Different Biomarker Profiles Identified in Study of Late Dupilumab Responders

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Changed
Fri, 10/18/2024 - 12:09

 

— A proteomics study designed to determine why some patients with atopic dermatitis (AD) respond quickly to dupilumab, others respond more slowly, and the remainder do not respond at all demonstrated that molecular responses in these three groups are very different.

A discovery that could lead to personalizing therapies, the data identified “distinct systemic biomarker profiles,” according to Ester Del Duca, MD, an instructor in the Laboratory of Inflammatory Skin Diseases at the Icahn School of Medicine at Mount Sinai, New York City.

The study was conducted with 67 patients with AD and 16 healthy controls. Serum was collected at two timepoints: An average of 20 weeks after starting dupilumab, then at a mean interval of about 9 months later. At these timepoints, called follow-up 1 and 2, a panel of more than 600 proteins, including unique markers for immunologic, cardiovascular, and neurologic activity, were evaluated.

The criterion for differentiating the three response groups was an Investigator Global Assessment (IGA) score of 0 or 1, signifying clear or almost clear skin (or at least a 2-point IGA reduction from baseline). Early responders were those who met the criterion at both follow-ups, late responders were those who met this criterion only at the second follow-up, and nonresponders never met the criterion.

“There were no significant differences at baseline in clinical severity, past medical history, or patient characteristics,” said Del Duca, who presented these data in a late breaking news session at the European Academy of Dermatology and Venereology (EADV) 2024 Congress.

Of the 67 patients with AD, 39 were early responders, 11 were late responders, and 17 were nonresponders.

The differences in proteomics were marked.
For early responders, there was an early normalization of the proteome, reported Del Duca, illustrating the differences in the proteome of the three groups with a color-coded chart of protein up-regulation and down-regulation relative to healthy controls. The normalization of the proteome persisted in early responders when assessed at the second follow-up.

In the late responders, the proteome dysregulation was substantial relative to healthy controls at the first follow-up, but there was considerable improvement by the second follow-up. Although the change at the second follow-up was still not as robust as that seen in the early responders at either follow-up, Del Duca described the proteomic profile as a 45% improvement from the first follow-up.

In contrast, nonresponders showed worsening in their blood proteome from follow-up 1 to 2. Nonresponders at first follow-up showed up-regulation relative to healthy controls for many proteins associated with the Th1 response, such as interferon gamma, CXCL9, and CXCL10, and Th2 response, such as interleukin-4 and Th17/22, and these did not normalize or worsen by the second follow-up.

“Uniquely to nonresponders, key Th1 biomarkers remained significantly up-regulated relative to controls at both follow-up 1 and 2,” with a P value < .05, Del Duca reported.

To achieve normalization of the proteome as defined by healthy controls, both up-regulation and down-regulation of protein activity were required, although more up-regulations than down-regulations were observed.

When evaluating the proteome changes most implicated in immunoregulation, the investigators were able to show a correlation between worsening in the proteome and greater severity of AD as defined by IGA, Eczema Area and Severity Index, and body surface area involvement.

“Spearman analysis revealed strong and positive correlations between improvements in biomarkers at follow-up 1 and 2 with improvements in clinical markers,” Del Duca said. As examples, she noted favorable changes in biomarkers specifically associated with T cells, dendritic cells, and natural killer cells as clinical outcomes improved.

Conversely, the worsening in T-cell activation among nonresponders, particularly Th1 biomarkers, also tracked with increasing AD symptoms over time.

The implications of the research are broad, and most importantly, it shows that therapeutic targets are likely to differ between patients with AD, according to Del Duca. Although proteomic studies have not yet been conducted with other treatments, these might provide further insight about how patients with AD differ in response across other drugs.

This is important work, according to Brigitte Dréno, MD, PhD, head of the Department of Dermatology, Nantes University Hospital in France. As moderator of the late-breaking news session, she suggested that there are many potential messages from these data, not least that treatment of AD likely involves targeting cytokines beyond those affected by dupilumab in at least some patients.

