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Developments in wound healing include different treatment options
ORLANDO – , Hadar Lev-Tov, MD, said at the ODAC Dermatology, Aesthetic & Surgery Conference.
At the meeting, Dr. Lev-Tov, associate professor of dermatology at the University of Miami, reviewed some of the latest developments in several conditions involving wound care.
Pyoderma gangrenosum (PG): In this condition, pustules or nodules become large ulcerations, and one-third of patients with PG have pathergy, exaggerated skin injury after a mild trauma such as a bump or a bruise.
“You want to look at the clues in the history because 20% of these patients had histories of PG elsewhere,” Dr. Lev-Tov said. “Ask them about other ulcers, maybe they had some wound dehiscence history.”
Criteria have been developed to help with the diagnosis of ulcerative PG, which includes one major criterion, a biopsy of the ulcer edge showing neutrophilic infiltrate, along with minor criteria, including exclusion of an infection, pathergy, and a history of inflammatory bowel disease or inflammatory arthritis.
“This is no longer a diagnosis of exclusion,” Dr. Lev-Tov said.
Cyclosporine and oral steroids have been found to work well, but it typically takes many months before healing occurs. Tacrolimus or topical steroids can work as well, but healing also takes a fairly long time with those medications, Dr. Lev-Tov said.
The tumor necrosis factor (TNF) blocker infliximab is another option. He had a patient who was referred to him who had been treated with cyclosporine for 3 years for PG on his feet, even though it had not been effective. Dr. Lev-Tov tried infliximab, and the wounds finally cleared, he said.
Apremilast, a phosphodiesterase 4 (PDE4)-inhibitor, is another option for treating PG, he said. “Anecdotally, I used apremilast on three patients with recurrent PG for long-term suppression, with success,” he noted.
Epidermal grafting using suction and heat is an approach that might deserve further exploration for PG, Dr. Lev-Tov suggested. With this procedure, described in an article in 2014, heat and suction are used to induce blistering to separate and remove the epidermis from the dermis at the dermal-epidermal junction, creating an epidermal graft is placed over the wound to promote healing. Patients with PG who are immunosuppressed but demonstrate pathergy do not tend to experience pathergy when epidermal skin grafting is performed, he said.
The heat-suction procedure is simple, painless, and scarless, but better controlled data on this approach are needed, he said.
Corona phlebectatica: This disease involving abnormally dilated veins near the ankle has received formal recognition as a sign of venous insufficiency, in a 2020 update of a classification system for describing patients with chronic venous disorders, Dr. Lev-Tov said.
“We knew about it for years, but now there’s some data that can actually predict the severity of disease,” and, he said, it is now a part of the diagnostic criteria for venous insufficiency .
Venous leg ulcers: These often painful sores on the inside of the leg typically take more than a month to heal. A systematic review of placebo-controlled studies of pentoxifylline as a treatment for venous leg ulcers, published in 2021, supports its use for healing venous leg ulcers, Dr. Lev-Tov said. “It improved the healing rate and increased what [the researchers] called ‘significant improvement,’ ” a category they created to account for the varying methods across the studies, he said.
Topical beta-blockers can improve epithelialization and fibroblast migration in wound healing, he said. A study on topical timolol for various wounds found that a 0.5% formulation of topical timolol, with one drop applied per square centimeter as frequently as possible, was effective in healing. But the healing process was prolonged – a median of 90 days, said Dr. Lev-Tov, one of the study authors.
“When you start this, I don’t want you to expect the wound to heal tomorrow,” he said. “You’ve got to educate your patient.”
Dr. Lev-Tov reports relevant financial relationships with Abbvie, Novartis, Pfizer and other companies.
ORLANDO – , Hadar Lev-Tov, MD, said at the ODAC Dermatology, Aesthetic & Surgery Conference.
At the meeting, Dr. Lev-Tov, associate professor of dermatology at the University of Miami, reviewed some of the latest developments in several conditions involving wound care.
Pyoderma gangrenosum (PG): In this condition, pustules or nodules become large ulcerations, and one-third of patients with PG have pathergy, exaggerated skin injury after a mild trauma such as a bump or a bruise.
“You want to look at the clues in the history because 20% of these patients had histories of PG elsewhere,” Dr. Lev-Tov said. “Ask them about other ulcers, maybe they had some wound dehiscence history.”
Criteria have been developed to help with the diagnosis of ulcerative PG, which includes one major criterion, a biopsy of the ulcer edge showing neutrophilic infiltrate, along with minor criteria, including exclusion of an infection, pathergy, and a history of inflammatory bowel disease or inflammatory arthritis.
“This is no longer a diagnosis of exclusion,” Dr. Lev-Tov said.
Cyclosporine and oral steroids have been found to work well, but it typically takes many months before healing occurs. Tacrolimus or topical steroids can work as well, but healing also takes a fairly long time with those medications, Dr. Lev-Tov said.
The tumor necrosis factor (TNF) blocker infliximab is another option. He had a patient who was referred to him who had been treated with cyclosporine for 3 years for PG on his feet, even though it had not been effective. Dr. Lev-Tov tried infliximab, and the wounds finally cleared, he said.
Apremilast, a phosphodiesterase 4 (PDE4)-inhibitor, is another option for treating PG, he said. “Anecdotally, I used apremilast on three patients with recurrent PG for long-term suppression, with success,” he noted.
Epidermal grafting using suction and heat is an approach that might deserve further exploration for PG, Dr. Lev-Tov suggested. With this procedure, described in an article in 2014, heat and suction are used to induce blistering to separate and remove the epidermis from the dermis at the dermal-epidermal junction, creating an epidermal graft is placed over the wound to promote healing. Patients with PG who are immunosuppressed but demonstrate pathergy do not tend to experience pathergy when epidermal skin grafting is performed, he said.
The heat-suction procedure is simple, painless, and scarless, but better controlled data on this approach are needed, he said.
Corona phlebectatica: This disease involving abnormally dilated veins near the ankle has received formal recognition as a sign of venous insufficiency, in a 2020 update of a classification system for describing patients with chronic venous disorders, Dr. Lev-Tov said.
“We knew about it for years, but now there’s some data that can actually predict the severity of disease,” and, he said, it is now a part of the diagnostic criteria for venous insufficiency .
Venous leg ulcers: These often painful sores on the inside of the leg typically take more than a month to heal. A systematic review of placebo-controlled studies of pentoxifylline as a treatment for venous leg ulcers, published in 2021, supports its use for healing venous leg ulcers, Dr. Lev-Tov said. “It improved the healing rate and increased what [the researchers] called ‘significant improvement,’ ” a category they created to account for the varying methods across the studies, he said.
Topical beta-blockers can improve epithelialization and fibroblast migration in wound healing, he said. A study on topical timolol for various wounds found that a 0.5% formulation of topical timolol, with one drop applied per square centimeter as frequently as possible, was effective in healing. But the healing process was prolonged – a median of 90 days, said Dr. Lev-Tov, one of the study authors.
“When you start this, I don’t want you to expect the wound to heal tomorrow,” he said. “You’ve got to educate your patient.”
Dr. Lev-Tov reports relevant financial relationships with Abbvie, Novartis, Pfizer and other companies.
ORLANDO – , Hadar Lev-Tov, MD, said at the ODAC Dermatology, Aesthetic & Surgery Conference.
At the meeting, Dr. Lev-Tov, associate professor of dermatology at the University of Miami, reviewed some of the latest developments in several conditions involving wound care.
Pyoderma gangrenosum (PG): In this condition, pustules or nodules become large ulcerations, and one-third of patients with PG have pathergy, exaggerated skin injury after a mild trauma such as a bump or a bruise.
“You want to look at the clues in the history because 20% of these patients had histories of PG elsewhere,” Dr. Lev-Tov said. “Ask them about other ulcers, maybe they had some wound dehiscence history.”
Criteria have been developed to help with the diagnosis of ulcerative PG, which includes one major criterion, a biopsy of the ulcer edge showing neutrophilic infiltrate, along with minor criteria, including exclusion of an infection, pathergy, and a history of inflammatory bowel disease or inflammatory arthritis.
“This is no longer a diagnosis of exclusion,” Dr. Lev-Tov said.
Cyclosporine and oral steroids have been found to work well, but it typically takes many months before healing occurs. Tacrolimus or topical steroids can work as well, but healing also takes a fairly long time with those medications, Dr. Lev-Tov said.
The tumor necrosis factor (TNF) blocker infliximab is another option. He had a patient who was referred to him who had been treated with cyclosporine for 3 years for PG on his feet, even though it had not been effective. Dr. Lev-Tov tried infliximab, and the wounds finally cleared, he said.
Apremilast, a phosphodiesterase 4 (PDE4)-inhibitor, is another option for treating PG, he said. “Anecdotally, I used apremilast on three patients with recurrent PG for long-term suppression, with success,” he noted.
Epidermal grafting using suction and heat is an approach that might deserve further exploration for PG, Dr. Lev-Tov suggested. With this procedure, described in an article in 2014, heat and suction are used to induce blistering to separate and remove the epidermis from the dermis at the dermal-epidermal junction, creating an epidermal graft is placed over the wound to promote healing. Patients with PG who are immunosuppressed but demonstrate pathergy do not tend to experience pathergy when epidermal skin grafting is performed, he said.
The heat-suction procedure is simple, painless, and scarless, but better controlled data on this approach are needed, he said.
Corona phlebectatica: This disease involving abnormally dilated veins near the ankle has received formal recognition as a sign of venous insufficiency, in a 2020 update of a classification system for describing patients with chronic venous disorders, Dr. Lev-Tov said.
“We knew about it for years, but now there’s some data that can actually predict the severity of disease,” and, he said, it is now a part of the diagnostic criteria for venous insufficiency .
Venous leg ulcers: These often painful sores on the inside of the leg typically take more than a month to heal. A systematic review of placebo-controlled studies of pentoxifylline as a treatment for venous leg ulcers, published in 2021, supports its use for healing venous leg ulcers, Dr. Lev-Tov said. “It improved the healing rate and increased what [the researchers] called ‘significant improvement,’ ” a category they created to account for the varying methods across the studies, he said.
Topical beta-blockers can improve epithelialization and fibroblast migration in wound healing, he said. A study on topical timolol for various wounds found that a 0.5% formulation of topical timolol, with one drop applied per square centimeter as frequently as possible, was effective in healing. But the healing process was prolonged – a median of 90 days, said Dr. Lev-Tov, one of the study authors.
“When you start this, I don’t want you to expect the wound to heal tomorrow,” he said. “You’ve got to educate your patient.”
Dr. Lev-Tov reports relevant financial relationships with Abbvie, Novartis, Pfizer and other companies.
AT ODAC 2023
Expert gives tips on less-discussed dermatologic diseases
ORLANDO – , according to Adam Friedman, MD, professor and chair of dermatology at George Washington University, Washington.
These semi-forsaken diseases are important not to miss and can “also be quite challenging when we think about their management,” he said at the ODAC Dermatology, Aesthetic & Surgical Conference.
Dr. Friedman, also director of the GW dermatology residency program, reviewed several of these diseases – along with tips for management – during a session at the meeting.
. It does not always have the classic ring pattern for which it is best known, he said. And in patients with darker skin tones, it is characterized by more of a brown or black color, rather than the pink-red color.
Dr. Friedman said that despite a kind of “Pavlovian response” linking GA with diabetes, this link might not be as strong as the field has come to believe, since the studies on which this belief was based included a patient population with narrow demographics. “Maybe GA and type 1 diabetes aren’t necessarily connected,” he said.
Dyslipidemia, on the other hand, has a strong connection with GA, he said. The disease is also linked to thyroid disease and is linked with malignancy, especially in older patients with generalized or atypical presentations of GA, he said.
Spontaneous resolution of the disease is seen within 2 years for 50% to 75% of patients, so “no treatment may be the best treatment,” but antimalarials can be effective, Dr. Friedman said. “I use antimalarials frequently in my practice,” he said. “The key is, they take time to work (4-5 months),” which should be explained to patients.
Antibiotics, he said, can be “somewhat effective,” but in the case of doxycycline at least, the disease can resolve within weeks but then may return when treatment is stopped.
There is some evidence to support using biologics and more recently, Janus kinase (JAK) inhibitors, off-label, to treat GA. Efficacy has been seen with the tumor necrosis factor (TNF) blocker infliximab and with the JAK inhibitor tofacitinib, he said.
Lichen planus (LP). This is another common disease that can go off-script with its presentation. The disease is often described with the “six P’s” indicating the following characteristics: pruritic, polygonal, planar or flat-topped, purple papules, and plaques. But LP “didn’t read the textbook,” Dr. Friedman said.
“The clinical presentation of lichen planus can be quite broad,” he said. “The P’s aren’t always followed as there are a variety of colors and configurations which can be witnessed.”
