, et al. A simple surgical technique for the treatment of steatocystoma multiplex. Int J Dermatol. 2001;40:785-788.
- Oertel YC, Scott DM. Cytologic-pathologic correlations: fine needle aspiration of three cases of steatocystoma multiplex. Ann Diagn Pathol. 1998;2:318-320.
- Egbert BM, Price NM, Segal RJ. Steatocystoma multiplex. Report of a florid case and a review. Arch Dermatol. 1979;115:334-335.
- Adams BB, Mutasim DF, Nordlund JJ. Steatocystoma multiplex: a quick removal technique. Cutis. 1999;64:127-130.
- Lee SJ, Choe YS, Park BC, et al. The vein hook successfully used for eradication of steatocystoma multiplex. Dermatol Surg. 2007;33:82-84.
- Bettes PSL, Lopes SL, Prestes MA, et al. Treatment of a facial variant of the multiple steatocystoma with skin graft: case report. Rev Bras Cir Plást. 1998;13:31-36
- Düzova AN, Sentürk GB. Suggestion for the treatment of steatocystoma multiplex located exclusively on the face. Int J Dermatol. 2004;43:60-62. doi:10.1111/j.1365-4632.2004.02068.x
- Choudhary S, Koley S, Salodkar A. A modified surgical technique for steatocystoma multiplex. J Cutan Aesthet Surg. 2010;3:25-28.
- Kaya TI, Ikizoglu G, Kokturk A, et al. A simple surgical technique for the treatment of steatocystoma multiplex. Int J Dermatol. 2001;40:785-788.
- Bakkour W, Madan V. Carbon dioxide laser perforation and extirpation of steatocystoma multiplex. Dermatol Surg. 2014;40:658-662.
- Mumcuog?lu CT, Gurel MS, Kiremitci U, et al. Er: yag laser therapy for steatocystoma multiplex. Indian J Dermatol. 2010;55:300-301.
- Moody MN, Landau JM, Goldberg LH, et al. 1,450-nm diode laser in combination with the 1550-nm fractionated erbium-doped fiber laser for the treatment of steatocystoma multiplex: a case report. Dermatol Surg. 2012;38(7 Pt 1):1104-1106.
- Cheon DU, Ko JY. 1927-nm fiber-optic diode laser: a novel therapeutic option for facial steatocystoma multiplex. J Cosmet Dermatol. 2019;18:1326-1329.
- Kim KT, Sun H, Chung EH. Comparison of complete surgical excision and minimally invasive excision using CO2 laser for removal of epidermal cysts on the face. Arch Craniofac Surg. 2019;20:84-88.
- Kassira S, Korta DZ, de Feraudy S, et al. Fractionated ablative carbon dioxide laser treatment of steatocystoma multiplex. J Cosmet Laser Ther. 2016;18:364-366.
- Dixit N, Sardana K, Paliwal P. The rationale of ideal pulse duration and pulse interval in the treatment of steatocystoma multiplex using the carbon dioxide laser in a super-pulse mode as opposedto the ultra-pulse mode. Indian J Dermatol Venereol Leprol. 2020;86:454-456.
Steatocystomas are small sebum-filled cysts that typically manifest in the dermis and originate from sebaceous follicles. Although commonly asymptomatic, these lesions can manifest with pruritus or become infected, predisposing patients to further complications.1 Steatocystomas can manifest as single (steatocystoma simplex [SS]) or numerous (steatocystoma multiplex [SM]) lesions; the lesions also can spontaneously rupture with characteristics that resemble hidradenitis suppurativa (HS)(steatocystoma multiplex suppurativa [SMS]).1,2
Steatocystomas are relatively rare, and there is limited consensus in the published literature on the etiology and management of this condition. In this article, we present a comprehensive review of steatocystomas in the current literature. We highlight important features to consider when making the diagnosis and also offer recommendations for best-practice treatment.
Historical Background
Although not explicitly identified by name, the first documentation of steatocystomas is a case report published in 1873. In this account, the author described a patient who presented with approximately 250 flesh-colored dermal cysts across the body that varied in size.3 In 1899, the term steatocystoma multiple—derived from Greek roots meaning “fatty bag”—was first used.4
In 1982, almost a century later, Brownstein5 reported some of the earliest cases of SS. This solitary subtype is identical to SM on a microscopic level; however, unlike SM, this variant occurs as a single lesion that typically forms in adulthood and in the absence of family history. Other benign adnexal tumors (eg, pilomatricomas, pilar cysts, and sebaceous hyperplasias) also can manifest as either solitary or multiple lesions.
In 1976, McDonald and Reed6 reported the first known cases of patients with both SM and HS. At the time, the co-occurrence of these conditions was viewed as coincidental, but there were postulations of a shared inflammatory process and hereditary link6; it was not until 1982 that the term steatocystoma multiplex suppurativum was coined to describe this variant.7 Although rare, there have been multiple documented instances of SMS since. It has been suggested that the convergence of these conditions may indicate a shared follicular proliferation defect.8 Ongoing investigation is warranted to explain the underlying pathogenesis of this unique variant.
Epidemiology
The available epidemiologic data primarily relate to SM, the most common steatocystoma variant. Nevertheless, SM is a relatively rare condition, and the exact incidence and prevalence remain unknown.8,9 Steatocystomas typically manifest in the first and second decades of life and have been observed in patients of both sexes, with studies demonstrating no notable sex bias.4,9
Etiology and Pathophysiology
Steatocystomas can occur sporadically or may be inherited as an autosomal-dominant condition.4 Typically, SS tends to manifest as an isolated occurrence without any inherent genetic predisposition.5 Alternatively, SM may develop sporadically or be associated with a mutation in the keratin 17 gene (KRT17).4 Steatocystoma multiplex also has been associated with at least 4 different missense mutations, including N92H, R94H, and R94C, located on the long (q) arm of chromosome 17.4,10-12
The keratin 17 gene is responsible for encoding the keratin 17 protein, a type I intermediate filament predominantly synthesized in the basal cells of epithelial tissue. This fibrous structural protein can regulate many processes, including inflammation and cell proliferation, and is found in regions such as the sebaceous glands, hair follicles, and eccrine sweat glands. Overexpression of KRT17 has been suggested in other cutaneous conditions, most notably psoriasis.12 Despite KRT17’s many roles, it remains unclear why SM typically manifests with a myriad of sebum-containing cysts as the primary symptom.12 Continued investigation into the genetic underpinnings of SM and the keratin 17 protein is necessary to further elucidate a more comprehensive understanding of this condition.
Hormonal influences have been suggested as a potential trigger for steatocystoma growth.4,13 This condition is associated with dysfunction of the sebaceous glands, and, correspondingly, the incidence of disease is highest in pubertal patients, in whom androgen levels and sebum production are elevated.4,13,14 Two cases of transgender men taking testosterone therapy presenting with steatocystomas provide additional clinical support for this association.15
Additionally, the use of immunomodulatory agents, such as ustekinumab (anti–interleukin 12/interleukin 23), has been shown to trigger SM. It is predicted that the reduced expression of certain interferons and interleukins may lead to downstream consequences in the keratin 17 pathway and lead to SM lesion formation in genetically susceptible individuals.16 Targeting these potential causes in the future may prove efficacious in the secondary prevention of familial SM manifestation or exacerbations.
Mutations in the KRT17 gene also have been implicated in pachyonychia congenita type 2 (PC-2).4 Marked by extensive systemic hyperkeratosis, PC-2 has been observed to coincide with SM in certain patients.4,5 Interestingly, the location of the KRT17 mutations are identical in both PC-2 and SM.4 Although most individuals with hereditary SM do not exhibit the characteristic features of PC-2, mild nail and dental abnormalities have been observed in some SM cases.4,10 This relationship suggests that SM may be a less severe variant of PC-2 or part of a complex polygenetic spectrum of disease.10 Further research is imperative to determine the exact nature and extent of the relationship between these conditions.
Clinical Manifestations
Steatocystomas are flesh-colored subcutaneous cysts that range in size from less than 3 mm to larger than 3 cm in diameter (Figure). They form within a single pilosebaceous unit and typically display firm attachment due to their origination in the dermis.2,7,17 Steatocystomas generally contain lipid material, and less frequently, keratin and hair shafts, distinguishing them as the only “true” sebaceous cysts.18 Their color can range from flesh-toned to yellow, with reports of occasional dark-blue shades and calcifications.19,20 Steatocystomas can persist indefinitely, and they usually are asymptomatic.
Diagnosis of steatocystoma is confirmed by biopsy.4 Steatocystomas are characterized by a dermal cyst lined by stratified squamous cell epithelium (eFigures 1 and 2).21 Classically they feature flattened sebaceous lobules, multinucleated giant cells, and abortive hair follicles. The lining of these cysts is marked by lymphocytic infiltrate and a dense, wrinkled, eosinophilic keratin cuticle that replaces the granular layer.22 The cyst maintains an epidermal connection through a follicular infundibulum characterized by clumps of keratinocytes, sebocytes, corneocytes, and/or hair follicles.7 Aspirated contents reveal crystalline structures and anucleate squamous cells upon microscopic analysis. That being said, variable histologic findings of steatocystomas have been described.23
Steatocystoma simplex, as the name implies, classifies a single isolated steatocystoma. This subtype exhibits similar histopathologic and clinical features to the other subtypes of steatocystomas. Notably, SS is not associated with a genetic mutation and is not an inherited condition within families.5 Steatocystoma multiplex manifests with many steatocystomas, often distributed widely across the body.3,4 The chest, axillae, and groin are the most common locations; however, these cysts can manifest on the face, back, abdomen, and extremities.4,18-22 Rare occurrences of SM limited to the face, scalp, and distal extremities have been documented.18,21,24,25 Due to the possibility of an autosomal-dominant inheritance, it is advisable to take a comprehensive family history in patients for whom SM is in the differential.17
Steatocystoma multiplex—especially familial variants—has been shown to develop in conjunction with other dermatologic conditions, including eruptive vellus hair (EVH) cysts, persistent infantile milia, and epidermoid/dermoid cysts.26 While some investigators regard these as separate entities due to their varied genetic etiology, it has been suggested that these conditions may be related and that the diagnosis is determined by the location of cyst origin along the sebaceous ducts.26,27 Other dermatologic conditions and lesions that frequently manifest comorbidly with SM include hidrocystomas, syringomas, pilonidal cysts, lichen planus, nodulocystic acne, trichotillomania, trichoblastomas, trichoepithelioma, HS, keratoacanthomas, acrokeratosis verruciformis of Hopf, and embryonal hair formation. Steatocystoma multiplex, manifesting comorbidly with dental and orofacial malformations (eg, partial noneruption of secondary teeth, natal and defective teeth, and bilateral preauricular sinuses) has been classified as SM natal teeth syndrome.6
Steatocystoma multiplex suppurativa is a rare and serious variant of SM characterized by inflammation, cyst rupture, sinus tract formation, and scarring.24 Patients with SMS typically have multiple intact SM cysts, which can aid in differentiation from HS.2,24 Steatocystoma multiplex suppurativa is associated with more complications than SS and SM, including cyst perforation, development of purulent and/or foul-smelling discharge, infection, scarring, pain, and overall discomfort.2
Given its rarity and the potential manifestations that overlap with other conditions, steatocystomas easily can be misdiagnosed. In some clinical instances, EVHs may share similar characteristics with SM; however, certain distinguishing features exist, including a central tuft of protruding hairs and different expressed contents, such as the vellus hair shafts, from the cyst’s lumen.28 Furthermore, histologic examination of EVHs reveals epidermoid keratinization of the lining as well as a lack of sebaceous glands within the wall.28,29 Other similar conditions include epidermoid cysts, pilar cysts, lipomas, epidermal inclusion cysts, dermoid cysts, sebaceous hyperplasia, folliculitis, xanthomas, neurofibromatosis, and syringomas.30 Occasionally, SMS can be mistaken for HS or acne conglobata, and SM lesions with a facial distribution can mimic acne vulgaris.1,31 These conditions should be excluded before a diagnosis of SS, SM, or SMS is made.
Importantly, SM is visually indistinguishable from subcutaneous metastasis on physical examination, and there are reports of oncologic conditions (eg, pulmonary adenocarcinoma metastasized to the skin) being mistaken for SS or SM.32 Therefore, a thorough clinical examination, histopathologic analysis, and potential use of other imaging modalities such as ultrasonography (US) are needed to ensure an accurate diagnosis.
Ultrasonography has demonstrated utility in diagnosing steatocystomas.33-35 Steatocystomas have incidentally been found on routine mammograms and can demonstrate well-defined circular nodules with radiolucent characteristics and a thin radiodense outline.33,36 Homogeneous hypoechoic nodules within the dermis without posterior acoustic features generally are observed (eFigure 3).33,37 In patients declining biopsy, US may be useful in further characterization of an unknown lesion. Color Doppler US can be used to distinguish SMS from HS. Specifically, SM typically exhibits an absence of Doppler signaling due to a lack of vascularity, providing a helpful diagnostic clue for the SMS variant.33
Management and Treatment Options
There is no established standard treatment for steatocystomas; therefore, the approach to management is contingent on clinical presentation and patient preferences. Various medical, surgical, and laser management options are available, each with its own advantages and limitations. Treatment of SM is difficult due to the large number of lesions.38 In many cases, continued observation is a viable treatment option, as most SS and SM lesions are asymptomatic; however, cosmetic concerns can be debilitating for patients with SM and may warrant intervention.39 More extensive medical and surgical management often are necessary in SMS due to associated morbidity. Discussing options and goals as well as setting realistic expectations with the patient are essential in determining the optimal approach.
Medical Management—In medical literature, oral isotretinoin (13-cis-retinoic acid) has been the mainstay of therapy for steatocystoma, as its effect on the size and activity of sebaceous glands is hypothesized to decrease disease activity.38,40 Interventional studies and case reports have exhibited varying degrees of effectiveness.1,38-41 Some reports depict a reduction in the formation of new lesions and a decrease in the size of pre-existing lesions, some show mild delayed therapeutic efficacy, and others suggest exacerbation of the condition.1,38-41 This outcome variability is attributed to isotretinoin’s preferential efficacy in treating inflammatory lesions.40,42
Tetracycline derivatives and intralesional steroid injections also have been employed with some efficacy in patients with focal inflammatory SM and SMS.43 There is limited evidence on the long-term outcomes of these interventions, and intralesional injections often are not recommended in conditions such as SM, in which there are many lesions present.
Surgical Management—Minimally invasive surgical procedures including drainage and resections have been used with varying efficacy in SS and SM. Typically, a 2- to 3-mm incision or sharp-tipped cautery is employed to puncture the cyst. Alternatively, radiofrequency probes with a 2.4-MHz frequency setting have been used to minimize incision size.44 The contents then are expressed with manual pressure or forceps, and the cyst sac is extracted using forceps and/or a vein hook (eFigure 4).44,45 The specific surgical techniques and their respective advantages and limitations are summarized in the eTable. Reported advantages and limitations of surgical techniques are derived from information provided by the authors of steatocystoma case reports, which are based on observations of a very limited sample size.
Laser Treatment—Various laser modalities have been used in the management of steatocystomas, including carbon dioxide lasers, erbium-doped yttrium aluminum garnet lasers, 1450-nm diode plus 1550-nm fractionated erbium-doped fiber lasers, and 1927-nm diode lasers.54,55-57 These lasers are used to perforate the cyst before extirpation and have displayed advantages in minimizing scar length.58 The super-pulse mode of carbon dioxide lasers demonstrates efficacy with minimal scarring and recurrence, and this mode is preferred to minimize thermal damage.54,59 Furthermore, this modality can be especially useful in patients whose condition is refractory to other noninvasive options.59 Similarly, the erbium-doped yttrium aluminum garnet laser was well tolerated with no complications noted.55 The 1927-nm diode laser also displayed good outcomes as well as no recurrence.57 With laser use, it is important to note that multiple treatments are needed to see optimal outcomes.54 Moreover, laser settings must be carefully considered, especially in patients with Fitzpatrick skin type III or higher, and topical anti-inflammatory agents should be considered posttreatment to minimize complications.54,59,60
Recommendations
For management of SS, we recommend conservative therapy of watchful observation, as scarring or postinflammatory pigment change may be brought on by medical or surgical therapy; however, if SS is cosmetically bothersome, laser or surgical excision can be done (eFigure 4).4,43-53 It is important to counsel the patient on risks/benefits. For SM, watchful observation also is indicated; however, systemic therapies aimed at prevention may be the most efficacious by limiting disease progression, and oral tetracycline or isotretinoin may be tried.4 Tetracyclines have the risk for photosensitivity and are teratogenic, while isotretinoin is extremely teratogenic, requires laboratory monitoring and regular pregnancy tests in women, and often causes substantial mucosal dryness. If lesions are bothersome or refractory to these therapies, intralesional steroids or surgical/laser procedures can be tried throughout multiple visits.43-53 For SMS, systemic therapies frequently are recommended. The risks of systemic tetracycline and isotretinoin therapies must be discussed. Patients with treatment-refractory SMS may require surgical excision or deroofing of sinus tracts.43-53 This management is similar to that of HS and must be tailored to the patient.