When Dréno asked Del Duca about what could be surmised about changes from baseline before treatment to the first follow-up, Del Duca said that the study was retrospective, so baseline data were not available.

This is an important missing piece of this investigation, according to Dréno.

“As you move this work forward,” she said that it would be “very important” to determine “if there are predictive markers for evaluating which patients will respond.”

This is a small study with many additional variables to consider in order to develop a clinically useful tool, Del Duca noted. However, this work not only has the potential to guide treatment selection but the biomarkers up-regulated in nonresponders are already “suggesting potential targets for refining therapeutic strategies,” she said.

The study received funding from Bristol-Myers Squibb. Del Duca reported no financial relationships with industry. Dréno reported financial relationships with La Roche–Posay, Pierre Fabré, and Galderma.

A version of this article appeared on Medscape.com.

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— A proteomics study designed to determine why some patients with atopic dermatitis (AD) respond quickly to dupilumab, others respond more slowly, and the remainder do not respond at all demonstrated that molecular responses in these three groups are very different.

A discovery that could lead to personalizing therapies, the data identified “distinct systemic biomarker profiles,” according to Ester Del Duca, MD, an instructor in the Laboratory of Inflammatory Skin Diseases at the Icahn School of Medicine at Mount Sinai, New York City.

The study was conducted with 67 patients with AD and 16 healthy controls. Serum was collected at two timepoints: An average of 20 weeks after starting dupilumab, then at a mean interval of about 9 months later. At these timepoints, called follow-up 1 and 2, a panel of more than 600 proteins, including unique markers for immunologic, cardiovascular, and neurologic activity, were evaluated.

The criterion for differentiating the three response groups was an Investigator Global Assessment (IGA) score of 0 or 1, signifying clear or almost clear skin (or at least a 2-point IGA reduction from baseline). Early responders were those who met the criterion at both follow-ups, late responders were those who met this criterion only at the second follow-up, and nonresponders never met the criterion.

“There were no significant differences at baseline in clinical severity, past medical history, or patient characteristics,” said Del Duca, who presented these data in a late breaking news session at the European Academy of Dermatology and Venereology (EADV) 2024 Congress.

Of the 67 patients with AD, 39 were early responders, 11 were late responders, and 17 were nonresponders.

The differences in proteomics were marked.
For early responders, there was an early normalization of the proteome, reported Del Duca, illustrating the differences in the proteome of the three groups with a color-coded chart of protein up-regulation and down-regulation relative to healthy controls. The normalization of the proteome persisted in early responders when assessed at the second follow-up.

In the late responders, the proteome dysregulation was substantial relative to healthy controls at the first follow-up, but there was considerable improvement by the second follow-up. Although the change at the second follow-up was still not as robust as that seen in the early responders at either follow-up, Del Duca described the proteomic profile as a 45% improvement from the first follow-up.

In contrast, nonresponders showed worsening in their blood proteome from follow-up 1 to 2. Nonresponders at first follow-up showed up-regulation relative to healthy controls for many proteins associated with the Th1 response, such as interferon gamma, CXCL9, and CXCL10, and Th2 response, such as interleukin-4 and Th17/22, and these did not normalize or worsen by the second follow-up.

“Uniquely to nonresponders, key Th1 biomarkers remained significantly up-regulated relative to controls at both follow-up 1 and 2,” with a P value < .05, Del Duca reported.

To achieve normalization of the proteome as defined by healthy controls, both up-regulation and down-regulation of protein activity were required, although more up-regulations than down-regulations were observed.

When evaluating the proteome changes most implicated in immunoregulation, the investigators were able to show a correlation between worsening in the proteome and greater severity of AD as defined by IGA, Eczema Area and Severity Index, and body surface area involvement.

“Spearman analysis revealed strong and positive correlations between improvements in biomarkers at follow-up 1 and 2 with improvements in clinical markers,” Del Duca said. As examples, she noted favorable changes in biomarkers specifically associated with T cells, dendritic cells, and natural killer cells as clinical outcomes improved.

Conversely, the worsening in T-cell activation among nonresponders, particularly Th1 biomarkers, also tracked with increasing AD symptoms over time.