With LP, there is a clear association with dyslipidemia and diabetes, so “asking the right questions is going to be important” when talking to the patient. There is also a higher risk of autoimmune diseases, especially of the thyroid type, associated with LP, he said.
No treatment has been Food and Drug Administration approved for LP, but some are expected in the future, he said.
For now, he emphasized creativity in the management of patients with LP. “I love oral retinoids for this,” he said. Antimalarials and methotrexate are also options.
In one case Dr. Friedman saw, nothing seemed to work: light therapy for a year; metronidazole; isotretinoin; halobetasol/tazarotene lotion; and the TNF-blocker adalimumab either weren’t effective or resulted in complications in the patient.
Knowing the recent implication of the interleukin (IL)-17 pathway in the pathophysiology of LP, he then tried the anti-IL17 antibody secukinumab. “This patient had a pretty robust response to treatment,” Dr. Friedman said. “He was very excited. The problem, as always, is access, especially for off-label therapies.”
Tumid lupus erythematosus. This disease is characterized by erythematous, edematous, nonscarring plaques on sun-exposed sites. For treatment, Dr. Friedman said antimalarials can be up to 90% effective, sometimes with rapid resolution of the lesions.
“You want to dose below that 5 mg per kg of true body weight to limit the small potential for ocular toxicity over time,” he said. And, he emphasized, “always combine treatment with good sun-protective measures.”
Dr. Friedman reported financial relationships with Sanova, Pfizer, Novartis, and other companies.
ORLANDO – , according to Adam Friedman, MD, professor and chair of dermatology at George Washington University, Washington.
These semi-forsaken diseases are important not to miss and can “also be quite challenging when we think about their management,” he said at the ODAC Dermatology, Aesthetic & Surgical Conference.
Dr. Friedman, also director of the GW dermatology residency program, reviewed several of these diseases – along with tips for management – during a session at the meeting.
. It does not always have the classic ring pattern for which it is best known, he said. And in patients with darker skin tones, it is characterized by more of a brown or black color, rather than the pink-red color.
Dr. Friedman said that despite a kind of “Pavlovian response” linking GA with diabetes, this link might not be as strong as the field has come to believe, since the studies on which this belief was based included a patient population with narrow demographics. “Maybe GA and type 1 diabetes aren’t necessarily connected,” he said.
Dyslipidemia, on the other hand, has a strong connection with GA, he said. The disease is also linked to thyroid disease and is linked with malignancy, especially in older patients with generalized or atypical presentations of GA, he said.
Spontaneous resolution of the disease is seen within 2 years for 50% to 75% of patients, so “no treatment may be the best treatment,” but antimalarials can be effective, Dr. Friedman said. “I use antimalarials frequently in my practice,” he said. “The key is, they take time to work (4-5 months),” which should be explained to patients.
Antibiotics, he said, can be “somewhat effective,” but in the case of doxycycline at least, the disease can resolve within weeks but then may return when treatment is stopped.
There is some evidence to support using biologics and more recently, Janus kinase (JAK) inhibitors, off-label, to treat GA. Efficacy has been seen with the tumor necrosis factor (TNF) blocker infliximab and with the JAK inhibitor tofacitinib, he said.
Lichen planus (LP). This is another common disease that can go off-script with its presentation. The disease is often described with the “six P’s” indicating the following characteristics: pruritic, polygonal, planar or flat-topped, purple papules, and plaques. But LP “didn’t read the textbook,” Dr. Friedman said.
“The clinical presentation of lichen planus can be quite broad,” he said. “The P’s aren’t always followed as there are a variety of colors and configurations which can be witnessed.”
With LP, there is a clear association with dyslipidemia and diabetes, so “asking the right questions is going to be important” when talking to the patient. There is also a higher risk of autoimmune diseases, especially of the thyroid type, associated with LP, he said.
No treatment has been Food and Drug Administration approved for LP, but some are expected in the future, he said.
For now, he emphasized creativity in the management of patients with LP. “I love oral retinoids for this,” he said. Antimalarials and methotrexate are also options.
In one case Dr. Friedman saw, nothing seemed to work: light therapy for a year; metronidazole; isotretinoin; halobetasol/tazarotene lotion; and the TNF-blocker adalimumab either weren’t effective or resulted in complications in the patient.
Knowing the recent implication of the interleukin (IL)-17 pathway in the pathophysiology of LP, he then tried the anti-IL17 antibody secukinumab. “This patient had a pretty robust response to treatment,” Dr. Friedman said. “He was very excited. The problem, as always, is access, especially for off-label therapies.”
Tumid lupus erythematosus. This disease is characterized by erythematous, edematous, nonscarring plaques on sun-exposed sites. For treatment, Dr. Friedman said antimalarials can be up to 90% effective, sometimes with rapid resolution of the lesions.
“You want to dose below that 5 mg per kg of true body weight to limit the small potential for ocular toxicity over time,” he said. And, he emphasized, “always combine treatment with good sun-protective measures.”
Dr. Friedman reported financial relationships with Sanova, Pfizer, Novartis, and other companies.
ORLANDO – , according to Adam Friedman, MD, professor and chair of dermatology at George Washington University, Washington.
These semi-forsaken diseases are important not to miss and can “also be quite challenging when we think about their management,” he said at the ODAC Dermatology, Aesthetic & Surgical Conference.
Dr. Friedman, also director of the GW dermatology residency program, reviewed several of these diseases – along with tips for management – during a session at the meeting.
. It does not always have the classic ring pattern for which it is best known, he said. And in patients with darker skin tones, it is characterized by more of a brown or black color, rather than the pink-red color.
Dr. Friedman said that despite a kind of “Pavlovian response” linking GA with diabetes, this link might not be as strong as the field has come to believe, since the studies on which this belief was based included a patient population with narrow demographics. “Maybe GA and type 1 diabetes aren’t necessarily connected,” he said.
Dyslipidemia, on the other hand, has a strong connection with GA, he said. The disease is also linked to thyroid disease and is linked with malignancy, especially in older patients with generalized or atypical presentations of GA, he said.
Spontaneous resolution of the disease is seen within 2 years for 50% to 75% of patients, so “no treatment may be the best treatment,” but antimalarials can be effective, Dr. Friedman said. “I use antimalarials frequently in my practice,” he said. “The key is, they take time to work (4-5 months),” which should be explained to patients.
Antibiotics, he said, can be “somewhat effective,” but in the case of doxycycline at least, the disease can resolve within weeks but then may return when treatment is stopped.
There is some evidence to support using biologics and more recently, Janus kinase (JAK) inhibitors, off-label, to treat GA. Efficacy has been seen with the tumor necrosis factor (TNF) blocker infliximab and with the JAK inhibitor tofacitinib, he said.
Lichen planus (LP). This is another common disease that can go off-script with its presentation. The disease is often described with the “six P’s” indicating the following characteristics: pruritic, polygonal, planar or flat-topped, purple papules, and plaques. But LP “didn’t read the textbook,” Dr. Friedman said.
“The clinical presentation of lichen planus can be quite broad,” he said. “The P’s aren’t always followed as there are a variety of colors and configurations which can be witnessed.”
With LP, there is a clear association with dyslipidemia and diabetes, so “asking the right questions is going to be important” when talking to the patient. There is also a higher risk of autoimmune diseases, especially of the thyroid type, associated with LP, he said.
No treatment has been Food and Drug Administration approved for LP, but some are expected in the future, he said.
For now, he emphasized creativity in the management of patients with LP. “I love oral retinoids for this,” he said. Antimalarials and methotrexate are also options.
In one case Dr. Friedman saw, nothing seemed to work: light therapy for a year; metronidazole; isotretinoin; halobetasol/tazarotene lotion; and the TNF-blocker adalimumab either weren’t effective or resulted in complications in the patient.
Knowing the recent implication of the interleukin (IL)-17 pathway in the pathophysiology of LP, he then tried the anti-IL17 antibody secukinumab. “This patient had a pretty robust response to treatment,” Dr. Friedman said. “He was very excited. The problem, as always, is access, especially for off-label therapies.”
Tumid lupus erythematosus. This disease is characterized by erythematous, edematous, nonscarring plaques on sun-exposed sites. For treatment, Dr. Friedman said antimalarials can be up to 90% effective, sometimes with rapid resolution of the lesions.
“You want to dose below that 5 mg per kg of true body weight to limit the small potential for ocular toxicity over time,” he said. And, he emphasized, “always combine treatment with good sun-protective measures.”
Dr. Friedman reported financial relationships with Sanova, Pfizer, Novartis, and other companies.
AT ODAC 2023
Expert offers insights on pediatric dermatology emergencies
ORLANDO – The eruption spread away from the head and her transaminase levels were “dramatic,” in the 700s, said Kalyani S. Marathe, MD, MPH, associate professor of dermatology and pediatrics at the University of Cincinnati.
Dr. Marathe, director of the division of dermatology at Cincinnati Children’s Hospital, reviewed this case in a presentation on pediatric dermatologic emergencies at the ODAC Dermatology, Aesthetic & Surgery Conference, pointing out potential pitfalls and important aspects that might require swift action.
The patient was diagnosed with drug reaction with eosinophilia and systemic symptoms (DRESS).
Facial involvement is common in pediatric cases of DRESS, but edema of the face is less common in children than adults, Dr. Marathe said.
Antiepileptic medications are the most common cause of DRESS, followed by antibiotics – most often, vancomycin and trimethoprim/sulfamethoxazole, she said. But sometimes the trigger is not clear, she noted, recalling a vexing case she once saw in which IV contrast was eventually identified as the cause.
When DRESS is suspected, she said, lab work should be done during the acute eruption and after resolution. This should include CBC, liver function tests, creatinine, and urinalysis, and human herpesvirus 6 (HHV-6) and thyroid testing.
Treatment typically includes supportive care, unless symptoms are systemic, or if there is impending liver failure, when steroids, cyclosporine, or IVIG can be used.
Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN): Mortality rates when these diseases overlap is 4%, Dr. Marathe said. Clues to diagnosing this other medication-induced condition include involvement of the palms and the soles of the feet; presence of the Nikolsky sign in which the top layers of the skin slip away from the lower layers when rubbed; mucosal involvement, which often precedes cutaneous involvement; and these symptoms occurring within the first 8 weeks of taking a medication, which are most commonly antibiotics and anti-epileptics.
Dr. Marathe underscored how important it is to get ophthalmology involved right away, because of the risk of vision loss. Amniotic membrane transfer to the eye at the time of diagnosis has been found to produce dramatically better outcomes, she said. The membrane has anti-inflammatory and antiscarring properties and can promote wound healing on the surface of the eye.
“I would recommend getting your ophthalmology team on board early because they have to advocate for these patients,” she said.
Corticosteroids and IVIG can improve ocular outcomes, but cyclosporine is associated with better mortality outcomes, she said. Emerging data on etanercept has also led to more use of that drug, she said.
Erythema multiforme (EM): unlike urticaria, multiforme EM can have mucosal involvement, Dr. Marathe said. Clinicians should look for three zones of color: A central duskiness, a rim of pallor, and a ring of erythema.
EM is triggered by a virus, which is usually herpes simplex virus (HSV). But she added that HSV is not always found. “So, there are certainly other triggers out there that we just haven’t identified,” she said.
If HSV is suspected, oral acyclovir is effective, she noted.
Other cases might not be as straightforward. Dr. Marathe said that during her fellowship, she saw a patient with EM that was controlled only by IVIG, so it was administered every 3 months. In that case, the trigger was never found.
Multisystem inflammatory syndrome in children (MIS-C): This syndrome can follow COVID-19 infection, and usually presents with 3-5 days of fever after COVID has resolved. It can include gastrointestinal, cardiorespiratory, and neurocognitive symptoms.
The skin presentation is mainly a morbilliform pattern, but clinicians might also see conjunctival involvement, mucosal involvement, and “COVID toes,” painful red or purple lesions on the toes.
Treatment is usually IVIG and systemic corticosteroids, with the treatment course depending on the severity.
MIS-C was initially thought to be Kawasaki’s disease, another autoinflammatory disorder, which is related but distinct, Dr. Marathe said.
Patients with MIS-C “are usually going to have COVID-positive antibodies,” she said. But since almost everybody may have COVID antibodies, “it’s not usually a helpful test for you now. But early on, that’s what we used as helpful indicator.”
Dr. Marathe reported no relevant financial relationships.
ORLANDO – The eruption spread away from the head and her transaminase levels were “dramatic,” in the 700s, said Kalyani S. Marathe, MD, MPH, associate professor of dermatology and pediatrics at the University of Cincinnati.
