Dermatology

Most patients with epidermolysis bullosa who use topical products choose antimicrobials, according to data from a survey of 202 children and adults.

Management of epidermolysis bullosa (EB) involves a combination of skin protection and infection management, but patient home care practices have not been well studied, wrote Leila Shayegan of Columbia University, New York, and colleagues.

In a study published in Pediatric Dermatology, the researchers surveyed 202 patients who were enrolled in the Epidermolysis Bullosa Clinical Characterization and Outcomes Database during 2017. The patients ranged in age from 1 month to 62 years with an average age of 11 years; 52% were female. The patients represented a range of EB subtypes, including 130 patients with dystrophic EB, 51 patients with EB simplex, 21 with junctional EB, and 3 patients each with Kindler syndrome and unspecified subtypes.

Overall, most of the patients reported cleaning their skin either every day (37%) or every other day (32%). Of the 188 patients who reported using topical products on their wounds, 131 (70%) said they used at least one antimicrobial product, while 125 patients (66%) reported using at least one emollient; 32 (17%) used emollients only, and 21(11%) reported no use of topical products.

The most popular topical antibiotics were mupirocin (31%) and bacitracin (31%). In addition, 14% of respondents used silver-containing products, and 16% used medical-grade honey. Roughly half (51%) of patients who reported use of at least one antimicrobial product used two or more different antimicrobial products.

A total of 38% of patients used only water for cleansing. Of the 131 patients who reported using additives in their cleansing water, 57% added salt, 54% added bleach, 27% added vinegar, and 26% reported “other” additive use, which could include Epsom salt, baking soda, oatmeal, or essential oils, the researchers said. The concentrations of these additives ranged from barely effective 0.002% sodium hypochlorite and 0.002% acetic acid solutions to potentially cytotoxic solutions of 0.09% sodium hypochlorite and 0.156% acetic acid.

“Although the survey was not designed to correlate skin care practices with wound culture results and resistance patterns, widespread use of topical antimicrobials described among EB patients highlights the need for increased emphasis on antibiotic stewardship,” the researchers noted. They added that health care providers should educate patients and families not only about mindful use of antibiotics, but also appropriate concentrations of cleansing additives.

“Optimizing EB patient home skin care routines, along with future longitudinal studies on the impact of EB skin care interventions on microbial resistance patterns, wound healing and [squamous cell carcinoma] risk are necessary to improve outcomes for patients with EB,” they emphasized.

The Epidermolysis Bullosa Clinical Characterization and Outcomes Database used in the study is funded by the Epidermolysis Bullosa Research Partnership and the Epidermolysis Bullosa Medical Research Foundation. Ms. Shayegan had no financial conflicts to disclose. Several coauthors disclosed relationships with multiple companies including Abeona Therapeutics, Castle Creek Pharmaceuticals, Fibrocell Science, ProQR, and Scioderm.

SOURCE: Shayegan L et al. Pediatr Dermatol. 2020. doi: 10.1111/pde.14102.

Most patients with epidermolysis bullosa who use topical products choose antimicrobials, according to data from a survey of 202 children and adults.

Management of epidermolysis bullosa (EB) involves a combination of skin protection and infection management, but patient home care practices have not been well studied, wrote Leila Shayegan of Columbia University, New York, and colleagues.

In a study published in Pediatric Dermatology, the researchers surveyed 202 patients who were enrolled in the Epidermolysis Bullosa Clinical Characterization and Outcomes Database during 2017. The patients ranged in age from 1 month to 62 years with an average age of 11 years; 52% were female. The patients represented a range of EB subtypes, including 130 patients with dystrophic EB, 51 patients with EB simplex, 21 with junctional EB, and 3 patients each with Kindler syndrome and unspecified subtypes.

Overall, most of the patients reported cleaning their skin either every day (37%) or every other day (32%). Of the 188 patients who reported using topical products on their wounds, 131 (70%) said they used at least one antimicrobial product, while 125 patients (66%) reported using at least one emollient; 32 (17%) used emollients only, and 21(11%) reported no use of topical products.

The most popular topical antibiotics were mupirocin (31%) and bacitracin (31%). In addition, 14% of respondents used silver-containing products, and 16% used medical-grade honey. Roughly half (51%) of patients who reported use of at least one antimicrobial product used two or more different antimicrobial products.

A total of 38% of patients used only water for cleansing. Of the 131 patients who reported using additives in their cleansing water, 57% added salt, 54% added bleach, 27% added vinegar, and 26% reported “other” additive use, which could include Epsom salt, baking soda, oatmeal, or essential oils, the researchers said. The concentrations of these additives ranged from barely effective 0.002% sodium hypochlorite and 0.002% acetic acid solutions to potentially cytotoxic solutions of 0.09% sodium hypochlorite and 0.156% acetic acid.

“Although the survey was not designed to correlate skin care practices with wound culture results and resistance patterns, widespread use of topical antimicrobials described among EB patients highlights the need for increased emphasis on antibiotic stewardship,” the researchers noted. They added that health care providers should educate patients and families not only about mindful use of antibiotics, but also appropriate concentrations of cleansing additives.

“Optimizing EB patient home skin care routines, along with future longitudinal studies on the impact of EB skin care interventions on microbial resistance patterns, wound healing and [squamous cell carcinoma] risk are necessary to improve outcomes for patients with EB,” they emphasized.

The Epidermolysis Bullosa Clinical Characterization and Outcomes Database used in the study is funded by the Epidermolysis Bullosa Research Partnership and the Epidermolysis Bullosa Medical Research Foundation. Ms. Shayegan had no financial conflicts to disclose. Several coauthors disclosed relationships with multiple companies including Abeona Therapeutics, Castle Creek Pharmaceuticals, Fibrocell Science, ProQR, and Scioderm.

SOURCE: Shayegan L et al. Pediatr Dermatol. 2020. doi: 10.1111/pde.14102.

Most patients with epidermolysis bullosa who use topical products choose antimicrobials, according to data from a survey of 202 children and adults.

Management of epidermolysis bullosa (EB) involves a combination of skin protection and infection management, but patient home care practices have not been well studied, wrote Leila Shayegan of Columbia University, New York, and colleagues.

In a study published in Pediatric Dermatology, the researchers surveyed 202 patients who were enrolled in the Epidermolysis Bullosa Clinical Characterization and Outcomes Database during 2017. The patients ranged in age from 1 month to 62 years with an average age of 11 years; 52% were female. The patients represented a range of EB subtypes, including 130 patients with dystrophic EB, 51 patients with EB simplex, 21 with junctional EB, and 3 patients each with Kindler syndrome and unspecified subtypes.

Overall, most of the patients reported cleaning their skin either every day (37%) or every other day (32%). Of the 188 patients who reported using topical products on their wounds, 131 (70%) said they used at least one antimicrobial product, while 125 patients (66%) reported using at least one emollient; 32 (17%) used emollients only, and 21(11%) reported no use of topical products.

The most popular topical antibiotics were mupirocin (31%) and bacitracin (31%). In addition, 14% of respondents used silver-containing products, and 16% used medical-grade honey. Roughly half (51%) of patients who reported use of at least one antimicrobial product used two or more different antimicrobial products.

A total of 38% of patients used only water for cleansing. Of the 131 patients who reported using additives in their cleansing water, 57% added salt, 54% added bleach, 27% added vinegar, and 26% reported “other” additive use, which could include Epsom salt, baking soda, oatmeal, or essential oils, the researchers said. The concentrations of these additives ranged from barely effective 0.002% sodium hypochlorite and 0.002% acetic acid solutions to potentially cytotoxic solutions of 0.09% sodium hypochlorite and 0.156% acetic acid.

“Although the survey was not designed to correlate skin care practices with wound culture results and resistance patterns, widespread use of topical antimicrobials described among EB patients highlights the need for increased emphasis on antibiotic stewardship,” the researchers noted. They added that health care providers should educate patients and families not only about mindful use of antibiotics, but also appropriate concentrations of cleansing additives.

“Optimizing EB patient home skin care routines, along with future longitudinal studies on the impact of EB skin care interventions on microbial resistance patterns, wound healing and [squamous cell carcinoma] risk are necessary to improve outcomes for patients with EB,” they emphasized.

The Epidermolysis Bullosa Clinical Characterization and Outcomes Database used in the study is funded by the Epidermolysis Bullosa Research Partnership and the Epidermolysis Bullosa Medical Research Foundation. Ms. Shayegan had no financial conflicts to disclose. Several coauthors disclosed relationships with multiple companies including Abeona Therapeutics, Castle Creek Pharmaceuticals, Fibrocell Science, ProQR, and Scioderm.

SOURCE: Shayegan L et al. Pediatr Dermatol. 2020. doi: 10.1111/pde.14102.

ORLANDO – Because Food and Drug Administration–approved treatment options for children and adolescents with severe dermatologic diseases are limited, systemic therapies for these patients often require the use of off-label medications. However, this scenario is changing, A. Yasmine Kirkorian, MD, said at the ODAC Dermatology, Aesthetic & Surgical Conference.

Jeff Craven/MDedge News

“I really would like to emphasize that children with severe disease need to be treated,” added Dr. Kirkorian, a pediatric dermatologist at George Washington University, Washington, and Children’s National Health System, where she is interim chief of the division of dermatology.

Current on-label systemic therapies for pediatric skin disease include etanercept for psoriasis (4 years and older), ustekinumab for psoriasis (12 years and older), adalimumab for hidradenitis suppurativa (12 years and older), and omalizumab for chronic idiopathic urticaria (12 years and older). A new addition to the list is dupilumab, which was approved for children and adolescents with atopic dermatitis (AD) aged 12 years and older in 2019, she noted.

Dupilumab is currently being studied in children aged 6 months to 12 years, and other clinical trials are evaluating more options for pediatric patients with AD, alopecia areata, and psoriasis. They include a clinical trial of the oral Janus kinase 3 (JAK3) inhibitor PF-06651600 in patients aged 12 years and older with alopecia areata. Six biologic therapies are being evaluated for psoriasis in patients beginning at 6 years: ixekizumab, secukinumab, ustekinumab, guselkumab, brodalumab, and apremilast.

Some systemic therapies are off-label “but used all the time” for dermatologic diseases in pediatrics, Dr. Kirkorian noted. One example is methotrexate, which is approved by the FDA for acute lymphoblastic leukemia, meningeal leukemia, and juvenile idiopathic arthritis down to infancy. Having existing efficacy and safety data for a medication in a pediatric population, even for a different disease, can be helpful when counseling parents of children with severe dermatologic disease. “If you have something, even in an older population of children, it can be reassuring, or you can use evidence from other diseases,” she said.

While methotrexate is a cheap option and approved by the FDA for other pediatric indications down to infancy, the cons of using it to treat AD in pediatric patients are numerous. Treatment requires a number of blood draws for lab testing, which can be discouraging for younger patients, and the reported adverse effect profile may be concerning to some parents, while “in practice doesn’t really occur,” she said. Methotrexate is a teratogen so is not appropriate for teenagers who are sexually active and not using contraception.

The “biggest problem,” though, is the issue of whether methotrexate is effective, since it doesn’t always work for AD, Dr. Kirkorian said. “Even at the highest doses, I often feel that we fail the atopic children,” as opposed to using it to treat psoriasis, “where you know I’m going to get you on something that works.”

In contrast, cyclosporine is FDA approved down to infancy, and works quickly as a bridge to other therapy, and is not expensive, Dr. Kirkorian said. Cons include the need for blood draws, blood pressure checks, drug interactions, and adverse effects, she noted, adding that she tries to use cyclosporine as a bridge to on-label and off-label dupilumab.

Even with FDA approval for dupilumab down to age 12 years, she said it can be difficult to get insurance approval for the on-label treatment for patients in this age group with AD, before they first fail other therapies (even with off-label systemic drugs). For patients under age 12 years, getting approval is even more challenging and requires rigorous documentation of what therapies the child has failed, and how it has affected their quality of life, she said.

“If you send in a letter to the insurance company without an IGA [Investigator Global Assessment] or SCORAD, you’re going to get rejected,” Dr. Kirkorian said. In addition to those two measures, she provides “everything else,” including the impact of the disease on quality of life of patients, and school, she said, adding, “Did they miss school, did they get hospitalized for infections? And do they have comorbid diseases that might help you get approval?”

In pediatric patients with psoriasis, common issues are more likely to be about how insurance dictates step therapy. She has often found that young children may stop responding to etanercept after a few years, which can justify a switch to ustekinumab or a new treatment in a clinical trial, she said. Adolescents with psoriasis can receive ustekinumab, which is approved for psoriasis in patients aged 12-17 years, she said, noting that the infrequent ustekinumab dosing schedule is often beneficial in this population.

When all other approved options fail for young patients with psoriasis, justifying off-label use isn’t always easy. “You just have to make a justification based on the literature, even though it’s off label,” citing available safety information for other diseases, and “demonstrate over and over the impact on quality of life,” which works “most of the time,” Dr. Kirkorian said.

She reported having no conflicts of interest.

ORLANDO – Because Food and Drug Administration–approved treatment options for children and adolescents with severe dermatologic diseases are limited, systemic therapies for these patients often require the use of off-label medications. However, this scenario is changing, A. Yasmine Kirkorian, MD, said at the ODAC Dermatology, Aesthetic & Surgical Conference.

Jeff Craven/MDedge News

“I really would like to emphasize that children with severe disease need to be treated,” added Dr. Kirkorian, a pediatric dermatologist at George Washington University, Washington, and Children’s National Health System, where she is interim chief of the division of dermatology.

Current on-label systemic therapies for pediatric skin disease include etanercept for psoriasis (4 years and older), ustekinumab for psoriasis (12 years and older), adalimumab for hidradenitis suppurativa (12 years and older), and omalizumab for chronic idiopathic urticaria (12 years and older). A new addition to the list is dupilumab, which was approved for children and adolescents with atopic dermatitis (AD) aged 12 years and older in 2019, she noted.

Dupilumab is currently being studied in children aged 6 months to 12 years, and other clinical trials are evaluating more options for pediatric patients with AD, alopecia areata, and psoriasis. They include a clinical trial of the oral Janus kinase 3 (JAK3) inhibitor PF-06651600 in patients aged 12 years and older with alopecia areata. Six biologic therapies are being evaluated for psoriasis in patients beginning at 6 years: ixekizumab, secukinumab, ustekinumab, guselkumab, brodalumab, and apremilast.

Some systemic therapies are off-label “but used all the time” for dermatologic diseases in pediatrics, Dr. Kirkorian noted. One example is methotrexate, which is approved by the FDA for acute lymphoblastic leukemia, meningeal leukemia, and juvenile idiopathic arthritis down to infancy. Having existing efficacy and safety data for a medication in a pediatric population, even for a different disease, can be helpful when counseling parents of children with severe dermatologic disease. “If you have something, even in an older population of children, it can be reassuring, or you can use evidence from other diseases,” she said.

While methotrexate is a cheap option and approved by the FDA for other pediatric indications down to infancy, the cons of using it to treat AD in pediatric patients are numerous. Treatment requires a number of blood draws for lab testing, which can be discouraging for younger patients, and the reported adverse effect profile may be concerning to some parents, while “in practice doesn’t really occur,” she said. Methotrexate is a teratogen so is not appropriate for teenagers who are sexually active and not using contraception.

The “biggest problem,” though, is the issue of whether methotrexate is effective, since it doesn’t always work for AD, Dr. Kirkorian said. “Even at the highest doses, I often feel that we fail the atopic children,” as opposed to using it to treat psoriasis, “where you know I’m going to get you on something that works.”

In contrast, cyclosporine is FDA approved down to infancy, and works quickly as a bridge to other therapy, and is not expensive, Dr. Kirkorian said. Cons include the need for blood draws, blood pressure checks, drug interactions, and adverse effects, she noted, adding that she tries to use cyclosporine as a bridge to on-label and off-label dupilumab.

Even with FDA approval for dupilumab down to age 12 years, she said it can be difficult to get insurance approval for the on-label treatment for patients in this age group with AD, before they first fail other therapies (even with off-label systemic drugs). For patients under age 12 years, getting approval is even more challenging and requires rigorous documentation of what therapies the child has failed, and how it has affected their quality of life, she said.

“If you send in a letter to the insurance company without an IGA [Investigator Global Assessment] or SCORAD, you’re going to get rejected,” Dr. Kirkorian said. In addition to those two measures, she provides “everything else,” including the impact of the disease on quality of life of patients, and school, she said, adding, “Did they miss school, did they get hospitalized for infections? And do they have comorbid diseases that might help you get approval?”

In pediatric patients with psoriasis, common issues are more likely to be about how insurance dictates step therapy. She has often found that young children may stop responding to etanercept after a few years, which can justify a switch to ustekinumab or a new treatment in a clinical trial, she said. Adolescents with psoriasis can receive ustekinumab, which is approved for psoriasis in patients aged 12-17 years, she said, noting that the infrequent ustekinumab dosing schedule is often beneficial in this population.

When all other approved options fail for young patients with psoriasis, justifying off-label use isn’t always easy. “You just have to make a justification based on the literature, even though it’s off label,” citing available safety information for other diseases, and “demonstrate over and over the impact on quality of life,” which works “most of the time,” Dr. Kirkorian said.

She reported having no conflicts of interest.

ORLANDO – Because Food and Drug Administration–approved treatment options for children and adolescents with severe dermatologic diseases are limited, systemic therapies for these patients often require the use of off-label medications. However, this scenario is changing, A. Yasmine Kirkorian, MD, said at the ODAC Dermatology, Aesthetic & Surgical Conference.

Jeff Craven/MDedge News

“I really would like to emphasize that children with severe disease need to be treated,” added Dr. Kirkorian, a pediatric dermatologist at George Washington University, Washington, and Children’s National Health System, where she is interim chief of the division of dermatology.

Current on-label systemic therapies for pediatric skin disease include etanercept for psoriasis (4 years and older), ustekinumab for psoriasis (12 years and older), adalimumab for hidradenitis suppurativa (12 years and older), and omalizumab for chronic idiopathic urticaria (12 years and older). A new addition to the list is dupilumab, which was approved for children and adolescents with atopic dermatitis (AD) aged 12 years and older in 2019, she noted.

Dupilumab is currently being studied in children aged 6 months to 12 years, and other clinical trials are evaluating more options for pediatric patients with AD, alopecia areata, and psoriasis. They include a clinical trial of the oral Janus kinase 3 (JAK3) inhibitor PF-06651600 in patients aged 12 years and older with alopecia areata. Six biologic therapies are being evaluated for psoriasis in patients beginning at 6 years: ixekizumab, secukinumab, ustekinumab, guselkumab, brodalumab, and apremilast.

Some systemic therapies are off-label “but used all the time” for dermatologic diseases in pediatrics, Dr. Kirkorian noted. One example is methotrexate, which is approved by the FDA for acute lymphoblastic leukemia, meningeal leukemia, and juvenile idiopathic arthritis down to infancy. Having existing efficacy and safety data for a medication in a pediatric population, even for a different disease, can be helpful when counseling parents of children with severe dermatologic disease. “If you have something, even in an older population of children, it can be reassuring, or you can use evidence from other diseases,” she said.

While methotrexate is a cheap option and approved by the FDA for other pediatric indications down to infancy, the cons of using it to treat AD in pediatric patients are numerous. Treatment requires a number of blood draws for lab testing, which can be discouraging for younger patients, and the reported adverse effect profile may be concerning to some parents, while “in practice doesn’t really occur,” she said. Methotrexate is a teratogen so is not appropriate for teenagers who are sexually active and not using contraception.

The “biggest problem,” though, is the issue of whether methotrexate is effective, since it doesn’t always work for AD, Dr. Kirkorian said. “Even at the highest doses, I often feel that we fail the atopic children,” as opposed to using it to treat psoriasis, “where you know I’m going to get you on something that works.”

In contrast, cyclosporine is FDA approved down to infancy, and works quickly as a bridge to other therapy, and is not expensive, Dr. Kirkorian said. Cons include the need for blood draws, blood pressure checks, drug interactions, and adverse effects, she noted, adding that she tries to use cyclosporine as a bridge to on-label and off-label dupilumab.

Even with FDA approval for dupilumab down to age 12 years, she said it can be difficult to get insurance approval for the on-label treatment for patients in this age group with AD, before they first fail other therapies (even with off-label systemic drugs). For patients under age 12 years, getting approval is even more challenging and requires rigorous documentation of what therapies the child has failed, and how it has affected their quality of life, she said.

“If you send in a letter to the insurance company without an IGA [Investigator Global Assessment] or SCORAD, you’re going to get rejected,” Dr. Kirkorian said. In addition to those two measures, she provides “everything else,” including the impact of the disease on quality of life of patients, and school, she said, adding, “Did they miss school, did they get hospitalized for infections? And do they have comorbid diseases that might help you get approval?”

In pediatric patients with psoriasis, common issues are more likely to be about how insurance dictates step therapy. She has often found that young children may stop responding to etanercept after a few years, which can justify a switch to ustekinumab or a new treatment in a clinical trial, she said. Adolescents with psoriasis can receive ustekinumab, which is approved for psoriasis in patients aged 12-17 years, she said, noting that the infrequent ustekinumab dosing schedule is often beneficial in this population.

When all other approved options fail for young patients with psoriasis, justifying off-label use isn’t always easy. “You just have to make a justification based on the literature, even though it’s off label,” citing available safety information for other diseases, and “demonstrate over and over the impact on quality of life,” which works “most of the time,” Dr. Kirkorian said.

She reported having no conflicts of interest.

A biopsy of the skin was consistent with folliculitis, but a dental panoramic x-ray revealed an abscess of tooth number 30, which is on the right side. This combination of findings was consistent with a dental sinus.

This unusual diagnosis is most common in adults and arises from dental disease in the mid mandibular pre-molars. It will appear as an abscess or crusted papule and can occur in the lower jaw, neck, or occasionally, the mid cheek. Children are rarely affected. Because the sinus opening relieves pressure from the dental abscess, there is often little to no pain.