The implications of the research are broad, and most importantly, it shows that therapeutic targets are likely to differ between patients with AD, according to Del Duca. Although proteomic studies have not yet been conducted with other treatments, these might provide further insight about how patients with AD differ in response across other drugs.

This is important work, according to Brigitte Dréno, MD, PhD, head of the Department of Dermatology, Nantes University Hospital in France. As moderator of the late-breaking news session, she suggested that there are many potential messages from these data, not least that treatment of AD likely involves targeting cytokines beyond those affected by dupilumab in at least some patients.

When Dréno asked Del Duca about what could be surmised about changes from baseline before treatment to the first follow-up, Del Duca said that the study was retrospective, so baseline data were not available.

This is an important missing piece of this investigation, according to Dréno.

“As you move this work forward,” she said that it would be “very important” to determine “if there are predictive markers for evaluating which patients will respond.”

This is a small study with many additional variables to consider in order to develop a clinically useful tool, Del Duca noted. However, this work not only has the potential to guide treatment selection but the biomarkers up-regulated in nonresponders are already “suggesting potential targets for refining therapeutic strategies,” she said.

The study received funding from Bristol-Myers Squibb. Del Duca reported no financial relationships with industry. Dréno reported financial relationships with La Roche–Posay, Pierre Fabré, and Galderma.

A version of this article appeared on Medscape.com.

 

— A proteomics study designed to determine why some patients with atopic dermatitis (AD) respond quickly to dupilumab, others respond more slowly, and the remainder do not respond at all demonstrated that molecular responses in these three groups are very different.

A discovery that could lead to personalizing therapies, the data identified “distinct systemic biomarker profiles,” according to Ester Del Duca, MD, an instructor in the Laboratory of Inflammatory Skin Diseases at the Icahn School of Medicine at Mount Sinai, New York City.

The study was conducted with 67 patients with AD and 16 healthy controls. Serum was collected at two timepoints: An average of 20 weeks after starting dupilumab, then at a mean interval of about 9 months later. At these timepoints, called follow-up 1 and 2, a panel of more than 600 proteins, including unique markers for immunologic, cardiovascular, and neurologic activity, were evaluated.

The criterion for differentiating the three response groups was an Investigator Global Assessment (IGA) score of 0 or 1, signifying clear or almost clear skin (or at least a 2-point IGA reduction from baseline). Early responders were those who met the criterion at both follow-ups, late responders were those who met this criterion only at the second follow-up, and nonresponders never met the criterion.

“There were no significant differences at baseline in clinical severity, past medical history, or patient characteristics,” said Del Duca, who presented these data in a late breaking news session at the European Academy of Dermatology and Venereology (EADV) 2024 Congress.

Of the 67 patients with AD, 39 were early responders, 11 were late responders, and 17 were nonresponders.

The differences in proteomics were marked.
For early responders, there was an early normalization of the proteome, reported Del Duca, illustrating the differences in the proteome of the three groups with a color-coded chart of protein up-regulation and down-regulation relative to healthy controls. The normalization of the proteome persisted in early responders when assessed at the second follow-up.

In the late responders, the proteome dysregulation was substantial relative to healthy controls at the first follow-up, but there was considerable improvement by the second follow-up. Although the change at the second follow-up was still not as robust as that seen in the early responders at either follow-up, Del Duca described the proteomic profile as a 45% improvement from the first follow-up.

In contrast, nonresponders showed worsening in their blood proteome from follow-up 1 to 2. Nonresponders at first follow-up showed up-regulation relative to healthy controls for many proteins associated with the Th1 response, such as interferon gamma, CXCL9, and CXCL10, and Th2 response, such as interleukin-4 and Th17/22, and these did not normalize or worsen by the second follow-up.

“Uniquely to nonresponders, key Th1 biomarkers remained significantly up-regulated relative to controls at both follow-up 1 and 2,” with a P value < .05, Del Duca reported.

To achieve normalization of the proteome as defined by healthy controls, both up-regulation and down-regulation of protein activity were required, although more up-regulations than down-regulations were observed.