Dr. Marathe, director of the division of dermatology at Cincinnati Children’s Hospital, reviewed this case in a presentation on pediatric dermatologic emergencies at the ODAC Dermatology, Aesthetic & Surgery Conference, pointing out potential pitfalls and important aspects that might require swift action.
The patient was diagnosed with drug reaction with eosinophilia and systemic symptoms (DRESS).
Facial involvement is common in pediatric cases of DRESS, but edema of the face is less common in children than adults, Dr. Marathe said.
Antiepileptic medications are the most common cause of DRESS, followed by antibiotics – most often, vancomycin and trimethoprim/sulfamethoxazole, she said. But sometimes the trigger is not clear, she noted, recalling a vexing case she once saw in which IV contrast was eventually identified as the cause.
When DRESS is suspected, she said, lab work should be done during the acute eruption and after resolution. This should include CBC, liver function tests, creatinine, and urinalysis, and human herpesvirus 6 (HHV-6) and thyroid testing.
Treatment typically includes supportive care, unless symptoms are systemic, or if there is impending liver failure, when steroids, cyclosporine, or IVIG can be used.
Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN): Mortality rates when these diseases overlap is 4%, Dr. Marathe said. Clues to diagnosing this other medication-induced condition include involvement of the palms and the soles of the feet; presence of the Nikolsky sign in which the top layers of the skin slip away from the lower layers when rubbed; mucosal involvement, which often precedes cutaneous involvement; and these symptoms occurring within the first 8 weeks of taking a medication, which are most commonly antibiotics and anti-epileptics.
Dr. Marathe underscored how important it is to get ophthalmology involved right away, because of the risk of vision loss. Amniotic membrane transfer to the eye at the time of diagnosis has been found to produce dramatically better outcomes, she said. The membrane has anti-inflammatory and antiscarring properties and can promote wound healing on the surface of the eye.
“I would recommend getting your ophthalmology team on board early because they have to advocate for these patients,” she said.
Corticosteroids and IVIG can improve ocular outcomes, but cyclosporine is associated with better mortality outcomes, she said. Emerging data on etanercept has also led to more use of that drug, she said.
Erythema multiforme (EM): unlike urticaria, multiforme EM can have mucosal involvement, Dr. Marathe said. Clinicians should look for three zones of color: A central duskiness, a rim of pallor, and a ring of erythema.
EM is triggered by a virus, which is usually herpes simplex virus (HSV). But she added that HSV is not always found. “So, there are certainly other triggers out there that we just haven’t identified,” she said.
If HSV is suspected, oral acyclovir is effective, she noted.
Other cases might not be as straightforward. Dr. Marathe said that during her fellowship, she saw a patient with EM that was controlled only by IVIG, so it was administered every 3 months. In that case, the trigger was never found.
Multisystem inflammatory syndrome in children (MIS-C): This syndrome can follow COVID-19 infection, and usually presents with 3-5 days of fever after COVID has resolved. It can include gastrointestinal, cardiorespiratory, and neurocognitive symptoms.
The skin presentation is mainly a morbilliform pattern, but clinicians might also see conjunctival involvement, mucosal involvement, and “COVID toes,” painful red or purple lesions on the toes.
Treatment is usually IVIG and systemic corticosteroids, with the treatment course depending on the severity.
MIS-C was initially thought to be Kawasaki’s disease, another autoinflammatory disorder, which is related but distinct, Dr. Marathe said.
Patients with MIS-C “are usually going to have COVID-positive antibodies,” she said. But since almost everybody may have COVID antibodies, “it’s not usually a helpful test for you now. But early on, that’s what we used as helpful indicator.”
Dr. Marathe reported no relevant financial relationships.
ORLANDO – The eruption spread away from the head and her transaminase levels were “dramatic,” in the 700s, said Kalyani S. Marathe, MD, MPH, associate professor of dermatology and pediatrics at the University of Cincinnati.
Dr. Marathe, director of the division of dermatology at Cincinnati Children’s Hospital, reviewed this case in a presentation on pediatric dermatologic emergencies at the ODAC Dermatology, Aesthetic & Surgery Conference, pointing out potential pitfalls and important aspects that might require swift action.
The patient was diagnosed with drug reaction with eosinophilia and systemic symptoms (DRESS).
Facial involvement is common in pediatric cases of DRESS, but edema of the face is less common in children than adults, Dr. Marathe said.
Antiepileptic medications are the most common cause of DRESS, followed by antibiotics – most often, vancomycin and trimethoprim/sulfamethoxazole, she said. But sometimes the trigger is not clear, she noted, recalling a vexing case she once saw in which IV contrast was eventually identified as the cause.
When DRESS is suspected, she said, lab work should be done during the acute eruption and after resolution. This should include CBC, liver function tests, creatinine, and urinalysis, and human herpesvirus 6 (HHV-6) and thyroid testing.
Treatment typically includes supportive care, unless symptoms are systemic, or if there is impending liver failure, when steroids, cyclosporine, or IVIG can be used.
Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN): Mortality rates when these diseases overlap is 4%, Dr. Marathe said. Clues to diagnosing this other medication-induced condition include involvement of the palms and the soles of the feet; presence of the Nikolsky sign in which the top layers of the skin slip away from the lower layers when rubbed; mucosal involvement, which often precedes cutaneous involvement; and these symptoms occurring within the first 8 weeks of taking a medication, which are most commonly antibiotics and anti-epileptics.
Dr. Marathe underscored how important it is to get ophthalmology involved right away, because of the risk of vision loss. Amniotic membrane transfer to the eye at the time of diagnosis has been found to produce dramatically better outcomes, she said. The membrane has anti-inflammatory and antiscarring properties and can promote wound healing on the surface of the eye.
“I would recommend getting your ophthalmology team on board early because they have to advocate for these patients,” she said.
Corticosteroids and IVIG can improve ocular outcomes, but cyclosporine is associated with better mortality outcomes, she said. Emerging data on etanercept has also led to more use of that drug, she said.
Erythema multiforme (EM): unlike urticaria, multiforme EM can have mucosal involvement, Dr. Marathe said. Clinicians should look for three zones of color: A central duskiness, a rim of pallor, and a ring of erythema.
EM is triggered by a virus, which is usually herpes simplex virus (HSV). But she added that HSV is not always found. “So, there are certainly other triggers out there that we just haven’t identified,” she said.
If HSV is suspected, oral acyclovir is effective, she noted.
Other cases might not be as straightforward. Dr. Marathe said that during her fellowship, she saw a patient with EM that was controlled only by IVIG, so it was administered every 3 months. In that case, the trigger was never found.
Multisystem inflammatory syndrome in children (MIS-C): This syndrome can follow COVID-19 infection, and usually presents with 3-5 days of fever after COVID has resolved. It can include gastrointestinal, cardiorespiratory, and neurocognitive symptoms.
The skin presentation is mainly a morbilliform pattern, but clinicians might also see conjunctival involvement, mucosal involvement, and “COVID toes,” painful red or purple lesions on the toes.
Treatment is usually IVIG and systemic corticosteroids, with the treatment course depending on the severity.
MIS-C was initially thought to be Kawasaki’s disease, another autoinflammatory disorder, which is related but distinct, Dr. Marathe said.
Patients with MIS-C “are usually going to have COVID-positive antibodies,” she said. But since almost everybody may have COVID antibodies, “it’s not usually a helpful test for you now. But early on, that’s what we used as helpful indicator.”
Dr. Marathe reported no relevant financial relationships.
AT ODAC 2023
First Humira biosimilar launches in U.S.
The first biosimilar for Humira, adalimumab-atto (Amjevita), is now available in the United States, according to an announcement on Jan. 31 by the manufacturer, Amgen. At least seven other U.S. Food and Drug Administration–approved Humira biosimilars are expected to become available later in 2023.
Amjevita was approved by the FDA in September 2016 for multiple inflammatory diseases, including rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, Crohn’s disease, ulcerative colitis, and plaque psoriasis. The delayed launch was part of a global settlement with Humira’s manufacturer, AbbVie.
Humira (adalimumab) has been available since 2002 and is consistently one of the top-selling drugs in the United States. A single 40-mg Amjevita pen device will be available at two prices: a list price (wholesale acquisition cost) of $1,557.59, 55% below the current Humira list price, and a list price of $3,288.24, 5% below the current Humira list price, according to Amgen.
“Amgen’s goal is to provide broad access for patients by offering two options to health plans and pharmacy benefit managers,” the company said in the press release.
Patients are less likely to benefit from the more significant discount, said Marta Wosinska, PhD, a health care economist at the Brookings Institute in Washington, DC. It's expected that insurance companies will use the higher list price for Amjevita, she said, as this higher price will also likely have higher rebates. Rebates are payments to health insurance payers provided by drug manufacturers to promote use of an expensive drug. Some pharmacy benefit managers have already said that they plan to charge patients the same amount for Humira as its biosimilars, Dr. Wosinska said.
"For an existing patient, there's really no incentive for them to switch," she said in an interview.
So far only one insurance company, Kaiser Permanente, has plans to switch patients over to biosimilars, according to the health policy podcast Tradeoffs, and the insurer will stop covering Humira by the end of this year.
A version of this article first appeared on Medscape.com.
*This story was updated 2/1/2023.
The first biosimilar for Humira, adalimumab-atto (Amjevita), is now available in the United States, according to an announcement on Jan. 31 by the manufacturer, Amgen. At least seven other U.S. Food and Drug Administration–approved Humira biosimilars are expected to become available later in 2023.
Amjevita was approved by the FDA in September 2016 for multiple inflammatory diseases, including rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, Crohn’s disease, ulcerative colitis, and plaque psoriasis. The delayed launch was part of a global settlement with Humira’s manufacturer, AbbVie.
Humira (adalimumab) has been available since 2002 and is consistently one of the top-selling drugs in the United States. A single 40-mg Amjevita pen device will be available at two prices: a list price (wholesale acquisition cost) of $1,557.59, 55% below the current Humira list price, and a list price of $3,288.24, 5% below the current Humira list price, according to Amgen.
“Amgen’s goal is to provide broad access for patients by offering two options to health plans and pharmacy benefit managers,” the company said in the press release.
Patients are less likely to benefit from the more significant discount, said Marta Wosinska, PhD, a health care economist at the Brookings Institute in Washington, DC. It's expected that insurance companies will use the higher list price for Amjevita, she said, as this higher price will also likely have higher rebates. Rebates are payments to health insurance payers provided by drug manufacturers to promote use of an expensive drug. Some pharmacy benefit managers have already said that they plan to charge patients the same amount for Humira as its biosimilars, Dr. Wosinska said.
"For an existing patient, there's really no incentive for them to switch," she said in an interview.
So far only one insurance company, Kaiser Permanente, has plans to switch patients over to biosimilars, according to the health policy podcast Tradeoffs, and the insurer will stop covering Humira by the end of this year.
A version of this article first appeared on Medscape.com.
*This story was updated 2/1/2023.
The first biosimilar for Humira, adalimumab-atto (Amjevita), is now available in the United States, according to an announcement on Jan. 31 by the manufacturer, Amgen. At least seven other U.S. Food and Drug Administration–approved Humira biosimilars are expected to become available later in 2023.
Amjevita was approved by the FDA in September 2016 for multiple inflammatory diseases, including rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, Crohn’s disease, ulcerative colitis, and plaque psoriasis. The delayed launch was part of a global settlement with Humira’s manufacturer, AbbVie.
Humira (adalimumab) has been available since 2002 and is consistently one of the top-selling drugs in the United States. A single 40-mg Amjevita pen device will be available at two prices: a list price (wholesale acquisition cost) of $1,557.59, 55% below the current Humira list price, and a list price of $3,288.24, 5% below the current Humira list price, according to Amgen.
“Amgen’s goal is to provide broad access for patients by offering two options to health plans and pharmacy benefit managers,” the company said in the press release.
Patients are less likely to benefit from the more significant discount, said Marta Wosinska, PhD, a health care economist at the Brookings Institute in Washington, DC. It's expected that insurance companies will use the higher list price for Amjevita, she said, as this higher price will also likely have higher rebates. Rebates are payments to health insurance payers provided by drug manufacturers to promote use of an expensive drug. Some pharmacy benefit managers have already said that they plan to charge patients the same amount for Humira as its biosimilars, Dr. Wosinska said.
"For an existing patient, there's really no incentive for them to switch," she said in an interview.
So far only one insurance company, Kaiser Permanente, has plans to switch patients over to biosimilars, according to the health policy podcast Tradeoffs, and the insurer will stop covering Humira by the end of this year.
A version of this article first appeared on Medscape.com.
*This story was updated 2/1/2023.
Scalp ridges
The gyrate or cerebriform pattern of inflammatory, often pus-filled, subcutaneous tracts of the scalp pointed to a diagnosis of dissecting cellulitis. This patient did not have the fluctuant tracts frequently seen in more active disease but did have the scarring and alopecia common with this disorder.