It can be challenging to convince a patient that his or her skin lesion derives from dental disease. Often, though, patients are glad it is not cancer. Patients should be referred to an endodontist for a work-up and a root canal, which is the preferred treatment. If a root canal is not feasible, dental extraction will lead to cure.

In this case, the patient promptly underwent a root canal and was cured in 2 weeks. The scar from the papule can have a depressed appearance (FIGURE 2), which can be addressed with excisional scar revision once the underlying abscess is cured.

‌

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 biopsy of the skin was consistent with folliculitis, but a dental panoramic x-ray revealed an abscess of tooth number 30, which is on the right side. This combination of findings was consistent with a dental sinus.

This unusual diagnosis is most common in adults and arises from dental disease in the mid mandibular pre-molars. It will appear as an abscess or crusted papule and can occur in the lower jaw, neck, or occasionally, the mid cheek. Children are rarely affected. Because the sinus opening relieves pressure from the dental abscess, there is often little to no pain.

It can be challenging to convince a patient that his or her skin lesion derives from dental disease. Often, though, patients are glad it is not cancer. Patients should be referred to an endodontist for a work-up and a root canal, which is the preferred treatment. If a root canal is not feasible, dental extraction will lead to cure.

In this case, the patient promptly underwent a root canal and was cured in 2 weeks. The scar from the papule can have a depressed appearance (FIGURE 2), which can be addressed with excisional scar revision once the underlying abscess is cured.

‌

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 biopsy of the skin was consistent with folliculitis, but a dental panoramic x-ray revealed an abscess of tooth number 30, which is on the right side. This combination of findings was consistent with a dental sinus.

This unusual diagnosis is most common in adults and arises from dental disease in the mid mandibular pre-molars. It will appear as an abscess or crusted papule and can occur in the lower jaw, neck, or occasionally, the mid cheek. Children are rarely affected. Because the sinus opening relieves pressure from the dental abscess, there is often little to no pain.

It can be challenging to convince a patient that his or her skin lesion derives from dental disease. Often, though, patients are glad it is not cancer. Patients should be referred to an endodontist for a work-up and a root canal, which is the preferred treatment. If a root canal is not feasible, dental extraction will lead to cure.

In this case, the patient promptly underwent a root canal and was cured in 2 weeks. The scar from the papule can have a depressed appearance (FIGURE 2), which can be addressed with excisional scar revision once the underlying abscess is cured.

‌

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.

Imagine a patient suffering with horrible psoriasis for decades having failed “every available treatment.” Imagine him living all that time with “flaking, cracking, painful, itchy skin,” only to develop cirrhosis after exposure to toxic therapies.

Then imagine the experience for that patient when, 2 weeks after initiating treatment with a new interleukin-17 inhibitor, his skin clears completely.

“Two weeks later it’s all gone – it was a moment to behold,” said Joel M. Gelfand, MD, professor of dermatology and epidemiology at the University of Pennsylvania, Philadelphia, who had cared for the man for many years before a psoriasis treatment revolution of sorts took the field of dermatology by storm.

“The progress has been breathtaking – there’s no other way to describe it – and it feels like a miracle every time I see a new patient who has tough disease and I have all these things to offer them,” he continued. “For most patients, I can really help them and make a major difference in their life.”

Much of the progress in psoriasis treatment in the past 50 years unfolded over the past 2 decades, with biologics emerging for psoriasis, said Mark Lebwohl, MD, Waldman professor of dermatology and chair of the Kimberly and Eric J. Waldman department of dermatology at the Icahn School of Medicine at Mount Sinai, New York.

Dr. Lebwohl recounted some of his own experiences with psoriasis patients before the advent of treatments – particularly biologics – that have transformed practice.

There was a time when psoriasis patients had little more to turn to than the effective – but “disgusting” – Goeckerman Regimen involving cycles of UVB light exposure and topical crude coal tar application. Initially, the regimen, which was introduced in the 1920s, was used around the clock on an inpatient basis until the skin cleared, Dr. Lebwohl said.

In the 1970s, the immunosuppressive chemotherapy drug methotrexate became the first oral systemic therapy approved for severe psoriasis. For those with disabling disease, it offered some hope for relief, but only about 40% of patients achieved at least a 75% reduction in the Psoriasis Area and Severity Index score (PASI 75), he said, adding that they did so at the expense of the liver and bone marrow. “But it was the only thing we had for severe psoriasis other than light treatments.”

In the 1980s and 1990s, oral retinoids emerged as a treatment for psoriasis, and the immunosuppressive drug cyclosporine used to prevent organ rejection in some transplant patients was found to clear psoriasis in affected transplant recipients. Although they brought relief to some patients with severe, disabling disease, these also came with a high price. “It’s not that effective, and it has lots of side effects ... and causes kidney damage in essentially 100% of patients,” Dr. Lebwohl said of cyclosporine.

“So we had treatments that worked, but because the side effects were sufficiently severe, a lot of patients were not treated,” he said.

Enter the biologics era

The early 2000s brought the first two approvals for psoriasis: alefacept (Amevive), a “modestly effective, but quite safe” immunosuppressive dimeric fusion protein approved in early 2003 for moderate to severe plaque psoriasis, and efalizumab (Raptiva), a recombinant humanized monoclonal antibody approved in October 2003; both were T-cell–targeted therapies. The former was withdrawn from the market voluntarily as newer agents became available, and the latter was withdrawn in 2009 because of a link with development of progressive multifocal leukoencephalopathy.

Tumor necrosis factor (TNF) blockers, which had been used effectively for RA and Crohn’s disease, emerged next, and were highly effective, much safer than the systemic treatments, and gained “very widespread use,” Dr. Lebwohl said.

Alan Menter, MD, chairman of the division of dermatology at Baylor University Medical Center, Dallas, also a prolific researcher – and chair of the guidelines committee that published two new sets of guidelines for psoriasis treatment in 2019 – said that the field of dermatology was “late to the biologic evolution,” as many of the early biologics were first approved for PsA.

“But over the last 10 years, things have changed dramatically,” he said. “After that we suddenly leapt ahead of everybody. ... We now have 11 biologic drugs approved for psoriasis, which is more than any other disease has available.”

It’s been “highly exciting” to see this “evolution and revolution,” he commented, adding that one of the next challenges is to address the comorbidities, such as cardiovascular disease, associated with psoriasis.

“The big question now ... is if you improve skin and you improve joints, can you potentially reduce the risk of coronary artery disease,” he said. “Everybody is looking at that, and to me it’s one of the most exciting things that we’re doing.”

Work is ongoing to look at whether the IL-17s and IL-23s have “other indications outside of the skin and joints,” both within and outside of dermatology.

Like Dr. Gottlieb, Dr. Menter also mentioned the potential for hidradenitis suppurativa, and also for a condition that is rarely discussed or studied: genital psoriasis. Ixekizumab has recently been shown to work in about 75% of patients with genital psoriasis, he noted.

Another important area of research is the identification of biomarkers for predicting response and relapse, he said. For now, biomarker research has disappointed, he added, predicting that it will take at least 3-5 years before biomarkers to help guide treatment are identified.

Indeed, Dr. Gelfand, who also is director of the Psoriasis and Phototherapy Treatment Center, vice chair of clinical research, and medical director of the dermatology clinical studies unit at the University of Pennsylvania, agreed there is a need for research to improve treatment selection.

Advances are being made in genetics – with more than 80 different genes now identified as being related to psoriasis – and in medical informatics – which allow thousands of patients to be followed for years, he said, noting that this could elucidate immunopathological features that can improve treatments, predict and prevent comorbidity, and further improve outcomes.

“We also need care that is more patient centered,” he said, describing the ongoing pragmatic LITE trial of home- or office-based phototherapy for which he is the lead investigator, and other studies that he hopes will expand access to care.

Kenneth Brian Gordon, MD, chair and professor of dermatology at the Medical College of Wisconsin, Milwaukee, whose career started in the basic science immunology arena, added the need for expanding benefit to patients with more-moderate disease. Like Dr. Menter, he identified psoriasis as the area in medicine that has had the greatest degree of advancement, except perhaps for hepatitis C.

He described the process not as a “bench-to-bedside” story, but as a bedside-to-bench, then “back-to-bedside” story.

It was really about taking those early T-cell–targeted biologics and anti-TNF agents from bedside to bench with the realization of the importance of the IL-23 and IL-17 pathways, and that understanding led back to the bedside with the development of the newest agents – and to a “huge difference in patient’s lives.”

“But we’ve gotten so good at treating patients with severe disease ... the question now is how to take care of those with more-moderate disease,” he said, noting that a focus on cost and better delivery systems will be needed for that population.

That research is underway, and the future looks bright – and clear.
 

“I think with psoriasis therapy and where we’ve come in the last 20 years ... we have a hard time remembering what it was like before we had biologic agents” he said. “Our perspective has changed a lot, and sometimes we forget that.”

In fact, “psoriasis has sort of dragged dermatology into the world of modern clinical trial science, and we can now apply that to all sorts of other diseases,” he said. “The psoriasis trials were the first really well-done large-scale trials in dermatology, and I think that has given dermatology a real leg up in how we do clinical research and how we do evidence-based medicine.”

All of the doctors interviewed for this story have received funds and/or honoraria from, consulted with, are employed with, or served on the advisory boards of manufacturers of biologics. Dr. Gelfand is a copatent holder of resiquimod for treatment of cutaneous T-cell lymphoma and is deputy editor of the Journal of Investigative Dermatology.

[email protected]
 

Imagine a patient suffering with horrible psoriasis for decades having failed “every available treatment.” Imagine him living all that time with “flaking, cracking, painful, itchy skin,” only to develop cirrhosis after exposure to toxic therapies.

Then imagine the experience for that patient when, 2 weeks after initiating treatment with a new interleukin-17 inhibitor, his skin clears completely.

“Two weeks later it’s all gone – it was a moment to behold,” said Joel M. Gelfand, MD, professor of dermatology and epidemiology at the University of Pennsylvania, Philadelphia, who had cared for the man for many years before a psoriasis treatment revolution of sorts took the field of dermatology by storm.

“The progress has been breathtaking – there’s no other way to describe it – and it feels like a miracle every time I see a new patient who has tough disease and I have all these things to offer them,” he continued. “For most patients, I can really help them and make a major difference in their life.”

Much of the progress in psoriasis treatment in the past 50 years unfolded over the past 2 decades, with biologics emerging for psoriasis, said Mark Lebwohl, MD, Waldman professor of dermatology and chair of the Kimberly and Eric J. Waldman department of dermatology at the Icahn School of Medicine at Mount Sinai, New York.

Dr. Lebwohl recounted some of his own experiences with psoriasis patients before the advent of treatments – particularly biologics – that have transformed practice.

There was a time when psoriasis patients had little more to turn to than the effective – but “disgusting” – Goeckerman Regimen involving cycles of UVB light exposure and topical crude coal tar application. Initially, the regimen, which was introduced in the 1920s, was used around the clock on an inpatient basis until the skin cleared, Dr. Lebwohl said.

In the 1970s, the immunosuppressive chemotherapy drug methotrexate became the first oral systemic therapy approved for severe psoriasis. For those with disabling disease, it offered some hope for relief, but only about 40% of patients achieved at least a 75% reduction in the Psoriasis Area and Severity Index score (PASI 75), he said, adding that they did so at the expense of the liver and bone marrow. “But it was the only thing we had for severe psoriasis other than light treatments.”

In the 1980s and 1990s, oral retinoids emerged as a treatment for psoriasis, and the immunosuppressive drug cyclosporine used to prevent organ rejection in some transplant patients was found to clear psoriasis in affected transplant recipients. Although they brought relief to some patients with severe, disabling disease, these also came with a high price. “It’s not that effective, and it has lots of side effects ... and causes kidney damage in essentially 100% of patients,” Dr. Lebwohl said of cyclosporine.

“So we had treatments that worked, but because the side effects were sufficiently severe, a lot of patients were not treated,” he said.

Enter the biologics era

The early 2000s brought the first two approvals for psoriasis: alefacept (Amevive), a “modestly effective, but quite safe” immunosuppressive dimeric fusion protein approved in early 2003 for moderate to severe plaque psoriasis, and efalizumab (Raptiva), a recombinant humanized monoclonal antibody approved in October 2003; both were T-cell–targeted therapies. The former was withdrawn from the market voluntarily as newer agents became available, and the latter was withdrawn in 2009 because of a link with development of progressive multifocal leukoencephalopathy.

Tumor necrosis factor (TNF) blockers, which had been used effectively for RA and Crohn’s disease, emerged next, and were highly effective, much safer than the systemic treatments, and gained “very widespread use,” Dr. Lebwohl said.

Alan Menter, MD, chairman of the division of dermatology at Baylor University Medical Center, Dallas, also a prolific researcher – and chair of the guidelines committee that published two new sets of guidelines for psoriasis treatment in 2019 – said that the field of dermatology was “late to the biologic evolution,” as many of the early biologics were first approved for PsA.

“But over the last 10 years, things have changed dramatically,” he said. “After that we suddenly leapt ahead of everybody. ... We now have 11 biologic drugs approved for psoriasis, which is more than any other disease has available.”

It’s been “highly exciting” to see this “evolution and revolution,” he commented, adding that one of the next challenges is to address the comorbidities, such as cardiovascular disease, associated with psoriasis.

“The big question now ... is if you improve skin and you improve joints, can you potentially reduce the risk of coronary artery disease,” he said. “Everybody is looking at that, and to me it’s one of the most exciting things that we’re doing.”

Work is ongoing to look at whether the IL-17s and IL-23s have “other indications outside of the skin and joints,” both within and outside of dermatology.

Like Dr. Gottlieb, Dr. Menter also mentioned the potential for hidradenitis suppurativa, and also for a condition that is rarely discussed or studied: genital psoriasis. Ixekizumab has recently been shown to work in about 75% of patients with genital psoriasis, he noted.

Another important area of research is the identification of biomarkers for predicting response and relapse, he said. For now, biomarker research has disappointed, he added, predicting that it will take at least 3-5 years before biomarkers to help guide treatment are identified.

Indeed, Dr. Gelfand, who also is director of the Psoriasis and Phototherapy Treatment Center, vice chair of clinical research, and medical director of the dermatology clinical studies unit at the University of Pennsylvania, agreed there is a need for research to improve treatment selection.

Advances are being made in genetics – with more than 80 different genes now identified as being related to psoriasis – and in medical informatics – which allow thousands of patients to be followed for years, he said, noting that this could elucidate immunopathological features that can improve treatments, predict and prevent comorbidity, and further improve outcomes.

“We also need care that is more patient centered,” he said, describing the ongoing pragmatic LITE trial of home- or office-based phototherapy for which he is the lead investigator, and other studies that he hopes will expand access to care.

Kenneth Brian Gordon, MD, chair and professor of dermatology at the Medical College of Wisconsin, Milwaukee, whose career started in the basic science immunology arena, added the need for expanding benefit to patients with more-moderate disease. Like Dr. Menter, he identified psoriasis as the area in medicine that has had the greatest degree of advancement, except perhaps for hepatitis C.

He described the process not as a “bench-to-bedside” story, but as a bedside-to-bench, then “back-to-bedside” story.

It was really about taking those early T-cell–targeted biologics and anti-TNF agents from bedside to bench with the realization of the importance of the IL-23 and IL-17 pathways, and that understanding led back to the bedside with the development of the newest agents – and to a “huge difference in patient’s lives.”

“But we’ve gotten so good at treating patients with severe disease ... the question now is how to take care of those with more-moderate disease,” he said, noting that a focus on cost and better delivery systems will be needed for that population.

That research is underway, and the future looks bright – and clear.
 

“I think with psoriasis therapy and where we’ve come in the last 20 years ... we have a hard time remembering what it was like before we had biologic agents” he said. “Our perspective has changed a lot, and sometimes we forget that.”

In fact, “psoriasis has sort of dragged dermatology into the world of modern clinical trial science, and we can now apply that to all sorts of other diseases,” he said. “The psoriasis trials were the first really well-done large-scale trials in dermatology, and I think that has given dermatology a real leg up in how we do clinical research and how we do evidence-based medicine.”

All of the doctors interviewed for this story have received funds and/or honoraria from, consulted with, are employed with, or served on the advisory boards of manufacturers of biologics. Dr. Gelfand is a copatent holder of resiquimod for treatment of cutaneous T-cell lymphoma and is deputy editor of the Journal of Investigative Dermatology.

[email protected]
 

Imagine a patient suffering with horrible psoriasis for decades having failed “every available treatment.” Imagine him living all that time with “flaking, cracking, painful, itchy skin,” only to develop cirrhosis after exposure to toxic therapies.

Then imagine the experience for that patient when, 2 weeks after initiating treatment with a new interleukin-17 inhibitor, his skin clears completely.

“Two weeks later it’s all gone – it was a moment to behold,” said Joel M. Gelfand, MD, professor of dermatology and epidemiology at the University of Pennsylvania, Philadelphia, who had cared for the man for many years before a psoriasis treatment revolution of sorts took the field of dermatology by storm.

“The progress has been breathtaking – there’s no other way to describe it – and it feels like a miracle every time I see a new patient who has tough disease and I have all these things to offer them,” he continued. “For most patients, I can really help them and make a major difference in their life.”

Much of the progress in psoriasis treatment in the past 50 years unfolded over the past 2 decades, with biologics emerging for psoriasis, said Mark Lebwohl, MD, Waldman professor of dermatology and chair of the Kimberly and Eric J. Waldman department of dermatology at the Icahn School of Medicine at Mount Sinai, New York.

Dr. Lebwohl recounted some of his own experiences with psoriasis patients before the advent of treatments – particularly biologics – that have transformed practice.

There was a time when psoriasis patients had little more to turn to than the effective – but “disgusting” – Goeckerman Regimen involving cycles of UVB light exposure and topical crude coal tar application. Initially, the regimen, which was introduced in the 1920s, was used around the clock on an inpatient basis until the skin cleared, Dr. Lebwohl said.

In the 1970s, the immunosuppressive chemotherapy drug methotrexate became the first oral systemic therapy approved for severe psoriasis. For those with disabling disease, it offered some hope for relief, but only about 40% of patients achieved at least a 75% reduction in the Psoriasis Area and Severity Index score (PASI 75), he said, adding that they did so at the expense of the liver and bone marrow. “But it was the only thing we had for severe psoriasis other than light treatments.”

In the 1980s and 1990s, oral retinoids emerged as a treatment for psoriasis, and the immunosuppressive drug cyclosporine used to prevent organ rejection in some transplant patients was found to clear psoriasis in affected transplant recipients. Although they brought relief to some patients with severe, disabling disease, these also came with a high price. “It’s not that effective, and it has lots of side effects ... and causes kidney damage in essentially 100% of patients,” Dr. Lebwohl said of cyclosporine.

“So we had treatments that worked, but because the side effects were sufficiently severe, a lot of patients were not treated,” he said.

Enter the biologics era

The early 2000s brought the first two approvals for psoriasis: alefacept (Amevive), a “modestly effective, but quite safe” immunosuppressive dimeric fusion protein approved in early 2003 for moderate to severe plaque psoriasis, and efalizumab (Raptiva), a recombinant humanized monoclonal antibody approved in October 2003; both were T-cell–targeted therapies. The former was withdrawn from the market voluntarily as newer agents became available, and the latter was withdrawn in 2009 because of a link with development of progressive multifocal leukoencephalopathy.

Tumor necrosis factor (TNF) blockers, which had been used effectively for RA and Crohn’s disease, emerged next, and were highly effective, much safer than the systemic treatments, and gained “very widespread use,” Dr. Lebwohl said.

Alan Menter, MD, chairman of the division of dermatology at Baylor University Medical Center, Dallas, also a prolific researcher – and chair of the guidelines committee that published two new sets of guidelines for psoriasis treatment in 2019 – said that the field of dermatology was “late to the biologic evolution,” as many of the early biologics were first approved for PsA.

“But over the last 10 years, things have changed dramatically,” he said. “After that we suddenly leapt ahead of everybody. ... We now have 11 biologic drugs approved for psoriasis, which is more than any other disease has available.”

It’s been “highly exciting” to see this “evolution and revolution,” he commented, adding that one of the next challenges is to address the comorbidities, such as cardiovascular disease, associated with psoriasis.

“The big question now ... is if you improve skin and you improve joints, can you potentially reduce the risk of coronary artery disease,” he said. “Everybody is looking at that, and to me it’s one of the most exciting things that we’re doing.”

Work is ongoing to look at whether the IL-17s and IL-23s have “other indications outside of the skin and joints,” both within and outside of dermatology.

Like Dr. Gottlieb, Dr. Menter also mentioned the potential for hidradenitis suppurativa, and also for a condition that is rarely discussed or studied: genital psoriasis. Ixekizumab has recently been shown to work in about 75% of patients with genital psoriasis, he noted.

Another important area of research is the identification of biomarkers for predicting response and relapse, he said. For now, biomarker research has disappointed, he added, predicting that it will take at least 3-5 years before biomarkers to help guide treatment are identified.

Indeed, Dr. Gelfand, who also is director of the Psoriasis and Phototherapy Treatment Center, vice chair of clinical research, and medical director of the dermatology clinical studies unit at the University of Pennsylvania, agreed there is a need for research to improve treatment selection.

Advances are being made in genetics – with more than 80 different genes now identified as being related to psoriasis – and in medical informatics – which allow thousands of patients to be followed for years, he said, noting that this could elucidate immunopathological features that can improve treatments, predict and prevent comorbidity, and further improve outcomes.

“We also need care that is more patient centered,” he said, describing the ongoing pragmatic LITE trial of home- or office-based phototherapy for which he is the lead investigator, and other studies that he hopes will expand access to care.