Conclusion
Overall, steatocystomas are a relatively rare pathology, with a limited consensus on their etiology and management. This review summarizes the current knowledge on the condition to support clinicians in diagnosis and management, ranging from watchful waiting to surgical removal. By individualizing treatment plans, clinicians ultimately can optimize outcomes in patients with steatocystomas.
Steatocystomas are small sebum-filled cysts that typically manifest in the dermis and originate from sebaceous follicles. Although commonly asymptomatic, these lesions can manifest with pruritus or become infected, predisposing patients to further complications.1 Steatocystomas can manifest as single (steatocystoma simplex [SS]) or numerous (steatocystoma multiplex [SM]) lesions; the lesions also can spontaneously rupture with characteristics that resemble hidradenitis suppurativa (HS)(steatocystoma multiplex suppurativa [SMS]).1,2
Steatocystomas are relatively rare, and there is limited consensus in the published literature on the etiology and management of this condition. In this article, we present a comprehensive review of steatocystomas in the current literature. We highlight important features to consider when making the diagnosis and also offer recommendations for best-practice treatment.
Historical Background
Although not explicitly identified by name, the first documentation of steatocystomas is a case report published in 1873. In this account, the author described a patient who presented with approximately 250 flesh-colored dermal cysts across the body that varied in size.3 In 1899, the term steatocystoma multiple—derived from Greek roots meaning “fatty bag”—was first used.4
In 1982, almost a century later, Brownstein5 reported some of the earliest cases of SS. This solitary subtype is identical to SM on a microscopic level; however, unlike SM, this variant occurs as a single lesion that typically forms in adulthood and in the absence of family history. Other benign adnexal tumors (eg, pilomatricomas, pilar cysts, and sebaceous hyperplasias) also can manifest as either solitary or multiple lesions.
In 1976, McDonald and Reed6 reported the first known cases of patients with both SM and HS. At the time, the co-occurrence of these conditions was viewed as coincidental, but there were postulations of a shared inflammatory process and hereditary link6; it was not until 1982 that the term steatocystoma multiplex suppurativum was coined to describe this variant.7 Although rare, there have been multiple documented instances of SMS since. It has been suggested that the convergence of these conditions may indicate a shared follicular proliferation defect.8 Ongoing investigation is warranted to explain the underlying pathogenesis of this unique variant.
Epidemiology
The available epidemiologic data primarily relate to SM, the most common steatocystoma variant. Nevertheless, SM is a relatively rare condition, and the exact incidence and prevalence remain unknown.8,9 Steatocystomas typically manifest in the first and second decades of life and have been observed in patients of both sexes, with studies demonstrating no notable sex bias.4,9
Etiology and Pathophysiology
Steatocystomas can occur sporadically or may be inherited as an autosomal-dominant condition.4 Typically, SS tends to manifest as an isolated occurrence without any inherent genetic predisposition.5 Alternatively, SM may develop sporadically or be associated with a mutation in the keratin 17 gene (KRT17).4 Steatocystoma multiplex also has been associated with at least 4 different missense mutations, including N92H, R94H, and R94C, located on the long (q) arm of chromosome 17.4,10-12
The keratin 17 gene is responsible for encoding the keratin 17 protein, a type I intermediate filament predominantly synthesized in the basal cells of epithelial tissue. This fibrous structural protein can regulate many processes, including inflammation and cell proliferation, and is found in regions such as the sebaceous glands, hair follicles, and eccrine sweat glands. Overexpression of KRT17 has been suggested in other cutaneous conditions, most notably psoriasis.12 Despite KRT17’s many roles, it remains unclear why SM typically manifests with a myriad of sebum-containing cysts as the primary symptom.12 Continued investigation into the genetic underpinnings of SM and the keratin 17 protein is necessary to further elucidate a more comprehensive understanding of this condition.
Hormonal influences have been suggested as a potential trigger for steatocystoma growth.4,13 This condition is associated with dysfunction of the sebaceous glands, and, correspondingly, the incidence of disease is highest in pubertal patients, in whom androgen levels and sebum production are elevated.4,13,14 Two cases of transgender men taking testosterone therapy presenting with steatocystomas provide additional clinical support for this association.15
Additionally, the use of immunomodulatory agents, such as ustekinumab (anti–interleukin 12/interleukin 23), has been shown to trigger SM. It is predicted that the reduced expression of certain interferons and interleukins may lead to downstream consequences in the keratin 17 pathway and lead to SM lesion formation in genetically susceptible individuals.16 Targeting these potential causes in the future may prove efficacious in the secondary prevention of familial SM manifestation or exacerbations.
Mutations in the KRT17 gene also have been implicated in pachyonychia congenita type 2 (PC-2).4 Marked by extensive systemic hyperkeratosis, PC-2 has been observed to coincide with SM in certain patients.4,5 Interestingly, the location of the KRT17 mutations are identical in both PC-2 and SM.4 Although most individuals with hereditary SM do not exhibit the characteristic features of PC-2, mild nail and dental abnormalities have been observed in some SM cases.4,10 This relationship suggests that SM may be a less severe variant of PC-2 or part of a complex polygenetic spectrum of disease.10 Further research is imperative to determine the exact nature and extent of the relationship between these conditions.
Clinical Manifestations
Steatocystomas are flesh-colored subcutaneous cysts that range in size from less than 3 mm to larger than 3 cm in diameter (Figure). They form within a single pilosebaceous unit and typically display firm attachment due to their origination in the dermis.2,7,17 Steatocystomas generally contain lipid material, and less frequently, keratin and hair shafts, distinguishing them as the only “true” sebaceous cysts.18 Their color can range from flesh-toned to yellow, with reports of occasional dark-blue shades and calcifications.19,20 Steatocystomas can persist indefinitely, and they usually are asymptomatic.
Diagnosis of steatocystoma is confirmed by biopsy.4 Steatocystomas are characterized by a dermal cyst lined by stratified squamous cell epithelium (eFigures 1 and 2).21 Classically they feature flattened sebaceous lobules, multinucleated giant cells, and abortive hair follicles. The lining of these cysts is marked by lymphocytic infiltrate and a dense, wrinkled, eosinophilic keratin cuticle that replaces the granular layer.22 The cyst maintains an epidermal connection through a follicular infundibulum characterized by clumps of keratinocytes, sebocytes, corneocytes, and/or hair follicles.7 Aspirated contents reveal crystalline structures and anucleate squamous cells upon microscopic analysis. That being said, variable histologic findings of steatocystomas have been described.23
Steatocystoma simplex, as the name implies, classifies a single isolated steatocystoma. This subtype exhibits similar histopathologic and clinical features to the other subtypes of steatocystomas. Notably, SS is not associated with a genetic mutation and is not an inherited condition within families.5 Steatocystoma multiplex manifests with many steatocystomas, often distributed widely across the body.3,4 The chest, axillae, and groin are the most common locations; however, these cysts can manifest on the face, back, abdomen, and extremities.4,18-22 Rare occurrences of SM limited to the face, scalp, and distal extremities have been documented.18,21,24,25 Due to the possibility of an autosomal-dominant inheritance, it is advisable to take a comprehensive family history in patients for whom SM is in the differential.17
Steatocystoma multiplex—especially familial variants—has been shown to develop in conjunction with other dermatologic conditions, including eruptive vellus hair (EVH) cysts, persistent infantile milia, and epidermoid/dermoid cysts.26 While some investigators regard these as separate entities due to their varied genetic etiology, it has been suggested that these conditions may be related and that the diagnosis is determined by the location of cyst origin along the sebaceous ducts.26,27 Other dermatologic conditions and lesions that frequently manifest comorbidly with SM include hidrocystomas, syringomas, pilonidal cysts, lichen planus, nodulocystic acne, trichotillomania, trichoblastomas, trichoepithelioma, HS, keratoacanthomas, acrokeratosis verruciformis of Hopf, and embryonal hair formation. Steatocystoma multiplex, manifesting comorbidly with dental and orofacial malformations (eg, partial noneruption of secondary teeth, natal and defective teeth, and bilateral preauricular sinuses) has been classified as SM natal teeth syndrome.6
Steatocystoma multiplex suppurativa is a rare and serious variant of SM characterized by inflammation, cyst rupture, sinus tract formation, and scarring.24 Patients with SMS typically have multiple intact SM cysts, which can aid in differentiation from HS.2,24 Steatocystoma multiplex suppurativa is associated with more complications than SS and SM, including cyst perforation, development of purulent and/or foul-smelling discharge, infection, scarring, pain, and overall discomfort.2
Given its rarity and the potential manifestations that overlap with other conditions, steatocystomas easily can be misdiagnosed. In some clinical instances, EVHs may share similar characteristics with SM; however, certain distinguishing features exist, including a central tuft of protruding hairs and different expressed contents, such as the vellus hair shafts, from the cyst’s lumen.28 Furthermore, histologic examination of EVHs reveals epidermoid keratinization of the lining as well as a lack of sebaceous glands within the wall.28,29 Other similar conditions include epidermoid cysts, pilar cysts, lipomas, epidermal inclusion cysts, dermoid cysts, sebaceous hyperplasia, folliculitis, xanthomas, neurofibromatosis, and syringomas.30 Occasionally, SMS can be mistaken for HS or acne conglobata, and SM lesions with a facial distribution can mimic acne vulgaris.1,31 These conditions should be excluded before a diagnosis of SS, SM, or SMS is made.
Importantly, SM is visually indistinguishable from subcutaneous metastasis on physical examination, and there are reports of oncologic conditions (eg, pulmonary adenocarcinoma metastasized to the skin) being mistaken for SS or SM.32 Therefore, a thorough clinical examination, histopathologic analysis, and potential use of other imaging modalities such as ultrasonography (US) are needed to ensure an accurate diagnosis.
Ultrasonography has demonstrated utility in diagnosing steatocystomas.33-35 Steatocystomas have incidentally been found on routine mammograms and can demonstrate well-defined circular nodules with radiolucent characteristics and a thin radiodense outline.33,36 Homogeneous hypoechoic nodules within the dermis without posterior acoustic features generally are observed (eFigure 3).33,37 In patients declining biopsy, US may be useful in further characterization of an unknown lesion. Color Doppler US can be used to distinguish SMS from HS. Specifically, SM typically exhibits an absence of Doppler signaling due to a lack of vascularity, providing a helpful diagnostic clue for the SMS variant.33
Management and Treatment Options
There is no established standard treatment for steatocystomas; therefore, the approach to management is contingent on clinical presentation and patient preferences. Various medical, surgical, and laser management options are available, each with its own advantages and limitations. Treatment of SM is difficult due to the large number of lesions.38 In many cases, continued observation is a viable treatment option, as most SS and SM lesions are asymptomatic; however, cosmetic concerns can be debilitating for patients with SM and may warrant intervention.39 More extensive medical and surgical management often are necessary in SMS due to associated morbidity. Discussing options and goals as well as setting realistic expectations with the patient are essential in determining the optimal approach.
Medical Management—In medical literature, oral isotretinoin (13-cis-retinoic acid) has been the mainstay of therapy for steatocystoma, as its effect on the size and activity of sebaceous glands is hypothesized to decrease disease activity.38,40 Interventional studies and case reports have exhibited varying degrees of effectiveness.1,38-41 Some reports depict a reduction in the formation of new lesions and a decrease in the size of pre-existing lesions, some show mild delayed therapeutic efficacy, and others suggest exacerbation of the condition.1,38-41 This outcome variability is attributed to isotretinoin’s preferential efficacy in treating inflammatory lesions.40,42
Tetracycline derivatives and intralesional steroid injections also have been employed with some efficacy in patients with focal inflammatory SM and SMS.43 There is limited evidence on the long-term outcomes of these interventions, and intralesional injections often are not recommended in conditions such as SM, in which there are many lesions present.
Surgical Management—Minimally invasive surgical procedures including drainage and resections have been used with varying efficacy in SS and SM. Typically, a 2- to 3-mm incision or sharp-tipped cautery is employed to puncture the cyst. Alternatively, radiofrequency probes with a 2.4-MHz frequency setting have been used to minimize incision size.44 The contents then are expressed with manual pressure or forceps, and the cyst sac is extracted using forceps and/or a vein hook (eFigure 4).44,45 The specific surgical techniques and their respective advantages and limitations are summarized in the eTable. Reported advantages and limitations of surgical techniques are derived from information provided by the authors of steatocystoma case reports, which are based on observations of a very limited sample size.
Laser Treatment—Various laser modalities have been used in the management of steatocystomas, including carbon dioxide lasers, erbium-doped yttrium aluminum garnet lasers, 1450-nm diode plus 1550-nm fractionated erbium-doped fiber lasers, and 1927-nm diode lasers.54,55-57 These lasers are used to perforate the cyst before extirpation and have displayed advantages in minimizing scar length.58 The super-pulse mode of carbon dioxide lasers demonstrates efficacy with minimal scarring and recurrence, and this mode is preferred to minimize thermal damage.54,59 Furthermore, this modality can be especially useful in patients whose condition is refractory to other noninvasive options.59 Similarly, the erbium-doped yttrium aluminum garnet laser was well tolerated with no complications noted.55 The 1927-nm diode laser also displayed good outcomes as well as no recurrence.57 With laser use, it is important to note that multiple treatments are needed to see optimal outcomes.54 Moreover, laser settings must be carefully considered, especially in patients with Fitzpatrick skin type III or higher, and topical anti-inflammatory agents should be considered posttreatment to minimize complications.54,59,60
Recommendations
For management of SS, we recommend conservative therapy of watchful observation, as scarring or postinflammatory pigment change may be brought on by medical or surgical therapy; however, if SS is cosmetically bothersome, laser or surgical excision can be done (eFigure 4).4,43-53 It is important to counsel the patient on risks/benefits. For SM, watchful observation also is indicated; however, systemic therapies aimed at prevention may be the most efficacious by limiting disease progression, and oral tetracycline or isotretinoin may be tried.4 Tetracyclines have the risk for photosensitivity and are teratogenic, while isotretinoin is extremely teratogenic, requires laboratory monitoring and regular pregnancy tests in women, and often causes substantial mucosal dryness. If lesions are bothersome or refractory to these therapies, intralesional steroids or surgical/laser procedures can be tried throughout multiple visits.43-53 For SMS, systemic therapies frequently are recommended. The risks of systemic tetracycline and isotretinoin therapies must be discussed. Patients with treatment-refractory SMS may require surgical excision or deroofing of sinus tracts.43-53 This management is similar to that of HS and must be tailored to the patient.
Conclusion
Overall, steatocystomas are a relatively rare pathology, with a limited consensus on their etiology and management. This review summarizes the current knowledge on the condition to support clinicians in diagnosis and management, ranging from watchful waiting to surgical removal. By individualizing treatment plans, clinicians ultimately can optimize outcomes in patients with steatocystomas.
- Santana CN, Pereira DD, Lisboa AP, et al. Steatocystoma multiplex suppurativa: case report of a rare condition. An Bras Dermatol. 2016;91(5 suppl 1):51-53.
- Atzori L, Zanniello R, Pilloni L, et al. Steatocystoma multiplex suppurativa associated with hidradenitis suppurativa successfully treated with adalimumab. J Eur Acad Dermatol Venereol. 2019;33(Suppl 6):42-44.
- Jamieson WA. Case of numerous cutaneous cysts scattered over the body. Edinb Med J. 1873;19:223-225.