Dissecting cellulitis is similar to acne and hidradenitis suppurativa in that it starts with follicular plugging. This plugging leads to inflammation, dilation and rupture of the follicle, and purulent sinus tract formation. The sinus tracts of the scalp can be extensive. Dissecting cellulitis is most common in 18- to 40-year-olds and more common in Black individuals.1 When it occurs in conjunction with cystic acne and hidradenitis suppurativa, it is known as the follicular occlusion triad syndrome.
While oral antibiotics are an option for the treatment of dissecting cellulitis, oral isotretinoin is the first-line approach. Tumor necrosis factor alfa inhibitors have also been used with success, according to case reports.1
Given that this patient had a small area of current inflammation, he was started on oral doxycycline 100 mg twice daily for 2 months. He was scheduled for a follow-up appointment in 3 months to reassess his progress and to explore treatment with isotretinoin if the condition worsened or did not improve.
Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.
1. Federico A, Rossi A, Caro G, et al. Are dissecting cellulitis and hidradenitis suppurativa different diseases? Clin Dermatol. 2021;39:496-499. doi: 10.1016/j.clindermatol.2021.01.002
The gyrate or cerebriform pattern of inflammatory, often pus-filled, subcutaneous tracts of the scalp pointed to a diagnosis of dissecting cellulitis. This patient did not have the fluctuant tracts frequently seen in more active disease but did have the scarring and alopecia common with this disorder.
Dissecting cellulitis is similar to acne and hidradenitis suppurativa in that it starts with follicular plugging. This plugging leads to inflammation, dilation and rupture of the follicle, and purulent sinus tract formation. The sinus tracts of the scalp can be extensive. Dissecting cellulitis is most common in 18- to 40-year-olds and more common in Black individuals.1 When it occurs in conjunction with cystic acne and hidradenitis suppurativa, it is known as the follicular occlusion triad syndrome.
While oral antibiotics are an option for the treatment of dissecting cellulitis, oral isotretinoin is the first-line approach. Tumor necrosis factor alfa inhibitors have also been used with success, according to case reports.1
Given that this patient had a small area of current inflammation, he was started on oral doxycycline 100 mg twice daily for 2 months. He was scheduled for a follow-up appointment in 3 months to reassess his progress and to explore treatment with isotretinoin if the condition worsened or did not improve.
Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.
The gyrate or cerebriform pattern of inflammatory, often pus-filled, subcutaneous tracts of the scalp pointed to a diagnosis of dissecting cellulitis. This patient did not have the fluctuant tracts frequently seen in more active disease but did have the scarring and alopecia common with this disorder.
Dissecting cellulitis is similar to acne and hidradenitis suppurativa in that it starts with follicular plugging. This plugging leads to inflammation, dilation and rupture of the follicle, and purulent sinus tract formation. The sinus tracts of the scalp can be extensive. Dissecting cellulitis is most common in 18- to 40-year-olds and more common in Black individuals.1 When it occurs in conjunction with cystic acne and hidradenitis suppurativa, it is known as the follicular occlusion triad syndrome.
While oral antibiotics are an option for the treatment of dissecting cellulitis, oral isotretinoin is the first-line approach. Tumor necrosis factor alfa inhibitors have also been used with success, according to case reports.1
Given that this patient had a small area of current inflammation, he was started on oral doxycycline 100 mg twice daily for 2 months. He was scheduled for a follow-up appointment in 3 months to reassess his progress and to explore treatment with isotretinoin if the condition worsened or did not improve.
Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.
1. Federico A, Rossi A, Caro G, et al. Are dissecting cellulitis and hidradenitis suppurativa different diseases? Clin Dermatol. 2021;39:496-499. doi: 10.1016/j.clindermatol.2021.01.002
1. Federico A, Rossi A, Caro G, et al. Are dissecting cellulitis and hidradenitis suppurativa different diseases? Clin Dermatol. 2021;39:496-499. doi: 10.1016/j.clindermatol.2021.01.002
Palmar rash
This patient’s targetoid and tingling skin lesions, in association with herpes simplex virus (HSV) infection, are a classic presentation of erythema multiforme (EM).
EM is an acute, self-limited, immune-mediated process that most commonly arises in a symmetrical pattern on acral surfaces. These lesions may be accompanied by eruptions on oral, anogenital, or ocular mucosa. EM is classified into 2 subtypes: major and minor. EM major refers to EM with significant mucosal involvement on at least 2 mucosal sites; it may also manifest with a prodrome of fevers, arthralgias, and malaise. EM minor is used to classify EM with minimal mucosal involvement.1
The term “multiforme” denotes the varied dermatologic changes, including macules, papules, and targetoid lesions with 3 identifiable zones, which are pathognomonic for EM. The classic 3 zones consist of an inner dusky, vesicular, or necrotic center; a middle elevated edematous surrounding ring; and an outer ring of macular erythema. Patients may also present with an atypical macular target lesion, characterized by fewer than 3 zones with an ill-defined border between the zones. The lesions may be asymptomatic, or patients may describe an itchy or burning sensation.
The differential diagnosis of EM includes urticaria, fixed drug eruption, subacute lupus erythematosus, Kawasaki disease, erythema annulare centrifugum, vasculitis, and Stevens-Johnson syndrome.
Infections with HSV types 1 or 2 are the leading cause of EM and are thought to involve a cell-mediated immune process directed against viral antigens in skin.2 Other infectious causes include cytomegalovirus, Epstein-Barr virus, influenza virus, and—rarely—newer strains of coronavirus.3 Pharmacologic reactions are the cause in a small percentage of patients, and may involve nonsteroidal anti-inflammatory drugs, antibiotics, sulfonamides, antiepileptics, and tumor necrosis factor-alpha inhibitors. Studies also link the development of EM to primary malignancy, autoimmune disease, and immunizations.1
The treatment of EM is dependent on the clinical course and severity of the disease. If a causative agent is identified, it should be discontinued (if a drug) or treated (if an infection). Topical antiseptic mouthwashes, antihistamines, and topical corticosteroids can be used to relieve cutaneous discomfort. Biologics and immunosuppressants can be used with patients who have severe symptoms or functional impairment. Patients who have recurrences associated with HSV should be given antiviral prophylaxis for 6 months consisting of oral acyclovir 10 mg/kg/d, valacyclovir 500 to 1000 mg/d, or famciclovir 250 mg twice daily.1
Given the recurrent nature of this patient’s disease, and its association with HSV outbreaks, he was prescribed prophylactic valacyclovir 1000 mg/d orally for 6 months to reduce HSV outbreaks and hopefully prevent future EM episodes.
Photo courtesy of Cyrelle F. Finan, MD. Text courtesy of Lynn Midani, BS, University of New Mexico School of Medicine, and Cyrelle F. Finan, MD, Department of Dermatology, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.
1. Trayes KP, Love G, Studdiford JS. Erythema multiforme: recognition and management. Am Fam Physician. 2019;100:82-88.
2. Hafsi W, Badri T. Erythema multiforme. StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing; 2022. Updated August 1, 2022. Accessed December 15, 2022. www.ncbi.nlm.nih.gov/books/NBK470259/
3. Bennardo L, Nisticò SP, Dastoli S, et al. Erythema multiforme and COVID-19: what do we know? Medicina. 2021;57:828. https://doi.org/10.3390/medicina57080828
This patient’s targetoid and tingling skin lesions, in association with herpes simplex virus (HSV) infection, are a classic presentation of erythema multiforme (EM).
EM is an acute, self-limited, immune-mediated process that most commonly arises in a symmetrical pattern on acral surfaces. These lesions may be accompanied by eruptions on oral, anogenital, or ocular mucosa. EM is classified into 2 subtypes: major and minor. EM major refers to EM with significant mucosal involvement on at least 2 mucosal sites; it may also manifest with a prodrome of fevers, arthralgias, and malaise. EM minor is used to classify EM with minimal mucosal involvement.1
The term “multiforme” denotes the varied dermatologic changes, including macules, papules, and targetoid lesions with 3 identifiable zones, which are pathognomonic for EM. The classic 3 zones consist of an inner dusky, vesicular, or necrotic center; a middle elevated edematous surrounding ring; and an outer ring of macular erythema. Patients may also present with an atypical macular target lesion, characterized by fewer than 3 zones with an ill-defined border between the zones. The lesions may be asymptomatic, or patients may describe an itchy or burning sensation.
The differential diagnosis of EM includes urticaria, fixed drug eruption, subacute lupus erythematosus, Kawasaki disease, erythema annulare centrifugum, vasculitis, and Stevens-Johnson syndrome.
Infections with HSV types 1 or 2 are the leading cause of EM and are thought to involve a cell-mediated immune process directed against viral antigens in skin.2 Other infectious causes include cytomegalovirus, Epstein-Barr virus, influenza virus, and—rarely—newer strains of coronavirus.3 Pharmacologic reactions are the cause in a small percentage of patients, and may involve nonsteroidal anti-inflammatory drugs, antibiotics, sulfonamides, antiepileptics, and tumor necrosis factor-alpha inhibitors. Studies also link the development of EM to primary malignancy, autoimmune disease, and immunizations.1
The treatment of EM is dependent on the clinical course and severity of the disease. If a causative agent is identified, it should be discontinued (if a drug) or treated (if an infection). Topical antiseptic mouthwashes, antihistamines, and topical corticosteroids can be used to relieve cutaneous discomfort. Biologics and immunosuppressants can be used with patients who have severe symptoms or functional impairment. Patients who have recurrences associated with HSV should be given antiviral prophylaxis for 6 months consisting of oral acyclovir 10 mg/kg/d, valacyclovir 500 to 1000 mg/d, or famciclovir 250 mg twice daily.1
Given the recurrent nature of this patient’s disease, and its association with HSV outbreaks, he was prescribed prophylactic valacyclovir 1000 mg/d orally for 6 months to reduce HSV outbreaks and hopefully prevent future EM episodes.
Photo courtesy of Cyrelle F. Finan, MD. Text courtesy of Lynn Midani, BS, University of New Mexico School of Medicine, and Cyrelle F. Finan, MD, Department of Dermatology, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.
This patient’s targetoid and tingling skin lesions, in association with herpes simplex virus (HSV) infection, are a classic presentation of erythema multiforme (EM).
EM is an acute, self-limited, immune-mediated process that most commonly arises in a symmetrical pattern on acral surfaces. These lesions may be accompanied by eruptions on oral, anogenital, or ocular mucosa. EM is classified into 2 subtypes: major and minor. EM major refers to EM with significant mucosal involvement on at least 2 mucosal sites; it may also manifest with a prodrome of fevers, arthralgias, and malaise. EM minor is used to classify EM with minimal mucosal involvement.1
The term “multiforme” denotes the varied dermatologic changes, including macules, papules, and targetoid lesions with 3 identifiable zones, which are pathognomonic for EM. The classic 3 zones consist of an inner dusky, vesicular, or necrotic center; a middle elevated edematous surrounding ring; and an outer ring of macular erythema. Patients may also present with an atypical macular target lesion, characterized by fewer than 3 zones with an ill-defined border between the zones. The lesions may be asymptomatic, or patients may describe an itchy or burning sensation.
The differential diagnosis of EM includes urticaria, fixed drug eruption, subacute lupus erythematosus, Kawasaki disease, erythema annulare centrifugum, vasculitis, and Stevens-Johnson syndrome.
Infections with HSV types 1 or 2 are the leading cause of EM and are thought to involve a cell-mediated immune process directed against viral antigens in skin.2 Other infectious causes include cytomegalovirus, Epstein-Barr virus, influenza virus, and—rarely—newer strains of coronavirus.3 Pharmacologic reactions are the cause in a small percentage of patients, and may involve nonsteroidal anti-inflammatory drugs, antibiotics, sulfonamides, antiepileptics, and tumor necrosis factor-alpha inhibitors. Studies also link the development of EM to primary malignancy, autoimmune disease, and immunizations.1
The treatment of EM is dependent on the clinical course and severity of the disease. If a causative agent is identified, it should be discontinued (if a drug) or treated (if an infection). Topical antiseptic mouthwashes, antihistamines, and topical corticosteroids can be used to relieve cutaneous discomfort. Biologics and immunosuppressants can be used with patients who have severe symptoms or functional impairment. Patients who have recurrences associated with HSV should be given antiviral prophylaxis for 6 months consisting of oral acyclovir 10 mg/kg/d, valacyclovir 500 to 1000 mg/d, or famciclovir 250 mg twice daily.1
Given the recurrent nature of this patient’s disease, and its association with HSV outbreaks, he was prescribed prophylactic valacyclovir 1000 mg/d orally for 6 months to reduce HSV outbreaks and hopefully prevent future EM episodes.