Kenneth Brian Gordon, MD, chair and professor of dermatology at the Medical College of Wisconsin, Milwaukee, whose career started in the basic science immunology arena, added the need for expanding benefit to patients with more-moderate disease. Like Dr. Menter, he identified psoriasis as the area in medicine that has had the greatest degree of advancement, except perhaps for hepatitis C.

He described the process not as a “bench-to-bedside” story, but as a bedside-to-bench, then “back-to-bedside” story.

It was really about taking those early T-cell–targeted biologics and anti-TNF agents from bedside to bench with the realization of the importance of the IL-23 and IL-17 pathways, and that understanding led back to the bedside with the development of the newest agents – and to a “huge difference in patient’s lives.”

“But we’ve gotten so good at treating patients with severe disease ... the question now is how to take care of those with more-moderate disease,” he said, noting that a focus on cost and better delivery systems will be needed for that population.

That research is underway, and the future looks bright – and clear.
 

“I think with psoriasis therapy and where we’ve come in the last 20 years ... we have a hard time remembering what it was like before we had biologic agents” he said. “Our perspective has changed a lot, and sometimes we forget that.”

In fact, “psoriasis has sort of dragged dermatology into the world of modern clinical trial science, and we can now apply that to all sorts of other diseases,” he said. “The psoriasis trials were the first really well-done large-scale trials in dermatology, and I think that has given dermatology a real leg up in how we do clinical research and how we do evidence-based medicine.”

All of the doctors interviewed for this story have received funds and/or honoraria from, consulted with, are employed with, or served on the advisory boards of manufacturers of biologics. Dr. Gelfand is a copatent holder of resiquimod for treatment of cutaneous T-cell lymphoma and is deputy editor of the Journal of Investigative Dermatology.

[email protected]
 

ATLANTA – Psoriasis type and patient age at presentation among patients with psoriatic arthritis predict the timing of arthritis symptom synchronicity, according to findings from the Psoriatic Arthritis Registry of Turkey International Database.

Sharon Worcester/MDedge News

However, in those who develop arthritis symptoms first, age at onset is not predictive of psoriatic arthritis (PsA) symptom synchronicity, Umut Kalyoncu, MD, reported at the annual meeting of the American College of Rheumatology.

Of 1,631 patients from the registry, 1,251 had psoriasis first, 71 had arthritis first, and 309 had synchronous onset, which was defined as the onset of both psoriasis and arthritis symptoms within a 12-month period. The time from skin disease to PsA was 155.6 months, –67.4 months, and 1.8 months, among the groups, respectively, and the mean age at PsA onset was similar, ranging from about 41 to 42 years in those who developed arthritis first, said Dr. Kalyoncu, of the department of rheumatology at Hacettepe University, Ankara, Turkey.

However, the mean age of PsA onset among those who developed psoriasis first was 29.4 years, compared with 46.3 years in those who developed arthritis first.

“So there is a really big difference between psoriasis beginning age,” he said.

PsA types also differed by onset symptoms: Axial involvement was more common with arthritis-first onset at 38.0%, compared with 28.8% for psoriasis first and 27.8% for synchronous onset). Oligoarthritis occurred more often with arthritis-first onset (45.1% vs. 30.7% and 29.4%, respectively), and polyarthritis occurred less often with arthritis-first onset (33.8% vs. 49.4% and 47.6%, respectively), he said.

Psoriasis type also differed among the groups: Pustular skin involvement was more common in arthritis-first patients (18.3% vs. 11.9% and 16.5% of psoriasis-first and synchronous-onset patients), scalp lesions as the initial lesion were more common in psoriasis-first patients (48.3% vs. 35.2% of arthritis-first patients and 39.8% of synchronous-onset patients), and genital involvement was present more often in arthritis-first patients (12.7% vs. 6.2% and 4.9% of psoriasis-first and synchronous-onset patients).

Early-onset (type 1) psoriasis was more common in psoriasis-first patients (74% vs. 28.1% and 51.8% of arthritis-first and synchronous-onset patients), whereas late-onset (type 2) psoriasis was more common in arthritis-first patients (71.9% vs. 26.0% and 48.2% for psoriasis-first and synchronous-onset patients).

A family history of psoriasis or PsA was more common in psoriasis-first patients (35.6% vs. 26.3% and 28.2% of arthritis-first and synchronous-onset patients), Dr. Kalyoncu said.

Treatment types did not differ between the groups.

Multiple linear regression analysis for the time elapsed from psoriasis to PsA symptom synchronicity, with all other independent variables set to baseline values, showed an overall intercept interval of 66 months, but with nail involvement, family history, or plaque psoriasis, the interval was extended by 28, 24, and 20 months, respectively. However, the presence of pustular psoriasis decreased the intercept interval by 28 months.

A temporal relationship between the onset of skin psoriasis and PsA is a well-known feature of psoriatic disease, with prior studies showing that the majority of cases involve psoriasis-first onset, Dr. Kalyoncu said, adding that heterogeneity in musculoskeletal and skin involvement is also a known feature.

However, little is known about the role of genetics, he noted.

Therefore, he and his colleagues used the Psoriatic Arthritis Registry of Turkey International Database, which was established in 2014 and now also includes data from patients in Canada and Italy, to explore the associations between disease characteristics and the temporal relationship of skin and musculoskeletal disease.

Based on the findings, age at the onset of psoriasis was the main factor that determined PsA symptom synchronicity, he said.

“We know that HLA-Cw6 is important in genetic susceptibility of psoriatic arthritis, but it is important only for early-onset arthritis, not late-onset psoriasis,” Dr. Kalyoncu said. “So our results make an indirect contribution [to the understanding of] these genetic and immunochemical differences between early-onset and late-onset psoriasis, and we need further future studies about this topic.”

Dr. Kalyoncu reported having no relevant disclosures.

[email protected]

SOURCE: Kalyoncu U et al. Arthritis Rheumatol. 2019;71(suppl 10), Abstract 2854.

ATLANTA – Psoriasis type and patient age at presentation among patients with psoriatic arthritis predict the timing of arthritis symptom synchronicity, according to findings from the Psoriatic Arthritis Registry of Turkey International Database.

Sharon Worcester/MDedge News

However, in those who develop arthritis symptoms first, age at onset is not predictive of psoriatic arthritis (PsA) symptom synchronicity, Umut Kalyoncu, MD, reported at the annual meeting of the American College of Rheumatology.

Of 1,631 patients from the registry, 1,251 had psoriasis first, 71 had arthritis first, and 309 had synchronous onset, which was defined as the onset of both psoriasis and arthritis symptoms within a 12-month period. The time from skin disease to PsA was 155.6 months, –67.4 months, and 1.8 months, among the groups, respectively, and the mean age at PsA onset was similar, ranging from about 41 to 42 years in those who developed arthritis first, said Dr. Kalyoncu, of the department of rheumatology at Hacettepe University, Ankara, Turkey.

However, the mean age of PsA onset among those who developed psoriasis first was 29.4 years, compared with 46.3 years in those who developed arthritis first.

“So there is a really big difference between psoriasis beginning age,” he said.

PsA types also differed by onset symptoms: Axial involvement was more common with arthritis-first onset at 38.0%, compared with 28.8% for psoriasis first and 27.8% for synchronous onset). Oligoarthritis occurred more often with arthritis-first onset (45.1% vs. 30.7% and 29.4%, respectively), and polyarthritis occurred less often with arthritis-first onset (33.8% vs. 49.4% and 47.6%, respectively), he said.

Psoriasis type also differed among the groups: Pustular skin involvement was more common in arthritis-first patients (18.3% vs. 11.9% and 16.5% of psoriasis-first and synchronous-onset patients), scalp lesions as the initial lesion were more common in psoriasis-first patients (48.3% vs. 35.2% of arthritis-first patients and 39.8% of synchronous-onset patients), and genital involvement was present more often in arthritis-first patients (12.7% vs. 6.2% and 4.9% of psoriasis-first and synchronous-onset patients).

Early-onset (type 1) psoriasis was more common in psoriasis-first patients (74% vs. 28.1% and 51.8% of arthritis-first and synchronous-onset patients), whereas late-onset (type 2) psoriasis was more common in arthritis-first patients (71.9% vs. 26.0% and 48.2% for psoriasis-first and synchronous-onset patients).

A family history of psoriasis or PsA was more common in psoriasis-first patients (35.6% vs. 26.3% and 28.2% of arthritis-first and synchronous-onset patients), Dr. Kalyoncu said.

Treatment types did not differ between the groups.

Multiple linear regression analysis for the time elapsed from psoriasis to PsA symptom synchronicity, with all other independent variables set to baseline values, showed an overall intercept interval of 66 months, but with nail involvement, family history, or plaque psoriasis, the interval was extended by 28, 24, and 20 months, respectively. However, the presence of pustular psoriasis decreased the intercept interval by 28 months.

A temporal relationship between the onset of skin psoriasis and PsA is a well-known feature of psoriatic disease, with prior studies showing that the majority of cases involve psoriasis-first onset, Dr. Kalyoncu said, adding that heterogeneity in musculoskeletal and skin involvement is also a known feature.

However, little is known about the role of genetics, he noted.

Therefore, he and his colleagues used the Psoriatic Arthritis Registry of Turkey International Database, which was established in 2014 and now also includes data from patients in Canada and Italy, to explore the associations between disease characteristics and the temporal relationship of skin and musculoskeletal disease.

Based on the findings, age at the onset of psoriasis was the main factor that determined PsA symptom synchronicity, he said.

“We know that HLA-Cw6 is important in genetic susceptibility of psoriatic arthritis, but it is important only for early-onset arthritis, not late-onset psoriasis,” Dr. Kalyoncu said. “So our results make an indirect contribution [to the understanding of] these genetic and immunochemical differences between early-onset and late-onset psoriasis, and we need further future studies about this topic.”

Dr. Kalyoncu reported having no relevant disclosures.

[email protected]

SOURCE: Kalyoncu U et al. Arthritis Rheumatol. 2019;71(suppl 10), Abstract 2854.

ATLANTA – Psoriasis type and patient age at presentation among patients with psoriatic arthritis predict the timing of arthritis symptom synchronicity, according to findings from the Psoriatic Arthritis Registry of Turkey International Database.

Sharon Worcester/MDedge News

However, in those who develop arthritis symptoms first, age at onset is not predictive of psoriatic arthritis (PsA) symptom synchronicity, Umut Kalyoncu, MD, reported at the annual meeting of the American College of Rheumatology.

Of 1,631 patients from the registry, 1,251 had psoriasis first, 71 had arthritis first, and 309 had synchronous onset, which was defined as the onset of both psoriasis and arthritis symptoms within a 12-month period. The time from skin disease to PsA was 155.6 months, –67.4 months, and 1.8 months, among the groups, respectively, and the mean age at PsA onset was similar, ranging from about 41 to 42 years in those who developed arthritis first, said Dr. Kalyoncu, of the department of rheumatology at Hacettepe University, Ankara, Turkey.

However, the mean age of PsA onset among those who developed psoriasis first was 29.4 years, compared with 46.3 years in those who developed arthritis first.

“So there is a really big difference between psoriasis beginning age,” he said.

PsA types also differed by onset symptoms: Axial involvement was more common with arthritis-first onset at 38.0%, compared with 28.8% for psoriasis first and 27.8% for synchronous onset). Oligoarthritis occurred more often with arthritis-first onset (45.1% vs. 30.7% and 29.4%, respectively), and polyarthritis occurred less often with arthritis-first onset (33.8% vs. 49.4% and 47.6%, respectively), he said.

Psoriasis type also differed among the groups: Pustular skin involvement was more common in arthritis-first patients (18.3% vs. 11.9% and 16.5% of psoriasis-first and synchronous-onset patients), scalp lesions as the initial lesion were more common in psoriasis-first patients (48.3% vs. 35.2% of arthritis-first patients and 39.8% of synchronous-onset patients), and genital involvement was present more often in arthritis-first patients (12.7% vs. 6.2% and 4.9% of psoriasis-first and synchronous-onset patients).

Early-onset (type 1) psoriasis was more common in psoriasis-first patients (74% vs. 28.1% and 51.8% of arthritis-first and synchronous-onset patients), whereas late-onset (type 2) psoriasis was more common in arthritis-first patients (71.9% vs. 26.0% and 48.2% for psoriasis-first and synchronous-onset patients).

A family history of psoriasis or PsA was more common in psoriasis-first patients (35.6% vs. 26.3% and 28.2% of arthritis-first and synchronous-onset patients), Dr. Kalyoncu said.

Treatment types did not differ between the groups.

Multiple linear regression analysis for the time elapsed from psoriasis to PsA symptom synchronicity, with all other independent variables set to baseline values, showed an overall intercept interval of 66 months, but with nail involvement, family history, or plaque psoriasis, the interval was extended by 28, 24, and 20 months, respectively. However, the presence of pustular psoriasis decreased the intercept interval by 28 months.

A temporal relationship between the onset of skin psoriasis and PsA is a well-known feature of psoriatic disease, with prior studies showing that the majority of cases involve psoriasis-first onset, Dr. Kalyoncu said, adding that heterogeneity in musculoskeletal and skin involvement is also a known feature.

However, little is known about the role of genetics, he noted.

Therefore, he and his colleagues used the Psoriatic Arthritis Registry of Turkey International Database, which was established in 2014 and now also includes data from patients in Canada and Italy, to explore the associations between disease characteristics and the temporal relationship of skin and musculoskeletal disease.

Based on the findings, age at the onset of psoriasis was the main factor that determined PsA symptom synchronicity, he said.

“We know that HLA-Cw6 is important in genetic susceptibility of psoriatic arthritis, but it is important only for early-onset arthritis, not late-onset psoriasis,” Dr. Kalyoncu said. “So our results make an indirect contribution [to the understanding of] these genetic and immunochemical differences between early-onset and late-onset psoriasis, and we need further future studies about this topic.”

Dr. Kalyoncu reported having no relevant disclosures.

[email protected]

SOURCE: Kalyoncu U et al. Arthritis Rheumatol. 2019;71(suppl 10), Abstract 2854.

Hand infections, if not treated properly, can cause severe chronic morbidity. The conditions I review here range from superficial to deep seated: herpetic whitlow located in the epidermis; felon in subcutaneous tissue; pyogenic flexor tenosynovitis (FTS) in the tendon sheath; and human bite infection at any level including possibly synovium and bone.

Superficial infections usually respond to nonsurgical management. However, antimicrobial therapy is not straightforward. There is no single regimen that covers all possible pathogens. Combination therapy must usually be started and then tailored once an organism and its susceptibility are known. Subcutaneous, tendon sheath, synovial, and bone infections frequently require surgical management.

Herpetic whitlow

Herpes simplex virus type 1 (HSV-1) is common, with as much as 90% of the population exposed by 60 years of age.¹ Initial infection usually occurs in the oropharynx and is known as a fever blister or cold sore. However, HSV-1 also can cause herpetic whitlow, a primary infection in the fingertip in which the virus penetrates the subcutaneous tissue, usually after a breakdown in the skin barrier either from infected saliva or the lips of an infected individual.¹

What you’ll see. The lesion is characterized by pain, swelling, erythema, and nonpurulent vesicle formation ­(FIGURE 1). The condition is usually self-limiting, with the inflammation resolving spontaneously, leaving normal healthy skin within 1 to 2 weeks. Herpetic whitlow is an occupational hazard for medical, nursing, paramedical, and dental personnel, and standard precautions should be used when handling secretions (Strength of Recommendation [SOR]: A).²

Herpetic whitlow is distinguished from a felon by its formation of vesicles, lack of a tense pulp space, and serous, not purulent, drainage.

Reactivation of HSV-1 (and HSV-2) is common, with a prodrome of a “tingling sensation” and subsequent blister formation in the same location as the previous infection. It can cause pain and discomfort and may render the individual unable to perform usual activities.^1,3 This lesion is often confused with bacterial (pyogenic) infections of the pulp of the finger or thumb (felon).¹ Herpetic whitlow can be distinguished from a felon by its formation of vesicles, lack of a tense pulp space, and serous, rather than purulent, drainage. Scarring is not associated with herpes infection because penetration is limited to the epidermal area. Superimposed bacterial infection can be mistaken for an abscess (felon) and lead to unnecessary incision and drainage, causing associated morbidity and potential scarring in the affected area.¹

How it’s treated. Treatment of herpetic whitlow is usually conservative, and topical application of acyclovir 5% appears to be beneficial (SOR: C).⁴ Two studies also suggest that oral acyclovir is beneficial for herpetic whitlow and may reduce the frequency of recurrence.^5,6 Controlled studies in the use of acyclovir for herpetic whitlow have not been conducted. Despite a lack of direct evidence, acyclovir, famciclovir, and valacyclovir are accepted therapies for herpetic whitlow (TABLE 1⁷) (SOR: B).^6,8

Felon

A felon is a closed-space infection affecting the pulp of the fingers or thumb. The anatomy of the finger is unique in that there are multiple septa attaching the periosteum to the skin, thereby creating several closed spaces prone to develop pockets of infection.

Continue to: What you'll see

What you’ll see. Clinical signs and symptoms include pain in the pulp of the finger with tenderness and swelling. Bacteria are usually introduced into fingertip space (fat pad) by a penetrating object. Some reported cases have involved individuals with diabetes who regularly check their blood sugar (FIGURE 2).⁹ A defining characteristic is that the infection usually does not extend past the interphalangeal joint. Radiologic evaluation may be necessary to detect the presence of foreign bodies or to assess bone involvement (osteomyelitis of the distal phalanx).¹⁰ The differential diagnosis includes paronychia, in which the infection starts in the nail area and pain is not as intense as in a felon infection.¹¹

How it’s treated. Surgical treatment of felon is controversial. There is no doubt that pus should be drained; how the incision is best performed, however, has been debated.¹² Before surgical debridement, obtain a sample of pus for Gram stain and for cultures of aerobic and anaerobic organisms, acid-fast bacilli (AFB), and fungi (SOR: A).^13,14 Several surgical techniques and their pitfalls are described in the literature.

Lateral and tip incisions may help avoid painful scars. However, multiple reports of this procedure describe injury to neurovascular bundles, leading to ischemia and anesthesia.¹² The “fish-mouth” incision and the “hockey stick” or “J” incision, as well as the transverse palmar incision, are no longer recommended due to painful sequelae, sensorial alterations, and risk of cutting the digital nerves.¹⁵ The preferred surgical procedure at this time is to make a very short incision over the area of maximum tenderness, then open and drain the abscess. Avoid placing ­packing in the affected area. Post-surgical management includes elevation, immobilization with an appropriate splint, and application of compresses until the wound has healed.^12,15,16

Since Staphylococcus aureus and Streptococcus sp are the most common bacteria causing felon, start empiric treatment with an antistaphylococcal penicillin, a first-generation cephalosporin, or clindamycin. Once a microbe has been isolated, treatment can be tailored as needed. Treatment may take up to 10 to 14 days and depends on the location and resolution of symptoms.¹³ Assess tetanus status and give prophylaxis as needed (SOR: A).¹⁷

Acute pyogenic flexor tenosynovitis

FTS is an aggressive closed-space bacterial infection that involves the flexor tendon synovial sheath. FTS accounts for up to 10% of acute hand infections and requires prompt medical attention with wound lavage, surgical management, and antimicrobial therapy to minimize serious consequences to the digit.¹⁸

Continue to: What you'll see

What you’ll see. FTS is diagnosed using clinical criteria^19,20: fusiform swelling of the finger; exquisite tenderness over the entire course of the flexor tendon sheath; pain on passive extension; and flexed posture of the digit (FIGURE 3). Patients usually recall some type of trauma or puncture wound to the affected area, but hematogenous spread of Neisseria gonorrhoeae also has been reported.²¹ The most common bacterial pathogens are Staphylococcus sp or Streptococcus sp. However, obtain a sample for Gram stain and culture for aerobic, anaerobic, AFB, and fungal agents before irrigating the wound with copious fluids and initiating empirical antibiotic therapy.¹⁴ Once a pathogen has been isolated, tailor antimicrobial therapy based on identified sensitivities and local ­antibiogram.¹³

How it’s treated. Early treatment of FTS is of utmost importance to avoid adverse outcomes. If FTS is diagnosed early, manage conservatively with elevation of the hand, splinting in a neutral position, and intravenous (IV) antibiotics. The use of adjunct antibiotics has improved range-of-motion outcomes compared with elevation and splinting alone (54% excellent vs 14% excellent) (SOR: A).²²In the most complex or fulminant cases, when conservative treatment has failed to show improvement (FIGURE 4), surgical management is indicated.²²

Surgical management of FTS has involved either an open or closed method. The open approach consists of open incision and drainage with exposure of the flexor tendon sheath, followed by large-volume sheath irrigation and closure of incision, in some cases over a drain. The closed approach with irrigation, rather than open washout, has been associated with improved outcomes (71% excellent vs 26% excellent).²² As a result, the procedure of choice is the closed approach, which uses closed catheter irrigation. An incision and placement of an angiocatheter allows for gentle irrigation of the wound until all purulent material has been evacuated (SOR: C).^22,23

Human bite injuries

A human bite injury occurs in 1 of 2 ways, and each has a distinct pattern.

What you’ll see

Closed-fist injury occurs when a clenched fist strikes the teeth of another person. The resulting lesion can easily fool a clinician by appearing to show very little damage. If not appropriately evaluated and treated, the lesion can cause considerable morbidity ­(FIGURE 5). Injury to the extensor mechanism and joint capsule can also damage the articular cartilage and bone, allowing bacteria to grow in a closed environment. This usually affects the metacarpophalangeal joint (MCP) due to its prominence when a hand is clenched. Initially the lesion seems to be minor, with a small laceration of 3 to 5 mm on the overlying skin, thus inoculating mouth flora deep in the hand tissue. Once the hand is relaxed, the broken skin retracts proximally, covering the wound and making it look innocuous.²⁴

Continue to: Occlusive bite injury...