- Kamra HT, Gadgil PA, Ovhal AG, et al. Steatocystoma multiplex-a rare genetic disorder: a case report and review of the literature. J Clin Diagn Res. 2013;7:166-168.
- Brownstein MH. Steatocystoma simplex. A solitary steatocystoma. Arch Dermatol. 1982;118:409-411.
- McDonald RM, Reed WB. Natal teeth and steatocystoma multiplex complicated by hidradenitis suppurativa. A new syndrome. Arch Dermatol. 1976;112:1132-1134.
- Plewig G, Wolff HH, Braun-Falco O. Steatocystoma multiplex: anatomic reevaluation, electron microscopy, and autoradiography. Arch Dermatol. 1982;272:363-380.
- Fletcher J, Posso-De Los Rios C, Jambrosic J, A, et al. Coexistence of hidradenitis suppurativa and steatocystoma multiplex: is it a new variant of hidradenitis suppurativa? J Cutan Med Surg. 2021;25:586-590.
- Cho S, Chang SE, Choi JH, et al. Clinical and histologic features of 64 cases of steatocystoma multiplex. J Dermatol. 2002;29:152-156.
- Covello SP, Smith FJ, Sillevis Smitt JH, et al. Keratin 17 mutations cause either steatocystoma multiplex or pachyonychia congenita type 2. Br J Dermatol. 1998;139:475-480.
- Liu Q, Wu W, Lu J, et al. Steatocystoma multiplex is associated with the R94C mutation in the KRTl7 gene. Mol Med Rep. 2015;12:5072-5076.
- Yang L, Zhang S, Wang G. Keratin 17 in disease pathogenesis: from cancer to dermatoses. J Pathol. 2019;247:158-165.
- Shamloul G, Khachemoune A. An updated review of the sebaceous gland and its role in health and diseases Part 1: embryology, evolution, structure, and function of sebaceous glands. Dermatol Ther. 2021;34:e14695.
- Del Rosso JQ, Kircik LH, Stein Gold L, et al. Androgens, androgen receptors, and the skin: from the laboratory to the clinic with emphasis on clinical and therapeutic implications. J Drugs Dermatol. 2020;19:30-35.
- Porras Fimbres DC, Wolfe SA, Kelley CE. Proliferation of steatocystomas in 2 transgender men. JAAD Case Rep. 2022;26:70-72.
- Marasca C, Megna M, Donnarumma M, et al. A case of steatocystoma multiplex in a psoriatic patient during treatment with anti-IL-12/23. Skin Appendage Disord. 2020;6:309-311.
- Gordon Spratt EA, Kaplan J, Patel RR, et al. Steatocystoma. Dermatol Online J. 2013;19:20721.
- Sharma A, Agrawal S, Dhurat R, et al. An unusual case of facial steatocystoma multiplex: a clinicopathologic and dermoscopic report. Dermatopathology (Basel). 2018;5:58-63.
- Rahman MH, Islam MS, Ansari NP. Atypical steatocystoma multiplex with calcification. ISRN Dermatol. 2011;2011:381901.
- Beyer AV, Vossmann D. Steatocystoma multiplex. Article in German. Hautarzt. 1996;47:469-471.
- Yanagi T, Matsumura T. Steatocystoma multiplex presenting as acral subcutaneous nodules. Acta Derm Venereol. 2006;86:374-375.
- Marzano AV, Tavecchio S, Balice Y, et al. Acral subcutaneous steatocystoma multiplex: a distinct subtype of the disease? Australas J Dermatol. 2012;53:198-201.
- Ferrandiz C, Peyri J. Steatocystoma multiplex. Article in Spanish. Med Cutan Ibero Lat Am. 1984;12:173-176.
- Alotaibi L, Alsaif M, Alhumidi A, et al. Steatocystoma multiplex suppurativa: a case with unusual giant cysts over the scalp and neck. Case Rep Dermatol. 2019;11:71-76.
- Kim SJ, Park HJ, Oh ST, et al. A case of steatocystoma multiplex limited to scalp. Ann Dermatol. 2009;21:106-109.
- Patrizi A, Neri I, Guerrini V, et al. Persistent milia, steatocystoma multiplex and eruptive vellus hair cysts: variable expression of multiple pilosebaceous cysts within an affected family. Dermatology. 1998;196:392-396.
- Tomková H, Fujimoto W, Arata J. Expression of keratins (K10 and K17) in steatocystoma multiplex, eruptive vellus hair cysts, and epidermoid and trichilemmal cysts. Am J Dermatopathol. 1997;19:250-253.
- Patokar AS, Holani AR, Khandait GH, et al. Eruptive vellus hair cysts: an underdiagnosed entity. Int J Trichology. 2022;14:31-33.
- Ohtake N, Kubota Y, Takayama O, et al. Relationship between steatocystoma multiplex and eruptive vellus hair cysts. J Am Acad Dermatol. 1992;26(5 Pt 2):876-878.
- Yoon H, Kang Y, Park H, et al. Sonographic appearance of steatocystoma: an analysis of 14 pathologically confirmed lesions. Taehan Yongsang Uihakhoe Chi. 2021;82:382-392.
- Varshney M, Aziz M, Maheshwari V, et al. Steatocystoma multiplex. BMJ Case Rep. 2011;2011:bcr0420114165.
- Tsai MH, Hsiao YP, Lin WL, et al. Steatocystoma multiplex as initial impression of non-small cell lung cancer with complete response to gefitinib. Chin J Cancer Res. 2014;26:E5-E9.
- Zussino M, Nazzaro G, Moltrasio C, et al. Coexistence of steatocystoma multiplex and hidradenitis suppurativa: assessment of this unique association by means of ultrasonography and color Doppler. Skin Res Technol. 2019;25:877-880.
- Whittle C, Silva-Hirschberg C, Loyola K, et al. Ultrasonographic spectrum of cutaneous cysts with stratified squamous epithelium in pediatric dermatology: pictorial essay. J Ultrasound Med. 2023;42:923-930.
- Arceu M, Martinez G, Alfaro D, et al. Ultrasound morphologic features of steatocystoma multiplex with clinical correlation. J Ultrasound Med. 2020;39:2255-2260.
- Reick-Mitrisin V, Reddy A, Shah BA. A breast imaging case of steatocystoma multiplex: a rare condition involving multiple anatomic regions. Cureus. 2022;14:E27756.
- Yoon H, Kang Y, Park H, et al. Sonographic appearance of steatocystoma: an analysis of 14 pathologically confirmed lesions. Taehan Yongsang Uihakhoe Chi. 2021;82:382-392.
- Apaydin R, Bilen N, Bayramgurler D, et al. Steatocystoma multiplex suppurativum: oral isotretinoin treatment combined with cryotherapy. Australas J Dermatol. 2000;41:98-100.
- Sharma A, Agrawal S, Dhurat R, et al. An unusual case of facial steatocystoma multiplex: a clinicopathologic and dermoscopic report. Dermatopathology (Basel). 2018;5:58-63.
- Moritz DL, Silverman RA. Steatocystoma multiplex treated with isotretinoin: a delayed response. Cutis. 1988;42:437-439.
- Schwartz JL, Goldsmith LA. Steatocystoma multiplex suppurativum: treatment with isotretinoin. Cutis. 1984;34:149-153.
- Kim SJ, Park HJ, Oh ST, et al. A case of steatocystoma multiplex limited to the scalp. Ann Dermatol. 2009;21:106-109.
- Fekete GL, Fekete JE. Steatocystoma multiplex generalisata partially suppurativa--case report. Acta Dermatovenerol Croat. 2010;18:114-119.
- Choudhary S, Koley S, Salodkar A. A modified surgical technique for steatocystoma multiplex. J Cutan Aesthet Surg. 2010;3:25-28.
- Kaya TI, Ikizoglu G, Kokturk A, et al. A simple surgical technique for the treatment of steatocystoma multiplex. Int J Dermatol. 2001;40:785-788.
- Oertel YC, Scott DM. Cytologic-pathologic correlations: fine needle aspiration of three cases of steatocystoma multiplex. Ann Diagn Pathol. 1998;2:318-320.
- Egbert BM, Price NM, Segal RJ. Steatocystoma multiplex. Report of a florid case and a review. Arch Dermatol. 1979;115:334-335.
- Adams BB, Mutasim DF, Nordlund JJ. Steatocystoma multiplex: a quick removal technique. Cutis. 1999;64:127-130.
- Lee SJ, Choe YS, Park BC, et al. The vein hook successfully used for eradication of steatocystoma multiplex. Dermatol Surg. 2007;33:82-84.
- Bettes PSL, Lopes SL, Prestes MA, et al. Treatment of a facial variant of the multiple steatocystoma with skin graft: case report. Rev Bras Cir Plást. 1998;13:31-36
- Düzova AN, Sentürk GB. Suggestion for the treatment of steatocystoma multiplex located exclusively on the face. Int J Dermatol. 2004;43:60-62. doi:10.1111/j.1365-4632.2004.02068.x
- Choudhary S, Koley S, Salodkar A. A modified surgical technique for steatocystoma multiplex. J Cutan Aesthet Surg. 2010;3:25-28.
- Kaya TI, Ikizoglu G, Kokturk A, et al. A simple surgical technique for the treatment of steatocystoma multiplex. Int J Dermatol. 2001;40:785-788.
- Bakkour W, Madan V. Carbon dioxide laser perforation and extirpation of steatocystoma multiplex. Dermatol Surg. 2014;40:658-662.
- Mumcuog?lu CT, Gurel MS, Kiremitci U, et al. Er: yag laser therapy for steatocystoma multiplex. Indian J Dermatol. 2010;55:300-301.
- Moody MN, Landau JM, Goldberg LH, et al. 1,450-nm diode laser in combination with the 1550-nm fractionated erbium-doped fiber laser for the treatment of steatocystoma multiplex: a case report. Dermatol Surg. 2012;38(7 Pt 1):1104-1106.
- Cheon DU, Ko JY. 1927-nm fiber-optic diode laser: a novel therapeutic option for facial steatocystoma multiplex. J Cosmet Dermatol. 2019;18:1326-1329.
- Kim KT, Sun H, Chung EH. Comparison of complete surgical excision and minimally invasive excision using CO2 laser for removal of epidermal cysts on the face. Arch Craniofac Surg. 2019;20:84-88.
- Kassira S, Korta DZ, de Feraudy S, et al. Fractionated ablative carbon dioxide laser treatment of steatocystoma multiplex. J Cosmet Laser Ther. 2016;18:364-366.
- Dixit N, Sardana K, Paliwal P. The rationale of ideal pulse duration and pulse interval in the treatment of steatocystoma multiplex using the carbon dioxide laser in a super-pulse mode as opposedto the ultra-pulse mode. Indian J Dermatol Venereol Leprol. 2020;86:454-456.
- Santana CN, Pereira DD, Lisboa AP, et al. Steatocystoma multiplex suppurativa: case report of a rare condition. An Bras Dermatol. 2016;91(5 suppl 1):51-53.
- Atzori L, Zanniello R, Pilloni L, et al. Steatocystoma multiplex suppurativa associated with hidradenitis suppurativa successfully treated with adalimumab. J Eur Acad Dermatol Venereol. 2019;33(Suppl 6):42-44.
- Jamieson WA. Case of numerous cutaneous cysts scattered over the body. Edinb Med J. 1873;19:223-225.
- Kamra HT, Gadgil PA, Ovhal AG, et al. Steatocystoma multiplex-a rare genetic disorder: a case report and review of the literature. J Clin Diagn Res. 2013;7:166-168.
- Brownstein MH. Steatocystoma simplex. A solitary steatocystoma. Arch Dermatol. 1982;118:409-411.
- McDonald RM, Reed WB. Natal teeth and steatocystoma multiplex complicated by hidradenitis suppurativa. A new syndrome. Arch Dermatol. 1976;112:1132-1134.
- Plewig G, Wolff HH, Braun-Falco O. Steatocystoma multiplex: anatomic reevaluation, electron microscopy, and autoradiography. Arch Dermatol. 1982;272:363-380.
- Fletcher J, Posso-De Los Rios C, Jambrosic J, A, et al. Coexistence of hidradenitis suppurativa and steatocystoma multiplex: is it a new variant of hidradenitis suppurativa? J Cutan Med Surg. 2021;25:586-590.
- Cho S, Chang SE, Choi JH, et al. Clinical and histologic features of 64 cases of steatocystoma multiplex. J Dermatol. 2002;29:152-156.
- Covello SP, Smith FJ, Sillevis Smitt JH, et al. Keratin 17 mutations cause either steatocystoma multiplex or pachyonychia congenita type 2. Br J Dermatol. 1998;139:475-480.
- Liu Q, Wu W, Lu J, et al. Steatocystoma multiplex is associated with the R94C mutation in the KRTl7 gene. Mol Med Rep. 2015;12:5072-5076.
- Yang L, Zhang S, Wang G. Keratin 17 in disease pathogenesis: from cancer to dermatoses. J Pathol. 2019;247:158-165.
- Shamloul G, Khachemoune A. An updated review of the sebaceous gland and its role in health and diseases Part 1: embryology, evolution, structure, and function of sebaceous glands. Dermatol Ther. 2021;34:e14695.
- Del Rosso JQ, Kircik LH, Stein Gold L, et al. Androgens, androgen receptors, and the skin: from the laboratory to the clinic with emphasis on clinical and therapeutic implications. J Drugs Dermatol. 2020;19:30-35.
- Porras Fimbres DC, Wolfe SA, Kelley CE. Proliferation of steatocystomas in 2 transgender men. JAAD Case Rep. 2022;26:70-72.
- Marasca C, Megna M, Donnarumma M, et al. A case of steatocystoma multiplex in a psoriatic patient during treatment with anti-IL-12/23. Skin Appendage Disord. 2020;6:309-311.
- Gordon Spratt EA, Kaplan J, Patel RR, et al. Steatocystoma. Dermatol Online J. 2013;19:20721.
- Sharma A, Agrawal S, Dhurat R, et al. An unusual case of facial steatocystoma multiplex: a clinicopathologic and dermoscopic report. Dermatopathology (Basel). 2018;5:58-63.
- Rahman MH, Islam MS, Ansari NP. Atypical steatocystoma multiplex with calcification. ISRN Dermatol. 2011;2011:381901.
- Beyer AV, Vossmann D. Steatocystoma multiplex. Article in German. Hautarzt. 1996;47:469-471.
- Yanagi T, Matsumura T. Steatocystoma multiplex presenting as acral subcutaneous nodules. Acta Derm Venereol. 2006;86:374-375.
- Marzano AV, Tavecchio S, Balice Y, et al. Acral subcutaneous steatocystoma multiplex: a distinct subtype of the disease? Australas J Dermatol. 2012;53:198-201.
- Ferrandiz C, Peyri J. Steatocystoma multiplex. Article in Spanish. Med Cutan Ibero Lat Am. 1984;12:173-176.
- Alotaibi L, Alsaif M, Alhumidi A, et al. Steatocystoma multiplex suppurativa: a case with unusual giant cysts over the scalp and neck. Case Rep Dermatol. 2019;11:71-76.
- Kim SJ, Park HJ, Oh ST, et al. A case of steatocystoma multiplex limited to scalp. Ann Dermatol. 2009;21:106-109.
- Patrizi A, Neri I, Guerrini V, et al. Persistent milia, steatocystoma multiplex and eruptive vellus hair cysts: variable expression of multiple pilosebaceous cysts within an affected family. Dermatology. 1998;196:392-396.
- Tomková H, Fujimoto W, Arata J. Expression of keratins (K10 and K17) in steatocystoma multiplex, eruptive vellus hair cysts, and epidermoid and trichilemmal cysts. Am J Dermatopathol. 1997;19:250-253.
- Patokar AS, Holani AR, Khandait GH, et al. Eruptive vellus hair cysts: an underdiagnosed entity. Int J Trichology. 2022;14:31-33.
- Ohtake N, Kubota Y, Takayama O, et al. Relationship between steatocystoma multiplex and eruptive vellus hair cysts. J Am Acad Dermatol. 1992;26(5 Pt 2):876-878.