Photo courtesy of Cyrelle F. Finan, MD. Text courtesy of Lynn Midani, BS, University of New Mexico School of Medicine, and Cyrelle F. Finan, MD, Department of Dermatology, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.
1. Trayes KP, Love G, Studdiford JS. Erythema multiforme: recognition and management. Am Fam Physician. 2019;100:82-88.
2. Hafsi W, Badri T. Erythema multiforme. StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing; 2022. Updated August 1, 2022. Accessed December 15, 2022. www.ncbi.nlm.nih.gov/books/NBK470259/
3. Bennardo L, Nisticò SP, Dastoli S, et al. Erythema multiforme and COVID-19: what do we know? Medicina. 2021;57:828. https://doi.org/10.3390/medicina57080828
1. Trayes KP, Love G, Studdiford JS. Erythema multiforme: recognition and management. Am Fam Physician. 2019;100:82-88.
2. Hafsi W, Badri T. Erythema multiforme. StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing; 2022. Updated August 1, 2022. Accessed December 15, 2022. www.ncbi.nlm.nih.gov/books/NBK470259/
3. Bennardo L, Nisticò SP, Dastoli S, et al. Erythema multiforme and COVID-19: what do we know? Medicina. 2021;57:828. https://doi.org/10.3390/medicina57080828
Elevated PCSK9 levels associated with psoriasis suggest new treatment target
A Mendelian randomization study employing data from nearly 300,000 individuals has linked elevated levels of the PCSK9 enzyme with an increased risk of psoriasis, suggesting it might be targetable as an intervention.
. Conversely, psoriasis risk did not appear to be affected when LDL-C was reduced by other pathways of lipid control.
This study “suggests that PCSK9 inhibition is causally associated with reduced risk of psoriasis,” reported a team of investigators led by Sizheng Steven Zhao, MD, PhD, of the division of musculoskeletal and dermatological sciences, University of Manchester (England). “Existing PCSK9 inhibitors hold potential as therapeutic targets for prevention, and possibly treatment, of psoriasis, although further clinical studies are needed,” they concluded.
In an interview, Dr. Zhao also noted that it will be interesting to look at psoriasis susceptibility in post hoc analyses of large randomized controlled trials of PCSK9 inhibitors for cardiovascular disease.
“Genetically proxied” inhibition of HMG-CoA reductase, which is targeted by statins, and NPC1L1 which is targeted by ezetimibe, “were not associated with psoriasis risk,” the investigators reported in the study, published in JAMA Dermatology.
Abnormal lipid metabolism is sufficiently common among people with psoriasis that screening in patients with moderate to severe disease is recommended in 2019 psoriasis guidelines from the American Academy of Dermatology and the National Psoriasis Foundation. However, the link between these diseases is unclear. This study was launched to explore genetically proxied relationships between psoriasis and LDL-C reductions as well as specific treatments for elevated LDL-C.
Mendelian randomizations were applied to deidentified data from two sources, a UK biobank and FinnGen, a Finnish-based project for identifying genotype-to-phenotype correlations. Genetic proxies for these variables were established on the basis of genomewide association studies on large population samples.
Ultimately, 34 genetic variants were selected to proxy for lipid lowering by PCSK9, 19 were selected to proxy for HMG-CoA reductase, and 9 for NPC1L1. In the Mendelian analyses performed on the two sources, genetically proxied PCSK9 inhibition was associated with about a 30% reduction in the odds ratio of psoriasis (OR, 0.69; P = .003). There were no robust associations with proxies for reductions in either HMG-CoA reductase or NPC1L1.
In sensitivity analyses, there was no evidence of bias from pleiotropy or genetic confounding, according to Dr. Zhao and his coauthors, who noted that the relationship between reductions in PCSK9 and reduced risk of psoriasis appeared to be independent of change in circulating LDL-C.
Given the prior evidence implicating the PCSK9 enzyme in psoriasis risk, “this is an exciting study that really highlights the importance of studying and targeting lipid metabolism in psoriasis for a few reasons,” according to Michael S. Garshick, MD, a researcher, cardiologist, and director of the cardio-rheumatology program, New York University Langone Health.
An investigator who has participated in several studies evaluating the relationship between cardiovascular risk and psoriasis, Dr. Garshick said there is increasing interest in PCSK9 as a biomarker or even a mediator of inflammation independent of blood lipid levels.
“In psoriasis regarding PCSK9, we and others have shown PCSK9 is elevated in psoriatic lesion skin, and studies are starting to investigate the unique lipidomic profile in psoriasis,” Dr. Garshick said in an interview. The study he led that showed elevated PCSK9 levels in psoriatic skin was published in 2021 in the Journal of Investigative Dermatology.
While the Mendelian randomization provides only “an inference” that PCSK9 plays a role in mediating risk of psoriasis, Dr. Zhao and coauthors cited numerous studies linking elevated PCSK9 to psoriasis pathophysiology. This not only includes the elevated PCSK9 expression in psoriatic plaques as shown by Dr. Garshick and others but several sets of experimental evidence linking PCSK9 to inflammatory pathways, including upregulation of interleukin-17 and stimulation of macrophage activation.
While Dr. Zhao and coauthors suggested that clinical trials are now needed to test the potential of PCSK9 inhibitors to modify the risk of psoriasis, Dr. Garshick indicated that there are numerous variables to unravel in the relationship between elevated lipids, PCSK9, and psoriasis.
“In our own studies, we did see a statistical correlation between circulating PCSK9 and psoriasis severity,” Dr. Garshick said. But he added, “I think we are just beginning to understand the functions of circulating (extrahepatic) PCSK9 independent of lipid metabolism.”
While he is intrigued by the evidence that PCSK9 is linked to systemic inflammation, he pointed out that several medications used to treat dyslipidemias, such as statins, are associated with an anti-inflammatory effect.
This study “further emphasizes the need to conduct clinical trials treating dyslipidemia in psoriasis, including the targeting of PCSK9, whether it is with statins with lipid lowering and potential pleiotropic anti-inflammatory properties or PCSK9 inhibition,” he said. If positive, “both would be exciting.“
From a cardiologist’s point of view, there is an upside for including patients with psoriasis in lipid-lowering trials even if the effect on psoriasis is modest. Either way, “you still get the lipid-lowering benefit, which is important for reducing atherosclerotic cardiovascular disease,” Dr. Garshick said.
Dr. Zhao reported financial relationships with UCB, although UCB did not provide funding for this study. One author reported grants from Versus Arthritis and the National Institute for Health Research Manchester Biomedical Research Centre during the study, grants from Bristol Myers Squibb, Galapagos, and Pfizer, and personal fees from Chugai Roche outside the submitted work. No other disclosures were reported. The study was supported by grants from Versus Arthritis and the NIHR Manchester Biomedical Research Centre. Dr. Garshick reported financial relationships with AbbVie and Horizon Therapeutics.
A Mendelian randomization study employing data from nearly 300,000 individuals has linked elevated levels of the PCSK9 enzyme with an increased risk of psoriasis, suggesting it might be targetable as an intervention.
. Conversely, psoriasis risk did not appear to be affected when LDL-C was reduced by other pathways of lipid control.
This study “suggests that PCSK9 inhibition is causally associated with reduced risk of psoriasis,” reported a team of investigators led by Sizheng Steven Zhao, MD, PhD, of the division of musculoskeletal and dermatological sciences, University of Manchester (England). “Existing PCSK9 inhibitors hold potential as therapeutic targets for prevention, and possibly treatment, of psoriasis, although further clinical studies are needed,” they concluded.
In an interview, Dr. Zhao also noted that it will be interesting to look at psoriasis susceptibility in post hoc analyses of large randomized controlled trials of PCSK9 inhibitors for cardiovascular disease.
“Genetically proxied” inhibition of HMG-CoA reductase, which is targeted by statins, and NPC1L1 which is targeted by ezetimibe, “were not associated with psoriasis risk,” the investigators reported in the study, published in JAMA Dermatology.
Abnormal lipid metabolism is sufficiently common among people with psoriasis that screening in patients with moderate to severe disease is recommended in 2019 psoriasis guidelines from the American Academy of Dermatology and the National Psoriasis Foundation. However, the link between these diseases is unclear. This study was launched to explore genetically proxied relationships between psoriasis and LDL-C reductions as well as specific treatments for elevated LDL-C.
Mendelian randomizations were applied to deidentified data from two sources, a UK biobank and FinnGen, a Finnish-based project for identifying genotype-to-phenotype correlations. Genetic proxies for these variables were established on the basis of genomewide association studies on large population samples.
Ultimately, 34 genetic variants were selected to proxy for lipid lowering by PCSK9, 19 were selected to proxy for HMG-CoA reductase, and 9 for NPC1L1. In the Mendelian analyses performed on the two sources, genetically proxied PCSK9 inhibition was associated with about a 30% reduction in the odds ratio of psoriasis (OR, 0.69; P = .003). There were no robust associations with proxies for reductions in either HMG-CoA reductase or NPC1L1.
In sensitivity analyses, there was no evidence of bias from pleiotropy or genetic confounding, according to Dr. Zhao and his coauthors, who noted that the relationship between reductions in PCSK9 and reduced risk of psoriasis appeared to be independent of change in circulating LDL-C.
Given the prior evidence implicating the PCSK9 enzyme in psoriasis risk, “this is an exciting study that really highlights the importance of studying and targeting lipid metabolism in psoriasis for a few reasons,” according to Michael S. Garshick, MD, a researcher, cardiologist, and director of the cardio-rheumatology program, New York University Langone Health.
An investigator who has participated in several studies evaluating the relationship between cardiovascular risk and psoriasis, Dr. Garshick said there is increasing interest in PCSK9 as a biomarker or even a mediator of inflammation independent of blood lipid levels.
“In psoriasis regarding PCSK9, we and others have shown PCSK9 is elevated in psoriatic lesion skin, and studies are starting to investigate the unique lipidomic profile in psoriasis,” Dr. Garshick said in an interview. The study he led that showed elevated PCSK9 levels in psoriatic skin was published in 2021 in the Journal of Investigative Dermatology.
While the Mendelian randomization provides only “an inference” that PCSK9 plays a role in mediating risk of psoriasis, Dr. Zhao and coauthors cited numerous studies linking elevated PCSK9 to psoriasis pathophysiology. This not only includes the elevated PCSK9 expression in psoriatic plaques as shown by Dr. Garshick and others but several sets of experimental evidence linking PCSK9 to inflammatory pathways, including upregulation of interleukin-17 and stimulation of macrophage activation.
While Dr. Zhao and coauthors suggested that clinical trials are now needed to test the potential of PCSK9 inhibitors to modify the risk of psoriasis, Dr. Garshick indicated that there are numerous variables to unravel in the relationship between elevated lipids, PCSK9, and psoriasis.
“In our own studies, we did see a statistical correlation between circulating PCSK9 and psoriasis severity,” Dr. Garshick said. But he added, “I think we are just beginning to understand the functions of circulating (extrahepatic) PCSK9 independent of lipid metabolism.”
While he is intrigued by the evidence that PCSK9 is linked to systemic inflammation, he pointed out that several medications used to treat dyslipidemias, such as statins, are associated with an anti-inflammatory effect.
This study “further emphasizes the need to conduct clinical trials treating dyslipidemia in psoriasis, including the targeting of PCSK9, whether it is with statins with lipid lowering and potential pleiotropic anti-inflammatory properties or PCSK9 inhibition,” he said. If positive, “both would be exciting.“
From a cardiologist’s point of view, there is an upside for including patients with psoriasis in lipid-lowering trials even if the effect on psoriasis is modest. Either way, “you still get the lipid-lowering benefit, which is important for reducing atherosclerotic cardiovascular disease,” Dr. Garshick said.
Dr. Zhao reported financial relationships with UCB, although UCB did not provide funding for this study. One author reported grants from Versus Arthritis and the National Institute for Health Research Manchester Biomedical Research Centre during the study, grants from Bristol Myers Squibb, Galapagos, and Pfizer, and personal fees from Chugai Roche outside the submitted work. No other disclosures were reported. The study was supported by grants from Versus Arthritis and the NIHR Manchester Biomedical Research Centre. Dr. Garshick reported financial relationships with AbbVie and Horizon Therapeutics.
A Mendelian randomization study employing data from nearly 300,000 individuals has linked elevated levels of the PCSK9 enzyme with an increased risk of psoriasis, suggesting it might be targetable as an intervention.
. Conversely, psoriasis risk did not appear to be affected when LDL-C was reduced by other pathways of lipid control.