Occlusive bite injury occurs when one individual forcibly bites another. Such wounds tend to be less penetrating than clenched-fist injuries. However, they can vary from superficial lacerations to wounds with tissue loss, including traumatic finger amputation.^24,25

One randomized prospective study compared mechanical wound care alone with combined mechanical wound care and oral or IV antibiotics and found that 47% of patients receiving wound care alone became infected vs no infection among those given oral or parenteral antibiotics (SOR: C).²⁶ Experts in the field advise examining the wound after administering a local anesthetic, thereby allowing better visualization of possible tendon damage, joint penetration, fracture, or deep-tissue infection. The procedure should be performed by a physician experienced in treating hand wounds, whether in the emergency department (ED) or in an operating suite.

How it’s treated. There is controversy regarding whether an affected patient can be adequately treated as an outpatient. Most traumatic bite lesions occur in men, and in those abusing drugs or alcohol.²⁵ In the latter case, individuals may be less likely to return for subsequent care or to finish the antibiotic course as prescribed. It is therefore strongly suggested that those individuals be admitted to receive IV antibiotics and physical therapy to expedite healing and avoid morbidity and sequelae of the lesions (SOR: C).^25,27

Obtain cultures from the wound after giving analgesia but before starting the procedure. The sample should be sent to the Microbiology Department or outpatient reference lab for aerobic, anaerobic, AFB, and fungal cultures. Recommend that the laboratory use 10% CO₂-enriched media for ­Eikenella ­corrodens isolation (SOR: A).^28,29

Among oral human flora are large concentrations of anaerobic bacteria such as Bacteroides sp (including B fragilis), ­Prevotella sp, Peptostreptococcus sp, Fusobacterium sp, Veillonella sp, Enterobateriaceae, and Clostridum. B fragilis accounts for up to 41% of isolates in some studies.³⁰ Most of them are beta-lactamase producers. The most common aerobic bacteria are alpha- and beta-hemolytic Streptococci, S aureus, Staphylococcus epidermis, Corynebacterium, and E corrodens. E corrodens accounts for up to 25% of bacteria isolated in clenched-fist injuries.^27,29

Continue to: HSV-1 and HSV-2...

HSV-1 and HSV-2, as well as hepatitis B and C and human immunodeficiency virus (HIV) can be isolated in saliva of infected individuals and can be transmitted when contaminated blood is exposed to an open wound. Still, the presence of HIV in saliva is unlikely to result in disease transmission, due to salivary inhibitors rendering the virus non-infective in most cases.²⁵ Obtain HIV and hepatitis B and C serology at baseline and at 3 and 6 months.²⁵ If HIV infection is known or suspected, or if there was exposure to blood in the wound, the Centers for Disease Control and Prevention recommends postexposure prophylaxis with a 28-day course of anti-­retroviral medication (SOR: A).^24,31

Hepatitis B virus has an infectivity ­100-fold greater than HIV.²⁷ If possible, the 2 people involved in the altercation should be tested for hepatitis B surface antigen. If the result is positive, the individual with the skin wound should receive hepatitis B immune globulin (0.06 mL/kg/dose),³² and the vaccination schedule started if not done previously (SOR: A).³³

Most experts recommend early antibiotic therapy given over 3 to 5 days for fresh, superficial wounds and specifically for wounds affecting hands, feet, joint, and genital area.¹¹ For treatment of cellulitis or abscess, 10 to 14 days is sufficient; tenosynovitis requires 2 to 3 weeks; osteomyelitis requires 4 to 6 weeks.²⁴ Wound care associated with daily dressing changes and antimicrobial therapy was superior to wound care alone (0% vs 47%).³⁰ Assess tetanus status in all cases (SOR: A).^17,33,34

Antimicrobial therapy for contamination with oral secretion is not straightforward. No one medication covers all possible pathogens. Use a combination therapy initially and then narrow coverage once the microorganism has been identified and susceptibilities are known. Empirical oral therapy with amoxicillin-clavulanate would be reasonable.

If IV therapy is needed, consider using ampicillin-sulbactam, cefazolin, or clindamycin. These antibiotics usually cover S aureus, Streptococcus sp, E corrodens and some anaerobes. Dicloxacillin will cover S aureus but provides poor coverage for E corrodens. First-generation cephalosporins cover S aureus, but E corrodens resistance is common. For penicillin-allergic individuals, use trimethoprim-sulfamethoxazole to cover E corrodens. Doxycycline can be used in children older than 8 years and in adults; avoid it in pregnant women.

Continue to: General principles guiding wound care, microbiology, and antibiotic management

General principles guiding wound care, microbiology, and antibiotic management

Elapsed time between injury and seeking medical attention is characterized as an early (24 hours), late (1-7 days), or delayed (> 7 days) presentation. The timing of an individual’s presentation and a determination of whether the wound is “clean” or “dirty” are both factors in the risk of infection and in ­associated morbidity and long-term ­sequelae.

General principles of surgery are important. The cornerstones of treatment are the use of topical anesthesia to provide pain control, which allows for better examination of the wound, debridement of devitalized tissue, collection of wound cultures, and irrigation of the wound with large volume of fluids to mechanically remove dirt, foreign bodies, and bacteria.

Surgical knowledge of hand anatomy increases the likelihood of favorable outcomes in morbidity and functionality. Depending on the circumstances and location, this procedure may be performed by an experienced hand surgeon or an ED physician. (Diversity in settings and available resources may explain why there is so much variability in the composition of patient populations and outcomes found in the medical literature.)

To maximize appropriate bacteriologic success, the Microbiology Department or lab needs to be informed of the type of samples that have been collected. Cultures should be sent for aerobic, anaerobic, AFB, and fungal cultures. Enrichment of aerobic culture with 10% CO₂ increases the likelihood of isolating E corrodens (fastidious bacterium), which has been identified in approximately 25% of clenched-fist wounds.

Populations at heightened risk for human bite injuries include alcohol and drug abusers and those of poor socioeconomic status who may not have the resources to visit a medical facility early enough to obtain appropriate medical care. These patients are at risk for being lost to follow-up as well as medication noncompliance, so inpatient admission may diminish the possibilities of incomplete medical treatment, complications, and adverse outcomes such as loss of functionality of the affected extremity.

Continue to: Antimicrobial therapy is not easy

Antimicrobial therapy is not easy. No single regimen covers all possibilities. Start antimicrobial treatment empirically with wide-spectrum coverage, and tailor the regimen, as needed, based on microbiology ­results.

In clean surgical procedures, S aureus is the most common pathogen. It is acceptable to start empirical treatment with an antistaphylococcal penicillin, first-generation cephalosporin, or clindamycin. In contaminated wounds, gram-negative bacteria, anaerobes, fungal organisms, and mixed infections are more commonly seen.^35-37

Felon has occurred in individuals with diabetes, who regularly check their blood-sugar level.

First-generation cephalosporin provides good coverage for gram-positive and gram-negative bacteria in clean wounds. However, in contaminated wounds with devitalized tissue, a more aggressive scheme is recommended: start with a penicillin and aminoglycoside.^35-37 In some cases, monotherapy with either ampicillin/sulbactam, imipenem, meropenem, piperacillin/tazobactam, or tigecylline may be sufficient until culture results are available; at that point, antibiotic coverage can be narrowed as indicated (TABLE 2⁷).^35,36

CORRESPONDENCE
Carlos A. Arango, MD, 8399 Bayberry Road, Jacksonville, FL 32256; [email protected].

Hand infections, if not treated properly, can cause severe chronic morbidity. The conditions I review here range from superficial to deep seated: herpetic whitlow located in the epidermis; felon in subcutaneous tissue; pyogenic flexor tenosynovitis (FTS) in the tendon sheath; and human bite infection at any level including possibly synovium and bone.

Superficial infections usually respond to nonsurgical management. However, antimicrobial therapy is not straightforward. There is no single regimen that covers all possible pathogens. Combination therapy must usually be started and then tailored once an organism and its susceptibility are known. Subcutaneous, tendon sheath, synovial, and bone infections frequently require surgical management.

Herpetic whitlow

Herpes simplex virus type 1 (HSV-1) is common, with as much as 90% of the population exposed by 60 years of age.¹ Initial infection usually occurs in the oropharynx and is known as a fever blister or cold sore. However, HSV-1 also can cause herpetic whitlow, a primary infection in the fingertip in which the virus penetrates the subcutaneous tissue, usually after a breakdown in the skin barrier either from infected saliva or the lips of an infected individual.¹

What you’ll see. The lesion is characterized by pain, swelling, erythema, and nonpurulent vesicle formation ­(FIGURE 1). The condition is usually self-limiting, with the inflammation resolving spontaneously, leaving normal healthy skin within 1 to 2 weeks. Herpetic whitlow is an occupational hazard for medical, nursing, paramedical, and dental personnel, and standard precautions should be used when handling secretions (Strength of Recommendation [SOR]: A).²

Herpetic whitlow is distinguished from a felon by its formation of vesicles, lack of a tense pulp space, and serous, not purulent, drainage.

Reactivation of HSV-1 (and HSV-2) is common, with a prodrome of a “tingling sensation” and subsequent blister formation in the same location as the previous infection. It can cause pain and discomfort and may render the individual unable to perform usual activities.^1,3 This lesion is often confused with bacterial (pyogenic) infections of the pulp of the finger or thumb (felon).¹ Herpetic whitlow can be distinguished from a felon by its formation of vesicles, lack of a tense pulp space, and serous, rather than purulent, drainage. Scarring is not associated with herpes infection because penetration is limited to the epidermal area. Superimposed bacterial infection can be mistaken for an abscess (felon) and lead to unnecessary incision and drainage, causing associated morbidity and potential scarring in the affected area.¹

How it’s treated. Treatment of herpetic whitlow is usually conservative, and topical application of acyclovir 5% appears to be beneficial (SOR: C).⁴ Two studies also suggest that oral acyclovir is beneficial for herpetic whitlow and may reduce the frequency of recurrence.^5,6 Controlled studies in the use of acyclovir for herpetic whitlow have not been conducted. Despite a lack of direct evidence, acyclovir, famciclovir, and valacyclovir are accepted therapies for herpetic whitlow (TABLE 1⁷) (SOR: B).^6,8

Felon

A felon is a closed-space infection affecting the pulp of the fingers or thumb. The anatomy of the finger is unique in that there are multiple septa attaching the periosteum to the skin, thereby creating several closed spaces prone to develop pockets of infection.

Continue to: What you'll see

What you’ll see. Clinical signs and symptoms include pain in the pulp of the finger with tenderness and swelling. Bacteria are usually introduced into fingertip space (fat pad) by a penetrating object. Some reported cases have involved individuals with diabetes who regularly check their blood sugar (FIGURE 2).⁹ A defining characteristic is that the infection usually does not extend past the interphalangeal joint. Radiologic evaluation may be necessary to detect the presence of foreign bodies or to assess bone involvement (osteomyelitis of the distal phalanx).¹⁰ The differential diagnosis includes paronychia, in which the infection starts in the nail area and pain is not as intense as in a felon infection.¹¹

How it’s treated. Surgical treatment of felon is controversial. There is no doubt that pus should be drained; how the incision is best performed, however, has been debated.¹² Before surgical debridement, obtain a sample of pus for Gram stain and for cultures of aerobic and anaerobic organisms, acid-fast bacilli (AFB), and fungi (SOR: A).^13,14 Several surgical techniques and their pitfalls are described in the literature.

Lateral and tip incisions may help avoid painful scars. However, multiple reports of this procedure describe injury to neurovascular bundles, leading to ischemia and anesthesia.¹² The “fish-mouth” incision and the “hockey stick” or “J” incision, as well as the transverse palmar incision, are no longer recommended due to painful sequelae, sensorial alterations, and risk of cutting the digital nerves.¹⁵ The preferred surgical procedure at this time is to make a very short incision over the area of maximum tenderness, then open and drain the abscess. Avoid placing ­packing in the affected area. Post-surgical management includes elevation, immobilization with an appropriate splint, and application of compresses until the wound has healed.^12,15,16

Since Staphylococcus aureus and Streptococcus sp are the most common bacteria causing felon, start empiric treatment with an antistaphylococcal penicillin, a first-generation cephalosporin, or clindamycin. Once a microbe has been isolated, treatment can be tailored as needed. Treatment may take up to 10 to 14 days and depends on the location and resolution of symptoms.¹³ Assess tetanus status and give prophylaxis as needed (SOR: A).¹⁷

Acute pyogenic flexor tenosynovitis

FTS is an aggressive closed-space bacterial infection that involves the flexor tendon synovial sheath. FTS accounts for up to 10% of acute hand infections and requires prompt medical attention with wound lavage, surgical management, and antimicrobial therapy to minimize serious consequences to the digit.¹⁸

Continue to: What you'll see

What you’ll see. FTS is diagnosed using clinical criteria^19,20: fusiform swelling of the finger; exquisite tenderness over the entire course of the flexor tendon sheath; pain on passive extension; and flexed posture of the digit (FIGURE 3). Patients usually recall some type of trauma or puncture wound to the affected area, but hematogenous spread of Neisseria gonorrhoeae also has been reported.²¹ The most common bacterial pathogens are Staphylococcus sp or Streptococcus sp. However, obtain a sample for Gram stain and culture for aerobic, anaerobic, AFB, and fungal agents before irrigating the wound with copious fluids and initiating empirical antibiotic therapy.¹⁴ Once a pathogen has been isolated, tailor antimicrobial therapy based on identified sensitivities and local ­antibiogram.¹³

How it’s treated. Early treatment of FTS is of utmost importance to avoid adverse outcomes. If FTS is diagnosed early, manage conservatively with elevation of the hand, splinting in a neutral position, and intravenous (IV) antibiotics. The use of adjunct antibiotics has improved range-of-motion outcomes compared with elevation and splinting alone (54% excellent vs 14% excellent) (SOR: A).²²In the most complex or fulminant cases, when conservative treatment has failed to show improvement (FIGURE 4), surgical management is indicated.²²

Surgical management of FTS has involved either an open or closed method. The open approach consists of open incision and drainage with exposure of the flexor tendon sheath, followed by large-volume sheath irrigation and closure of incision, in some cases over a drain. The closed approach with irrigation, rather than open washout, has been associated with improved outcomes (71% excellent vs 26% excellent).²² As a result, the procedure of choice is the closed approach, which uses closed catheter irrigation. An incision and placement of an angiocatheter allows for gentle irrigation of the wound until all purulent material has been evacuated (SOR: C).^22,23

Human bite injuries

A human bite injury occurs in 1 of 2 ways, and each has a distinct pattern.

What you’ll see

Closed-fist injury occurs when a clenched fist strikes the teeth of another person. The resulting lesion can easily fool a clinician by appearing to show very little damage. If not appropriately evaluated and treated, the lesion can cause considerable morbidity ­(FIGURE 5). Injury to the extensor mechanism and joint capsule can also damage the articular cartilage and bone, allowing bacteria to grow in a closed environment. This usually affects the metacarpophalangeal joint (MCP) due to its prominence when a hand is clenched. Initially the lesion seems to be minor, with a small laceration of 3 to 5 mm on the overlying skin, thus inoculating mouth flora deep in the hand tissue. Once the hand is relaxed, the broken skin retracts proximally, covering the wound and making it look innocuous.²⁴

Continue to: Occlusive bite injury...

Occlusive bite injury occurs when one individual forcibly bites another. Such wounds tend to be less penetrating than clenched-fist injuries. However, they can vary from superficial lacerations to wounds with tissue loss, including traumatic finger amputation.^24,25

One randomized prospective study compared mechanical wound care alone with combined mechanical wound care and oral or IV antibiotics and found that 47% of patients receiving wound care alone became infected vs no infection among those given oral or parenteral antibiotics (SOR: C).²⁶ Experts in the field advise examining the wound after administering a local anesthetic, thereby allowing better visualization of possible tendon damage, joint penetration, fracture, or deep-tissue infection. The procedure should be performed by a physician experienced in treating hand wounds, whether in the emergency department (ED) or in an operating suite.

How it’s treated. There is controversy regarding whether an affected patient can be adequately treated as an outpatient. Most traumatic bite lesions occur in men, and in those abusing drugs or alcohol.²⁵ In the latter case, individuals may be less likely to return for subsequent care or to finish the antibiotic course as prescribed. It is therefore strongly suggested that those individuals be admitted to receive IV antibiotics and physical therapy to expedite healing and avoid morbidity and sequelae of the lesions (SOR: C).^25,27

Obtain cultures from the wound after giving analgesia but before starting the procedure. The sample should be sent to the Microbiology Department or outpatient reference lab for aerobic, anaerobic, AFB, and fungal cultures. Recommend that the laboratory use 10% CO₂-enriched media for ­Eikenella ­corrodens isolation (SOR: A).^28,29

Among oral human flora are large concentrations of anaerobic bacteria such as Bacteroides sp (including B fragilis), ­Prevotella sp, Peptostreptococcus sp, Fusobacterium sp, Veillonella sp, Enterobateriaceae, and Clostridum. B fragilis accounts for up to 41% of isolates in some studies.³⁰ Most of them are beta-lactamase producers. The most common aerobic bacteria are alpha- and beta-hemolytic Streptococci, S aureus, Staphylococcus epidermis, Corynebacterium, and E corrodens. E corrodens accounts for up to 25% of bacteria isolated in clenched-fist injuries.^27,29

Continue to: HSV-1 and HSV-2...

HSV-1 and HSV-2, as well as hepatitis B and C and human immunodeficiency virus (HIV) can be isolated in saliva of infected individuals and can be transmitted when contaminated blood is exposed to an open wound. Still, the presence of HIV in saliva is unlikely to result in disease transmission, due to salivary inhibitors rendering the virus non-infective in most cases.²⁵ Obtain HIV and hepatitis B and C serology at baseline and at 3 and 6 months.²⁵ If HIV infection is known or suspected, or if there was exposure to blood in the wound, the Centers for Disease Control and Prevention recommends postexposure prophylaxis with a 28-day course of anti-­retroviral medication (SOR: A).^24,31

Hepatitis B virus has an infectivity ­100-fold greater than HIV.²⁷ If possible, the 2 people involved in the altercation should be tested for hepatitis B surface antigen. If the result is positive, the individual with the skin wound should receive hepatitis B immune globulin (0.06 mL/kg/dose),³² and the vaccination schedule started if not done previously (SOR: A).³³

Most experts recommend early antibiotic therapy given over 3 to 5 days for fresh, superficial wounds and specifically for wounds affecting hands, feet, joint, and genital area.¹¹ For treatment of cellulitis or abscess, 10 to 14 days is sufficient; tenosynovitis requires 2 to 3 weeks; osteomyelitis requires 4 to 6 weeks.²⁴ Wound care associated with daily dressing changes and antimicrobial therapy was superior to wound care alone (0% vs 47%).³⁰ Assess tetanus status in all cases (SOR: A).^17,33,34

Antimicrobial therapy for contamination with oral secretion is not straightforward. No one medication covers all possible pathogens. Use a combination therapy initially and then narrow coverage once the microorganism has been identified and susceptibilities are known. Empirical oral therapy with amoxicillin-clavulanate would be reasonable.

If IV therapy is needed, consider using ampicillin-sulbactam, cefazolin, or clindamycin. These antibiotics usually cover S aureus, Streptococcus sp, E corrodens and some anaerobes. Dicloxacillin will cover S aureus but provides poor coverage for E corrodens. First-generation cephalosporins cover S aureus, but E corrodens resistance is common. For penicillin-allergic individuals, use trimethoprim-sulfamethoxazole to cover E corrodens. Doxycycline can be used in children older than 8 years and in adults; avoid it in pregnant women.

Continue to: General principles guiding wound care, microbiology, and antibiotic management

General principles guiding wound care, microbiology, and antibiotic management

Elapsed time between injury and seeking medical attention is characterized as an early (24 hours), late (1-7 days), or delayed (> 7 days) presentation. The timing of an individual’s presentation and a determination of whether the wound is “clean” or “dirty” are both factors in the risk of infection and in ­associated morbidity and long-term ­sequelae.

General principles of surgery are important. The cornerstones of treatment are the use of topical anesthesia to provide pain control, which allows for better examination of the wound, debridement of devitalized tissue, collection of wound cultures, and irrigation of the wound with large volume of fluids to mechanically remove dirt, foreign bodies, and bacteria.

Surgical knowledge of hand anatomy increases the likelihood of favorable outcomes in morbidity and functionality. Depending on the circumstances and location, this procedure may be performed by an experienced hand surgeon or an ED physician. (Diversity in settings and available resources may explain why there is so much variability in the composition of patient populations and outcomes found in the medical literature.)

To maximize appropriate bacteriologic success, the Microbiology Department or lab needs to be informed of the type of samples that have been collected. Cultures should be sent for aerobic, anaerobic, AFB, and fungal cultures. Enrichment of aerobic culture with 10% CO₂ increases the likelihood of isolating E corrodens (fastidious bacterium), which has been identified in approximately 25% of clenched-fist wounds.

Populations at heightened risk for human bite injuries include alcohol and drug abusers and those of poor socioeconomic status who may not have the resources to visit a medical facility early enough to obtain appropriate medical care. These patients are at risk for being lost to follow-up as well as medication noncompliance, so inpatient admission may diminish the possibilities of incomplete medical treatment, complications, and adverse outcomes such as loss of functionality of the affected extremity.

Continue to: Antimicrobial therapy is not easy

Antimicrobial therapy is not easy. No single regimen covers all possibilities. Start antimicrobial treatment empirically with wide-spectrum coverage, and tailor the regimen, as needed, based on microbiology ­results.

In clean surgical procedures, S aureus is the most common pathogen. It is acceptable to start empirical treatment with an antistaphylococcal penicillin, first-generation cephalosporin, or clindamycin. In contaminated wounds, gram-negative bacteria, anaerobes, fungal organisms, and mixed infections are more commonly seen.^35-37

Felon has occurred in individuals with diabetes, who regularly check their blood-sugar level.