- Yoon H, Kang Y, Park H, et al. Sonographic appearance of steatocystoma: an analysis of 14 pathologically confirmed lesions. Taehan Yongsang Uihakhoe Chi. 2021;82:382-392.
- Varshney M, Aziz M, Maheshwari V, et al. Steatocystoma multiplex. BMJ Case Rep. 2011;2011:bcr0420114165.
- Tsai MH, Hsiao YP, Lin WL, et al. Steatocystoma multiplex as initial impression of non-small cell lung cancer with complete response to gefitinib. Chin J Cancer Res. 2014;26:E5-E9.
- Zussino M, Nazzaro G, Moltrasio C, et al. Coexistence of steatocystoma multiplex and hidradenitis suppurativa: assessment of this unique association by means of ultrasonography and color Doppler. Skin Res Technol. 2019;25:877-880.
- Whittle C, Silva-Hirschberg C, Loyola K, et al. Ultrasonographic spectrum of cutaneous cysts with stratified squamous epithelium in pediatric dermatology: pictorial essay. J Ultrasound Med. 2023;42:923-930.
- Arceu M, Martinez G, Alfaro D, et al. Ultrasound morphologic features of steatocystoma multiplex with clinical correlation. J Ultrasound Med. 2020;39:2255-2260.
- Reick-Mitrisin V, Reddy A, Shah BA. A breast imaging case of steatocystoma multiplex: a rare condition involving multiple anatomic regions. Cureus. 2022;14:E27756.
- Yoon H, Kang Y, Park H, et al. Sonographic appearance of steatocystoma: an analysis of 14 pathologically confirmed lesions. Taehan Yongsang Uihakhoe Chi. 2021;82:382-392.
- Apaydin R, Bilen N, Bayramgurler D, et al. Steatocystoma multiplex suppurativum: oral isotretinoin treatment combined with cryotherapy. Australas J Dermatol. 2000;41:98-100.
- Sharma A, Agrawal S, Dhurat R, et al. An unusual case of facial steatocystoma multiplex: a clinicopathologic and dermoscopic report. Dermatopathology (Basel). 2018;5:58-63.
- Moritz DL, Silverman RA. Steatocystoma multiplex treated with isotretinoin: a delayed response. Cutis. 1988;42:437-439.
- Schwartz JL, Goldsmith LA. Steatocystoma multiplex suppurativum: treatment with isotretinoin. Cutis. 1984;34:149-153.
- Kim SJ, Park HJ, Oh ST, et al. A case of steatocystoma multiplex limited to the scalp. Ann Dermatol. 2009;21:106-109.
- Fekete GL, Fekete JE. Steatocystoma multiplex generalisata partially suppurativa--case report. Acta Dermatovenerol Croat. 2010;18:114-119.
- Choudhary S, Koley S, Salodkar A. A modified surgical technique for steatocystoma multiplex. J Cutan Aesthet Surg. 2010;3:25-28.
- Kaya TI, Ikizoglu G, Kokturk A, et al. A simple surgical technique for the treatment of steatocystoma multiplex. Int J Dermatol. 2001;40:785-788.
- Oertel YC, Scott DM. Cytologic-pathologic correlations: fine needle aspiration of three cases of steatocystoma multiplex. Ann Diagn Pathol. 1998;2:318-320.
- Egbert BM, Price NM, Segal RJ. Steatocystoma multiplex. Report of a florid case and a review. Arch Dermatol. 1979;115:334-335.
- Adams BB, Mutasim DF, Nordlund JJ. Steatocystoma multiplex: a quick removal technique. Cutis. 1999;64:127-130.
- Lee SJ, Choe YS, Park BC, et al. The vein hook successfully used for eradication of steatocystoma multiplex. Dermatol Surg. 2007;33:82-84.
- Bettes PSL, Lopes SL, Prestes MA, et al. Treatment of a facial variant of the multiple steatocystoma with skin graft: case report. Rev Bras Cir Plást. 1998;13:31-36
- Düzova AN, Sentürk GB. Suggestion for the treatment of steatocystoma multiplex located exclusively on the face. Int J Dermatol. 2004;43:60-62. doi:10.1111/j.1365-4632.2004.02068.x
- Choudhary S, Koley S, Salodkar A. A modified surgical technique for steatocystoma multiplex. J Cutan Aesthet Surg. 2010;3:25-28.
- Kaya TI, Ikizoglu G, Kokturk A, et al. A simple surgical technique for the treatment of steatocystoma multiplex. Int J Dermatol. 2001;40:785-788.
- Bakkour W, Madan V. Carbon dioxide laser perforation and extirpation of steatocystoma multiplex. Dermatol Surg. 2014;40:658-662.
- Mumcuog?lu CT, Gurel MS, Kiremitci U, et al. Er: yag laser therapy for steatocystoma multiplex. Indian J Dermatol. 2010;55:300-301.
- Moody MN, Landau JM, Goldberg LH, et al. 1,450-nm diode laser in combination with the 1550-nm fractionated erbium-doped fiber laser for the treatment of steatocystoma multiplex: a case report. Dermatol Surg. 2012;38(7 Pt 1):1104-1106.
- Cheon DU, Ko JY. 1927-nm fiber-optic diode laser: a novel therapeutic option for facial steatocystoma multiplex. J Cosmet Dermatol. 2019;18:1326-1329.
- Kim KT, Sun H, Chung EH. Comparison of complete surgical excision and minimally invasive excision using CO2 laser for removal of epidermal cysts on the face. Arch Craniofac Surg. 2019;20:84-88.
- Kassira S, Korta DZ, de Feraudy S, et al. Fractionated ablative carbon dioxide laser treatment of steatocystoma multiplex. J Cosmet Laser Ther. 2016;18:364-366.
- Dixit N, Sardana K, Paliwal P. The rationale of ideal pulse duration and pulse interval in the treatment of steatocystoma multiplex using the carbon dioxide laser in a super-pulse mode as opposedto the ultra-pulse mode. Indian J Dermatol Venereol Leprol. 2020;86:454-456.
Steatocystomas: Update on Clinical Manifestations, Diagnosis, and Management
Steatocystomas: Update on Clinical Manifestations, Diagnosis, and Management
Practice Points
- Steatocystomas, which manifest as single or multiple flesh-colored subcutaneous cysts ranging from less than 3 mm to more than 3 cm, typically are asymptomatic and can persist indefinitely.
- Treatment options for steatocystomas include oral isotretinoin, tetracycline derivatives, and intralesional steroid injections. Minimally invasive procedures such as drainage and resection also are available, employing techniques such as blade incision, radiofrequency probes, and laser treatments to minimize scarring and recurrence.
- Conservative therapies such as watchful waiting are recommended for the simplex and multiplex variants, while more aggressive management such as surgical removal is recommended for the multiplex suppurativa variant due to its elevated risk for complications.
Operational Risk Management in Dermatologic Procedures
Operational Risk Management in Dermatologic Procedures
Operational risk management (ORM) refers to the systematic identification and assessment of daily operational risks within an organization designed to mitigate negative financial, reputational, and safety outcomes while maximizing efficiency and achievement of objectives.1 Operational risk management is indispensable to modern military operations, optimizing mission readiness while minimizing complications and personnel morbidity. Application of ORM in medicine holds considerable promise due to the emphasis on precise and efficient decision-making in high-stakes environments, where the margin for error is minimal. In this article, we propose integrating ORM principles into dermatologic surgery to enhance patient-centered care through improved counseling, risk assessment, and procedural outcomes.
Principles and Processes of ORM
The ORM framework is built on 4 fundamental principles: accept risk when benefits outweigh the cost, accept no unnecessary risk, anticipate and manage risk by planning, and make risk decisions at the right level.2 These principles form the foundation of the ORM’s systematic 5-step approach to identify hazards, assess hazards, make risk decisions, implement controls, and supervise. Key to the ORM process is the use of risk assessment codes and the risk assessment matrix to quantify and prioritize risks. Risk assessment codes are numerical values assigned to hazards based on their assessed severity and probability. The risk assessment matrix is a tool that plots the severity of a hazard against its probability. By locating a hazard on the matrix, users can visualize its risk level in terms of severity and probability. Building and using the risk assessment matrix begins with determining severity by assessing the potential impact of a hazard and categorizing it into levels (catastrophic, critical, moderate, or negligible). Next, probability is determined by evaluating the likelihood of occurrence (frequent, likely, occasional, seldom, or unlikely). Finally, the severity and probability are combined to assign a risk assessment code, which indicates the risk level and helps visualize criticality. Systematically applying these principles and processes enables users to make informed decisions that balance mission objectives with safety.
Proposed Framework for ORM in Dermatology Surgery
Current risk mitigation in dermatologic surgery includes strict medication oversight, sterilization protocols, and photography to prevent wrong-site surgeries. Preoperative risk assessment through conducting a thorough patient history is vital, considering factors such as pregnancy, allergies, bleeding history, cardiac devices, and keloid propensity, all of which impact surgical outcomes.3-5 After gathering the patient’s history, dermatologists determine appropriateness for surgery and its inherent risks, typically via an informed consent process outlining the diagnosis and procedure purpose as well as a list of risks, benefits, and alternatives, including forgoing treatment.
Importantly, the standard process for dermatologic risk evaluation often lacks a comprehensive systematic approach seen in other higher-risk surgical fields. For example, general surgeons frequently utilize risk assessment calculators such as the one developed by the American College of Surgeons’ National Surgical Quality Improvement Program to estimate surgical complications.6 While specific guidelines exist for evaluating factors such as hypertension or anticoagulant use, no single tool synthesizes all patient risk factors for a unified assessment. Therefore, we propose integrating ORM as a structured decision-making process that offers a more consistent means for dermatologists to evaluate, synthesize, categorize, and present risks to patients. Our proposed process includes translating military mishap severity into a framework that helps patients better understand decisions about their health care when using ORM (eTable 1). The proposed process also provides dermatologists with a systematic, proactive, and iterative approach to assessing risks that allows them to consistently qualify medical decisions (eTable 2).
Patients often struggle to understand surgical risk severity, including overestimating the risks of routine minor procedures or underestimating the risks of more intensive procedures.7,8 Incorporating ORM into patient communication mirrors the provider’s process but uses patient-friendly terminology—it is discussion based and integrates patient preferences and tolerances (eTable 2). These steps often occur informally in dermatologic counseling; however, an organized structured approach, especially using a visual aid such as a risk assessment matrix, enhances patient comprehension, recall, and satisfaction.9
Practical Scenarios
Integrating ORM into dermatologic surgery is a proactive iterative process for both provider decision-making and patient communication. Leveraging a risk assessment matrix as a visual aid allows for clear identification, evaluation, and mitigation of hazards, fostering collaborative choices with regard to the treatment approach. Here we provide 2 case scenarios highlighting how ORM and the risk assessment matrix can be used in the management of a complex patient with a lesion in a high-risk location as well as to address patient anxiety and comorbidities. It is important to note that the way the matrices are completed in the examples provided may differ compared to other providers. The purpose of ORM is not to dictate risk categories but to serve as a tool for providers to take their own experiences and knowledge of the patient to guide their decision-making and counseling processes.
Case Scenario 1—An elderly man with a history of diabetes, cardiovascular accident, coronary artery bypass grafting, and multiple squamous cell carcinoma excisions presents for evaluation of a 1-cm squamous cell carcinoma in situ on the left leg. His current medications include an anticoagulant and antihypertensives.
In this scenario, the provider would apply ORM by identifying and assessing hazards, making risk decisions, implementing controls, and supervising care.
General hazards for excision on the leg include bleeding, infection, scarring, pain, delayed healing, activity limitations, and possible further procedures. Before the visit, the provider should prepare baseline risk matrices for 2 potential treatment options: wide local excision and electrodessication and curettage. For example, surgical bleeding may be assessed as negligible severity and almost certain probability for a general excision.
Next, the provider would incorporate the patient’s unique history in the risk matrices (eFigures 1 and 2). The patient’s use of an anticoagulant indicates a bleeding risk; therefore, the provider may shift the severity to minimal clinical concern, understanding the need for enhanced perioperative management. The history of diabetes also has a considerable impact on wound healing, so the provider might elevate the probability of delayed wound healing from rare to unlikely and the severity from moderate to severe. The prior cardiovascular accident also raises concerns about mobility and activity limitations during recovery, which could be escalated from minimal to moderate clinical concern if postoperative limitations on ambulation increase the risk for new clots. Based on this internal assessment, the provider identifies which risks are elevated and require further attention and discussion with the patient, helping tailor the counseling approach and potential treatment plan. The provider should begin to consider initial control measures such as coordinating anticoagulant management, ensuring diabetes is well controlled, and planning for postoperative ambulation support.
Once the provider has conducted the internal assessment, the ORM matrices become powerful tools for shared decision-making with the patient. The provider can walk the patient through the procedures and their common risks and then explain how their individual situation modifies the risks. The visual and explicit upgrade on the matrices allows the patient to clearly see how unique factors influence their personal risk profile, moving beyond a generic list of complications. The provider then should engage the patient in a discussion about their risk tolerance, which is crucial for mutual agreement on whether to proceed with treatment and, if so, which procedure is most appropriate given the patient’s comfort level with their individualized risk profile. Then the provider should reinforce the proactive steps planned to mitigate the identified risks to provide assurance and reinforce the collaborative approach to safety.
Finally, throughout the preoperative and postoperative phases, the provider should continuously monitor the patient’s condition and the effectiveness of the control measures, adjusting the plan as needed.
In this scenario, both the provider and the patient participated in the risk assessment, with the provider completing the assessment before the visit and presenting it to the patient or performing the assessment in real time with the patient present to explain the reasoning behind assignment of risk based on each procedure and the patient’s unique risk factors.
Case Scenario 2—A 38-year-old woman with a history of hypertension and procedural anxiety presents for evaluation of a biopsy-proven basal cell carcinoma on the nasal ala. The patient is taking diltiazem for hypertension and is compliant with her medication. Her blood pressure at the current visit is 148/96 mm Hg, which she attributes to white coat syndrome. Mohs micrographic surgery generally is the gold standard treatment for this case.
The provider’s ORM process, conducted either before or in real time during the visit, would begin with identification and assessment of the hazards. For Mohs surgery on the nasal ala, common hazards would include scarring, pain, infection, bleeding, and potential cosmetic distortion. Unique to this patient are the procedural anxiety and hypertension.
To populate the risk assessment matrix (eFigure 3), the provider would first map the baseline risks of Mohs surgery, which include considerable scarring as a moderate clinical concern but a seldom probability. Because the patient’s procedural anxiety directly increases the probability of intraoperative distress or elevated blood pressure during the procedure, the provider might assess patient distress/anxiety as a moderate clinical concern with a likely probability. While the patient’s blood pressure is controlled, the white coat syndrome raises the probability of hypertensive urgency/emergency during surgery; this might be elevated from unlikely to occasional or likely probability, and severity might increase from minimal to moderate due to its potential impact on procedural safety. The provider should consider strategies to address these elevated risks during the consultation. Then, as part of preprocedure planning, the provider should consider discussing anxiolytics, emphasizing medication compliance, and ensuring a calm environment for the patient’s surgery.
For this patient, the risk assessment matrix becomes a powerful tool to address fears and proactively manage her unique risk factors. To start the counseling process, the provider should explain the procedure, its benefits, and potential adverse effects. Then, the patient’s individualized risks can be visualized using the matrix, which also is an opportunity for reassurance, as it can alleviate patient fears by contextualizing rare but impactful outcomes.9
Now the provider can assess the patient’s risk tolerance. This discussion ensures that the patient’s comfort level and preferences are central to the treatment decision, even for a gold-standard procedure such as Mohs surgery. By listening and responding to the patient’s input, the provider can build trust and discuss strategies that can help control for some risk factors.
Finally, the provider would re-evaluate throughout the procedure by continuously monitoring the patient’s anxiety and vital signs. The provider should also be ready to adjust pain management or employ anxiety-reduction techniques.
Final Thoughts
Reviewing the risk assessment matrix can be an effective way to nonjudgmentally discuss a patient’s unique risk factors and provide a complete understanding of the planned treatment or procedure. It conveys to the patient that, as the provider, you are taking their health seriously when considering treatment options and can be a means to build patient rapport and trust. This approach mirrors risk communication strategies long employed in military operational planning, where transparency and structured risk evaluation are essential to maintaining mission readiness and unit cohesion.