This study “suggests that PCSK9 inhibition is causally associated with reduced risk of psoriasis,” reported a team of investigators led by Sizheng Steven Zhao, MD, PhD, of the division of musculoskeletal and dermatological sciences, University of Manchester (England). “Existing PCSK9 inhibitors hold potential as therapeutic targets for prevention, and possibly treatment, of psoriasis, although further clinical studies are needed,” they concluded.
In an interview, Dr. Zhao also noted that it will be interesting to look at psoriasis susceptibility in post hoc analyses of large randomized controlled trials of PCSK9 inhibitors for cardiovascular disease.
“Genetically proxied” inhibition of HMG-CoA reductase, which is targeted by statins, and NPC1L1 which is targeted by ezetimibe, “were not associated with psoriasis risk,” the investigators reported in the study, published in JAMA Dermatology.
Abnormal lipid metabolism is sufficiently common among people with psoriasis that screening in patients with moderate to severe disease is recommended in 2019 psoriasis guidelines from the American Academy of Dermatology and the National Psoriasis Foundation. However, the link between these diseases is unclear. This study was launched to explore genetically proxied relationships between psoriasis and LDL-C reductions as well as specific treatments for elevated LDL-C.
Mendelian randomizations were applied to deidentified data from two sources, a UK biobank and FinnGen, a Finnish-based project for identifying genotype-to-phenotype correlations. Genetic proxies for these variables were established on the basis of genomewide association studies on large population samples.
Ultimately, 34 genetic variants were selected to proxy for lipid lowering by PCSK9, 19 were selected to proxy for HMG-CoA reductase, and 9 for NPC1L1. In the Mendelian analyses performed on the two sources, genetically proxied PCSK9 inhibition was associated with about a 30% reduction in the odds ratio of psoriasis (OR, 0.69; P = .003). There were no robust associations with proxies for reductions in either HMG-CoA reductase or NPC1L1.
In sensitivity analyses, there was no evidence of bias from pleiotropy or genetic confounding, according to Dr. Zhao and his coauthors, who noted that the relationship between reductions in PCSK9 and reduced risk of psoriasis appeared to be independent of change in circulating LDL-C.
Given the prior evidence implicating the PCSK9 enzyme in psoriasis risk, “this is an exciting study that really highlights the importance of studying and targeting lipid metabolism in psoriasis for a few reasons,” according to Michael S. Garshick, MD, a researcher, cardiologist, and director of the cardio-rheumatology program, New York University Langone Health.
An investigator who has participated in several studies evaluating the relationship between cardiovascular risk and psoriasis, Dr. Garshick said there is increasing interest in PCSK9 as a biomarker or even a mediator of inflammation independent of blood lipid levels.
“In psoriasis regarding PCSK9, we and others have shown PCSK9 is elevated in psoriatic lesion skin, and studies are starting to investigate the unique lipidomic profile in psoriasis,” Dr. Garshick said in an interview. The study he led that showed elevated PCSK9 levels in psoriatic skin was published in 2021 in the Journal of Investigative Dermatology.
While the Mendelian randomization provides only “an inference” that PCSK9 plays a role in mediating risk of psoriasis, Dr. Zhao and coauthors cited numerous studies linking elevated PCSK9 to psoriasis pathophysiology. This not only includes the elevated PCSK9 expression in psoriatic plaques as shown by Dr. Garshick and others but several sets of experimental evidence linking PCSK9 to inflammatory pathways, including upregulation of interleukin-17 and stimulation of macrophage activation.
While Dr. Zhao and coauthors suggested that clinical trials are now needed to test the potential of PCSK9 inhibitors to modify the risk of psoriasis, Dr. Garshick indicated that there are numerous variables to unravel in the relationship between elevated lipids, PCSK9, and psoriasis.
“In our own studies, we did see a statistical correlation between circulating PCSK9 and psoriasis severity,” Dr. Garshick said. But he added, “I think we are just beginning to understand the functions of circulating (extrahepatic) PCSK9 independent of lipid metabolism.”
While he is intrigued by the evidence that PCSK9 is linked to systemic inflammation, he pointed out that several medications used to treat dyslipidemias, such as statins, are associated with an anti-inflammatory effect.
This study “further emphasizes the need to conduct clinical trials treating dyslipidemia in psoriasis, including the targeting of PCSK9, whether it is with statins with lipid lowering and potential pleiotropic anti-inflammatory properties or PCSK9 inhibition,” he said. If positive, “both would be exciting.“
From a cardiologist’s point of view, there is an upside for including patients with psoriasis in lipid-lowering trials even if the effect on psoriasis is modest. Either way, “you still get the lipid-lowering benefit, which is important for reducing atherosclerotic cardiovascular disease,” Dr. Garshick said.
Dr. Zhao reported financial relationships with UCB, although UCB did not provide funding for this study. One author reported grants from Versus Arthritis and the National Institute for Health Research Manchester Biomedical Research Centre during the study, grants from Bristol Myers Squibb, Galapagos, and Pfizer, and personal fees from Chugai Roche outside the submitted work. No other disclosures were reported. The study was supported by grants from Versus Arthritis and the NIHR Manchester Biomedical Research Centre. Dr. Garshick reported financial relationships with AbbVie and Horizon Therapeutics.
FROM JAMA DERMATOLOGY
Infant with red eyelid lesion
A 4-MONTH-OLD HISPANIC INFANT was brought to her pediatrician by her parents for evaluation of a dark red lesion over her right eyelid. The mother said that the lesion appeared when the child was 4 weeks old and started as a small red dot. As the baby grew, so did the red dot. The mother said the lesion appeared redder and darker when the baby got fussy and cried. The mother noted that some of the child’s eyelashes on the affected eyelid had fallen out. The infant was still able to use her eyes to follow the movements of her parents and siblings.
The mother denied any complications during pregnancy and delivered the child vaginally. No one else in the family had a similar lesion. When asked, the mother said that when her daughter was born, she was missing hair on her scalp and had dark spots on her lower backside. The mother had taken the baby to all wellness checks. The child was up to date on her vaccines, had no known drug allergies, and was otherwise healthy.
The pediatrician referred the baby to our skin clinic for further evaluation and treatment of the right eyelid lesion. Skin examination showed a 2.1-cm focal/localized, vascular, violaceous/dark red plaque over the right upper eyelid with an irregular border causing mild drooping of the right eyelid and some missing eyelashes (FIGURE 1). Multiple hyperpigmented patches on the upper and lower back were clinically consistent with Mongolian spots. Hair thinning was observed on the posterior and left posterior scalp.
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Infantile hemangioma
The diagnosis of an infantile hemangioma was made clinically, based on the lesion’s appearance and when it became noticeable (during the child’s first few weeks of life).
Infantile hemangiomas are the most common benign tumors of infancy, and the majority are not present at birth.1,2 Infantile periocular hemangioma, which our patient had, is typically unilateral and involves the upper eyelid.1 Infantile hemangiomas appear in the first few weeks of life with an area of pallor and later a faint red patch, which the mother first noted in our patient. Lesions grow rapidly in the first 3 to 6 months.2 Superficial lesions appear as bright red papules or patches that may have a flat or rough surface and are sharply demarcated, while deep lesions tend to be bluish and dome shaped.1,2
Infantile hemangiomas continue to grow until 9 to 12 months of age, at which time the growth rate slows to parallel the growth of the child. Involution typically begins by the time the child is 1 year old. Most infantile hemangiomas do not improve significantly after 3.5 years of age.3
Differential includes congenital hemangiomas, pyogenic granulomas
Clinical presentation, histology, and lesion evolution distinguish infantile hemangioma from other diagnoses, notably the following:
Congenital hemangiomas (CH) are fully formed vascular tumors present at birth; they occur less frequently than infantile hemangiomas. CHs are divided into 2 categories: rapidly involuting CHs and noninvoluting CHs.4
Continue to: Pyogenic granulomas
Pyogenic granulomas are usually small (< 1 cm), sessile or pedunculated red papules or nodules. They are friable, bleed easily, and grow rapidly.
Capillary malformations can manifest at birth as flat, red/purple, cutaneous patches with irregular borders that are painless and can spontaneously bleed; they can be found in any part of the body but mainly occur in the cervicofacial area.5 Capillary malformations are commonly known as stork bites on the nape of the neck or angel kisses if found on the forehead. Lateral lesions, known as port wine stains, persist and do not resolve without treatment.5
Tufted angioma and kaposiform hemangioendothelioma manifest as expanding ecchymotic firm masses with purpura and accompanying lymphedema.4 Magnetic resonance imaging, including magnetic resonance angiography, is recommended for management and treatment.4
Venous malformations can be noted at birth as a dark blue or purple discoloration and manifest as a deep mass.5 Venous malformations grow with the patient and have a rapid growth phase during puberty, pregnancy, or traumatic injury.5
Arteriovenous malformations (AVMs) may be present at birth as a slight blush hypervascular lesion. AVMs can be quiescent for many years and grow with the patient. AVMs have a palpable warmth, pulse, or thrill due to high vascular flow.5
Continue to: Individualize treatment when it's needed
Individualize treatment when it’s needed
The majority of infantile hemangiomas do not require treatment because they can resolve spontaneously over time.2 That said, children with periocular infantile hemangiomas may require treatment because the lesions may result in amblyopia and visual impairment if not properly treated.6 Treatment should be individualized, depending on the size, rate of growth, morphology, number, and location of the lesions; existing or potential complications; benefits and adverse events associated with the treatment; age of the patient; level of parental concern; and the physician’s comfort level with the various treatment options.
Predictive factors for ocular complications in patients with periocular infantile hemangiomas are diameter > 1 cm, a deep component, and upper eyelid involvement. Patients at risk for ocular complications should be promptly referred to an ophthalmologist, and treatment should be strongly considered.6 Currently, oral propranolol is the treatment of choice for high-risk and complicated infantile hemangiomas.2 This is a very safe treatment. Only rarely do the following adverse effects occur: bronchospasm, bradycardia, hypotension, nightmares, cold hands, and hypoglycemia. If these adverse effects do occur, they are reversible with discontinuation of propranolol. Hypoglycemia can be prevented by giving propranolol during or right after feeding.
Our patient was started on propranolol 1 mg/kg/d for 1 month. The medication was administered by syringe for precise measurement. After the initial dose was tolerated, this was increased to 2 mg/kg/d for 1 month, then continued sequentially another month on 2.5 mg/kg/d, 2 months on 3 mg/kg/d, and finally 2 months on 3.4 mg/kg/d. All doses were divided twice per day between feedings.
After 7 months of total treatment time (FIGURE 2), we began titrating down the patient’s dose over the next several months. After 3 months, treatment was stopped altogether. At the time treatment was completed, only a faint pink blush remained.
1. Tavakoli M, Yadegari S, Mosallaei M, et al. Infantile periocular hemangioma. J Ophthalmic Vis Res. 2017;12:205-211. doi: 10.4103/jovr.jovr_66_17
2. Leung AKC, Lam JM, Leong KF, et al. Infantile hemangioma: an updated review. Curr Pediatr Rev. 2021;17:55-69. doi: 10.2174/1573396316666200508100038
3. Couto RA, Maclellan RA, Zurakowski D, et al. Infantile hemangioma: clinical assessment of the involuting phase and implications for management. Plast Reconstr Surg. 2012;130:619-624. doi: 10.1097/PRS.0b013e31825dc129
4. Wildgruber M, Sadick M, Müller-Wille R, et al. Vascular tumors in infants and adolescents. Insights Imaging. 2019;10:30. doi: 10.1186/s13244-019-0718-6
5. Richter GT, Friedman AB. Hemangiomas and vascular malformations: current theory and management. Int J Pediatr. 2012;2012:645678. doi: 10.1155/2012/645678
6. Samuelov L, Kinori M, Rychlik K, et al. Risk factors for ocular complications in periocular infantile hemangiomas. Pediatr Dermatol. 2018;35:458-462. doi: 10.1111/pde.13525
A 4-MONTH-OLD HISPANIC INFANT was brought to her pediatrician by her parents for evaluation of a dark red lesion over her right eyelid. The mother said that the lesion appeared when the child was 4 weeks old and started as a small red dot. As the baby grew, so did the red dot. The mother said the lesion appeared redder and darker when the baby got fussy and cried. The mother noted that some of the child’s eyelashes on the affected eyelid had fallen out. The infant was still able to use her eyes to follow the movements of her parents and siblings.
The mother denied any complications during pregnancy and delivered the child vaginally. No one else in the family had a similar lesion. When asked, the mother said that when her daughter was born, she was missing hair on her scalp and had dark spots on her lower backside. The mother had taken the baby to all wellness checks. The child was up to date on her vaccines, had no known drug allergies, and was otherwise healthy.