First-generation cephalosporin provides good coverage for gram-positive and gram-negative bacteria in clean wounds. However, in contaminated wounds with devitalized tissue, a more aggressive scheme is recommended: start with a penicillin and aminoglycoside.^35-37 In some cases, monotherapy with either ampicillin/sulbactam, imipenem, meropenem, piperacillin/tazobactam, or tigecylline may be sufficient until culture results are available; at that point, antibiotic coverage can be narrowed as indicated (TABLE 2⁷).^35,36

CORRESPONDENCE
Carlos A. Arango, MD, 8399 Bayberry Road, Jacksonville, FL 32256; [email protected].

Hand infections, if not treated properly, can cause severe chronic morbidity. The conditions I review here range from superficial to deep seated: herpetic whitlow located in the epidermis; felon in subcutaneous tissue; pyogenic flexor tenosynovitis (FTS) in the tendon sheath; and human bite infection at any level including possibly synovium and bone.

Superficial infections usually respond to nonsurgical management. However, antimicrobial therapy is not straightforward. There is no single regimen that covers all possible pathogens. Combination therapy must usually be started and then tailored once an organism and its susceptibility are known. Subcutaneous, tendon sheath, synovial, and bone infections frequently require surgical management.

Herpetic whitlow

Herpes simplex virus type 1 (HSV-1) is common, with as much as 90% of the population exposed by 60 years of age.¹ Initial infection usually occurs in the oropharynx and is known as a fever blister or cold sore. However, HSV-1 also can cause herpetic whitlow, a primary infection in the fingertip in which the virus penetrates the subcutaneous tissue, usually after a breakdown in the skin barrier either from infected saliva or the lips of an infected individual.¹

What you’ll see. The lesion is characterized by pain, swelling, erythema, and nonpurulent vesicle formation ­(FIGURE 1). The condition is usually self-limiting, with the inflammation resolving spontaneously, leaving normal healthy skin within 1 to 2 weeks. Herpetic whitlow is an occupational hazard for medical, nursing, paramedical, and dental personnel, and standard precautions should be used when handling secretions (Strength of Recommendation [SOR]: A).²

Herpetic whitlow is distinguished from a felon by its formation of vesicles, lack of a tense pulp space, and serous, not purulent, drainage.

Reactivation of HSV-1 (and HSV-2) is common, with a prodrome of a “tingling sensation” and subsequent blister formation in the same location as the previous infection. It can cause pain and discomfort and may render the individual unable to perform usual activities.^1,3 This lesion is often confused with bacterial (pyogenic) infections of the pulp of the finger or thumb (felon).¹ Herpetic whitlow can be distinguished from a felon by its formation of vesicles, lack of a tense pulp space, and serous, rather than purulent, drainage. Scarring is not associated with herpes infection because penetration is limited to the epidermal area. Superimposed bacterial infection can be mistaken for an abscess (felon) and lead to unnecessary incision and drainage, causing associated morbidity and potential scarring in the affected area.¹

How it’s treated. Treatment of herpetic whitlow is usually conservative, and topical application of acyclovir 5% appears to be beneficial (SOR: C).⁴ Two studies also suggest that oral acyclovir is beneficial for herpetic whitlow and may reduce the frequency of recurrence.^5,6 Controlled studies in the use of acyclovir for herpetic whitlow have not been conducted. Despite a lack of direct evidence, acyclovir, famciclovir, and valacyclovir are accepted therapies for herpetic whitlow (TABLE 1⁷) (SOR: B).^6,8

Felon

A felon is a closed-space infection affecting the pulp of the fingers or thumb. The anatomy of the finger is unique in that there are multiple septa attaching the periosteum to the skin, thereby creating several closed spaces prone to develop pockets of infection.

Continue to: What you'll see

What you’ll see. Clinical signs and symptoms include pain in the pulp of the finger with tenderness and swelling. Bacteria are usually introduced into fingertip space (fat pad) by a penetrating object. Some reported cases have involved individuals with diabetes who regularly check their blood sugar (FIGURE 2).⁹ A defining characteristic is that the infection usually does not extend past the interphalangeal joint. Radiologic evaluation may be necessary to detect the presence of foreign bodies or to assess bone involvement (osteomyelitis of the distal phalanx).¹⁰ The differential diagnosis includes paronychia, in which the infection starts in the nail area and pain is not as intense as in a felon infection.¹¹

How it’s treated. Surgical treatment of felon is controversial. There is no doubt that pus should be drained; how the incision is best performed, however, has been debated.¹² Before surgical debridement, obtain a sample of pus for Gram stain and for cultures of aerobic and anaerobic organisms, acid-fast bacilli (AFB), and fungi (SOR: A).^13,14 Several surgical techniques and their pitfalls are described in the literature.

Lateral and tip incisions may help avoid painful scars. However, multiple reports of this procedure describe injury to neurovascular bundles, leading to ischemia and anesthesia.¹² The “fish-mouth” incision and the “hockey stick” or “J” incision, as well as the transverse palmar incision, are no longer recommended due to painful sequelae, sensorial alterations, and risk of cutting the digital nerves.¹⁵ The preferred surgical procedure at this time is to make a very short incision over the area of maximum tenderness, then open and drain the abscess. Avoid placing ­packing in the affected area. Post-surgical management includes elevation, immobilization with an appropriate splint, and application of compresses until the wound has healed.^12,15,16

Since Staphylococcus aureus and Streptococcus sp are the most common bacteria causing felon, start empiric treatment with an antistaphylococcal penicillin, a first-generation cephalosporin, or clindamycin. Once a microbe has been isolated, treatment can be tailored as needed. Treatment may take up to 10 to 14 days and depends on the location and resolution of symptoms.¹³ Assess tetanus status and give prophylaxis as needed (SOR: A).¹⁷

Acute pyogenic flexor tenosynovitis

FTS is an aggressive closed-space bacterial infection that involves the flexor tendon synovial sheath. FTS accounts for up to 10% of acute hand infections and requires prompt medical attention with wound lavage, surgical management, and antimicrobial therapy to minimize serious consequences to the digit.¹⁸

Continue to: What you'll see

What you’ll see. FTS is diagnosed using clinical criteria^19,20: fusiform swelling of the finger; exquisite tenderness over the entire course of the flexor tendon sheath; pain on passive extension; and flexed posture of the digit (FIGURE 3). Patients usually recall some type of trauma or puncture wound to the affected area, but hematogenous spread of Neisseria gonorrhoeae also has been reported.²¹ The most common bacterial pathogens are Staphylococcus sp or Streptococcus sp. However, obtain a sample for Gram stain and culture for aerobic, anaerobic, AFB, and fungal agents before irrigating the wound with copious fluids and initiating empirical antibiotic therapy.¹⁴ Once a pathogen has been isolated, tailor antimicrobial therapy based on identified sensitivities and local ­antibiogram.¹³

How it’s treated. Early treatment of FTS is of utmost importance to avoid adverse outcomes. If FTS is diagnosed early, manage conservatively with elevation of the hand, splinting in a neutral position, and intravenous (IV) antibiotics. The use of adjunct antibiotics has improved range-of-motion outcomes compared with elevation and splinting alone (54% excellent vs 14% excellent) (SOR: A).²²In the most complex or fulminant cases, when conservative treatment has failed to show improvement (FIGURE 4), surgical management is indicated.²²

Surgical management of FTS has involved either an open or closed method. The open approach consists of open incision and drainage with exposure of the flexor tendon sheath, followed by large-volume sheath irrigation and closure of incision, in some cases over a drain. The closed approach with irrigation, rather than open washout, has been associated with improved outcomes (71% excellent vs 26% excellent).²² As a result, the procedure of choice is the closed approach, which uses closed catheter irrigation. An incision and placement of an angiocatheter allows for gentle irrigation of the wound until all purulent material has been evacuated (SOR: C).^22,23

Human bite injuries

A human bite injury occurs in 1 of 2 ways, and each has a distinct pattern.

What you’ll see

Closed-fist injury occurs when a clenched fist strikes the teeth of another person. The resulting lesion can easily fool a clinician by appearing to show very little damage. If not appropriately evaluated and treated, the lesion can cause considerable morbidity ­(FIGURE 5). Injury to the extensor mechanism and joint capsule can also damage the articular cartilage and bone, allowing bacteria to grow in a closed environment. This usually affects the metacarpophalangeal joint (MCP) due to its prominence when a hand is clenched. Initially the lesion seems to be minor, with a small laceration of 3 to 5 mm on the overlying skin, thus inoculating mouth flora deep in the hand tissue. Once the hand is relaxed, the broken skin retracts proximally, covering the wound and making it look innocuous.²⁴

Continue to: Occlusive bite injury...

Occlusive bite injury occurs when one individual forcibly bites another. Such wounds tend to be less penetrating than clenched-fist injuries. However, they can vary from superficial lacerations to wounds with tissue loss, including traumatic finger amputation.^24,25

One randomized prospective study compared mechanical wound care alone with combined mechanical wound care and oral or IV antibiotics and found that 47% of patients receiving wound care alone became infected vs no infection among those given oral or parenteral antibiotics (SOR: C).²⁶ Experts in the field advise examining the wound after administering a local anesthetic, thereby allowing better visualization of possible tendon damage, joint penetration, fracture, or deep-tissue infection. The procedure should be performed by a physician experienced in treating hand wounds, whether in the emergency department (ED) or in an operating suite.

How it’s treated. There is controversy regarding whether an affected patient can be adequately treated as an outpatient. Most traumatic bite lesions occur in men, and in those abusing drugs or alcohol.²⁵ In the latter case, individuals may be less likely to return for subsequent care or to finish the antibiotic course as prescribed. It is therefore strongly suggested that those individuals be admitted to receive IV antibiotics and physical therapy to expedite healing and avoid morbidity and sequelae of the lesions (SOR: C).^25,27

Obtain cultures from the wound after giving analgesia but before starting the procedure. The sample should be sent to the Microbiology Department or outpatient reference lab for aerobic, anaerobic, AFB, and fungal cultures. Recommend that the laboratory use 10% CO₂-enriched media for ­Eikenella ­corrodens isolation (SOR: A).^28,29

Among oral human flora are large concentrations of anaerobic bacteria such as Bacteroides sp (including B fragilis), ­Prevotella sp, Peptostreptococcus sp, Fusobacterium sp, Veillonella sp, Enterobateriaceae, and Clostridum. B fragilis accounts for up to 41% of isolates in some studies.³⁰ Most of them are beta-lactamase producers. The most common aerobic bacteria are alpha- and beta-hemolytic Streptococci, S aureus, Staphylococcus epidermis, Corynebacterium, and E corrodens. E corrodens accounts for up to 25% of bacteria isolated in clenched-fist injuries.^27,29

Continue to: HSV-1 and HSV-2...

HSV-1 and HSV-2, as well as hepatitis B and C and human immunodeficiency virus (HIV) can be isolated in saliva of infected individuals and can be transmitted when contaminated blood is exposed to an open wound. Still, the presence of HIV in saliva is unlikely to result in disease transmission, due to salivary inhibitors rendering the virus non-infective in most cases.²⁵ Obtain HIV and hepatitis B and C serology at baseline and at 3 and 6 months.²⁵ If HIV infection is known or suspected, or if there was exposure to blood in the wound, the Centers for Disease Control and Prevention recommends postexposure prophylaxis with a 28-day course of anti-­retroviral medication (SOR: A).^24,31

Hepatitis B virus has an infectivity ­100-fold greater than HIV.²⁷ If possible, the 2 people involved in the altercation should be tested for hepatitis B surface antigen. If the result is positive, the individual with the skin wound should receive hepatitis B immune globulin (0.06 mL/kg/dose),³² and the vaccination schedule started if not done previously (SOR: A).³³

Most experts recommend early antibiotic therapy given over 3 to 5 days for fresh, superficial wounds and specifically for wounds affecting hands, feet, joint, and genital area.¹¹ For treatment of cellulitis or abscess, 10 to 14 days is sufficient; tenosynovitis requires 2 to 3 weeks; osteomyelitis requires 4 to 6 weeks.²⁴ Wound care associated with daily dressing changes and antimicrobial therapy was superior to wound care alone (0% vs 47%).³⁰ Assess tetanus status in all cases (SOR: A).^17,33,34

Antimicrobial therapy for contamination with oral secretion is not straightforward. No one medication covers all possible pathogens. Use a combination therapy initially and then narrow coverage once the microorganism has been identified and susceptibilities are known. Empirical oral therapy with amoxicillin-clavulanate would be reasonable.

If IV therapy is needed, consider using ampicillin-sulbactam, cefazolin, or clindamycin. These antibiotics usually cover S aureus, Streptococcus sp, E corrodens and some anaerobes. Dicloxacillin will cover S aureus but provides poor coverage for E corrodens. First-generation cephalosporins cover S aureus, but E corrodens resistance is common. For penicillin-allergic individuals, use trimethoprim-sulfamethoxazole to cover E corrodens. Doxycycline can be used in children older than 8 years and in adults; avoid it in pregnant women.

Continue to: General principles guiding wound care, microbiology, and antibiotic management

General principles guiding wound care, microbiology, and antibiotic management

Elapsed time between injury and seeking medical attention is characterized as an early (24 hours), late (1-7 days), or delayed (> 7 days) presentation. The timing of an individual’s presentation and a determination of whether the wound is “clean” or “dirty” are both factors in the risk of infection and in ­associated morbidity and long-term ­sequelae.

General principles of surgery are important. The cornerstones of treatment are the use of topical anesthesia to provide pain control, which allows for better examination of the wound, debridement of devitalized tissue, collection of wound cultures, and irrigation of the wound with large volume of fluids to mechanically remove dirt, foreign bodies, and bacteria.

Surgical knowledge of hand anatomy increases the likelihood of favorable outcomes in morbidity and functionality. Depending on the circumstances and location, this procedure may be performed by an experienced hand surgeon or an ED physician. (Diversity in settings and available resources may explain why there is so much variability in the composition of patient populations and outcomes found in the medical literature.)

To maximize appropriate bacteriologic success, the Microbiology Department or lab needs to be informed of the type of samples that have been collected. Cultures should be sent for aerobic, anaerobic, AFB, and fungal cultures. Enrichment of aerobic culture with 10% CO₂ increases the likelihood of isolating E corrodens (fastidious bacterium), which has been identified in approximately 25% of clenched-fist wounds.

Populations at heightened risk for human bite injuries include alcohol and drug abusers and those of poor socioeconomic status who may not have the resources to visit a medical facility early enough to obtain appropriate medical care. These patients are at risk for being lost to follow-up as well as medication noncompliance, so inpatient admission may diminish the possibilities of incomplete medical treatment, complications, and adverse outcomes such as loss of functionality of the affected extremity.

Continue to: Antimicrobial therapy is not easy

Antimicrobial therapy is not easy. No single regimen covers all possibilities. Start antimicrobial treatment empirically with wide-spectrum coverage, and tailor the regimen, as needed, based on microbiology ­results.

In clean surgical procedures, S aureus is the most common pathogen. It is acceptable to start empirical treatment with an antistaphylococcal penicillin, first-generation cephalosporin, or clindamycin. In contaminated wounds, gram-negative bacteria, anaerobes, fungal organisms, and mixed infections are more commonly seen.^35-37

Felon has occurred in individuals with diabetes, who regularly check their blood-sugar level.

First-generation cephalosporin provides good coverage for gram-positive and gram-negative bacteria in clean wounds. However, in contaminated wounds with devitalized tissue, a more aggressive scheme is recommended: start with a penicillin and aminoglycoside.^35-37 In some cases, monotherapy with either ampicillin/sulbactam, imipenem, meropenem, piperacillin/tazobactam, or tigecylline may be sufficient until culture results are available; at that point, antibiotic coverage can be narrowed as indicated (TABLE 2⁷).^35,36

CORRESPONDENCE
Carlos A. Arango, MD, 8399 Bayberry Road, Jacksonville, FL 32256; [email protected].

It is estimated that up to 45% of cases of scabies are misdiagnosed as another condition.¹ This can occur when common clinical features are overlooked, a skin exam is rushed (and the rash is chalked up to dermatitis), or the wrong part of the pruritic lesion is scraped (the papule, rather than the burrow). There are also atypical presentations of scabies, which can confound even the most astute clinician.¹ Misdiagnosis can increase health care costs due to repeat office visits or multiple referrals. In this article, we review the typical and atypical presentations of scabies and provide recommendations to aid physicians in its early recognition and correct diagnosis.

The scope of scabies infection, and its clinical stages

The prevalence of scabies, a common skin infection caused by the mite Sarcoptes scabiei, is estimated at 300 million cases worldwide annually, with the greatest incidence occurring in children and adolescents.¹ In the developing world, its clinical burden is highest among the homeless, those of lower socioeconomic status, and those with poor hygiene. In the developed world, the clinical burden is highest among hospitalized patients and residents of long-term living facilities.

The S scabiei mite is an obligate parasite that elicits an adaptive immune response in susceptible hosts. The female mite lays 60 to 90 eggs that mature into adult mites after completing the mite life cycle in human hosts. In immunocompetent patients, roughly 10 to 15 surviving mites can be found at any given point in the disease process.² In crusted or disseminated scabies, which often occur in immunocompromised patients, thousands of mites may be found at any given point in the disease process. ²

Scabies infection has 2 stages: the latent primary infection and the symptomatic secondary infection.

The primary infection starts with the initial mite invasion, typically with the transfer of impregnated females during person-to-person contact. Females deposit eggs as they burrow into the epidermis at the level of the stratum corneum with the use of proteolytic enzymes (creating the mite burrow). Surviving eggs hatch into larvae that then mature into nymphs and adult mites. After these adult mites mate, the impregnated females create new burrows and lay additional eggs.³ Patients may be asymptomatic during this initial stage and the infection may be transmitted from person to person through direct skin contact.

In children with scabies, vesicles, pustules, and nodular pruritic lesions may coexist with eczema and impetigo.

The second stage of infection is when patients experience severe pruritus with inflammatory papules seen on exam. The pruritus associated with scabies results from a delayed type IV hypersensitivity reaction to mite infestation. This requires host sensitization to the scabies mite. Clinically, there is a delayed onset (weeks) of numerous erythematous papules and, later, excoriated papules.

Conditions that scabies can mimic

The differential of typical scabies includes diagnoses manifesting with moderate to severe pruritus. In the immunocompetent adult, conditions to consider are atopic dermatitis, tinea corporis, papular urticaria, seborrheic dermatitis, poison ivy and other causes of contact dermatitis, drug eruptions, and irritant dermatitis. In immunocompetent infants, think of seborrheic dermatitis, atopic dermatitis, acropustulosis, and viral exanthems.

Continue to: Nodular scabies variants...

Nodular scabies variants can masquerade as pseudolymphoma, lymphoma, or leukemia cutis. In immunocompromised and elderly individuals, crusted scabies is often mistaken for psoriasis, atopic dermatitis, keratoderma, and lichen planus.^2,4,5

Scabies’ classic presentation

Typically, scabies causes intensely pruritic erythematous papules. Areas commonly affected are the webs and sides of fingers ­(FIGURE 1A and 1B), proximal palm and wrist flexors, extensor aspects of the arms and legs, axillary folds, periumbilical areas, the peri-areolar region in women, buttocks and thigh creases, and, in males, the genitals. The head may also be affected in children (FIGURE 1C), but seldom in adults. Interestingly, the back is usually spared across all age groups, though not always (FIGURE 2).

IMAGE COURTESY OF VISUALDX.COM

Mites are not found near pruritic papules. Scrape the mite burrows, which are small, linear, serpiginous lines, to discover the mature scabies mite.

The classic presentation also varies across age groups and populations.² In children, vesicles, pustules, and nodular pruritic lesions may coexist with eczema and impetigo. Among homeless individuals, coinfection with impetigo and eczema is common. Elderly patients are more likely to exhibit atypical lesions.⁶ Immunocompromised patients present with atypical papular scabies, crusted scabies, or scabies that may be only mildly pruritic or nonpruritic. In underdeveloped countries, indigenous populations are more susceptible to endemic scabies, with a high risk of scabies superinfection with Streptococcus.

Scabies subtypes with varying presentations

Clinical manifestations of scabies subtypes may make it difficult to diagnose the disease. These subtypes include nodular, pustular, vesiculobullous, and crusted scabies (Norwegian scabies). Although rare, these subtypes merit acknowledgement, as atypical cases contribute to the high rate of misdiagnosis.

Nodular scabies is a clinical variant that accounts for about 7% of scabies cases.⁷ It can resist traditional scabies treatment (permethrin cream, ivermectin—which we’ll discuss in a bit) and often requires topical or intralesional corticosteroid management. Nodular scabies most commonly affects male genitalia. Patients may have multiple excoriated skin-colored erythematous papules and nodules in areas involving the classic distribution of scabies (web spaces of fingers, flexural areas [FIGURE 3], scrotum, and groin).⁸

IMAGE COURTESY OF VISUALDX.COM

Continue to: Pustular scabies...

Pustular scabies is commonly seen in children and adolescents but can occur in all age groups. Patients may present with vesicular pustular lesions (FIGURE 4A and 4B).⁷ In some cases, topical corticosteroids have modified the classic clinical presentation into a pustular variant. However, scabies alone can cause pustular lesions.

IMAGES COURTESY OF VISUALDX.COM

Vesiculobullous scabies (FIGURE 5A and 5B) is a clinical subtype that may be mistaken for pemphigus vulgaris⁹ or bullous pemphigoid¹⁰ because of its strikingly similar clinical presentation to those disorders.

IMAGES COURTESY OF VISUALDX.COM

Crusted scabies (Norwegian scabies) is a severe, disseminated form of scabies that commonly affects immunocompromised patients, although cases are also seen in immunocompetent hosts. Afflicted immunocompetent patients often have a history of diabetes mellitus, liver cirrhosis, malnutrition, or alcohol abuse.¹¹ Patients present with a thick powdery or crusted white or yellow scale involving the feet or hands (FIGURE 6) that sometimes extends onto the limbs. Severe ­cases can involve wide body surfaces. One unusual presentation also included a desquamating rash without pruritus.¹²

IMAGE COURTESY OF VISUALDX.COM

Highly atypical cases

Distal white or yellow, thick, scaly, or crusted plaques can suggest psoriasis or dermatitis, but you should include scabies in the differential diagnosis.