- The OR Society. The history of OR. The OR Society. Published 2023.
- Naval Postgraduate School. ORM: operational risk management. Accessed September 12, 2025. https://nps.edu/web/safety/orm
- Smith C, Srivastava D, Nijhawan RI. Optimizing patient safety in dermatologic surgery. Dermatol Clin. 2019;37:319-328.
- Minkis K, Whittington A, Alam M. Dermatologic surgery emergencies: complications caused by systemic reactions, high-energy systems, and trauma. J Am Acad Dermatol. 2016;75:265-284.
- Pomerantz RG, Lee DA, Siegel DM. Risk assessment in surgical patients: balancing iatrogenic risks and benefits. Clin Dermatol. 2011;29:669-677.
- Bilimoria KY, Liu Y, Paruch JL, et al. Development and evaluation of the universal ACS NSQIP surgical risk calculator: a decision aid and informed consent tool for patients and surgeons. J Am Coll Surgeons. 2013;217:833-842.
- Lloyd AJ. The extent of patients’ understanding of the risk of treatments. BMJ Qual Saf. 2001;10:i14-i18.
- Falagas ME, Korbila IP, Giannopoulou KP, et al. Informed consent: how much and what do patients understand? Am J Surg. 2009;198:420-435.
- Cohen SM, Baimas-George M, Ponce C, et al. Is a picture worth a thousand words? a scoping review of the impact of visual aids on patients undergoing surgery. J Surg Educ. 2024;81:1276-1292.
Operational risk management (ORM) refers to the systematic identification and assessment of daily operational risks within an organization designed to mitigate negative financial, reputational, and safety outcomes while maximizing efficiency and achievement of objectives.1 Operational risk management is indispensable to modern military operations, optimizing mission readiness while minimizing complications and personnel morbidity. Application of ORM in medicine holds considerable promise due to the emphasis on precise and efficient decision-making in high-stakes environments, where the margin for error is minimal. In this article, we propose integrating ORM principles into dermatologic surgery to enhance patient-centered care through improved counseling, risk assessment, and procedural outcomes.
Principles and Processes of ORM
The ORM framework is built on 4 fundamental principles: accept risk when benefits outweigh the cost, accept no unnecessary risk, anticipate and manage risk by planning, and make risk decisions at the right level.2 These principles form the foundation of the ORM’s systematic 5-step approach to identify hazards, assess hazards, make risk decisions, implement controls, and supervise. Key to the ORM process is the use of risk assessment codes and the risk assessment matrix to quantify and prioritize risks. Risk assessment codes are numerical values assigned to hazards based on their assessed severity and probability. The risk assessment matrix is a tool that plots the severity of a hazard against its probability. By locating a hazard on the matrix, users can visualize its risk level in terms of severity and probability. Building and using the risk assessment matrix begins with determining severity by assessing the potential impact of a hazard and categorizing it into levels (catastrophic, critical, moderate, or negligible). Next, probability is determined by evaluating the likelihood of occurrence (frequent, likely, occasional, seldom, or unlikely). Finally, the severity and probability are combined to assign a risk assessment code, which indicates the risk level and helps visualize criticality. Systematically applying these principles and processes enables users to make informed decisions that balance mission objectives with safety.
Proposed Framework for ORM in Dermatology Surgery
Current risk mitigation in dermatologic surgery includes strict medication oversight, sterilization protocols, and photography to prevent wrong-site surgeries. Preoperative risk assessment through conducting a thorough patient history is vital, considering factors such as pregnancy, allergies, bleeding history, cardiac devices, and keloid propensity, all of which impact surgical outcomes.3-5 After gathering the patient’s history, dermatologists determine appropriateness for surgery and its inherent risks, typically via an informed consent process outlining the diagnosis and procedure purpose as well as a list of risks, benefits, and alternatives, including forgoing treatment.
Importantly, the standard process for dermatologic risk evaluation often lacks a comprehensive systematic approach seen in other higher-risk surgical fields. For example, general surgeons frequently utilize risk assessment calculators such as the one developed by the American College of Surgeons’ National Surgical Quality Improvement Program to estimate surgical complications.6 While specific guidelines exist for evaluating factors such as hypertension or anticoagulant use, no single tool synthesizes all patient risk factors for a unified assessment. Therefore, we propose integrating ORM as a structured decision-making process that offers a more consistent means for dermatologists to evaluate, synthesize, categorize, and present risks to patients. Our proposed process includes translating military mishap severity into a framework that helps patients better understand decisions about their health care when using ORM (eTable 1). The proposed process also provides dermatologists with a systematic, proactive, and iterative approach to assessing risks that allows them to consistently qualify medical decisions (eTable 2).
Patients often struggle to understand surgical risk severity, including overestimating the risks of routine minor procedures or underestimating the risks of more intensive procedures.7,8 Incorporating ORM into patient communication mirrors the provider’s process but uses patient-friendly terminology—it is discussion based and integrates patient preferences and tolerances (eTable 2). These steps often occur informally in dermatologic counseling; however, an organized structured approach, especially using a visual aid such as a risk assessment matrix, enhances patient comprehension, recall, and satisfaction.9
Practical Scenarios
Integrating ORM into dermatologic surgery is a proactive iterative process for both provider decision-making and patient communication. Leveraging a risk assessment matrix as a visual aid allows for clear identification, evaluation, and mitigation of hazards, fostering collaborative choices with regard to the treatment approach. Here we provide 2 case scenarios highlighting how ORM and the risk assessment matrix can be used in the management of a complex patient with a lesion in a high-risk location as well as to address patient anxiety and comorbidities. It is important to note that the way the matrices are completed in the examples provided may differ compared to other providers. The purpose of ORM is not to dictate risk categories but to serve as a tool for providers to take their own experiences and knowledge of the patient to guide their decision-making and counseling processes.
Case Scenario 1—An elderly man with a history of diabetes, cardiovascular accident, coronary artery bypass grafting, and multiple squamous cell carcinoma excisions presents for evaluation of a 1-cm squamous cell carcinoma in situ on the left leg. His current medications include an anticoagulant and antihypertensives.
In this scenario, the provider would apply ORM by identifying and assessing hazards, making risk decisions, implementing controls, and supervising care.
General hazards for excision on the leg include bleeding, infection, scarring, pain, delayed healing, activity limitations, and possible further procedures. Before the visit, the provider should prepare baseline risk matrices for 2 potential treatment options: wide local excision and electrodessication and curettage. For example, surgical bleeding may be assessed as negligible severity and almost certain probability for a general excision.
Next, the provider would incorporate the patient’s unique history in the risk matrices (eFigures 1 and 2). The patient’s use of an anticoagulant indicates a bleeding risk; therefore, the provider may shift the severity to minimal clinical concern, understanding the need for enhanced perioperative management. The history of diabetes also has a considerable impact on wound healing, so the provider might elevate the probability of delayed wound healing from rare to unlikely and the severity from moderate to severe. The prior cardiovascular accident also raises concerns about mobility and activity limitations during recovery, which could be escalated from minimal to moderate clinical concern if postoperative limitations on ambulation increase the risk for new clots. Based on this internal assessment, the provider identifies which risks are elevated and require further attention and discussion with the patient, helping tailor the counseling approach and potential treatment plan. The provider should begin to consider initial control measures such as coordinating anticoagulant management, ensuring diabetes is well controlled, and planning for postoperative ambulation support.
Once the provider has conducted the internal assessment, the ORM matrices become powerful tools for shared decision-making with the patient. The provider can walk the patient through the procedures and their common risks and then explain how their individual situation modifies the risks. The visual and explicit upgrade on the matrices allows the patient to clearly see how unique factors influence their personal risk profile, moving beyond a generic list of complications. The provider then should engage the patient in a discussion about their risk tolerance, which is crucial for mutual agreement on whether to proceed with treatment and, if so, which procedure is most appropriate given the patient’s comfort level with their individualized risk profile. Then the provider should reinforce the proactive steps planned to mitigate the identified risks to provide assurance and reinforce the collaborative approach to safety.
Finally, throughout the preoperative and postoperative phases, the provider should continuously monitor the patient’s condition and the effectiveness of the control measures, adjusting the plan as needed.
In this scenario, both the provider and the patient participated in the risk assessment, with the provider completing the assessment before the visit and presenting it to the patient or performing the assessment in real time with the patient present to explain the reasoning behind assignment of risk based on each procedure and the patient’s unique risk factors.
Case Scenario 2—A 38-year-old woman with a history of hypertension and procedural anxiety presents for evaluation of a biopsy-proven basal cell carcinoma on the nasal ala. The patient is taking diltiazem for hypertension and is compliant with her medication. Her blood pressure at the current visit is 148/96 mm Hg, which she attributes to white coat syndrome. Mohs micrographic surgery generally is the gold standard treatment for this case.
The provider’s ORM process, conducted either before or in real time during the visit, would begin with identification and assessment of the hazards. For Mohs surgery on the nasal ala, common hazards would include scarring, pain, infection, bleeding, and potential cosmetic distortion. Unique to this patient are the procedural anxiety and hypertension.
To populate the risk assessment matrix (eFigure 3), the provider would first map the baseline risks of Mohs surgery, which include considerable scarring as a moderate clinical concern but a seldom probability. Because the patient’s procedural anxiety directly increases the probability of intraoperative distress or elevated blood pressure during the procedure, the provider might assess patient distress/anxiety as a moderate clinical concern with a likely probability. While the patient’s blood pressure is controlled, the white coat syndrome raises the probability of hypertensive urgency/emergency during surgery; this might be elevated from unlikely to occasional or likely probability, and severity might increase from minimal to moderate due to its potential impact on procedural safety. The provider should consider strategies to address these elevated risks during the consultation. Then, as part of preprocedure planning, the provider should consider discussing anxiolytics, emphasizing medication compliance, and ensuring a calm environment for the patient’s surgery.
For this patient, the risk assessment matrix becomes a powerful tool to address fears and proactively manage her unique risk factors. To start the counseling process, the provider should explain the procedure, its benefits, and potential adverse effects. Then, the patient’s individualized risks can be visualized using the matrix, which also is an opportunity for reassurance, as it can alleviate patient fears by contextualizing rare but impactful outcomes.9
Now the provider can assess the patient’s risk tolerance. This discussion ensures that the patient’s comfort level and preferences are central to the treatment decision, even for a gold-standard procedure such as Mohs surgery. By listening and responding to the patient’s input, the provider can build trust and discuss strategies that can help control for some risk factors.
Finally, the provider would re-evaluate throughout the procedure by continuously monitoring the patient’s anxiety and vital signs. The provider should also be ready to adjust pain management or employ anxiety-reduction techniques.
Final Thoughts
Reviewing the risk assessment matrix can be an effective way to nonjudgmentally discuss a patient’s unique risk factors and provide a complete understanding of the planned treatment or procedure. It conveys to the patient that, as the provider, you are taking their health seriously when considering treatment options and can be a means to build patient rapport and trust. This approach mirrors risk communication strategies long employed in military operational planning, where transparency and structured risk evaluation are essential to maintaining mission readiness and unit cohesion.
Operational risk management (ORM) refers to the systematic identification and assessment of daily operational risks within an organization designed to mitigate negative financial, reputational, and safety outcomes while maximizing efficiency and achievement of objectives.1 Operational risk management is indispensable to modern military operations, optimizing mission readiness while minimizing complications and personnel morbidity. Application of ORM in medicine holds considerable promise due to the emphasis on precise and efficient decision-making in high-stakes environments, where the margin for error is minimal. In this article, we propose integrating ORM principles into dermatologic surgery to enhance patient-centered care through improved counseling, risk assessment, and procedural outcomes.
Principles and Processes of ORM
The ORM framework is built on 4 fundamental principles: accept risk when benefits outweigh the cost, accept no unnecessary risk, anticipate and manage risk by planning, and make risk decisions at the right level.2 These principles form the foundation of the ORM’s systematic 5-step approach to identify hazards, assess hazards, make risk decisions, implement controls, and supervise. Key to the ORM process is the use of risk assessment codes and the risk assessment matrix to quantify and prioritize risks. Risk assessment codes are numerical values assigned to hazards based on their assessed severity and probability. The risk assessment matrix is a tool that plots the severity of a hazard against its probability. By locating a hazard on the matrix, users can visualize its risk level in terms of severity and probability. Building and using the risk assessment matrix begins with determining severity by assessing the potential impact of a hazard and categorizing it into levels (catastrophic, critical, moderate, or negligible). Next, probability is determined by evaluating the likelihood of occurrence (frequent, likely, occasional, seldom, or unlikely). Finally, the severity and probability are combined to assign a risk assessment code, which indicates the risk level and helps visualize criticality. Systematically applying these principles and processes enables users to make informed decisions that balance mission objectives with safety.
Proposed Framework for ORM in Dermatology Surgery
Current risk mitigation in dermatologic surgery includes strict medication oversight, sterilization protocols, and photography to prevent wrong-site surgeries. Preoperative risk assessment through conducting a thorough patient history is vital, considering factors such as pregnancy, allergies, bleeding history, cardiac devices, and keloid propensity, all of which impact surgical outcomes.3-5 After gathering the patient’s history, dermatologists determine appropriateness for surgery and its inherent risks, typically via an informed consent process outlining the diagnosis and procedure purpose as well as a list of risks, benefits, and alternatives, including forgoing treatment.
Importantly, the standard process for dermatologic risk evaluation often lacks a comprehensive systematic approach seen in other higher-risk surgical fields. For example, general surgeons frequently utilize risk assessment calculators such as the one developed by the American College of Surgeons’ National Surgical Quality Improvement Program to estimate surgical complications.6 While specific guidelines exist for evaluating factors such as hypertension or anticoagulant use, no single tool synthesizes all patient risk factors for a unified assessment. Therefore, we propose integrating ORM as a structured decision-making process that offers a more consistent means for dermatologists to evaluate, synthesize, categorize, and present risks to patients. Our proposed process includes translating military mishap severity into a framework that helps patients better understand decisions about their health care when using ORM (eTable 1). The proposed process also provides dermatologists with a systematic, proactive, and iterative approach to assessing risks that allows them to consistently qualify medical decisions (eTable 2).
Patients often struggle to understand surgical risk severity, including overestimating the risks of routine minor procedures or underestimating the risks of more intensive procedures.7,8 Incorporating ORM into patient communication mirrors the provider’s process but uses patient-friendly terminology—it is discussion based and integrates patient preferences and tolerances (eTable 2). These steps often occur informally in dermatologic counseling; however, an organized structured approach, especially using a visual aid such as a risk assessment matrix, enhances patient comprehension, recall, and satisfaction.9
Practical Scenarios
Integrating ORM into dermatologic surgery is a proactive iterative process for both provider decision-making and patient communication. Leveraging a risk assessment matrix as a visual aid allows for clear identification, evaluation, and mitigation of hazards, fostering collaborative choices with regard to the treatment approach. Here we provide 2 case scenarios highlighting how ORM and the risk assessment matrix can be used in the management of a complex patient with a lesion in a high-risk location as well as to address patient anxiety and comorbidities. It is important to note that the way the matrices are completed in the examples provided may differ compared to other providers. The purpose of ORM is not to dictate risk categories but to serve as a tool for providers to take their own experiences and knowledge of the patient to guide their decision-making and counseling processes.
Case Scenario 1—An elderly man with a history of diabetes, cardiovascular accident, coronary artery bypass grafting, and multiple squamous cell carcinoma excisions presents for evaluation of a 1-cm squamous cell carcinoma in situ on the left leg. His current medications include an anticoagulant and antihypertensives.
In this scenario, the provider would apply ORM by identifying and assessing hazards, making risk decisions, implementing controls, and supervising care.
General hazards for excision on the leg include bleeding, infection, scarring, pain, delayed healing, activity limitations, and possible further procedures. Before the visit, the provider should prepare baseline risk matrices for 2 potential treatment options: wide local excision and electrodessication and curettage. For example, surgical bleeding may be assessed as negligible severity and almost certain probability for a general excision.