The pediatrician referred the baby to our skin clinic for further evaluation and treatment of the right eyelid lesion. Skin examination showed a 2.1-cm focal/localized, vascular, violaceous/dark red plaque over the right upper eyelid with an irregular border causing mild drooping of the right eyelid and some missing eyelashes (FIGURE 1). Multiple hyperpigmented patches on the upper and lower back were clinically consistent with Mongolian spots. Hair thinning was observed on the posterior and left posterior scalp.
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Infantile hemangioma
The diagnosis of an infantile hemangioma was made clinically, based on the lesion’s appearance and when it became noticeable (during the child’s first few weeks of life).
Infantile hemangiomas are the most common benign tumors of infancy, and the majority are not present at birth.1,2 Infantile periocular hemangioma, which our patient had, is typically unilateral and involves the upper eyelid.1 Infantile hemangiomas appear in the first few weeks of life with an area of pallor and later a faint red patch, which the mother first noted in our patient. Lesions grow rapidly in the first 3 to 6 months.2 Superficial lesions appear as bright red papules or patches that may have a flat or rough surface and are sharply demarcated, while deep lesions tend to be bluish and dome shaped.1,2
Infantile hemangiomas continue to grow until 9 to 12 months of age, at which time the growth rate slows to parallel the growth of the child. Involution typically begins by the time the child is 1 year old. Most infantile hemangiomas do not improve significantly after 3.5 years of age.3
Differential includes congenital hemangiomas, pyogenic granulomas
Clinical presentation, histology, and lesion evolution distinguish infantile hemangioma from other diagnoses, notably the following:
Congenital hemangiomas (CH) are fully formed vascular tumors present at birth; they occur less frequently than infantile hemangiomas. CHs are divided into 2 categories: rapidly involuting CHs and noninvoluting CHs.4
Continue to: Pyogenic granulomas
Pyogenic granulomas are usually small (< 1 cm), sessile or pedunculated red papules or nodules. They are friable, bleed easily, and grow rapidly.
Capillary malformations can manifest at birth as flat, red/purple, cutaneous patches with irregular borders that are painless and can spontaneously bleed; they can be found in any part of the body but mainly occur in the cervicofacial area.5 Capillary malformations are commonly known as stork bites on the nape of the neck or angel kisses if found on the forehead. Lateral lesions, known as port wine stains, persist and do not resolve without treatment.5
Tufted angioma and kaposiform hemangioendothelioma manifest as expanding ecchymotic firm masses with purpura and accompanying lymphedema.4 Magnetic resonance imaging, including magnetic resonance angiography, is recommended for management and treatment.4
Venous malformations can be noted at birth as a dark blue or purple discoloration and manifest as a deep mass.5 Venous malformations grow with the patient and have a rapid growth phase during puberty, pregnancy, or traumatic injury.5
Arteriovenous malformations (AVMs) may be present at birth as a slight blush hypervascular lesion. AVMs can be quiescent for many years and grow with the patient. AVMs have a palpable warmth, pulse, or thrill due to high vascular flow.5
Continue to: Individualize treatment when it's needed
Individualize treatment when it’s needed
The majority of infantile hemangiomas do not require treatment because they can resolve spontaneously over time.2 That said, children with periocular infantile hemangiomas may require treatment because the lesions may result in amblyopia and visual impairment if not properly treated.6 Treatment should be individualized, depending on the size, rate of growth, morphology, number, and location of the lesions; existing or potential complications; benefits and adverse events associated with the treatment; age of the patient; level of parental concern; and the physician’s comfort level with the various treatment options.
Predictive factors for ocular complications in patients with periocular infantile hemangiomas are diameter > 1 cm, a deep component, and upper eyelid involvement. Patients at risk for ocular complications should be promptly referred to an ophthalmologist, and treatment should be strongly considered.6 Currently, oral propranolol is the treatment of choice for high-risk and complicated infantile hemangiomas.2 This is a very safe treatment. Only rarely do the following adverse effects occur: bronchospasm, bradycardia, hypotension, nightmares, cold hands, and hypoglycemia. If these adverse effects do occur, they are reversible with discontinuation of propranolol. Hypoglycemia can be prevented by giving propranolol during or right after feeding.
Our patient was started on propranolol 1 mg/kg/d for 1 month. The medication was administered by syringe for precise measurement. After the initial dose was tolerated, this was increased to 2 mg/kg/d for 1 month, then continued sequentially another month on 2.5 mg/kg/d, 2 months on 3 mg/kg/d, and finally 2 months on 3.4 mg/kg/d. All doses were divided twice per day between feedings.
After 7 months of total treatment time (FIGURE 2), we began titrating down the patient’s dose over the next several months. After 3 months, treatment was stopped altogether. At the time treatment was completed, only a faint pink blush remained.
A 4-MONTH-OLD HISPANIC INFANT was brought to her pediatrician by her parents for evaluation of a dark red lesion over her right eyelid. The mother said that the lesion appeared when the child was 4 weeks old and started as a small red dot. As the baby grew, so did the red dot. The mother said the lesion appeared redder and darker when the baby got fussy and cried. The mother noted that some of the child’s eyelashes on the affected eyelid had fallen out. The infant was still able to use her eyes to follow the movements of her parents and siblings.
The mother denied any complications during pregnancy and delivered the child vaginally. No one else in the family had a similar lesion. When asked, the mother said that when her daughter was born, she was missing hair on her scalp and had dark spots on her lower backside. The mother had taken the baby to all wellness checks. The child was up to date on her vaccines, had no known drug allergies, and was otherwise healthy.
The pediatrician referred the baby to our skin clinic for further evaluation and treatment of the right eyelid lesion. Skin examination showed a 2.1-cm focal/localized, vascular, violaceous/dark red plaque over the right upper eyelid with an irregular border causing mild drooping of the right eyelid and some missing eyelashes (FIGURE 1). Multiple hyperpigmented patches on the upper and lower back were clinically consistent with Mongolian spots. Hair thinning was observed on the posterior and left posterior scalp.
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Infantile hemangioma
The diagnosis of an infantile hemangioma was made clinically, based on the lesion’s appearance and when it became noticeable (during the child’s first few weeks of life).
Infantile hemangiomas are the most common benign tumors of infancy, and the majority are not present at birth.1,2 Infantile periocular hemangioma, which our patient had, is typically unilateral and involves the upper eyelid.1 Infantile hemangiomas appear in the first few weeks of life with an area of pallor and later a faint red patch, which the mother first noted in our patient. Lesions grow rapidly in the first 3 to 6 months.2 Superficial lesions appear as bright red papules or patches that may have a flat or rough surface and are sharply demarcated, while deep lesions tend to be bluish and dome shaped.1,2
Infantile hemangiomas continue to grow until 9 to 12 months of age, at which time the growth rate slows to parallel the growth of the child. Involution typically begins by the time the child is 1 year old. Most infantile hemangiomas do not improve significantly after 3.5 years of age.3
Differential includes congenital hemangiomas, pyogenic granulomas
Clinical presentation, histology, and lesion evolution distinguish infantile hemangioma from other diagnoses, notably the following:
Congenital hemangiomas (CH) are fully formed vascular tumors present at birth; they occur less frequently than infantile hemangiomas. CHs are divided into 2 categories: rapidly involuting CHs and noninvoluting CHs.4
Continue to: Pyogenic granulomas
Pyogenic granulomas are usually small (< 1 cm), sessile or pedunculated red papules or nodules. They are friable, bleed easily, and grow rapidly.
Capillary malformations can manifest at birth as flat, red/purple, cutaneous patches with irregular borders that are painless and can spontaneously bleed; they can be found in any part of the body but mainly occur in the cervicofacial area.5 Capillary malformations are commonly known as stork bites on the nape of the neck or angel kisses if found on the forehead. Lateral lesions, known as port wine stains, persist and do not resolve without treatment.5
Tufted angioma and kaposiform hemangioendothelioma manifest as expanding ecchymotic firm masses with purpura and accompanying lymphedema.4 Magnetic resonance imaging, including magnetic resonance angiography, is recommended for management and treatment.4
Venous malformations can be noted at birth as a dark blue or purple discoloration and manifest as a deep mass.5 Venous malformations grow with the patient and have a rapid growth phase during puberty, pregnancy, or traumatic injury.5
Arteriovenous malformations (AVMs) may be present at birth as a slight blush hypervascular lesion. AVMs can be quiescent for many years and grow with the patient. AVMs have a palpable warmth, pulse, or thrill due to high vascular flow.5
Continue to: Individualize treatment when it's needed
Individualize treatment when it’s needed
The majority of infantile hemangiomas do not require treatment because they can resolve spontaneously over time.2 That said, children with periocular infantile hemangiomas may require treatment because the lesions may result in amblyopia and visual impairment if not properly treated.6 Treatment should be individualized, depending on the size, rate of growth, morphology, number, and location of the lesions; existing or potential complications; benefits and adverse events associated with the treatment; age of the patient; level of parental concern; and the physician’s comfort level with the various treatment options.
Predictive factors for ocular complications in patients with periocular infantile hemangiomas are diameter > 1 cm, a deep component, and upper eyelid involvement. Patients at risk for ocular complications should be promptly referred to an ophthalmologist, and treatment should be strongly considered.6 Currently, oral propranolol is the treatment of choice for high-risk and complicated infantile hemangiomas.2 This is a very safe treatment. Only rarely do the following adverse effects occur: bronchospasm, bradycardia, hypotension, nightmares, cold hands, and hypoglycemia. If these adverse effects do occur, they are reversible with discontinuation of propranolol. Hypoglycemia can be prevented by giving propranolol during or right after feeding.
Our patient was started on propranolol 1 mg/kg/d for 1 month. The medication was administered by syringe for precise measurement. After the initial dose was tolerated, this was increased to 2 mg/kg/d for 1 month, then continued sequentially another month on 2.5 mg/kg/d, 2 months on 3 mg/kg/d, and finally 2 months on 3.4 mg/kg/d. All doses were divided twice per day between feedings.
After 7 months of total treatment time (FIGURE 2), we began titrating down the patient’s dose over the next several months. After 3 months, treatment was stopped altogether. At the time treatment was completed, only a faint pink blush remained.
1. Tavakoli M, Yadegari S, Mosallaei M, et al. Infantile periocular hemangioma. J Ophthalmic Vis Res. 2017;12:205-211. doi: 10.4103/jovr.jovr_66_17
2. Leung AKC, Lam JM, Leong KF, et al. Infantile hemangioma: an updated review. Curr Pediatr Rev. 2021;17:55-69. doi: 10.2174/1573396316666200508100038
3. Couto RA, Maclellan RA, Zurakowski D, et al. Infantile hemangioma: clinical assessment of the involuting phase and implications for management. Plast Reconstr Surg. 2012;130:619-624. doi: 10.1097/PRS.0b013e31825dc129
4. Wildgruber M, Sadick M, Müller-Wille R, et al. Vascular tumors in infants and adolescents. Insights Imaging. 2019;10:30. doi: 10.1186/s13244-019-0718-6
5. Richter GT, Friedman AB. Hemangiomas and vascular malformations: current theory and management. Int J Pediatr. 2012;2012:645678. doi: 10.1155/2012/645678
6. Samuelov L, Kinori M, Rychlik K, et al. Risk factors for ocular complications in periocular infantile hemangiomas. Pediatr Dermatol. 2018;35:458-462. doi: 10.1111/pde.13525
1. Tavakoli M, Yadegari S, Mosallaei M, et al. Infantile periocular hemangioma. J Ophthalmic Vis Res. 2017;12:205-211. doi: 10.4103/jovr.jovr_66_17
2. Leung AKC, Lam JM, Leong KF, et al. Infantile hemangioma: an updated review. Curr Pediatr Rev. 2021;17:55-69. doi: 10.2174/1573396316666200508100038
3. Couto RA, Maclellan RA, Zurakowski D, et al. Infantile hemangioma: clinical assessment of the involuting phase and implications for management. Plast Reconstr Surg. 2012;130:619-624. doi: 10.1097/PRS.0b013e31825dc129
4. Wildgruber M, Sadick M, Müller-Wille R, et al. Vascular tumors in infants and adolescents. Insights Imaging. 2019;10:30. doi: 10.1186/s13244-019-0718-6
5. Richter GT, Friedman AB. Hemangiomas and vascular malformations: current theory and management. Int J Pediatr. 2012;2012:645678. doi: 10.1155/2012/645678
6. Samuelov L, Kinori M, Rychlik K, et al. Risk factors for ocular complications in periocular infantile hemangiomas. Pediatr Dermatol. 2018;35:458-462. doi: 10.1111/pde.13525
How should PRAME be used to evaluate melanocytic lesions?
SAN DIEGO – , according to Cora Humberson, MD.
“I’m a fan, but there are issues with it,” Dr. Humberson, dermatopathology coordinator in the department of pathology at Scripps MD Anderson Cancer Center, San Diego, said at the annual Cutaneous Malignancy Update. “It’s all in how you use it.”