Atypical presentations include lesions that appear outside of the classic distribution areas of scabies, lesions with uncharacteristic morphology, cases with coinfections, and instances in which patients are immunocompromised.¹³ Examples include scabies of the scalp coexisting with seborrheic dermatitis or dermatomyositis,¹⁴ scabies mimicking mastocytoma,^15,16 and scabies with coinfections of impetigo or eczema.¹⁷ These coinfections and clinical variations can be particularly challenging. Other reports of atypical scabies leading to misdiagnosis include a case of crusted scabies mimicking erythrodermic psoriasis¹⁸ and a case initially attributed to suppurative folliculitis and prurigo nodularis.¹⁹

Decisive diagnostic measures

Identifying the mite’s burrow on clinical exam is essential to making the diagnosis of scabies. Microscopic examinations of burrow scrapings remain the diagnostic gold standard. Frequently, nondermatologists perform skin scrapings of the pruritic papules of scabies instead of the burrows. These papules are a hypersensitivity reaction to the mites, and no scabetic mites will be found there. Burrows appear on exam as small, linear, serpiginous lines (FIGURE 7A and 7B).

IMAGES COURTESY OF VISUALDX.COM

Continue to: Handheld illumination with a dermatoscope...

Handheld illumination with a dermatoscope will allow visualization of the mite ­(FIGURE 8). (See “How fast do scabies mites move? Dermoscopy video answers that question.”) Dermatoscope findings consistent with scabies include a “delta ­glider,” a dark triangular shape that is the mite’s head hidden in the burrow,²⁰ or the classic “jet with contrail” (FIGURE 8).²¹ Scrape the burrow to discover the mature scabies mite (FIGURE 9) and confirm the diagnosis.

COURTESY OF ROMAN BRONFENBRENER, MD

Microscopic examination of scrapings has a reported sensitivity and specificity of up to 90% and 100%, respectively, when collection of scrapings is performed accurately and contains ova, feces, or mites.^14,20,22 Dermatologists increasingly use dermatoscopes to diagnose scabies. Dermoscopy's sensitivity is 91% and specificity is 85% to 86%,¹⁴ which is a reassuring frame of reference for physicians who do not routinely use dermatoscopes and instead rely on scrapings.

Continue to: How fast do scabies mites move? Dermoscopy video answers that question

SIDEBAR
How fast do scabies mites move? Dermoscopy video answers that question

Richard Usatine, MD; Ashfaq Marghoob, MD
University of Texas Health San Antonio (Dr. Usatine); Memorial Sloan Kettering Skin Cancer Center, Hauppauge, NY (Dr. Marghoob).

Dr. Marghoob reported that he has received honoraria for speaking for 3GEN. Dr. Usatine reported no potential conflict of interest relevant to this article.

A 22-year-old man infected with human immunodeficiency virus presented to a clinic with a 6-month history of intense pruritus. Physical examination revealed scale crust on the hands and wrists (FIGURE) and in the pubic region.

Dermoscopic examination of the rash on the wrist revealed scabies mites actively crawling on the surface of the skin. A superficial skin scraping revealed the Sarcoptes scabiei mite, several eggs, and scybala under the microscope. The extensive infestation in this patient with crusted scabies was related to his immunocompromised state. (The patient was successfully treated with oral ivermectin and topical permethrin.)

Unprecedented documentation of mite speed a clue to infectivity. The 36-second VIDEO captured an adult mite travelling a distance of 3 mm, translating to a speed of 5 mm/ min. Six younger adults/larvae were moving more rapidly with a maximum distance of 6 mm in 36 seconds (1 cm/min). The movement of a mite within the epidermis is slower, as the mite consumes keratin in creating burrows. The more rapid rate of movement on the skin surface may help to explain the contagious nature of scabies.

Vidyard Video

In this case, the mites and larvae were viewed on the screen of a smartphone to which a dermatoscope was attached magnetically. The mites were first visualized in the standard photo mode. Video mode was then used to capture the motion using the maximum zoom feature of the phone, to a magnification factor of 13.3×.

Literature to date has been silent on mites’ rate of motion. A Medline search yielded only 3 papers that addressed the issue of in vivo movement of scabies mites. None viewed the mites other than in their burrows and none calculated a rate of motion.

• In one study using videodermotoscopy, Micali stated that in most of the 16 cases identified, it was possible to observe the mites moving inside the burrows.1 No video images were published, and there was no mention of speed or characterization of the movement.¹
• A second study used reflectance confocal microscopy (RCM) to examine a single patient with crusted scabies. The authors claim to have viewed the ectoparasite's motion within the human host but provided no details of that motion.²
• In the third study, videodermoscopy showed a slightly higher sensitivity for scabies detection than RCM (95% vs. 92%).³ The authors did not mention visualization of movement of mites in their work but did quote the Micali paper for its mention of movements of the mite.

Applying digital dermoscopy in practice. It appears that this is the first published video documenting the movement of scabies mites and larvae in vivo using dermoscopy. This should pave the way for additional observations of scabies movement on and below the skin using dermoscopy with video. We recommend using the maximum zoom capability of the device along with the dermatoscope to view this movement. What has been surmised before—that the mite must move above the skin to infect human contacts—has now been captured in vivo using the power of dermoscopy.

CORRESPONDENCE
Richard P. Usatine, MD, 903 West Martin Street, San Antonio, TX 78207; [email protected].

REFERENCES
1. Micali G, Lacarrubba F, Lo Guzzo G. Scraping versus videodermatoscopy for the diagnosis of scabies: a comparative study. Acta Derm Venereol. 1999; 79:396.

2. Gürel MS, Turgut Erdemir AV, Tekin B. A case report of real-time in vivo demonstration of Sarcoptes scabiei. Turkiye Parazitol Derg. 2017; 41:229-232.

3. Cinotti E, Labeille B, Cambazard F, et al. Videodermoscopy compared to reflectance confocal microscopy for the diagnosis of scabies. J Eur Acad Dermatol Venereol. 2016; 30:1573-1577.

Continue to: 3 diagnostic missteps to avoid

 

 

3 diagnostic missteps to avoid

Misdiagnosis is often due to an overreliance on the clinical history without performing an adequate physical exam. In such cases, the physician often diagnoses a form of dermatitis as the cause of pruritic rash. (Admittedly, diagnostic error can result in either false-­positive or false-negative findings, and many patients are diagnosed with scabies when they have dermatitis.)

A second misstep? Scabies may be overlooked in a patient whose lesions are nonpruritic, such as someone with an immunocompromising condition.

And finally, crusted scabies is frequently mistaken for psoriasis or chronic dermatitis.⁸

Diagnostic errors are exceedingly troublesome for patients and caregivers. It is not unusual for a hospital or long-term care facility to lose significant employee work hours due to a scabies epidemic or fear of a scabies epidemic. In a 2003 outbreak of scabies in a Canadian long-term care facility, an estimated $200,000 was needed to control disease spread.²³

A topical agent is a mainstay of treatment

Watch the video of a scabies mite on the skin surface.

Permethrin cream is usually the first-line treatment choice.²⁴ Ivermectin, topical (cream) or systemic (pill), is the commonly used alternative for patients who do not respond to, or cannot tolerate, permethrin cream. A recent meta-analysis examined the effectiveness of 5% permethrin cream, 1% ivermectin cream, and oral ivermectin (200 mcg/kg single or double dose).²⁴ Overall, findings suggested there was no difference in the efficacy or in adverse effects of permethrin cream compared with ivermectin (topical or systemic) among adults. One study reported that permethrin cream was slightly more effective than ivermectin (cream or oral) because of the more rapid treatment response (approximately 94% clearance within 2 weeks of treatment, compared with 90%).²⁵

Continue to: Adjust treatment for special populations

 

 

Adjust treatment for special populations. Treatment of severe cases, such as crusted scabies, calls for combination therapy with oral ivermectin (200 mcg/kg) and 5% permethrin cream.²⁶

Five percent permethrin cream is the preferred treatment for children weighing < 15 kg and pregnant women; oral ivermectin has not been studied for efficacy and safety in these populations.²⁷

Effective response to treatment in these studies was measured by resolution of active scabies lesions and improvement in pruritus 1 to 2 weeks after treatment.

 

Anticipate these 3 clinical scenarios

The classic appearance of scabies usually triggers suspicion of its presence, leading to prompt identification of mite burrows and a correct diagnosis. Unfortunately, though, this is not always the case. And atypical presentations heighten the chance of diagnostic error, which overall occurs in nearly half of cases.¹ Keep in mind the following common scenarios, to help improve diagnosis.

1. When a patient presents with a severe pruritic eruption, the clinician may be tempted to settle early on a form of dermatitis and not consider the possibility of scabies. When the patient is later seen by an expert, the burrows are easily identified. Solution: Whenever a patient complains of severe pruritus, use a dermatoscope to carefully examine the digits, web spaces, proximal palms, wrists, and ankles for burrows.

Continue to: A patient with distal white or yellow, thick, scaly, or crusted plaques

 

 

2. A patient with distal white or yellow, thick, scaly, or crusted plaques is often thought to have psoriasis or dermatitis. But scabies should be included in the differential diagnosis. In particular, worsening thick, scaly plaques in an immunocompromised patient should prompt consideration of scabies.

3. Smooth nodules of the genitals in males, or pruritic smooth papules and plaques in other locations, should lead to the consideration of scabies. These presentations can be mistaken for lichen planus, folliculitis, papular urticaria, insect bites, or atopic dermatitis.

Due to the limited amount of mite burrows early in the disease process of scabies, and the gross similarities to a patient with dermatitis with skin excoriations, a thorough exam is needed—one that goes beyond the traditional web spaces and includes hidden/atypical locations such as margins of the feet and hands, the scalp, and neck creases. Careful and deliberate inspection for burrows is critical before ruling out the diagnosis.

CORRESPONDENCE
Art Papier, MD, 400 Red Creek Drive, Suite 200, Rochester, NY 14623; [email protected].

ACKNOWLEDGEMENT
We thank Angela Delacenserie, MA, for reviewing the manuscript and providing editing suggestions.

It is estimated that up to 45% of cases of scabies are misdiagnosed as another condition.¹ This can occur when common clinical features are overlooked, a skin exam is rushed (and the rash is chalked up to dermatitis), or the wrong part of the pruritic lesion is scraped (the papule, rather than the burrow). There are also atypical presentations of scabies, which can confound even the most astute clinician.¹ Misdiagnosis can increase health care costs due to repeat office visits or multiple referrals. In this article, we review the typical and atypical presentations of scabies and provide recommendations to aid physicians in its early recognition and correct diagnosis.

The scope of scabies infection, and its clinical stages

The prevalence of scabies, a common skin infection caused by the mite Sarcoptes scabiei, is estimated at 300 million cases worldwide annually, with the greatest incidence occurring in children and adolescents.¹ In the developing world, its clinical burden is highest among the homeless, those of lower socioeconomic status, and those with poor hygiene. In the developed world, the clinical burden is highest among hospitalized patients and residents of long-term living facilities.

The S scabiei mite is an obligate parasite that elicits an adaptive immune response in susceptible hosts. The female mite lays 60 to 90 eggs that mature into adult mites after completing the mite life cycle in human hosts. In immunocompetent patients, roughly 10 to 15 surviving mites can be found at any given point in the disease process.² In crusted or disseminated scabies, which often occur in immunocompromised patients, thousands of mites may be found at any given point in the disease process. ²

Scabies infection has 2 stages: the latent primary infection and the symptomatic secondary infection.

The primary infection starts with the initial mite invasion, typically with the transfer of impregnated females during person-to-person contact. Females deposit eggs as they burrow into the epidermis at the level of the stratum corneum with the use of proteolytic enzymes (creating the mite burrow). Surviving eggs hatch into larvae that then mature into nymphs and adult mites. After these adult mites mate, the impregnated females create new burrows and lay additional eggs.³ Patients may be asymptomatic during this initial stage and the infection may be transmitted from person to person through direct skin contact.

In children with scabies, vesicles, pustules, and nodular pruritic lesions may coexist with eczema and impetigo.

The second stage of infection is when patients experience severe pruritus with inflammatory papules seen on exam. The pruritus associated with scabies results from a delayed type IV hypersensitivity reaction to mite infestation. This requires host sensitization to the scabies mite. Clinically, there is a delayed onset (weeks) of numerous erythematous papules and, later, excoriated papules.

Conditions that scabies can mimic

The differential of typical scabies includes diagnoses manifesting with moderate to severe pruritus. In the immunocompetent adult, conditions to consider are atopic dermatitis, tinea corporis, papular urticaria, seborrheic dermatitis, poison ivy and other causes of contact dermatitis, drug eruptions, and irritant dermatitis. In immunocompetent infants, think of seborrheic dermatitis, atopic dermatitis, acropustulosis, and viral exanthems.

Continue to: Nodular scabies variants...

Nodular scabies variants can masquerade as pseudolymphoma, lymphoma, or leukemia cutis. In immunocompromised and elderly individuals, crusted scabies is often mistaken for psoriasis, atopic dermatitis, keratoderma, and lichen planus.^2,4,5

Scabies’ classic presentation

Typically, scabies causes intensely pruritic erythematous papules. Areas commonly affected are the webs and sides of fingers ­(FIGURE 1A and 1B), proximal palm and wrist flexors, extensor aspects of the arms and legs, axillary folds, periumbilical areas, the peri-areolar region in women, buttocks and thigh creases, and, in males, the genitals. The head may also be affected in children (FIGURE 1C), but seldom in adults. Interestingly, the back is usually spared across all age groups, though not always (FIGURE 2).

IMAGE COURTESY OF VISUALDX.COM

Mites are not found near pruritic papules. Scrape the mite burrows, which are small, linear, serpiginous lines, to discover the mature scabies mite.

The classic presentation also varies across age groups and populations.² In children, vesicles, pustules, and nodular pruritic lesions may coexist with eczema and impetigo. Among homeless individuals, coinfection with impetigo and eczema is common. Elderly patients are more likely to exhibit atypical lesions.⁶ Immunocompromised patients present with atypical papular scabies, crusted scabies, or scabies that may be only mildly pruritic or nonpruritic. In underdeveloped countries, indigenous populations are more susceptible to endemic scabies, with a high risk of scabies superinfection with Streptococcus.

Scabies subtypes with varying presentations

Clinical manifestations of scabies subtypes may make it difficult to diagnose the disease. These subtypes include nodular, pustular, vesiculobullous, and crusted scabies (Norwegian scabies). Although rare, these subtypes merit acknowledgement, as atypical cases contribute to the high rate of misdiagnosis.

Nodular scabies is a clinical variant that accounts for about 7% of scabies cases.⁷ It can resist traditional scabies treatment (permethrin cream, ivermectin—which we’ll discuss in a bit) and often requires topical or intralesional corticosteroid management. Nodular scabies most commonly affects male genitalia. Patients may have multiple excoriated skin-colored erythematous papules and nodules in areas involving the classic distribution of scabies (web spaces of fingers, flexural areas [FIGURE 3], scrotum, and groin).⁸

IMAGE COURTESY OF VISUALDX.COM

Continue to: Pustular scabies...

Pustular scabies is commonly seen in children and adolescents but can occur in all age groups. Patients may present with vesicular pustular lesions (FIGURE 4A and 4B).⁷ In some cases, topical corticosteroids have modified the classic clinical presentation into a pustular variant. However, scabies alone can cause pustular lesions.

IMAGES COURTESY OF VISUALDX.COM

Vesiculobullous scabies (FIGURE 5A and 5B) is a clinical subtype that may be mistaken for pemphigus vulgaris⁹ or bullous pemphigoid¹⁰ because of its strikingly similar clinical presentation to those disorders.

IMAGES COURTESY OF VISUALDX.COM

Crusted scabies (Norwegian scabies) is a severe, disseminated form of scabies that commonly affects immunocompromised patients, although cases are also seen in immunocompetent hosts. Afflicted immunocompetent patients often have a history of diabetes mellitus, liver cirrhosis, malnutrition, or alcohol abuse.¹¹ Patients present with a thick powdery or crusted white or yellow scale involving the feet or hands (FIGURE 6) that sometimes extends onto the limbs. Severe ­cases can involve wide body surfaces. One unusual presentation also included a desquamating rash without pruritus.¹²

IMAGE COURTESY OF VISUALDX.COM

Highly atypical cases

Distal white or yellow, thick, scaly, or crusted plaques can suggest psoriasis or dermatitis, but you should include scabies in the differential diagnosis.

Atypical presentations include lesions that appear outside of the classic distribution areas of scabies, lesions with uncharacteristic morphology, cases with coinfections, and instances in which patients are immunocompromised.¹³ Examples include scabies of the scalp coexisting with seborrheic dermatitis or dermatomyositis,¹⁴ scabies mimicking mastocytoma,^15,16 and scabies with coinfections of impetigo or eczema.¹⁷ These coinfections and clinical variations can be particularly challenging. Other reports of atypical scabies leading to misdiagnosis include a case of crusted scabies mimicking erythrodermic psoriasis¹⁸ and a case initially attributed to suppurative folliculitis and prurigo nodularis.¹⁹

Decisive diagnostic measures

Identifying the mite’s burrow on clinical exam is essential to making the diagnosis of scabies. Microscopic examinations of burrow scrapings remain the diagnostic gold standard. Frequently, nondermatologists perform skin scrapings of the pruritic papules of scabies instead of the burrows. These papules are a hypersensitivity reaction to the mites, and no scabetic mites will be found there. Burrows appear on exam as small, linear, serpiginous lines (FIGURE 7A and 7B).

IMAGES COURTESY OF VISUALDX.COM

Continue to: Handheld illumination with a dermatoscope...

Handheld illumination with a dermatoscope will allow visualization of the mite ­(FIGURE 8). (See “How fast do scabies mites move? Dermoscopy video answers that question.”) Dermatoscope findings consistent with scabies include a “delta ­glider,” a dark triangular shape that is the mite’s head hidden in the burrow,²⁰ or the classic “jet with contrail” (FIGURE 8).²¹ Scrape the burrow to discover the mature scabies mite (FIGURE 9) and confirm the diagnosis.

COURTESY OF ROMAN BRONFENBRENER, MD

Microscopic examination of scrapings has a reported sensitivity and specificity of up to 90% and 100%, respectively, when collection of scrapings is performed accurately and contains ova, feces, or mites.^14,20,22 Dermatologists increasingly use dermatoscopes to diagnose scabies. Dermoscopy's sensitivity is 91% and specificity is 85% to 86%,¹⁴ which is a reassuring frame of reference for physicians who do not routinely use dermatoscopes and instead rely on scrapings.

Continue to: How fast do scabies mites move? Dermoscopy video answers that question

SIDEBAR
How fast do scabies mites move? Dermoscopy video answers that question

Richard Usatine, MD; Ashfaq Marghoob, MD
University of Texas Health San Antonio (Dr. Usatine); Memorial Sloan Kettering Skin Cancer Center, Hauppauge, NY (Dr. Marghoob).

Dr. Marghoob reported that he has received honoraria for speaking for 3GEN. Dr. Usatine reported no potential conflict of interest relevant to this article.

A 22-year-old man infected with human immunodeficiency virus presented to a clinic with a 6-month history of intense pruritus. Physical examination revealed scale crust on the hands and wrists (FIGURE) and in the pubic region.

Dermoscopic examination of the rash on the wrist revealed scabies mites actively crawling on the surface of the skin. A superficial skin scraping revealed the Sarcoptes scabiei mite, several eggs, and scybala under the microscope. The extensive infestation in this patient with crusted scabies was related to his immunocompromised state. (The patient was successfully treated with oral ivermectin and topical permethrin.)

Unprecedented documentation of mite speed a clue to infectivity. The 36-second VIDEO captured an adult mite travelling a distance of 3 mm, translating to a speed of 5 mm/ min. Six younger adults/larvae were moving more rapidly with a maximum distance of 6 mm in 36 seconds (1 cm/min). The movement of a mite within the epidermis is slower, as the mite consumes keratin in creating burrows. The more rapid rate of movement on the skin surface may help to explain the contagious nature of scabies.

Vidyard Video

In this case, the mites and larvae were viewed on the screen of a smartphone to which a dermatoscope was attached magnetically. The mites were first visualized in the standard photo mode. Video mode was then used to capture the motion using the maximum zoom feature of the phone, to a magnification factor of 13.3×.

Literature to date has been silent on mites’ rate of motion. A Medline search yielded only 3 papers that addressed the issue of in vivo movement of scabies mites. None viewed the mites other than in their burrows and none calculated a rate of motion.

• In one study using videodermotoscopy, Micali stated that in most of the 16 cases identified, it was possible to observe the mites moving inside the burrows.1 No video images were published, and there was no mention of speed or characterization of the movement.¹
• A second study used reflectance confocal microscopy (RCM) to examine a single patient with crusted scabies. The authors claim to have viewed the ectoparasite's motion within the human host but provided no details of that motion.²
• In the third study, videodermoscopy showed a slightly higher sensitivity for scabies detection than RCM (95% vs. 92%).³ The authors did not mention visualization of movement of mites in their work but did quote the Micali paper for its mention of movements of the mite.

Applying digital dermoscopy in practice. It appears that this is the first published video documenting the movement of scabies mites and larvae in vivo using dermoscopy. This should pave the way for additional observations of scabies movement on and below the skin using dermoscopy with video. We recommend using the maximum zoom capability of the device along with the dermatoscope to view this movement. What has been surmised before—that the mite must move above the skin to infect human contacts—has now been captured in vivo using the power of dermoscopy.

CORRESPONDENCE
Richard P. Usatine, MD, 903 West Martin Street, San Antonio, TX 78207; [email protected].