Next, the provider would incorporate the patient’s unique history in the risk matrices (eFigures 1 and 2). The patient’s use of an anticoagulant indicates a bleeding risk; therefore, the provider may shift the severity to minimal clinical concern, understanding the need for enhanced perioperative management. The history of diabetes also has a considerable impact on wound healing, so the provider might elevate the probability of delayed wound healing from rare to unlikely and the severity from moderate to severe. The prior cardiovascular accident also raises concerns about mobility and activity limitations during recovery, which could be escalated from minimal to moderate clinical concern if postoperative limitations on ambulation increase the risk for new clots. Based on this internal assessment, the provider identifies which risks are elevated and require further attention and discussion with the patient, helping tailor the counseling approach and potential treatment plan. The provider should begin to consider initial control measures such as coordinating anticoagulant management, ensuring diabetes is well controlled, and planning for postoperative ambulation support.
Once the provider has conducted the internal assessment, the ORM matrices become powerful tools for shared decision-making with the patient. The provider can walk the patient through the procedures and their common risks and then explain how their individual situation modifies the risks. The visual and explicit upgrade on the matrices allows the patient to clearly see how unique factors influence their personal risk profile, moving beyond a generic list of complications. The provider then should engage the patient in a discussion about their risk tolerance, which is crucial for mutual agreement on whether to proceed with treatment and, if so, which procedure is most appropriate given the patient’s comfort level with their individualized risk profile. Then the provider should reinforce the proactive steps planned to mitigate the identified risks to provide assurance and reinforce the collaborative approach to safety.
Finally, throughout the preoperative and postoperative phases, the provider should continuously monitor the patient’s condition and the effectiveness of the control measures, adjusting the plan as needed.
In this scenario, both the provider and the patient participated in the risk assessment, with the provider completing the assessment before the visit and presenting it to the patient or performing the assessment in real time with the patient present to explain the reasoning behind assignment of risk based on each procedure and the patient’s unique risk factors.
Case Scenario 2—A 38-year-old woman with a history of hypertension and procedural anxiety presents for evaluation of a biopsy-proven basal cell carcinoma on the nasal ala. The patient is taking diltiazem for hypertension and is compliant with her medication. Her blood pressure at the current visit is 148/96 mm Hg, which she attributes to white coat syndrome. Mohs micrographic surgery generally is the gold standard treatment for this case.
The provider’s ORM process, conducted either before or in real time during the visit, would begin with identification and assessment of the hazards. For Mohs surgery on the nasal ala, common hazards would include scarring, pain, infection, bleeding, and potential cosmetic distortion. Unique to this patient are the procedural anxiety and hypertension.
To populate the risk assessment matrix (eFigure 3), the provider would first map the baseline risks of Mohs surgery, which include considerable scarring as a moderate clinical concern but a seldom probability. Because the patient’s procedural anxiety directly increases the probability of intraoperative distress or elevated blood pressure during the procedure, the provider might assess patient distress/anxiety as a moderate clinical concern with a likely probability. While the patient’s blood pressure is controlled, the white coat syndrome raises the probability of hypertensive urgency/emergency during surgery; this might be elevated from unlikely to occasional or likely probability, and severity might increase from minimal to moderate due to its potential impact on procedural safety. The provider should consider strategies to address these elevated risks during the consultation. Then, as part of preprocedure planning, the provider should consider discussing anxiolytics, emphasizing medication compliance, and ensuring a calm environment for the patient’s surgery.
For this patient, the risk assessment matrix becomes a powerful tool to address fears and proactively manage her unique risk factors. To start the counseling process, the provider should explain the procedure, its benefits, and potential adverse effects. Then, the patient’s individualized risks can be visualized using the matrix, which also is an opportunity for reassurance, as it can alleviate patient fears by contextualizing rare but impactful outcomes.9
Now the provider can assess the patient’s risk tolerance. This discussion ensures that the patient’s comfort level and preferences are central to the treatment decision, even for a gold-standard procedure such as Mohs surgery. By listening and responding to the patient’s input, the provider can build trust and discuss strategies that can help control for some risk factors.
Finally, the provider would re-evaluate throughout the procedure by continuously monitoring the patient’s anxiety and vital signs. The provider should also be ready to adjust pain management or employ anxiety-reduction techniques.
Final Thoughts
Reviewing the risk assessment matrix can be an effective way to nonjudgmentally discuss a patient’s unique risk factors and provide a complete understanding of the planned treatment or procedure. It conveys to the patient that, as the provider, you are taking their health seriously when considering treatment options and can be a means to build patient rapport and trust. This approach mirrors risk communication strategies long employed in military operational planning, where transparency and structured risk evaluation are essential to maintaining mission readiness and unit cohesion.
- The OR Society. The history of OR. The OR Society. Published 2023.
- Naval Postgraduate School. ORM: operational risk management. Accessed September 12, 2025. https://nps.edu/web/safety/orm
- Smith C, Srivastava D, Nijhawan RI. Optimizing patient safety in dermatologic surgery. Dermatol Clin. 2019;37:319-328.
- Minkis K, Whittington A, Alam M. Dermatologic surgery emergencies: complications caused by systemic reactions, high-energy systems, and trauma. J Am Acad Dermatol. 2016;75:265-284.
- Pomerantz RG, Lee DA, Siegel DM. Risk assessment in surgical patients: balancing iatrogenic risks and benefits. Clin Dermatol. 2011;29:669-677.
- Bilimoria KY, Liu Y, Paruch JL, et al. Development and evaluation of the universal ACS NSQIP surgical risk calculator: a decision aid and informed consent tool for patients and surgeons. J Am Coll Surgeons. 2013;217:833-842.
- Lloyd AJ. The extent of patients’ understanding of the risk of treatments. BMJ Qual Saf. 2001;10:i14-i18.
- Falagas ME, Korbila IP, Giannopoulou KP, et al. Informed consent: how much and what do patients understand? Am J Surg. 2009;198:420-435.
- Cohen SM, Baimas-George M, Ponce C, et al. Is a picture worth a thousand words? a scoping review of the impact of visual aids on patients undergoing surgery. J Surg Educ. 2024;81:1276-1292.
- The OR Society. The history of OR. The OR Society. Published 2023.
- Naval Postgraduate School. ORM: operational risk management. Accessed September 12, 2025. https://nps.edu/web/safety/orm
- Smith C, Srivastava D, Nijhawan RI. Optimizing patient safety in dermatologic surgery. Dermatol Clin. 2019;37:319-328.
- Minkis K, Whittington A, Alam M. Dermatologic surgery emergencies: complications caused by systemic reactions, high-energy systems, and trauma. J Am Acad Dermatol. 2016;75:265-284.
- Pomerantz RG, Lee DA, Siegel DM. Risk assessment in surgical patients: balancing iatrogenic risks and benefits. Clin Dermatol. 2011;29:669-677.
- Bilimoria KY, Liu Y, Paruch JL, et al. Development and evaluation of the universal ACS NSQIP surgical risk calculator: a decision aid and informed consent tool for patients and surgeons. J Am Coll Surgeons. 2013;217:833-842.
- Lloyd AJ. The extent of patients’ understanding of the risk of treatments. BMJ Qual Saf. 2001;10:i14-i18.
- Falagas ME, Korbila IP, Giannopoulou KP, et al. Informed consent: how much and what do patients understand? Am J Surg. 2009;198:420-435.
- Cohen SM, Baimas-George M, Ponce C, et al. Is a picture worth a thousand words? a scoping review of the impact of visual aids on patients undergoing surgery. J Surg Educ. 2024;81:1276-1292.
Operational Risk Management in Dermatologic Procedures
Operational Risk Management in Dermatologic Procedures
Dermoscopic Documentation of a No-see-um Bite
Dermoscopic Documentation of a No-see-um Bite
Biting midges, commonly known as no-see-ums, are true flies (order Diptera) and members of the Ceratopogonidae family. Regionally, they are known as punkies in the Northeast, pinyon gnats in the Southwest, moose flies in Canada, and sand gnats in Georgia, among other names.1 There are 6206 species found worldwide except for Antarctica.2 The 3 genera of greatest importance to human and livestock health in the United States are Culicoides, Leptoconops, and Forcipomyia.1 Forty-seven species of the genus Culicoides are known to be present in Florida.3 Species belonging to the genus Leptoconops also are present in coastal areas of southeast Florida as well as in the tropics, subtropics, and Caribbean.3 In the United States, biting midges primarily are a nuisance; the major medical issue associated with Culicoides insects are allergic reactions to their bites. Even though no-see-ums are not known to transmit disease in humans, they have an impact on other animal species in the United States as biting pests and vectors of disease-causing pathogens.1 Biting midges pose quite a nuisance for the proper enjoyment of outdoor spaces in the southeastern United States.
Characteristics
Morphologically, no-see-ums are gray flies measuring 1 to 3 mm in length (eFigure 1). Adults have 2 wings with distinctive patterns, large compound eyes, a thorax that extends slightly over the head, an abdomen with 9 segments, and antennae with 15 segments (eFigure 2).1,3,4 Females have modified mouth parts including mandibles that lacerate the skin during feeding, which is mainly on blood from vertebrate hosts (primarily mammals but also birds, reptiles, and amphibians).1,4 They also can feed on invertebrate hosts. Both male and female no-see-ums feed on nectar, but adult females require a blood meal to develop their eggs.2 Their life cycle progresses in stages from egg to larva to pupa to adult. Larval habitats include salt marshes, swamps, shores of streams and ponds, water-holding plants, rotting fruit, and saturated wood- and manure-enriched soil. Adults can live 2 to 7 weeks. They are weak fliers, particularly in windy conditions.1
In Florida, no-see-ums are more active during the rainy months of May to October but are active year-round in the southeastern United States and the Gulf Coast from Florida to West Texas. They are active throughout the United States in the warmer months of June and July.5 Their peak feeding activity occurs at dawn and dusk, but different species of biting midges such as Leptoconops and Culicoides also can feed during daylight hours and at night, respectively.1,6,7
Case Report
One of the authors (M.J.S.), a healthy 54-year-old man with no remarkable medical history or current use of medications, documented the natural progression of a no-see-um bite by sitting in an outdoor Florida space at 8:00
Clinical Manifestations
Although no-see-ums are not known to transmit disease in the United States, they are important biting pests that can affect tourism and prevent enjoyment of outdoor spaces and activities.2 The bite reactions on the host can range from wheal-like lesions to papules measuring 2 to 3 mm (at times with overlying vesicles) to nodules up to 1 cm in diameter.8 In our reported case, the small wheals disappeared within hours, but pruritic papules have been described to last from weeks to months. Published histopathologic correlation of biopsied indurated papules within 3 days of bite occurrence have revealed a superficial infiltrate composed of lymphocytes and histiocytes, while eosinophils were found in the deeper dermis and subcutaneous fat. Within 2 weeks, as the lesions aged, the infiltrate contained a smaller percentage of eosinophils and predominantly was present in only the superficial dermis.8 Delayed-type hypersensitivity reactions including pustules and bullous lesions also have been described.9,10 Host immune reaction to the saliva introduced during the bite dictates the severity of the response, and lesions may become secondarily infected due to scratching.11
Management Recommendations
Management consists of cleaning the bite site with soap and water to prevent infection, applying cold compresses or ice packs to relieve the intense itch, and avoiding scratching.11 Application of over-the-counter calamine lotion or hydrocortisone cream can relieve itch, and mid- to high-potency topical corticosteroids also can be prescribed for 1 to 2 weeks for more intense bite reactions in conjunction with oral antihistamines. Topical or oral antibiotics may be indicated if redness and swelling progress at the bite site or if breaks in the skin become secondarily infected.
Final Thoughts
Because of the wide-ranging habitats of no-see-ums, eradication programs using insecticides have been inefficient or environmentally suboptimal. Emptying all standing water in outdoor spaces will reduce the number of no-see-ums. Avoidance of the outdoors at dawn and dusk when no-see-ums are most active is helpful, as well as protecting exposed skin by wearing long-sleeved shirts and long pants when outside. Insect repellents containing DEET (N-N-diethyl-meta-toluamide) or picaridin can offer additional protection on the remaining exposed skin. Oil of lemon eucalyptus, or active compound p-menthane-3,8-diol, has been shown to be effective against no-see-ums. Use of DEET should be avoided in children younger than 2 years and p-menthane-3,8-diol in those younger than 3 years. Picaridin is safe for use in children.12 Citronella oil is ineffective. Installing window and patio screens with a mesh size less than 16 can prevent no-see-ums from passing through the netting but will restrict air flow.3 Turning off porch lights also is helpful, as no-see-ums are attracted to light sources.6 Since no-see-ums are weak flyers, setting ceiling or window fans at high speeds can minimize exposure; similarly, being outdoors on a windy day may decrease the likelihood of being bitten. Ultimately, the best remedy for a bite is to prevent them from happening.
- Hill CA, MacDonald JF. Biting midges: biology and public health risk. Purdue University. Published July 2013. Accessed September 3, 2025. http://extension.entm.purdue.edu/publichealth/insects/bitingmidge.html
- Borkent A, Dominiak P. Catalog of the biting midges of the world (Diptera: Ceratopogonidae). Zootaxa. 2020;4787:1-377.
- Connelly CR. Biting midges, no-see-ums Culicoides spp. (Insecta: Diptera: Ceratopogonidae). University of Florida publication #EENY 349. Published August 2, 2022. Accessed September 3, 2025. https://edis.ifas.ufl.edu/publication/IN626
- Mullen GR, Murphree CS. Biting midges (Ceratopogonidae). In: Mullen GR, Durden LA, eds. Medical and Veterinary Entomology. 3rd ed. Academic Press; 2019:213-236.
- Best Bee Brothers. No-see-um seasonality range map & season information. Published March 4, 2022. Accessed September 3, 2025. https://bestbeebrothers.com/blogs/blog/no-see-um-season
- Biology Insights. Is there a season for no see ums in Florida? Published August 28, 2025. Accessed September 16, 2025. https://biologyinsights.com/is-there-a-season-for-no-see-ums-in-florida/
- Burris S. Florida no see ums: how to navigate the woes of no see ums in Florida. The Bug Agenda. Published February 2, 2022. Accessed September 3, 2025. https://thebugagenda.com/no-see-ums-in-florida/
- Steffen C. Clinical and histopathologic correlation of midge bites. Arch Dermatol. 1981;117:785-787.
- Krakowski AC, Ho B. Arthropod assault from biting midges. J Pediatr. 2013;163:298.
- Maves RC, Reaves EJ, Martin GJ. Images in clinical tropical medicine: bullous leg lesions caused by Culicoides midges after travel in the Amazon basin. Am J Trop Med Hyg. 2010;83:447.
- Swank B. How long do no-see-ums live? Pest Source. Updated March 17, 2025. Accessed September 3, 2025. https://pestsource.com/no-see-um/lifespan/
- Nguyen QD, Vu MN, Herbert AA. Insect repellents: an updated review for the clinician. J Am Acad Dermatol. 2023;88:123-130.
Biting midges, commonly known as no-see-ums, are true flies (order Diptera) and members of the Ceratopogonidae family. Regionally, they are known as punkies in the Northeast, pinyon gnats in the Southwest, moose flies in Canada, and sand gnats in Georgia, among other names.1 There are 6206 species found worldwide except for Antarctica.2 The 3 genera of greatest importance to human and livestock health in the United States are Culicoides, Leptoconops, and Forcipomyia.1 Forty-seven species of the genus Culicoides are known to be present in Florida.3 Species belonging to the genus Leptoconops also are present in coastal areas of southeast Florida as well as in the tropics, subtropics, and Caribbean.3 In the United States, biting midges primarily are a nuisance; the major medical issue associated with Culicoides insects are allergic reactions to their bites. Even though no-see-ums are not known to transmit disease in humans, they have an impact on other animal species in the United States as biting pests and vectors of disease-causing pathogens.1 Biting midges pose quite a nuisance for the proper enjoyment of outdoor spaces in the southeastern United States.