PRAME is part of the cancer/testis (CT) antigens, of which more than 40 have now been identified. They are encoded by genes that are normally expressed only in the human germ line, but are also expressed in various tumor types, including melanoma and carcinomas of the bladder, lung, and liver. “The biological function of these antigens is not fully understood, but they may act as a repressor of retinoic acid, potentially inhibiting differentiation, inhibiting proliferation arrest – things that we associate with malignancy,” she said at the meeting, which was hosted by Scripps MD Anderson Cancer Center. “These immunogenic proteins are being pursued as targets for therapeutic cancer vaccines,” she noted.
CT antigens are also being evaluated for their role in oncogenesis, she added. Recapitulation of portions of the germline gene-expression might contribute characteristic features to the neoplastic phenotype, including immortality, invasiveness, immune evasion, and metastatic capacity.
According to Dr. Humberson, PRAME can be used to differentiate comingled nevus and melanoma, to distinguish between nevoid melanoma and nevus, and for melanoma margin assessment in sun-damaged skin. One potential pitfall is that sun-damaged melanocytes may express PRAME. “The older the person and the more sun damage [they have], the more likely you are to see this, but the melanocytes won’t be grouped, they’ll be scattered,” she said.
Another pitfall is that less than 15% of nevi may express PRAME. “PRAME can be expressed in scars, so if you’re looking at a spindle cell lesion, be aware that you might be looking at a scar if you’re seeing PRAME expression,” she added. She also noted that PRAME immunohistochemistry (IHC) expression is not a prognostic biomarker in thin melanomas.
If fewer than 25% of cells in a melanocytic lesion express PRAME, most published assessments of PRAME IHC favor nevi as the diagnosis. “If more than 75% are expressing it, it favors melanoma,” Dr. Humberson said. “There’s a big category in between. It’s not that 30% is more likely benign or that 60% is more likely malignant; you can’t really depend upon [PRAME] if you’re in this range.”
A diagnostic accuracy study found that when more than 75% of cells express PRAME, the marker has a sensitivity of 0.63 and a specificity of 0.97.
Selected PRAME-related published references she recommended include: J Cutan Pathol. 2021;48(9):1115-23; Diagnostics. 2022 Sep 9; 12(9):2197, and J Cutan Pathol. 2022;49(9):829-32.
Dr. Humberson reported having no relevant disclosures.
SAN DIEGO – , according to Cora Humberson, MD.
“I’m a fan, but there are issues with it,” Dr. Humberson, dermatopathology coordinator in the department of pathology at Scripps MD Anderson Cancer Center, San Diego, said at the annual Cutaneous Malignancy Update. “It’s all in how you use it.”
PRAME is part of the cancer/testis (CT) antigens, of which more than 40 have now been identified. They are encoded by genes that are normally expressed only in the human germ line, but are also expressed in various tumor types, including melanoma and carcinomas of the bladder, lung, and liver. “The biological function of these antigens is not fully understood, but they may act as a repressor of retinoic acid, potentially inhibiting differentiation, inhibiting proliferation arrest – things that we associate with malignancy,” she said at the meeting, which was hosted by Scripps MD Anderson Cancer Center. “These immunogenic proteins are being pursued as targets for therapeutic cancer vaccines,” she noted.
CT antigens are also being evaluated for their role in oncogenesis, she added. Recapitulation of portions of the germline gene-expression might contribute characteristic features to the neoplastic phenotype, including immortality, invasiveness, immune evasion, and metastatic capacity.
According to Dr. Humberson, PRAME can be used to differentiate comingled nevus and melanoma, to distinguish between nevoid melanoma and nevus, and for melanoma margin assessment in sun-damaged skin. One potential pitfall is that sun-damaged melanocytes may express PRAME. “The older the person and the more sun damage [they have], the more likely you are to see this, but the melanocytes won’t be grouped, they’ll be scattered,” she said.
Another pitfall is that less than 15% of nevi may express PRAME. “PRAME can be expressed in scars, so if you’re looking at a spindle cell lesion, be aware that you might be looking at a scar if you’re seeing PRAME expression,” she added. She also noted that PRAME immunohistochemistry (IHC) expression is not a prognostic biomarker in thin melanomas.
If fewer than 25% of cells in a melanocytic lesion express PRAME, most published assessments of PRAME IHC favor nevi as the diagnosis. “If more than 75% are expressing it, it favors melanoma,” Dr. Humberson said. “There’s a big category in between. It’s not that 30% is more likely benign or that 60% is more likely malignant; you can’t really depend upon [PRAME] if you’re in this range.”
A diagnostic accuracy study found that when more than 75% of cells express PRAME, the marker has a sensitivity of 0.63 and a specificity of 0.97.
Selected PRAME-related published references she recommended include: J Cutan Pathol. 2021;48(9):1115-23; Diagnostics. 2022 Sep 9; 12(9):2197, and J Cutan Pathol. 2022;49(9):829-32.
Dr. Humberson reported having no relevant disclosures.
SAN DIEGO – , according to Cora Humberson, MD.
“I’m a fan, but there are issues with it,” Dr. Humberson, dermatopathology coordinator in the department of pathology at Scripps MD Anderson Cancer Center, San Diego, said at the annual Cutaneous Malignancy Update. “It’s all in how you use it.”
PRAME is part of the cancer/testis (CT) antigens, of which more than 40 have now been identified. They are encoded by genes that are normally expressed only in the human germ line, but are also expressed in various tumor types, including melanoma and carcinomas of the bladder, lung, and liver. “The biological function of these antigens is not fully understood, but they may act as a repressor of retinoic acid, potentially inhibiting differentiation, inhibiting proliferation arrest – things that we associate with malignancy,” she said at the meeting, which was hosted by Scripps MD Anderson Cancer Center. “These immunogenic proteins are being pursued as targets for therapeutic cancer vaccines,” she noted.
CT antigens are also being evaluated for their role in oncogenesis, she added. Recapitulation of portions of the germline gene-expression might contribute characteristic features to the neoplastic phenotype, including immortality, invasiveness, immune evasion, and metastatic capacity.
According to Dr. Humberson, PRAME can be used to differentiate comingled nevus and melanoma, to distinguish between nevoid melanoma and nevus, and for melanoma margin assessment in sun-damaged skin. One potential pitfall is that sun-damaged melanocytes may express PRAME. “The older the person and the more sun damage [they have], the more likely you are to see this, but the melanocytes won’t be grouped, they’ll be scattered,” she said.
Another pitfall is that less than 15% of nevi may express PRAME. “PRAME can be expressed in scars, so if you’re looking at a spindle cell lesion, be aware that you might be looking at a scar if you’re seeing PRAME expression,” she added. She also noted that PRAME immunohistochemistry (IHC) expression is not a prognostic biomarker in thin melanomas.
If fewer than 25% of cells in a melanocytic lesion express PRAME, most published assessments of PRAME IHC favor nevi as the diagnosis. “If more than 75% are expressing it, it favors melanoma,” Dr. Humberson said. “There’s a big category in between. It’s not that 30% is more likely benign or that 60% is more likely malignant; you can’t really depend upon [PRAME] if you’re in this range.”
A diagnostic accuracy study found that when more than 75% of cells express PRAME, the marker has a sensitivity of 0.63 and a specificity of 0.97.
Selected PRAME-related published references she recommended include: J Cutan Pathol. 2021;48(9):1115-23; Diagnostics. 2022 Sep 9; 12(9):2197, and J Cutan Pathol. 2022;49(9):829-32.
Dr. Humberson reported having no relevant disclosures.
AT MELANOMA 2023
Circular patch on chest
A skin scraping and potassium hydroxide (KOH) prep confirmed the presence of branching hyphae, consistent with tinea corporis. The large size of this plaque could have easily made this diagnosis more difficult. When tinea corporis is suspected, look at the edge of the plaque; there is often thin scale and sometimes small pustules corresponding to follicular involvement.
Commonly called by the misnomer “ringworm,” tinea corporis is a skin infection caused by a wide variety of dermatophytes and affects all ages, sexes, and skin types. Trichophyton, Microsporum, and Epidermophyton species are frequently isolated.1 Patients with atopic dermatitis or weakened immunity may be more susceptible to more frequent or long-lasting episodes. Diabetes may have contributed to the extent of the disease in this case.
Patients with tinea corporis present with one or several annular patches to plaques that grow in size. When the source of contagion is an animal, inflammation can be dramatic. In the case above, there was minimal to no itching and the patient didn’t notice the rash; thus, it was able to enlarge for months.
Treatment options include systemic and topical antifungal therapy. Consideration should be given to the severity of the disease and causal organism. Azoles, terbinafine, and ciclopirox are common treatment options. Topical therapy with an appropriately selected antifungal for 1 to 6 weeks, based on clinical response, is safe and effective. It is important to consider other foci of infection, including the feet and hands. More extensive disease may be treated with oral therapy such as terbinafine, fluconazole, or itraconazole.
Because of the extent of the disease and the challenge of effective coverage with topical therapy, this patient was treated with oral terbinafine 250 mg daily for 3 weeks. The plaque cleared completely.
Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.
1. Leung AK, Lam JM, Leong KF, et al. Tinea corporis: an updated review. Drugs Context. 2020;9:2020-5-6. doi: 10.7573/dic.2020-5-6
A skin scraping and potassium hydroxide (KOH) prep confirmed the presence of branching hyphae, consistent with tinea corporis. The large size of this plaque could have easily made this diagnosis more difficult. When tinea corporis is suspected, look at the edge of the plaque; there is often thin scale and sometimes small pustules corresponding to follicular involvement.
Commonly called by the misnomer “ringworm,” tinea corporis is a skin infection caused by a wide variety of dermatophytes and affects all ages, sexes, and skin types. Trichophyton, Microsporum, and Epidermophyton species are frequently isolated.1 Patients with atopic dermatitis or weakened immunity may be more susceptible to more frequent or long-lasting episodes. Diabetes may have contributed to the extent of the disease in this case.
Patients with tinea corporis present with one or several annular patches to plaques that grow in size. When the source of contagion is an animal, inflammation can be dramatic. In the case above, there was minimal to no itching and the patient didn’t notice the rash; thus, it was able to enlarge for months.
Treatment options include systemic and topical antifungal therapy. Consideration should be given to the severity of the disease and causal organism. Azoles, terbinafine, and ciclopirox are common treatment options. Topical therapy with an appropriately selected antifungal for 1 to 6 weeks, based on clinical response, is safe and effective. It is important to consider other foci of infection, including the feet and hands. More extensive disease may be treated with oral therapy such as terbinafine, fluconazole, or itraconazole.
Because of the extent of the disease and the challenge of effective coverage with topical therapy, this patient was treated with oral terbinafine 250 mg daily for 3 weeks. The plaque cleared completely.
Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.
A skin scraping and potassium hydroxide (KOH) prep confirmed the presence of branching hyphae, consistent with tinea corporis. The large size of this plaque could have easily made this diagnosis more difficult. When tinea corporis is suspected, look at the edge of the plaque; there is often thin scale and sometimes small pustules corresponding to follicular involvement.
Commonly called by the misnomer “ringworm,” tinea corporis is a skin infection caused by a wide variety of dermatophytes and affects all ages, sexes, and skin types. Trichophyton, Microsporum, and Epidermophyton species are frequently isolated.1 Patients with atopic dermatitis or weakened immunity may be more susceptible to more frequent or long-lasting episodes. Diabetes may have contributed to the extent of the disease in this case.
Patients with tinea corporis present with one or several annular patches to plaques that grow in size. When the source of contagion is an animal, inflammation can be dramatic. In the case above, there was minimal to no itching and the patient didn’t notice the rash; thus, it was able to enlarge for months.
Treatment options include systemic and topical antifungal therapy. Consideration should be given to the severity of the disease and causal organism. Azoles, terbinafine, and ciclopirox are common treatment options. Topical therapy with an appropriately selected antifungal for 1 to 6 weeks, based on clinical response, is safe and effective. It is important to consider other foci of infection, including the feet and hands. More extensive disease may be treated with oral therapy such as terbinafine, fluconazole, or itraconazole.
Because of the extent of the disease and the challenge of effective coverage with topical therapy, this patient was treated with oral terbinafine 250 mg daily for 3 weeks. The plaque cleared completely.
Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.
1. Leung AK, Lam JM, Leong KF, et al. Tinea corporis: an updated review. Drugs Context. 2020;9:2020-5-6. doi: 10.7573/dic.2020-5-6
1. Leung AK, Lam JM, Leong KF, et al. Tinea corporis: an updated review. Drugs Context. 2020;9:2020-5-6. doi: 10.7573/dic.2020-5-6