REFERENCES
1. Micali G, Lacarrubba F, Lo Guzzo G. Scraping versus videodermatoscopy for the diagnosis of scabies: a comparative study. Acta Derm Venereol. 1999; 79:396.

2. Gürel MS, Turgut Erdemir AV, Tekin B. A case report of real-time in vivo demonstration of Sarcoptes scabiei. Turkiye Parazitol Derg. 2017; 41:229-232.

3. Cinotti E, Labeille B, Cambazard F, et al. Videodermoscopy compared to reflectance confocal microscopy for the diagnosis of scabies. J Eur Acad Dermatol Venereol. 2016; 30:1573-1577.

Continue to: 3 diagnostic missteps to avoid

 

 

3 diagnostic missteps to avoid

Misdiagnosis is often due to an overreliance on the clinical history without performing an adequate physical exam. In such cases, the physician often diagnoses a form of dermatitis as the cause of pruritic rash. (Admittedly, diagnostic error can result in either false-­positive or false-negative findings, and many patients are diagnosed with scabies when they have dermatitis.)

A second misstep? Scabies may be overlooked in a patient whose lesions are nonpruritic, such as someone with an immunocompromising condition.

And finally, crusted scabies is frequently mistaken for psoriasis or chronic dermatitis.⁸

Diagnostic errors are exceedingly troublesome for patients and caregivers. It is not unusual for a hospital or long-term care facility to lose significant employee work hours due to a scabies epidemic or fear of a scabies epidemic. In a 2003 outbreak of scabies in a Canadian long-term care facility, an estimated $200,000 was needed to control disease spread.²³

A topical agent is a mainstay of treatment

Watch the video of a scabies mite on the skin surface.

Permethrin cream is usually the first-line treatment choice.²⁴ Ivermectin, topical (cream) or systemic (pill), is the commonly used alternative for patients who do not respond to, or cannot tolerate, permethrin cream. A recent meta-analysis examined the effectiveness of 5% permethrin cream, 1% ivermectin cream, and oral ivermectin (200 mcg/kg single or double dose).²⁴ Overall, findings suggested there was no difference in the efficacy or in adverse effects of permethrin cream compared with ivermectin (topical or systemic) among adults. One study reported that permethrin cream was slightly more effective than ivermectin (cream or oral) because of the more rapid treatment response (approximately 94% clearance within 2 weeks of treatment, compared with 90%).²⁵

Continue to: Adjust treatment for special populations

 

 

Adjust treatment for special populations. Treatment of severe cases, such as crusted scabies, calls for combination therapy with oral ivermectin (200 mcg/kg) and 5% permethrin cream.²⁶

Five percent permethrin cream is the preferred treatment for children weighing < 15 kg and pregnant women; oral ivermectin has not been studied for efficacy and safety in these populations.²⁷

Effective response to treatment in these studies was measured by resolution of active scabies lesions and improvement in pruritus 1 to 2 weeks after treatment.

 

Anticipate these 3 clinical scenarios

The classic appearance of scabies usually triggers suspicion of its presence, leading to prompt identification of mite burrows and a correct diagnosis. Unfortunately, though, this is not always the case. And atypical presentations heighten the chance of diagnostic error, which overall occurs in nearly half of cases.¹ Keep in mind the following common scenarios, to help improve diagnosis.

1. When a patient presents with a severe pruritic eruption, the clinician may be tempted to settle early on a form of dermatitis and not consider the possibility of scabies. When the patient is later seen by an expert, the burrows are easily identified. Solution: Whenever a patient complains of severe pruritus, use a dermatoscope to carefully examine the digits, web spaces, proximal palms, wrists, and ankles for burrows.

Continue to: A patient with distal white or yellow, thick, scaly, or crusted plaques

 

 

2. A patient with distal white or yellow, thick, scaly, or crusted plaques is often thought to have psoriasis or dermatitis. But scabies should be included in the differential diagnosis. In particular, worsening thick, scaly plaques in an immunocompromised patient should prompt consideration of scabies.

3. Smooth nodules of the genitals in males, or pruritic smooth papules and plaques in other locations, should lead to the consideration of scabies. These presentations can be mistaken for lichen planus, folliculitis, papular urticaria, insect bites, or atopic dermatitis.

Due to the limited amount of mite burrows early in the disease process of scabies, and the gross similarities to a patient with dermatitis with skin excoriations, a thorough exam is needed—one that goes beyond the traditional web spaces and includes hidden/atypical locations such as margins of the feet and hands, the scalp, and neck creases. Careful and deliberate inspection for burrows is critical before ruling out the diagnosis.

CORRESPONDENCE
Art Papier, MD, 400 Red Creek Drive, Suite 200, Rochester, NY 14623; [email protected].

ACKNOWLEDGEMENT
We thank Angela Delacenserie, MA, for reviewing the manuscript and providing editing suggestions.

It is estimated that up to 45% of cases of scabies are misdiagnosed as another condition.¹ This can occur when common clinical features are overlooked, a skin exam is rushed (and the rash is chalked up to dermatitis), or the wrong part of the pruritic lesion is scraped (the papule, rather than the burrow). There are also atypical presentations of scabies, which can confound even the most astute clinician.¹ Misdiagnosis can increase health care costs due to repeat office visits or multiple referrals. In this article, we review the typical and atypical presentations of scabies and provide recommendations to aid physicians in its early recognition and correct diagnosis.

The scope of scabies infection, and its clinical stages

The prevalence of scabies, a common skin infection caused by the mite Sarcoptes scabiei, is estimated at 300 million cases worldwide annually, with the greatest incidence occurring in children and adolescents.¹ In the developing world, its clinical burden is highest among the homeless, those of lower socioeconomic status, and those with poor hygiene. In the developed world, the clinical burden is highest among hospitalized patients and residents of long-term living facilities.

The S scabiei mite is an obligate parasite that elicits an adaptive immune response in susceptible hosts. The female mite lays 60 to 90 eggs that mature into adult mites after completing the mite life cycle in human hosts. In immunocompetent patients, roughly 10 to 15 surviving mites can be found at any given point in the disease process.² In crusted or disseminated scabies, which often occur in immunocompromised patients, thousands of mites may be found at any given point in the disease process. ²

Scabies infection has 2 stages: the latent primary infection and the symptomatic secondary infection.

The primary infection starts with the initial mite invasion, typically with the transfer of impregnated females during person-to-person contact. Females deposit eggs as they burrow into the epidermis at the level of the stratum corneum with the use of proteolytic enzymes (creating the mite burrow). Surviving eggs hatch into larvae that then mature into nymphs and adult mites. After these adult mites mate, the impregnated females create new burrows and lay additional eggs.³ Patients may be asymptomatic during this initial stage and the infection may be transmitted from person to person through direct skin contact.

In children with scabies, vesicles, pustules, and nodular pruritic lesions may coexist with eczema and impetigo.

The second stage of infection is when patients experience severe pruritus with inflammatory papules seen on exam. The pruritus associated with scabies results from a delayed type IV hypersensitivity reaction to mite infestation. This requires host sensitization to the scabies mite. Clinically, there is a delayed onset (weeks) of numerous erythematous papules and, later, excoriated papules.

Conditions that scabies can mimic

The differential of typical scabies includes diagnoses manifesting with moderate to severe pruritus. In the immunocompetent adult, conditions to consider are atopic dermatitis, tinea corporis, papular urticaria, seborrheic dermatitis, poison ivy and other causes of contact dermatitis, drug eruptions, and irritant dermatitis. In immunocompetent infants, think of seborrheic dermatitis, atopic dermatitis, acropustulosis, and viral exanthems.

Continue to: Nodular scabies variants...

Nodular scabies variants can masquerade as pseudolymphoma, lymphoma, or leukemia cutis. In immunocompromised and elderly individuals, crusted scabies is often mistaken for psoriasis, atopic dermatitis, keratoderma, and lichen planus.^2,4,5

Scabies’ classic presentation

Typically, scabies causes intensely pruritic erythematous papules. Areas commonly affected are the webs and sides of fingers ­(FIGURE 1A and 1B), proximal palm and wrist flexors, extensor aspects of the arms and legs, axillary folds, periumbilical areas, the peri-areolar region in women, buttocks and thigh creases, and, in males, the genitals. The head may also be affected in children (FIGURE 1C), but seldom in adults. Interestingly, the back is usually spared across all age groups, though not always (FIGURE 2).

IMAGE COURTESY OF VISUALDX.COM

Mites are not found near pruritic papules. Scrape the mite burrows, which are small, linear, serpiginous lines, to discover the mature scabies mite.

The classic presentation also varies across age groups and populations.² In children, vesicles, pustules, and nodular pruritic lesions may coexist with eczema and impetigo. Among homeless individuals, coinfection with impetigo and eczema is common. Elderly patients are more likely to exhibit atypical lesions.⁶ Immunocompromised patients present with atypical papular scabies, crusted scabies, or scabies that may be only mildly pruritic or nonpruritic. In underdeveloped countries, indigenous populations are more susceptible to endemic scabies, with a high risk of scabies superinfection with Streptococcus.

Scabies subtypes with varying presentations

Clinical manifestations of scabies subtypes may make it difficult to diagnose the disease. These subtypes include nodular, pustular, vesiculobullous, and crusted scabies (Norwegian scabies). Although rare, these subtypes merit acknowledgement, as atypical cases contribute to the high rate of misdiagnosis.

Nodular scabies is a clinical variant that accounts for about 7% of scabies cases.⁷ It can resist traditional scabies treatment (permethrin cream, ivermectin—which we’ll discuss in a bit) and often requires topical or intralesional corticosteroid management. Nodular scabies most commonly affects male genitalia. Patients may have multiple excoriated skin-colored erythematous papules and nodules in areas involving the classic distribution of scabies (web spaces of fingers, flexural areas [FIGURE 3], scrotum, and groin).⁸

IMAGE COURTESY OF VISUALDX.COM

Continue to: Pustular scabies...

Pustular scabies is commonly seen in children and adolescents but can occur in all age groups. Patients may present with vesicular pustular lesions (FIGURE 4A and 4B).⁷ In some cases, topical corticosteroids have modified the classic clinical presentation into a pustular variant. However, scabies alone can cause pustular lesions.

IMAGES COURTESY OF VISUALDX.COM

Vesiculobullous scabies (FIGURE 5A and 5B) is a clinical subtype that may be mistaken for pemphigus vulgaris⁹ or bullous pemphigoid¹⁰ because of its strikingly similar clinical presentation to those disorders.

IMAGES COURTESY OF VISUALDX.COM

Crusted scabies (Norwegian scabies) is a severe, disseminated form of scabies that commonly affects immunocompromised patients, although cases are also seen in immunocompetent hosts. Afflicted immunocompetent patients often have a history of diabetes mellitus, liver cirrhosis, malnutrition, or alcohol abuse.¹¹ Patients present with a thick powdery or crusted white or yellow scale involving the feet or hands (FIGURE 6) that sometimes extends onto the limbs. Severe ­cases can involve wide body surfaces. One unusual presentation also included a desquamating rash without pruritus.¹²

IMAGE COURTESY OF VISUALDX.COM

Highly atypical cases

Distal white or yellow, thick, scaly, or crusted plaques can suggest psoriasis or dermatitis, but you should include scabies in the differential diagnosis.

Atypical presentations include lesions that appear outside of the classic distribution areas of scabies, lesions with uncharacteristic morphology, cases with coinfections, and instances in which patients are immunocompromised.¹³ Examples include scabies of the scalp coexisting with seborrheic dermatitis or dermatomyositis,¹⁴ scabies mimicking mastocytoma,^15,16 and scabies with coinfections of impetigo or eczema.¹⁷ These coinfections and clinical variations can be particularly challenging. Other reports of atypical scabies leading to misdiagnosis include a case of crusted scabies mimicking erythrodermic psoriasis¹⁸ and a case initially attributed to suppurative folliculitis and prurigo nodularis.¹⁹

Decisive diagnostic measures

Identifying the mite’s burrow on clinical exam is essential to making the diagnosis of scabies. Microscopic examinations of burrow scrapings remain the diagnostic gold standard. Frequently, nondermatologists perform skin scrapings of the pruritic papules of scabies instead of the burrows. These papules are a hypersensitivity reaction to the mites, and no scabetic mites will be found there. Burrows appear on exam as small, linear, serpiginous lines (FIGURE 7A and 7B).

IMAGES COURTESY OF VISUALDX.COM

Continue to: Handheld illumination with a dermatoscope...

Handheld illumination with a dermatoscope will allow visualization of the mite ­(FIGURE 8). (See “How fast do scabies mites move? Dermoscopy video answers that question.”) Dermatoscope findings consistent with scabies include a “delta ­glider,” a dark triangular shape that is the mite’s head hidden in the burrow,²⁰ or the classic “jet with contrail” (FIGURE 8).²¹ Scrape the burrow to discover the mature scabies mite (FIGURE 9) and confirm the diagnosis.

COURTESY OF ROMAN BRONFENBRENER, MD

Microscopic examination of scrapings has a reported sensitivity and specificity of up to 90% and 100%, respectively, when collection of scrapings is performed accurately and contains ova, feces, or mites.^14,20,22 Dermatologists increasingly use dermatoscopes to diagnose scabies. Dermoscopy's sensitivity is 91% and specificity is 85% to 86%,¹⁴ which is a reassuring frame of reference for physicians who do not routinely use dermatoscopes and instead rely on scrapings.

Continue to: How fast do scabies mites move? Dermoscopy video answers that question

SIDEBAR
How fast do scabies mites move? Dermoscopy video answers that question

Richard Usatine, MD; Ashfaq Marghoob, MD
University of Texas Health San Antonio (Dr. Usatine); Memorial Sloan Kettering Skin Cancer Center, Hauppauge, NY (Dr. Marghoob).

Dr. Marghoob reported that he has received honoraria for speaking for 3GEN. Dr. Usatine reported no potential conflict of interest relevant to this article.

A 22-year-old man infected with human immunodeficiency virus presented to a clinic with a 6-month history of intense pruritus. Physical examination revealed scale crust on the hands and wrists (FIGURE) and in the pubic region.

Dermoscopic examination of the rash on the wrist revealed scabies mites actively crawling on the surface of the skin. A superficial skin scraping revealed the Sarcoptes scabiei mite, several eggs, and scybala under the microscope. The extensive infestation in this patient with crusted scabies was related to his immunocompromised state. (The patient was successfully treated with oral ivermectin and topical permethrin.)

Unprecedented documentation of mite speed a clue to infectivity. The 36-second VIDEO captured an adult mite travelling a distance of 3 mm, translating to a speed of 5 mm/ min. Six younger adults/larvae were moving more rapidly with a maximum distance of 6 mm in 36 seconds (1 cm/min). The movement of a mite within the epidermis is slower, as the mite consumes keratin in creating burrows. The more rapid rate of movement on the skin surface may help to explain the contagious nature of scabies.

Vidyard Video

In this case, the mites and larvae were viewed on the screen of a smartphone to which a dermatoscope was attached magnetically. The mites were first visualized in the standard photo mode. Video mode was then used to capture the motion using the maximum zoom feature of the phone, to a magnification factor of 13.3×.

Literature to date has been silent on mites’ rate of motion. A Medline search yielded only 3 papers that addressed the issue of in vivo movement of scabies mites. None viewed the mites other than in their burrows and none calculated a rate of motion.

• In one study using videodermotoscopy, Micali stated that in most of the 16 cases identified, it was possible to observe the mites moving inside the burrows.1 No video images were published, and there was no mention of speed or characterization of the movement.¹
• A second study used reflectance confocal microscopy (RCM) to examine a single patient with crusted scabies. The authors claim to have viewed the ectoparasite's motion within the human host but provided no details of that motion.²
• In the third study, videodermoscopy showed a slightly higher sensitivity for scabies detection than RCM (95% vs. 92%).³ The authors did not mention visualization of movement of mites in their work but did quote the Micali paper for its mention of movements of the mite.

Applying digital dermoscopy in practice. It appears that this is the first published video documenting the movement of scabies mites and larvae in vivo using dermoscopy. This should pave the way for additional observations of scabies movement on and below the skin using dermoscopy with video. We recommend using the maximum zoom capability of the device along with the dermatoscope to view this movement. What has been surmised before—that the mite must move above the skin to infect human contacts—has now been captured in vivo using the power of dermoscopy.

CORRESPONDENCE
Richard P. Usatine, MD, 903 West Martin Street, San Antonio, TX 78207; [email protected].

REFERENCES
1. Micali G, Lacarrubba F, Lo Guzzo G. Scraping versus videodermatoscopy for the diagnosis of scabies: a comparative study. Acta Derm Venereol. 1999; 79:396.

2. Gürel MS, Turgut Erdemir AV, Tekin B. A case report of real-time in vivo demonstration of Sarcoptes scabiei. Turkiye Parazitol Derg. 2017; 41:229-232.

3. Cinotti E, Labeille B, Cambazard F, et al. Videodermoscopy compared to reflectance confocal microscopy for the diagnosis of scabies. J Eur Acad Dermatol Venereol. 2016; 30:1573-1577.

Continue to: 3 diagnostic missteps to avoid

 

 

3 diagnostic missteps to avoid

Misdiagnosis is often due to an overreliance on the clinical history without performing an adequate physical exam. In such cases, the physician often diagnoses a form of dermatitis as the cause of pruritic rash. (Admittedly, diagnostic error can result in either false-­positive or false-negative findings, and many patients are diagnosed with scabies when they have dermatitis.)

A second misstep? Scabies may be overlooked in a patient whose lesions are nonpruritic, such as someone with an immunocompromising condition.

And finally, crusted scabies is frequently mistaken for psoriasis or chronic dermatitis.⁸

Diagnostic errors are exceedingly troublesome for patients and caregivers. It is not unusual for a hospital or long-term care facility to lose significant employee work hours due to a scabies epidemic or fear of a scabies epidemic. In a 2003 outbreak of scabies in a Canadian long-term care facility, an estimated $200,000 was needed to control disease spread.²³

A topical agent is a mainstay of treatment

Watch the video of a scabies mite on the skin surface.

Permethrin cream is usually the first-line treatment choice.²⁴ Ivermectin, topical (cream) or systemic (pill), is the commonly used alternative for patients who do not respond to, or cannot tolerate, permethrin cream. A recent meta-analysis examined the effectiveness of 5% permethrin cream, 1% ivermectin cream, and oral ivermectin (200 mcg/kg single or double dose).²⁴ Overall, findings suggested there was no difference in the efficacy or in adverse effects of permethrin cream compared with ivermectin (topical or systemic) among adults. One study reported that permethrin cream was slightly more effective than ivermectin (cream or oral) because of the more rapid treatment response (approximately 94% clearance within 2 weeks of treatment, compared with 90%).²⁵

Continue to: Adjust treatment for special populations

 

 

Adjust treatment for special populations. Treatment of severe cases, such as crusted scabies, calls for combination therapy with oral ivermectin (200 mcg/kg) and 5% permethrin cream.²⁶

Five percent permethrin cream is the preferred treatment for children weighing < 15 kg and pregnant women; oral ivermectin has not been studied for efficacy and safety in these populations.²⁷

Effective response to treatment in these studies was measured by resolution of active scabies lesions and improvement in pruritus 1 to 2 weeks after treatment.

 

Anticipate these 3 clinical scenarios

The classic appearance of scabies usually triggers suspicion of its presence, leading to prompt identification of mite burrows and a correct diagnosis. Unfortunately, though, this is not always the case. And atypical presentations heighten the chance of diagnostic error, which overall occurs in nearly half of cases.¹ Keep in mind the following common scenarios, to help improve diagnosis.

1. When a patient presents with a severe pruritic eruption, the clinician may be tempted to settle early on a form of dermatitis and not consider the possibility of scabies. When the patient is later seen by an expert, the burrows are easily identified. Solution: Whenever a patient complains of severe pruritus, use a dermatoscope to carefully examine the digits, web spaces, proximal palms, wrists, and ankles for burrows.

Continue to: A patient with distal white or yellow, thick, scaly, or crusted plaques

 

 

2. A patient with distal white or yellow, thick, scaly, or crusted plaques is often thought to have psoriasis or dermatitis. But scabies should be included in the differential diagnosis. In particular, worsening thick, scaly plaques in an immunocompromised patient should prompt consideration of scabies.

3. Smooth nodules of the genitals in males, or pruritic smooth papules and plaques in other locations, should lead to the consideration of scabies. These presentations can be mistaken for lichen planus, folliculitis, papular urticaria, insect bites, or atopic dermatitis.

Due to the limited amount of mite burrows early in the disease process of scabies, and the gross similarities to a patient with dermatitis with skin excoriations, a thorough exam is needed—one that goes beyond the traditional web spaces and includes hidden/atypical locations such as margins of the feet and hands, the scalp, and neck creases. Careful and deliberate inspection for burrows is critical before ruling out the diagnosis.

CORRESPONDENCE
Art Papier, MD, 400 Red Creek Drive, Suite 200, Rochester, NY 14623; [email protected].

ACKNOWLEDGEMENT
We thank Angela Delacenserie, MA, for reviewing the manuscript and providing editing suggestions.

The Food and Drug Administration has granted accelerated approval to tazemetostat (Tazverik) for the treatment of adults and pediatric patients aged 16 years and older with metastatic or locally advanced epithelioid sarcoma not eligible for complete resection.

Olivier Le Moal/Getty Images

Approval was based on overall response rate in a trial enrolling 62 patients with metastatic or locally advanced epithelioid sarcoma. The overall response rate was 15%, with 1.6% of patients having a complete response and 13% having a partial response. Of the nine patients that had a response, six (67%) had a response lasting 6 months or longer, the FDA said in a press statement.

The most common side effects for patients taking tazemetostat were pain, fatigue, nausea, decreased appetite, vomiting, and constipation. Patients treated with tazemetostat are at increased risk of developing secondary malignancies, including T-cell lymphoblastic lymphoma, myelodysplastic syndrome, and acute myeloid leukemia.