Characteristics
Morphologically, no-see-ums are gray flies measuring 1 to 3 mm in length (eFigure 1). Adults have 2 wings with distinctive patterns, large compound eyes, a thorax that extends slightly over the head, an abdomen with 9 segments, and antennae with 15 segments (eFigure 2).1,3,4 Females have modified mouth parts including mandibles that lacerate the skin during feeding, which is mainly on blood from vertebrate hosts (primarily mammals but also birds, reptiles, and amphibians).1,4 They also can feed on invertebrate hosts. Both male and female no-see-ums feed on nectar, but adult females require a blood meal to develop their eggs.2 Their life cycle progresses in stages from egg to larva to pupa to adult. Larval habitats include salt marshes, swamps, shores of streams and ponds, water-holding plants, rotting fruit, and saturated wood- and manure-enriched soil. Adults can live 2 to 7 weeks. They are weak fliers, particularly in windy conditions.1
In Florida, no-see-ums are more active during the rainy months of May to October but are active year-round in the southeastern United States and the Gulf Coast from Florida to West Texas. They are active throughout the United States in the warmer months of June and July.5 Their peak feeding activity occurs at dawn and dusk, but different species of biting midges such as Leptoconops and Culicoides also can feed during daylight hours and at night, respectively.1,6,7
Case Report
One of the authors (M.J.S.), a healthy 54-year-old man with no remarkable medical history or current use of medications, documented the natural progression of a no-see-um bite by sitting in an outdoor Florida space at 8:00
Clinical Manifestations
Although no-see-ums are not known to transmit disease in the United States, they are important biting pests that can affect tourism and prevent enjoyment of outdoor spaces and activities.2 The bite reactions on the host can range from wheal-like lesions to papules measuring 2 to 3 mm (at times with overlying vesicles) to nodules up to 1 cm in diameter.8 In our reported case, the small wheals disappeared within hours, but pruritic papules have been described to last from weeks to months. Published histopathologic correlation of biopsied indurated papules within 3 days of bite occurrence have revealed a superficial infiltrate composed of lymphocytes and histiocytes, while eosinophils were found in the deeper dermis and subcutaneous fat. Within 2 weeks, as the lesions aged, the infiltrate contained a smaller percentage of eosinophils and predominantly was present in only the superficial dermis.8 Delayed-type hypersensitivity reactions including pustules and bullous lesions also have been described.9,10 Host immune reaction to the saliva introduced during the bite dictates the severity of the response, and lesions may become secondarily infected due to scratching.11
Management Recommendations
Management consists of cleaning the bite site with soap and water to prevent infection, applying cold compresses or ice packs to relieve the intense itch, and avoiding scratching.11 Application of over-the-counter calamine lotion or hydrocortisone cream can relieve itch, and mid- to high-potency topical corticosteroids also can be prescribed for 1 to 2 weeks for more intense bite reactions in conjunction with oral antihistamines. Topical or oral antibiotics may be indicated if redness and swelling progress at the bite site or if breaks in the skin become secondarily infected.
Final Thoughts
Because of the wide-ranging habitats of no-see-ums, eradication programs using insecticides have been inefficient or environmentally suboptimal. Emptying all standing water in outdoor spaces will reduce the number of no-see-ums. Avoidance of the outdoors at dawn and dusk when no-see-ums are most active is helpful, as well as protecting exposed skin by wearing long-sleeved shirts and long pants when outside. Insect repellents containing DEET (N-N-diethyl-meta-toluamide) or picaridin can offer additional protection on the remaining exposed skin. Oil of lemon eucalyptus, or active compound p-menthane-3,8-diol, has been shown to be effective against no-see-ums. Use of DEET should be avoided in children younger than 2 years and p-menthane-3,8-diol in those younger than 3 years. Picaridin is safe for use in children.12 Citronella oil is ineffective. Installing window and patio screens with a mesh size less than 16 can prevent no-see-ums from passing through the netting but will restrict air flow.3 Turning off porch lights also is helpful, as no-see-ums are attracted to light sources.6 Since no-see-ums are weak flyers, setting ceiling or window fans at high speeds can minimize exposure; similarly, being outdoors on a windy day may decrease the likelihood of being bitten. Ultimately, the best remedy for a bite is to prevent them from happening.
Biting midges, commonly known as no-see-ums, are true flies (order Diptera) and members of the Ceratopogonidae family. Regionally, they are known as punkies in the Northeast, pinyon gnats in the Southwest, moose flies in Canada, and sand gnats in Georgia, among other names.1 There are 6206 species found worldwide except for Antarctica.2 The 3 genera of greatest importance to human and livestock health in the United States are Culicoides, Leptoconops, and Forcipomyia.1 Forty-seven species of the genus Culicoides are known to be present in Florida.3 Species belonging to the genus Leptoconops also are present in coastal areas of southeast Florida as well as in the tropics, subtropics, and Caribbean.3 In the United States, biting midges primarily are a nuisance; the major medical issue associated with Culicoides insects are allergic reactions to their bites. Even though no-see-ums are not known to transmit disease in humans, they have an impact on other animal species in the United States as biting pests and vectors of disease-causing pathogens.1 Biting midges pose quite a nuisance for the proper enjoyment of outdoor spaces in the southeastern United States.
Characteristics
Morphologically, no-see-ums are gray flies measuring 1 to 3 mm in length (eFigure 1). Adults have 2 wings with distinctive patterns, large compound eyes, a thorax that extends slightly over the head, an abdomen with 9 segments, and antennae with 15 segments (eFigure 2).1,3,4 Females have modified mouth parts including mandibles that lacerate the skin during feeding, which is mainly on blood from vertebrate hosts (primarily mammals but also birds, reptiles, and amphibians).1,4 They also can feed on invertebrate hosts. Both male and female no-see-ums feed on nectar, but adult females require a blood meal to develop their eggs.2 Their life cycle progresses in stages from egg to larva to pupa to adult. Larval habitats include salt marshes, swamps, shores of streams and ponds, water-holding plants, rotting fruit, and saturated wood- and manure-enriched soil. Adults can live 2 to 7 weeks. They are weak fliers, particularly in windy conditions.1
In Florida, no-see-ums are more active during the rainy months of May to October but are active year-round in the southeastern United States and the Gulf Coast from Florida to West Texas. They are active throughout the United States in the warmer months of June and July.5 Their peak feeding activity occurs at dawn and dusk, but different species of biting midges such as Leptoconops and Culicoides also can feed during daylight hours and at night, respectively.1,6,7
Case Report
One of the authors (M.J.S.), a healthy 54-year-old man with no remarkable medical history or current use of medications, documented the natural progression of a no-see-um bite by sitting in an outdoor Florida space at 8:00
Clinical Manifestations
Although no-see-ums are not known to transmit disease in the United States, they are important biting pests that can affect tourism and prevent enjoyment of outdoor spaces and activities.2 The bite reactions on the host can range from wheal-like lesions to papules measuring 2 to 3 mm (at times with overlying vesicles) to nodules up to 1 cm in diameter.8 In our reported case, the small wheals disappeared within hours, but pruritic papules have been described to last from weeks to months. Published histopathologic correlation of biopsied indurated papules within 3 days of bite occurrence have revealed a superficial infiltrate composed of lymphocytes and histiocytes, while eosinophils were found in the deeper dermis and subcutaneous fat. Within 2 weeks, as the lesions aged, the infiltrate contained a smaller percentage of eosinophils and predominantly was present in only the superficial dermis.8 Delayed-type hypersensitivity reactions including pustules and bullous lesions also have been described.9,10 Host immune reaction to the saliva introduced during the bite dictates the severity of the response, and lesions may become secondarily infected due to scratching.11
Management Recommendations
Management consists of cleaning the bite site with soap and water to prevent infection, applying cold compresses or ice packs to relieve the intense itch, and avoiding scratching.11 Application of over-the-counter calamine lotion or hydrocortisone cream can relieve itch, and mid- to high-potency topical corticosteroids also can be prescribed for 1 to 2 weeks for more intense bite reactions in conjunction with oral antihistamines. Topical or oral antibiotics may be indicated if redness and swelling progress at the bite site or if breaks in the skin become secondarily infected.
Final Thoughts
Because of the wide-ranging habitats of no-see-ums, eradication programs using insecticides have been inefficient or environmentally suboptimal. Emptying all standing water in outdoor spaces will reduce the number of no-see-ums. Avoidance of the outdoors at dawn and dusk when no-see-ums are most active is helpful, as well as protecting exposed skin by wearing long-sleeved shirts and long pants when outside. Insect repellents containing DEET (N-N-diethyl-meta-toluamide) or picaridin can offer additional protection on the remaining exposed skin. Oil of lemon eucalyptus, or active compound p-menthane-3,8-diol, has been shown to be effective against no-see-ums. Use of DEET should be avoided in children younger than 2 years and p-menthane-3,8-diol in those younger than 3 years. Picaridin is safe for use in children.12 Citronella oil is ineffective. Installing window and patio screens with a mesh size less than 16 can prevent no-see-ums from passing through the netting but will restrict air flow.3 Turning off porch lights also is helpful, as no-see-ums are attracted to light sources.6 Since no-see-ums are weak flyers, setting ceiling or window fans at high speeds can minimize exposure; similarly, being outdoors on a windy day may decrease the likelihood of being bitten. Ultimately, the best remedy for a bite is to prevent them from happening.
- Hill CA, MacDonald JF. Biting midges: biology and public health risk. Purdue University. Published July 2013. Accessed September 3, 2025. http://extension.entm.purdue.edu/publichealth/insects/bitingmidge.html
- Borkent A, Dominiak P. Catalog of the biting midges of the world (Diptera: Ceratopogonidae). Zootaxa. 2020;4787:1-377.
- Connelly CR. Biting midges, no-see-ums Culicoides spp. (Insecta: Diptera: Ceratopogonidae). University of Florida publication #EENY 349. Published August 2, 2022. Accessed September 3, 2025. https://edis.ifas.ufl.edu/publication/IN626
- Mullen GR, Murphree CS. Biting midges (Ceratopogonidae). In: Mullen GR, Durden LA, eds. Medical and Veterinary Entomology. 3rd ed. Academic Press; 2019:213-236.
- Best Bee Brothers. No-see-um seasonality range map & season information. Published March 4, 2022. Accessed September 3, 2025. https://bestbeebrothers.com/blogs/blog/no-see-um-season
- Biology Insights. Is there a season for no see ums in Florida? Published August 28, 2025. Accessed September 16, 2025. https://biologyinsights.com/is-there-a-season-for-no-see-ums-in-florida/
- Burris S. Florida no see ums: how to navigate the woes of no see ums in Florida. The Bug Agenda. Published February 2, 2022. Accessed September 3, 2025. https://thebugagenda.com/no-see-ums-in-florida/
- Steffen C. Clinical and histopathologic correlation of midge bites. Arch Dermatol. 1981;117:785-787.
- Krakowski AC, Ho B. Arthropod assault from biting midges. J Pediatr. 2013;163:298.
- Maves RC, Reaves EJ, Martin GJ. Images in clinical tropical medicine: bullous leg lesions caused by Culicoides midges after travel in the Amazon basin. Am J Trop Med Hyg. 2010;83:447.
- Swank B. How long do no-see-ums live? Pest Source. Updated March 17, 2025. Accessed September 3, 2025. https://pestsource.com/no-see-um/lifespan/
- Nguyen QD, Vu MN, Herbert AA. Insect repellents: an updated review for the clinician. J Am Acad Dermatol. 2023;88:123-130.
- Hill CA, MacDonald JF. Biting midges: biology and public health risk. Purdue University. Published July 2013. Accessed September 3, 2025. http://extension.entm.purdue.edu/publichealth/insects/bitingmidge.html
- Borkent A, Dominiak P. Catalog of the biting midges of the world (Diptera: Ceratopogonidae). Zootaxa. 2020;4787:1-377.
- Connelly CR. Biting midges, no-see-ums Culicoides spp. (Insecta: Diptera: Ceratopogonidae). University of Florida publication #EENY 349. Published August 2, 2022. Accessed September 3, 2025. https://edis.ifas.ufl.edu/publication/IN626
- Mullen GR, Murphree CS. Biting midges (Ceratopogonidae). In: Mullen GR, Durden LA, eds. Medical and Veterinary Entomology. 3rd ed. Academic Press; 2019:213-236.
- Best Bee Brothers. No-see-um seasonality range map & season information. Published March 4, 2022. Accessed September 3, 2025. https://bestbeebrothers.com/blogs/blog/no-see-um-season
- Biology Insights. Is there a season for no see ums in Florida? Published August 28, 2025. Accessed September 16, 2025. https://biologyinsights.com/is-there-a-season-for-no-see-ums-in-florida/
- Burris S. Florida no see ums: how to navigate the woes of no see ums in Florida. The Bug Agenda. Published February 2, 2022. Accessed September 3, 2025. https://thebugagenda.com/no-see-ums-in-florida/
- Steffen C. Clinical and histopathologic correlation of midge bites. Arch Dermatol. 1981;117:785-787.
- Krakowski AC, Ho B. Arthropod assault from biting midges. J Pediatr. 2013;163:298.
- Maves RC, Reaves EJ, Martin GJ. Images in clinical tropical medicine: bullous leg lesions caused by Culicoides midges after travel in the Amazon basin. Am J Trop Med Hyg. 2010;83:447.
- Swank B. How long do no-see-ums live? Pest Source. Updated March 17, 2025. Accessed September 3, 2025. https://pestsource.com/no-see-um/lifespan/
- Nguyen QD, Vu MN, Herbert AA. Insect repellents: an updated review for the clinician. J Am Acad Dermatol. 2023;88:123-130.
Dermoscopic Documentation of a No-see-um Bite
Dermoscopic Documentation of a No-see-um Bite
Practice Points
- Biting midges, commonly known as no-see-ums, are extremely small flies whose bites can cause a burning sensation, mild pain, and reactions ranging from small wheals to intensely pruritic papules.
- Medical management of no-see-um bites is based on the severity of the skin reaction.
Botulinum Toxin as a Tool to Reduce Hyperhidrosis in Amputees
Botulinum Toxin as a Tool to Reduce Hyperhidrosis in Amputees
Practice Gap
Hyperhidrosis poses a considerable challenge for many amputees who use prosthetic devices, particularly at the interface between the residual limb and the prosthetic socket. The enclosed environment of the socket often leads to excessive sweating, which can compromise suction fit and increase the risk for skin chafing, irritation, and slippage. Persistent moisture also promotes bacterial and fungal growth, raising the likelihood of infections and foul odors within the socket. Research has shown that skin complications are highly prevalent among amputees, affecting up to 73.9% of this population in the United States.1 Commonly reported complications include wounds, abscesses, and blisters, many of which can be triggered or worsened by hyperhidrosis.2 Current treatment options for residual limb sweating include topical antiperspirants, botulinum toxin (BTX) injections, iontophoresis, and liner-liner socks.
While BTX commonly is used to treat hyperhidrosis in areas such as the palms and axillae, it typically is not considered as a first-line therapy for residual limb sweating; however, both BTX type A and type B have shown safety and effectiveness in managing hyperhidrosis in amputees, enhancing prosthetic use, and improving overall quality of life.3 Despite these benefits, BTX remains relatively underutilized for
Tools and Techniques
A 64-year-old man initially presented to our dermatology clinic after undergoing an above-the-knee amputation of the left leg 1 year prior. The amputation had been performed due to chronic prosthetic joint infections with Escherichia coli. He reported persistent sweating of the residual limb, which severely limited his use of a prosthesis and led to frequent falls.
During the initial visit, treatment options for primary hyperhidrosis including topical and injectable therapies were discussed. Due to a fear of needles, the patient chose topical treatment, with the option to pursue BTX injections later if better control was needed. An aluminum chloride hexahydrate prosthetic antiperspirant was prescribed for nightly application on the anterior and posterior
Botulinum toxin injections were administered in a grid-like pattern across the surface area where the residual limb made contact with the prosthetic. Using a surgical marker, the patient assisted the medical team in identifying the areas where sweating occurred most frequently. The area was divided into 4 equal sections, with each section treated per weekly interval sequentially over 4 weeks. The targeted areas included the left anterior (extending from the anterior tensor fasciae latae band to the lateral thigh) and left posterior residual limb (Figure 1 and eFigure 1, respectively).
The treated section was cleaned with an alcohol wipe prior to each injection, and 50 units of BTX (diluted to 2.5 units per 0.1 mL in bacteriostatic saline) were injected intradermally into each section (Figure 2 and eFigure 2). The injections were administered in rows, with the needle inserted at evenly spaced intervals approximately 1 inch apart. A total of 100 units were administered per section at each weekly appointment. The patient tolerated the procedure well, and no complications were observed.