“Epithelioid sarcoma accounts for less than 1% of all soft-tissue sarcomas,” said Richard Pazdur, MD, director of the FDA’s Oncology Center of Excellence and acting director of the Office of Oncologic Diseases in the Center for Drug Evaluation and Research. “Until today, there were no treatment options specifically for patients with epithelioid sarcoma. The approval of Tazverik provides a treatment option that specifically targets this disease.”

Tazemetostat must be dispensed with a patient medication guide that describes important information about the drug’s uses and risks, the FDA said.

[email protected]

The Food and Drug Administration has granted accelerated approval to tazemetostat (Tazverik) for the treatment of adults and pediatric patients aged 16 years and older with metastatic or locally advanced epithelioid sarcoma not eligible for complete resection.

Olivier Le Moal/Getty Images

Approval was based on overall response rate in a trial enrolling 62 patients with metastatic or locally advanced epithelioid sarcoma. The overall response rate was 15%, with 1.6% of patients having a complete response and 13% having a partial response. Of the nine patients that had a response, six (67%) had a response lasting 6 months or longer, the FDA said in a press statement.

The most common side effects for patients taking tazemetostat were pain, fatigue, nausea, decreased appetite, vomiting, and constipation. Patients treated with tazemetostat are at increased risk of developing secondary malignancies, including T-cell lymphoblastic lymphoma, myelodysplastic syndrome, and acute myeloid leukemia.

“Epithelioid sarcoma accounts for less than 1% of all soft-tissue sarcomas,” said Richard Pazdur, MD, director of the FDA’s Oncology Center of Excellence and acting director of the Office of Oncologic Diseases in the Center for Drug Evaluation and Research. “Until today, there were no treatment options specifically for patients with epithelioid sarcoma. The approval of Tazverik provides a treatment option that specifically targets this disease.”

Tazemetostat must be dispensed with a patient medication guide that describes important information about the drug’s uses and risks, the FDA said.

[email protected]

The Food and Drug Administration has granted accelerated approval to tazemetostat (Tazverik) for the treatment of adults and pediatric patients aged 16 years and older with metastatic or locally advanced epithelioid sarcoma not eligible for complete resection.

Olivier Le Moal/Getty Images

Approval was based on overall response rate in a trial enrolling 62 patients with metastatic or locally advanced epithelioid sarcoma. The overall response rate was 15%, with 1.6% of patients having a complete response and 13% having a partial response. Of the nine patients that had a response, six (67%) had a response lasting 6 months or longer, the FDA said in a press statement.

The most common side effects for patients taking tazemetostat were pain, fatigue, nausea, decreased appetite, vomiting, and constipation. Patients treated with tazemetostat are at increased risk of developing secondary malignancies, including T-cell lymphoblastic lymphoma, myelodysplastic syndrome, and acute myeloid leukemia.

“Epithelioid sarcoma accounts for less than 1% of all soft-tissue sarcomas,” said Richard Pazdur, MD, director of the FDA’s Oncology Center of Excellence and acting director of the Office of Oncologic Diseases in the Center for Drug Evaluation and Research. “Until today, there were no treatment options specifically for patients with epithelioid sarcoma. The approval of Tazverik provides a treatment option that specifically targets this disease.”

Tazemetostat must be dispensed with a patient medication guide that describes important information about the drug’s uses and risks, the FDA said.

[email protected]

Given the constellation of non-scarring alopecia on the patient’s posterior scalp (with no scale, papules, or plaques), the physician diagnosed alopecia areata (AA) with associated nail pitting in this patient. Although a scalp biopsy could have confirmed the diagnosis, it was not needed because the clinical picture was sufficient.

Nail pitting is commonly associated with psoriasis (although it is often less dense in presentation), but it can occur with alopecia areata. It may occur concurrently or separately from active alopecia. Pitting of the nails may occur in one or multiple fingernails and occurs in up to a third of patients with AA.

The patient’s scalp was treated with intralesional triamcinolone diluted with normal saline to a concentration of 5 mg/mL (0.5%) and injected in dermal blebs over every square centimeter of involvement. Not every 10-year-old can tolerate this modality, and many families prefer observation or topical steroids. Other topical treatments for AA of the scalp include anthralin, minoxidil, and immunotherapy with squaric acid dibutyl ester or diphencyprone. None of these therapies are approved by the Food and Drug Administration for the treatment of nail disease. There are case reports of systemic tofacitinib clearing significant AA associated nail pitting in adults.

The physician counseled the family to observe the nails and not pursue any antifungal therapies for the nails.

‌

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.

Given the constellation of non-scarring alopecia on the patient’s posterior scalp (with no scale, papules, or plaques), the physician diagnosed alopecia areata (AA) with associated nail pitting in this patient. Although a scalp biopsy could have confirmed the diagnosis, it was not needed because the clinical picture was sufficient.

Nail pitting is commonly associated with psoriasis (although it is often less dense in presentation), but it can occur with alopecia areata. It may occur concurrently or separately from active alopecia. Pitting of the nails may occur in one or multiple fingernails and occurs in up to a third of patients with AA.

The patient’s scalp was treated with intralesional triamcinolone diluted with normal saline to a concentration of 5 mg/mL (0.5%) and injected in dermal blebs over every square centimeter of involvement. Not every 10-year-old can tolerate this modality, and many families prefer observation or topical steroids. Other topical treatments for AA of the scalp include anthralin, minoxidil, and immunotherapy with squaric acid dibutyl ester or diphencyprone. None of these therapies are approved by the Food and Drug Administration for the treatment of nail disease. There are case reports of systemic tofacitinib clearing significant AA associated nail pitting in adults.

The physician counseled the family to observe the nails and not pursue any antifungal therapies for the nails.

‌

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.

Given the constellation of non-scarring alopecia on the patient’s posterior scalp (with no scale, papules, or plaques), the physician diagnosed alopecia areata (AA) with associated nail pitting in this patient. Although a scalp biopsy could have confirmed the diagnosis, it was not needed because the clinical picture was sufficient.

Nail pitting is commonly associated with psoriasis (although it is often less dense in presentation), but it can occur with alopecia areata. It may occur concurrently or separately from active alopecia. Pitting of the nails may occur in one or multiple fingernails and occurs in up to a third of patients with AA.

The patient’s scalp was treated with intralesional triamcinolone diluted with normal saline to a concentration of 5 mg/mL (0.5%) and injected in dermal blebs over every square centimeter of involvement. Not every 10-year-old can tolerate this modality, and many families prefer observation or topical steroids. Other topical treatments for AA of the scalp include anthralin, minoxidil, and immunotherapy with squaric acid dibutyl ester or diphencyprone. None of these therapies are approved by the Food and Drug Administration for the treatment of nail disease. There are case reports of systemic tofacitinib clearing significant AA associated nail pitting in adults.

The physician counseled the family to observe the nails and not pursue any antifungal therapies for the nails.

‌

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.

Six active ingredients used in sunscreen products in the United States showed systemic skin absorption with geometric mean plasma concentrations greater than 0.5 ng/mL in a randomized trial including four product types. The results were published in JAMA.

The testing was done as part of a proposed rule on sunscreen, published in February 2019, which requested additional information on sunscreen ingredients. Murali K. Matta, PhD, of the Food and Drug Administration and coauthors wrote that these plasma concentrations “surpassed the FDA threshold for potentially waiving additional safety studies for sunscreens.” But, they added, the findings “do not indicate that individuals should refrain from the use of sunscreen.”

This was a follow-up study to a smaller study of 24 health volunteers published last year that determined that the sunscreen active ingredients tested were absorbed systemically (JAMA. 2019;321[21]:2082-91). “This follow-up study expanded the sample size, tested additional sunscreen active ingredients and formulations, and confirmed the finding that sunscreen active ingredients are systemically absorbed,” the authors wrote.

To gather information on the absorption of active ingredients in sunscreens, the investigators randomized 48 adults to one of four sunscreen products (lotion, aerosol spray, nonaerosol spray, or pump spray) with one of six active ingredients (avobenzone, oxybenzone, octocrylene, homosalate, octisalate, and octinoxate). Not all products contained each of the ingredients.

The participants applied the products in amounts of 2 mg/cm² to 75% of body surface area at baseline, no use on day 1 and four times a day at 2-hour intervals on days 2 through 4. The researchers collected blood samples over 21 days and measured the maximum plasma concentrations. The average age of the participants was 37 years, and half were women. The study was conducted in a clinical pharmacology unit.

The geometric mean maximum plasma concentrations for the primary endpoint of avobenzone in lotion, aerosol spray, nonaerosol spray, and pump spray were 7.1 ng/mL, 3.5 ng/mL, 3.5 ng/mL, and 3.3 ng/mL, respectively.

For oxybenzone, the concentrations were 258.1 ng/mL and 180.1 ng/mL, respectively, for lotion and aerosol spray. The concentrations for octocrylene were 7.8 ng/mL, 6.6 ng/mL, and 6.6 ng/mL, respectively, for lotion, aerosol spray, and nonaerosol spray.

For homosalate, the geometric mean plasma concentrations were 23.1 ng/mL for aerosol spray, 17.9 for nonaerosol spray, and 13.9 for pump spray. For octisalate, the concentrations were 5.1 ng/mL, 5.8 ng/mL, and 4.6 ng/mL, respectively, for aerosol spray, nonaerosol spray, and pump spray. For octinoxate, the concentrations were 7.9 ng/mL for nonaerosol spray and 5.2 ng/mL for pump spray.

“The systemic exposures, as measured by geometric mean maximum plasma concentrations, of all the tested active ingredients were higher than 0.5 ng/mL after a single application,” the researchers noted.

Overall, the most common event was rash, which was reported in 14 participants.

The study findings were limited by several factors including the use of an indoor clinical setting, rather than outdoor exposure; the inability to assess absorption differences by formulation and Fitzpatrick skin type; and the variation in amounts of ingredients among products, the researchers noted. However, the results can be used to design additional studies needed to research the effects of systemic exposure to sunscreen ingredients, they said.

In an accompanying editorial (JAMA. 2020;323:223-4), Adewole S. Adamson, MD, of the University of Texas at Austin, and Kanade Shinkai, MD, of the University of California, San Francisco, wrote that “the study did not address key questions about sunscreen safety,” including the length of time it takes “for plasma concentrations of sunscreen ingredients to fall below the FDA threshold for safety testing.” Dr. Shinkai is also editor in chief of JAMA Dermatology.

“In making an informed decision, clinicians must determine whether the magnitude of the benefit exceeds the risk of potential harm for a specific individual,” they said. “Importantly, this balance may be different, depending on characteristics of the sunscreen user (e.g., for individuals with darker skin types and for children) and may depend on the frequency and duration of application (e.g., daily vs. intermittent use; starting in infancy or later in life),” they noted.

“In the absence of clear data demonstrating harm, the use of chemical sunscreen may still be considered appropriate; the use of mineral-based sunscreen is a well-established safe alternative,” although the potential harms remain uncertain until the sunscreen industry conducts the safety studies recommended by the FDA, Dr. Adamson and Dr. Shinkai concluded.

In a statement released by the FDA on Jan 21, the day the study was published, Janet Woodcock, MD, director of the FDA’s Center for Drug Evaluation and Research, said that, considering the “recognized public health benefits” of using sunscreen, the FDA “urges Americans to use sunscreens in conjunction with other sun protective measures (such as protective clothing).”

Commenting on the study, she said, “results from our study released today show there is evidence that some sunscreen active ingredients may be absorbed. However, the fact that an ingredient is absorbed through the skin and into the body does not mean that the ingredient is unsafe, nor does the FDA seeking further information indicate such. Rather, this finding calls for further industry testing to determine the safety and effect of systemic exposure of sunscreen ingredients, especially with chronic use.”

The study was supported by the FDA. The researchers and editorial authors had no financial conflicts to disclose.

SOURCES: Matta MK et al. JAMA. 2020;323:256-267.

Six active ingredients used in sunscreen products in the United States showed systemic skin absorption with geometric mean plasma concentrations greater than 0.5 ng/mL in a randomized trial including four product types. The results were published in JAMA.

The testing was done as part of a proposed rule on sunscreen, published in February 2019, which requested additional information on sunscreen ingredients. Murali K. Matta, PhD, of the Food and Drug Administration and coauthors wrote that these plasma concentrations “surpassed the FDA threshold for potentially waiving additional safety studies for sunscreens.” But, they added, the findings “do not indicate that individuals should refrain from the use of sunscreen.”

This was a follow-up study to a smaller study of 24 health volunteers published last year that determined that the sunscreen active ingredients tested were absorbed systemically (JAMA. 2019;321[21]:2082-91). “This follow-up study expanded the sample size, tested additional sunscreen active ingredients and formulations, and confirmed the finding that sunscreen active ingredients are systemically absorbed,” the authors wrote.

To gather information on the absorption of active ingredients in sunscreens, the investigators randomized 48 adults to one of four sunscreen products (lotion, aerosol spray, nonaerosol spray, or pump spray) with one of six active ingredients (avobenzone, oxybenzone, octocrylene, homosalate, octisalate, and octinoxate). Not all products contained each of the ingredients.

The participants applied the products in amounts of 2 mg/cm² to 75% of body surface area at baseline, no use on day 1 and four times a day at 2-hour intervals on days 2 through 4. The researchers collected blood samples over 21 days and measured the maximum plasma concentrations. The average age of the participants was 37 years, and half were women. The study was conducted in a clinical pharmacology unit.

The geometric mean maximum plasma concentrations for the primary endpoint of avobenzone in lotion, aerosol spray, nonaerosol spray, and pump spray were 7.1 ng/mL, 3.5 ng/mL, 3.5 ng/mL, and 3.3 ng/mL, respectively.

For oxybenzone, the concentrations were 258.1 ng/mL and 180.1 ng/mL, respectively, for lotion and aerosol spray. The concentrations for octocrylene were 7.8 ng/mL, 6.6 ng/mL, and 6.6 ng/mL, respectively, for lotion, aerosol spray, and nonaerosol spray.

For homosalate, the geometric mean plasma concentrations were 23.1 ng/mL for aerosol spray, 17.9 for nonaerosol spray, and 13.9 for pump spray. For octisalate, the concentrations were 5.1 ng/mL, 5.8 ng/mL, and 4.6 ng/mL, respectively, for aerosol spray, nonaerosol spray, and pump spray. For octinoxate, the concentrations were 7.9 ng/mL for nonaerosol spray and 5.2 ng/mL for pump spray.

“The systemic exposures, as measured by geometric mean maximum plasma concentrations, of all the tested active ingredients were higher than 0.5 ng/mL after a single application,” the researchers noted.

Overall, the most common event was rash, which was reported in 14 participants.

The study findings were limited by several factors including the use of an indoor clinical setting, rather than outdoor exposure; the inability to assess absorption differences by formulation and Fitzpatrick skin type; and the variation in amounts of ingredients among products, the researchers noted. However, the results can be used to design additional studies needed to research the effects of systemic exposure to sunscreen ingredients, they said.

In an accompanying editorial (JAMA. 2020;323:223-4), Adewole S. Adamson, MD, of the University of Texas at Austin, and Kanade Shinkai, MD, of the University of California, San Francisco, wrote that “the study did not address key questions about sunscreen safety,” including the length of time it takes “for plasma concentrations of sunscreen ingredients to fall below the FDA threshold for safety testing.” Dr. Shinkai is also editor in chief of JAMA Dermatology.

“In making an informed decision, clinicians must determine whether the magnitude of the benefit exceeds the risk of potential harm for a specific individual,” they said. “Importantly, this balance may be different, depending on characteristics of the sunscreen user (e.g., for individuals with darker skin types and for children) and may depend on the frequency and duration of application (e.g., daily vs. intermittent use; starting in infancy or later in life),” they noted.

“In the absence of clear data demonstrating harm, the use of chemical sunscreen may still be considered appropriate; the use of mineral-based sunscreen is a well-established safe alternative,” although the potential harms remain uncertain until the sunscreen industry conducts the safety studies recommended by the FDA, Dr. Adamson and Dr. Shinkai concluded.

In a statement released by the FDA on Jan 21, the day the study was published, Janet Woodcock, MD, director of the FDA’s Center for Drug Evaluation and Research, said that, considering the “recognized public health benefits” of using sunscreen, the FDA “urges Americans to use sunscreens in conjunction with other sun protective measures (such as protective clothing).”

Commenting on the study, she said, “results from our study released today show there is evidence that some sunscreen active ingredients may be absorbed. However, the fact that an ingredient is absorbed through the skin and into the body does not mean that the ingredient is unsafe, nor does the FDA seeking further information indicate such. Rather, this finding calls for further industry testing to determine the safety and effect of systemic exposure of sunscreen ingredients, especially with chronic use.”

The study was supported by the FDA. The researchers and editorial authors had no financial conflicts to disclose.

SOURCES: Matta MK et al. JAMA. 2020;323:256-267.

Six active ingredients used in sunscreen products in the United States showed systemic skin absorption with geometric mean plasma concentrations greater than 0.5 ng/mL in a randomized trial including four product types. The results were published in JAMA.

The testing was done as part of a proposed rule on sunscreen, published in February 2019, which requested additional information on sunscreen ingredients. Murali K. Matta, PhD, of the Food and Drug Administration and coauthors wrote that these plasma concentrations “surpassed the FDA threshold for potentially waiving additional safety studies for sunscreens.” But, they added, the findings “do not indicate that individuals should refrain from the use of sunscreen.”

This was a follow-up study to a smaller study of 24 health volunteers published last year that determined that the sunscreen active ingredients tested were absorbed systemically (JAMA. 2019;321[21]:2082-91). “This follow-up study expanded the sample size, tested additional sunscreen active ingredients and formulations, and confirmed the finding that sunscreen active ingredients are systemically absorbed,” the authors wrote.

To gather information on the absorption of active ingredients in sunscreens, the investigators randomized 48 adults to one of four sunscreen products (lotion, aerosol spray, nonaerosol spray, or pump spray) with one of six active ingredients (avobenzone, oxybenzone, octocrylene, homosalate, octisalate, and octinoxate). Not all products contained each of the ingredients.

The participants applied the products in amounts of 2 mg/cm² to 75% of body surface area at baseline, no use on day 1 and four times a day at 2-hour intervals on days 2 through 4. The researchers collected blood samples over 21 days and measured the maximum plasma concentrations. The average age of the participants was 37 years, and half were women. The study was conducted in a clinical pharmacology unit.

The geometric mean maximum plasma concentrations for the primary endpoint of avobenzone in lotion, aerosol spray, nonaerosol spray, and pump spray were 7.1 ng/mL, 3.5 ng/mL, 3.5 ng/mL, and 3.3 ng/mL, respectively.

For oxybenzone, the concentrations were 258.1 ng/mL and 180.1 ng/mL, respectively, for lotion and aerosol spray. The concentrations for octocrylene were 7.8 ng/mL, 6.6 ng/mL, and 6.6 ng/mL, respectively, for lotion, aerosol spray, and nonaerosol spray.

For homosalate, the geometric mean plasma concentrations were 23.1 ng/mL for aerosol spray, 17.9 for nonaerosol spray, and 13.9 for pump spray. For octisalate, the concentrations were 5.1 ng/mL, 5.8 ng/mL, and 4.6 ng/mL, respectively, for aerosol spray, nonaerosol spray, and pump spray. For octinoxate, the concentrations were 7.9 ng/mL for nonaerosol spray and 5.2 ng/mL for pump spray.

“The systemic exposures, as measured by geometric mean maximum plasma concentrations, of all the tested active ingredients were higher than 0.5 ng/mL after a single application,” the researchers noted.

Overall, the most common event was rash, which was reported in 14 participants.

The study findings were limited by several factors including the use of an indoor clinical setting, rather than outdoor exposure; the inability to assess absorption differences by formulation and Fitzpatrick skin type; and the variation in amounts of ingredients among products, the researchers noted. However, the results can be used to design additional studies needed to research the effects of systemic exposure to sunscreen ingredients, they said.

In an accompanying editorial (JAMA. 2020;323:223-4), Adewole S. Adamson, MD, of the University of Texas at Austin, and Kanade Shinkai, MD, of the University of California, San Francisco, wrote that “the study did not address key questions about sunscreen safety,” including the length of time it takes “for plasma concentrations of sunscreen ingredients to fall below the FDA threshold for safety testing.” Dr. Shinkai is also editor in chief of JAMA Dermatology.

“In making an informed decision, clinicians must determine whether the magnitude of the benefit exceeds the risk of potential harm for a specific individual,” they said. “Importantly, this balance may be different, depending on characteristics of the sunscreen user (e.g., for individuals with darker skin types and for children) and may depend on the frequency and duration of application (e.g., daily vs. intermittent use; starting in infancy or later in life),” they noted.

“In the absence of clear data demonstrating harm, the use of chemical sunscreen may still be considered appropriate; the use of mineral-based sunscreen is a well-established safe alternative,” although the potential harms remain uncertain until the sunscreen industry conducts the safety studies recommended by the FDA, Dr. Adamson and Dr. Shinkai concluded.

In a statement released by the FDA on Jan 21, the day the study was published, Janet Woodcock, MD, director of the FDA’s Center for Drug Evaluation and Research, said that, considering the “recognized public health benefits” of using sunscreen, the FDA “urges Americans to use sunscreens in conjunction with other sun protective measures (such as protective clothing).”

Commenting on the study, she said, “results from our study released today show there is evidence that some sunscreen active ingredients may be absorbed. However, the fact that an ingredient is absorbed through the skin and into the body does not mean that the ingredient is unsafe, nor does the FDA seeking further information indicate such. Rather, this finding calls for further industry testing to determine the safety and effect of systemic exposure of sunscreen ingredients, especially with chronic use.”

The study was supported by the FDA. The researchers and editorial authors had no financial conflicts to disclose.

SOURCES: Matta MK et al. JAMA. 2020;323:256-267.