Practice Implications
This staged approach to administering BTX ensures even distribution of the injections, optimizes hyperhidrosis control, minimizes the risk for complications, and allows for precise targeting of the affected areas to maximize therapeutic benefit. Following the initial procedure, our patient was scheduled for follow-ups approximately every 3 to 4 months starting from the first set of injections for each area. Over 9 months, the patient successfully completed 3 treatment sessions using this method. The patient reported improved quality of life after starting the BTX injections.
After evaluating the initial treatment outcomes with 100 units per section, the dosage was increased to 200 units per section to reduce the number of visits from 4 every 3 months to cover the entire area to 2 visits every 3 months. This adjustment aimed to optimize results and better manage the patient’s ongoing symptoms. At about 1 to 2 weeks after beginning treatment, the patient noticed decreased sweating and discomfort during his daily activities and reduced friction with his prosthetic leg. No adverse effects were noted with the increased dosage during a clinical visit.
Our case highlights the importance of ensuring equitable access to hyperhidrosis treatment. Dermatologists should prioritize patient-centered care by factoring in financial constraints when recommending therapies. In this patient’s case, offering a range of options including over-the-counter antiperspirants and prescription treatments allowed for a management plan tailored to his individual needs and circumstances.
DaxibotulinumtoxinA, known for its longer duration of action compared to other BTX formulations, presents a promising alternative for treating hyperhidrosis.4 However, a gap in care emerged for our patient when prescription antiperspirant was not covered by his insurance, and daxibotulinumtoxinA, which could have offered a more durable solution, was not yet available at our clinic for hyperhidrosis management. Expanding insurance coverage for effective prescription treatments and improving access to newer treatment options are crucial for enhancing patient outcomes and ensuring more equitable care.
Focusing dermatologic care on amputees presents distinct challenges and opportunities for improving their care and decreasing discomfort. Amputees, particularly those with residual limb hyperhidrosis, often experience additional discomfort and difficulty while using prosthetics, as excessive sweating can interfere with fit and function.5,6 Dermatologists should proactively address these specific needs by tailoring treatment accordingly. Incorporating targeted therapies, such as BTX injections, in addition to education on lifestyle modifications and managing treatment expectations, ensures comprehensive care that enhances both quality of life and functional outcomes. Engaging patients in discussions about all available options, including emerging therapies, is essential for improving care for this underserved population.
- Koc E, Tunca M, Akar A, et al. Skin problems in amputees: a descriptive study. Int J Dermatol. 2008;47:463–466. doi:10.1111/j.1365-4632.2008.03604.x
- Bui KM, Raugi GJ, Nguyen VQ, et al. Skin problems in individuals with lower-limb loss: literature review and proposed classification system. J Rehabil Res Dev. 2009;46:1085-1090. doi:10.1682/jrrd.2009.04.0052
- Rocha Melo J, Rodrigues MA, Caetano M, et al. Botulinum toxin in the treatment of residual limb hyperhidrosis: a systematic review. Rehabilitacion (Madr). 2023;57:100754. doi:10.1016/j.rh.2022.07.003
- Hansen C, Godfrey B, Wixom J, et al. Incidence, severity, and impact of hyperhidrosis in people with lower-limb amputation. J Rehabil Res Dev. 2015;52:31-40. doi:10.1682/JRRD.2014.04.0108
- Lannan FM, Powell J, Kim GM, et al. Hyperhidrosis of the residual limb: a narrative review of the measurement and treatment of excess perspiration affecting individuals with amputation. Prosthet Orthot Int. 2021;45:477-486. doi:10.1097/PXR.0000000000000040
- Pace S, Kentosh J. Managing residual limb hyperhidrosis in wounded warriors. Cutis. 2016;97:401-403.
Practice Gap
Hyperhidrosis poses a considerable challenge for many amputees who use prosthetic devices, particularly at the interface between the residual limb and the prosthetic socket. The enclosed environment of the socket often leads to excessive sweating, which can compromise suction fit and increase the risk for skin chafing, irritation, and slippage. Persistent moisture also promotes bacterial and fungal growth, raising the likelihood of infections and foul odors within the socket. Research has shown that skin complications are highly prevalent among amputees, affecting up to 73.9% of this population in the United States.1 Commonly reported complications include wounds, abscesses, and blisters, many of which can be triggered or worsened by hyperhidrosis.2 Current treatment options for residual limb sweating include topical antiperspirants, botulinum toxin (BTX) injections, iontophoresis, and liner-liner socks.
While BTX commonly is used to treat hyperhidrosis in areas such as the palms and axillae, it typically is not considered as a first-line therapy for residual limb sweating; however, both BTX type A and type B have shown safety and effectiveness in managing hyperhidrosis in amputees, enhancing prosthetic use, and improving overall quality of life.3 Despite these benefits, BTX remains relatively underutilized for
Tools and Techniques
A 64-year-old man initially presented to our dermatology clinic after undergoing an above-the-knee amputation of the left leg 1 year prior. The amputation had been performed due to chronic prosthetic joint infections with Escherichia coli. He reported persistent sweating of the residual limb, which severely limited his use of a prosthesis and led to frequent falls.
During the initial visit, treatment options for primary hyperhidrosis including topical and injectable therapies were discussed. Due to a fear of needles, the patient chose topical treatment, with the option to pursue BTX injections later if better control was needed. An aluminum chloride hexahydrate prosthetic antiperspirant was prescribed for nightly application on the anterior and posterior
Botulinum toxin injections were administered in a grid-like pattern across the surface area where the residual limb made contact with the prosthetic. Using a surgical marker, the patient assisted the medical team in identifying the areas where sweating occurred most frequently. The area was divided into 4 equal sections, with each section treated per weekly interval sequentially over 4 weeks. The targeted areas included the left anterior (extending from the anterior tensor fasciae latae band to the lateral thigh) and left posterior residual limb (Figure 1 and eFigure 1, respectively).
The treated section was cleaned with an alcohol wipe prior to each injection, and 50 units of BTX (diluted to 2.5 units per 0.1 mL in bacteriostatic saline) were injected intradermally into each section (Figure 2 and eFigure 2). The injections were administered in rows, with the needle inserted at evenly spaced intervals approximately 1 inch apart. A total of 100 units were administered per section at each weekly appointment. The patient tolerated the procedure well, and no complications were observed.
Practice Implications
This staged approach to administering BTX ensures even distribution of the injections, optimizes hyperhidrosis control, minimizes the risk for complications, and allows for precise targeting of the affected areas to maximize therapeutic benefit. Following the initial procedure, our patient was scheduled for follow-ups approximately every 3 to 4 months starting from the first set of injections for each area. Over 9 months, the patient successfully completed 3 treatment sessions using this method. The patient reported improved quality of life after starting the BTX injections.
After evaluating the initial treatment outcomes with 100 units per section, the dosage was increased to 200 units per section to reduce the number of visits from 4 every 3 months to cover the entire area to 2 visits every 3 months. This adjustment aimed to optimize results and better manage the patient’s ongoing symptoms. At about 1 to 2 weeks after beginning treatment, the patient noticed decreased sweating and discomfort during his daily activities and reduced friction with his prosthetic leg. No adverse effects were noted with the increased dosage during a clinical visit.
Our case highlights the importance of ensuring equitable access to hyperhidrosis treatment. Dermatologists should prioritize patient-centered care by factoring in financial constraints when recommending therapies. In this patient’s case, offering a range of options including over-the-counter antiperspirants and prescription treatments allowed for a management plan tailored to his individual needs and circumstances.
DaxibotulinumtoxinA, known for its longer duration of action compared to other BTX formulations, presents a promising alternative for treating hyperhidrosis.4 However, a gap in care emerged for our patient when prescription antiperspirant was not covered by his insurance, and daxibotulinumtoxinA, which could have offered a more durable solution, was not yet available at our clinic for hyperhidrosis management. Expanding insurance coverage for effective prescription treatments and improving access to newer treatment options are crucial for enhancing patient outcomes and ensuring more equitable care.
Focusing dermatologic care on amputees presents distinct challenges and opportunities for improving their care and decreasing discomfort. Amputees, particularly those with residual limb hyperhidrosis, often experience additional discomfort and difficulty while using prosthetics, as excessive sweating can interfere with fit and function.5,6 Dermatologists should proactively address these specific needs by tailoring treatment accordingly. Incorporating targeted therapies, such as BTX injections, in addition to education on lifestyle modifications and managing treatment expectations, ensures comprehensive care that enhances both quality of life and functional outcomes. Engaging patients in discussions about all available options, including emerging therapies, is essential for improving care for this underserved population.
Practice Gap
Hyperhidrosis poses a considerable challenge for many amputees who use prosthetic devices, particularly at the interface between the residual limb and the prosthetic socket. The enclosed environment of the socket often leads to excessive sweating, which can compromise suction fit and increase the risk for skin chafing, irritation, and slippage. Persistent moisture also promotes bacterial and fungal growth, raising the likelihood of infections and foul odors within the socket. Research has shown that skin complications are highly prevalent among amputees, affecting up to 73.9% of this population in the United States.1 Commonly reported complications include wounds, abscesses, and blisters, many of which can be triggered or worsened by hyperhidrosis.2 Current treatment options for residual limb sweating include topical antiperspirants, botulinum toxin (BTX) injections, iontophoresis, and liner-liner socks.
While BTX commonly is used to treat hyperhidrosis in areas such as the palms and axillae, it typically is not considered as a first-line therapy for residual limb sweating; however, both BTX type A and type B have shown safety and effectiveness in managing hyperhidrosis in amputees, enhancing prosthetic use, and improving overall quality of life.3 Despite these benefits, BTX remains relatively underutilized for
Tools and Techniques
A 64-year-old man initially presented to our dermatology clinic after undergoing an above-the-knee amputation of the left leg 1 year prior. The amputation had been performed due to chronic prosthetic joint infections with Escherichia coli. He reported persistent sweating of the residual limb, which severely limited his use of a prosthesis and led to frequent falls.
During the initial visit, treatment options for primary hyperhidrosis including topical and injectable therapies were discussed. Due to a fear of needles, the patient chose topical treatment, with the option to pursue BTX injections later if better control was needed. An aluminum chloride hexahydrate prosthetic antiperspirant was prescribed for nightly application on the anterior and posterior
Botulinum toxin injections were administered in a grid-like pattern across the surface area where the residual limb made contact with the prosthetic. Using a surgical marker, the patient assisted the medical team in identifying the areas where sweating occurred most frequently. The area was divided into 4 equal sections, with each section treated per weekly interval sequentially over 4 weeks. The targeted areas included the left anterior (extending from the anterior tensor fasciae latae band to the lateral thigh) and left posterior residual limb (Figure 1 and eFigure 1, respectively).
The treated section was cleaned with an alcohol wipe prior to each injection, and 50 units of BTX (diluted to 2.5 units per 0.1 mL in bacteriostatic saline) were injected intradermally into each section (Figure 2 and eFigure 2). The injections were administered in rows, with the needle inserted at evenly spaced intervals approximately 1 inch apart. A total of 100 units were administered per section at each weekly appointment. The patient tolerated the procedure well, and no complications were observed.
Practice Implications
This staged approach to administering BTX ensures even distribution of the injections, optimizes hyperhidrosis control, minimizes the risk for complications, and allows for precise targeting of the affected areas to maximize therapeutic benefit. Following the initial procedure, our patient was scheduled for follow-ups approximately every 3 to 4 months starting from the first set of injections for each area. Over 9 months, the patient successfully completed 3 treatment sessions using this method. The patient reported improved quality of life after starting the BTX injections.
After evaluating the initial treatment outcomes with 100 units per section, the dosage was increased to 200 units per section to reduce the number of visits from 4 every 3 months to cover the entire area to 2 visits every 3 months. This adjustment aimed to optimize results and better manage the patient’s ongoing symptoms. At about 1 to 2 weeks after beginning treatment, the patient noticed decreased sweating and discomfort during his daily activities and reduced friction with his prosthetic leg. No adverse effects were noted with the increased dosage during a clinical visit.
Our case highlights the importance of ensuring equitable access to hyperhidrosis treatment. Dermatologists should prioritize patient-centered care by factoring in financial constraints when recommending therapies. In this patient’s case, offering a range of options including over-the-counter antiperspirants and prescription treatments allowed for a management plan tailored to his individual needs and circumstances.
DaxibotulinumtoxinA, known for its longer duration of action compared to other BTX formulations, presents a promising alternative for treating hyperhidrosis.4 However, a gap in care emerged for our patient when prescription antiperspirant was not covered by his insurance, and daxibotulinumtoxinA, which could have offered a more durable solution, was not yet available at our clinic for hyperhidrosis management. Expanding insurance coverage for effective prescription treatments and improving access to newer treatment options are crucial for enhancing patient outcomes and ensuring more equitable care.
Focusing dermatologic care on amputees presents distinct challenges and opportunities for improving their care and decreasing discomfort. Amputees, particularly those with residual limb hyperhidrosis, often experience additional discomfort and difficulty while using prosthetics, as excessive sweating can interfere with fit and function.5,6 Dermatologists should proactively address these specific needs by tailoring treatment accordingly. Incorporating targeted therapies, such as BTX injections, in addition to education on lifestyle modifications and managing treatment expectations, ensures comprehensive care that enhances both quality of life and functional outcomes. Engaging patients in discussions about all available options, including emerging therapies, is essential for improving care for this underserved population.
- Koc E, Tunca M, Akar A, et al. Skin problems in amputees: a descriptive study. Int J Dermatol. 2008;47:463–466. doi:10.1111/j.1365-4632.2008.03604.x
- Bui KM, Raugi GJ, Nguyen VQ, et al. Skin problems in individuals with lower-limb loss: literature review and proposed classification system. J Rehabil Res Dev. 2009;46:1085-1090. doi:10.1682/jrrd.2009.04.0052
- Rocha Melo J, Rodrigues MA, Caetano M, et al. Botulinum toxin in the treatment of residual limb hyperhidrosis: a systematic review. Rehabilitacion (Madr). 2023;57:100754. doi:10.1016/j.rh.2022.07.003
- Hansen C, Godfrey B, Wixom J, et al. Incidence, severity, and impact of hyperhidrosis in people with lower-limb amputation. J Rehabil Res Dev. 2015;52:31-40. doi:10.1682/JRRD.2014.04.0108
- Lannan FM, Powell J, Kim GM, et al. Hyperhidrosis of the residual limb: a narrative review of the measurement and treatment of excess perspiration affecting individuals with amputation. Prosthet Orthot Int. 2021;45:477-486. doi:10.1097/PXR.0000000000000040
- Pace S, Kentosh J. Managing residual limb hyperhidrosis in wounded warriors. Cutis. 2016;97:401-403.
- Koc E, Tunca M, Akar A, et al. Skin problems in amputees: a descriptive study. Int J Dermatol. 2008;47:463–466. doi:10.1111/j.1365-4632.2008.03604.x
- Bui KM, Raugi GJ, Nguyen VQ, et al. Skin problems in individuals with lower-limb loss: literature review and proposed classification system. J Rehabil Res Dev. 2009;46:1085-1090. doi:10.1682/jrrd.2009.04.0052
- Rocha Melo J, Rodrigues MA, Caetano M, et al. Botulinum toxin in the treatment of residual limb hyperhidrosis: a systematic review. Rehabilitacion (Madr). 2023;57:100754. doi:10.1016/j.rh.2022.07.003
- Hansen C, Godfrey B, Wixom J, et al. Incidence, severity, and impact of hyperhidrosis in people with lower-limb amputation. J Rehabil Res Dev. 2015;52:31-40. doi:10.1682/JRRD.2014.04.0108
- Lannan FM, Powell J, Kim GM, et al. Hyperhidrosis of the residual limb: a narrative review of the measurement and treatment of excess perspiration affecting individuals with amputation. Prosthet Orthot Int. 2021;45:477-486. doi:10.1097/PXR.0000000000000040
- Pace S, Kentosh J. Managing residual limb hyperhidrosis in wounded warriors. Cutis. 2016;97:401-403.
Botulinum Toxin as a Tool to Reduce Hyperhidrosis in Amputees
Botulinum Toxin as a Tool to Reduce Hyperhidrosis in Amputees