When evaluating the proteome changes most implicated in immunoregulation, the investigators were able to show a correlation between worsening in the proteome and greater severity of AD as defined by IGA, Eczema Area and Severity Index, and body surface area involvement.

“Spearman analysis revealed strong and positive correlations between improvements in biomarkers at follow-up 1 and 2 with improvements in clinical markers,” Del Duca said. As examples, she noted favorable changes in biomarkers specifically associated with T cells, dendritic cells, and natural killer cells as clinical outcomes improved.

Conversely, the worsening in T-cell activation among nonresponders, particularly Th1 biomarkers, also tracked with increasing AD symptoms over time.

The implications of the research are broad, and most importantly, it shows that therapeutic targets are likely to differ between patients with AD, according to Del Duca. Although proteomic studies have not yet been conducted with other treatments, these might provide further insight about how patients with AD differ in response across other drugs.

This is important work, according to Brigitte Dréno, MD, PhD, head of the Department of Dermatology, Nantes University Hospital in France. As moderator of the late-breaking news session, she suggested that there are many potential messages from these data, not least that treatment of AD likely involves targeting cytokines beyond those affected by dupilumab in at least some patients.

When Dréno asked Del Duca about what could be surmised about changes from baseline before treatment to the first follow-up, Del Duca said that the study was retrospective, so baseline data were not available.

This is an important missing piece of this investigation, according to Dréno.

“As you move this work forward,” she said that it would be “very important” to determine “if there are predictive markers for evaluating which patients will respond.”

This is a small study with many additional variables to consider in order to develop a clinically useful tool, Del Duca noted. However, this work not only has the potential to guide treatment selection but the biomarkers up-regulated in nonresponders are already “suggesting potential targets for refining therapeutic strategies,” she said.

The study received funding from Bristol-Myers Squibb. Del Duca reported no financial relationships with industry. Dréno reported financial relationships with La Roche–Posay, Pierre Fabré, and Galderma.

A version of this article appeared on Medscape.com.

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Hidradenitis Suppurativa: Nodules Respond to As Needed Topical JAK Inhibitor

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Changed
Fri, 10/18/2024 - 11:36

 

— Following the report of results from a randomized trial in which a topically applied Janus kinase (JAK) inhibitor was highly active in patients with mild to moderate hidradenitis suppurativa (HS), an open-label extension showed that 16 more weeks of treatment on as-needed basis provided complete or near complete clearance of lesions in up to 38.5% of patients.

“Ruxolitinib cream may be a novel approach to address an unmet medical need in the treatment of milder HS for which there are no currently approved treatments,” reported Martina L. Porter, MD, assistant professor of dermatology, Harvard Medical School, and Beth Israel Deaconess Medical Center, both in Boston, Massachusetts.

In the earlier 16-week, double-blind, randomized period of this phase 2b study, 69 adults with mild to moderate HS were randomized to 1.5% ruxolitinib cream or vehicle, applied twice daily for 16 weeks. The new results are from the open-label extension period, where those on the vehicle were crossed over to topical ruxolitinib and treatment was continued for another 16 weeks.
 

Over 80% Meet Primary Endpoint at 32 Weeks

Entry criteria for the study included Hurley stage I or II HS with no draining tunnels. Hurley stage III patients were not eligible. Patients had to have an abscess or inflammatory nodule (AN) count of 3 lesions concentrated in a single anatomic area or up to 10 lesions if disseminated. The median AN count of those enrolled was 5.4. 

In the randomized portion of the study and in the open-label extension, the recommendation for application was to apply the medication to nodules and a 1-cm area of surrounding skin. As-needed treatment was only recommended in the extension portion of the study and rescue medication was not allowed.

The goal of the open-label extension was to evaluate how long the improvements were sustained, according to Dr. Porter, who presented the results at the 2024 European Academy of Dermatology and Venereology (EADV) meeting.

The primary endpoints of AN50, signaling at least a 50% reduction in AN count from baseline, among those initially randomized to ruxolitinib cream climbed slightly from 79.2% at the end of 16 weeks to 81.0% at the end of 32 weeks.

This shows that the benefits recorded in the randomized phase of the trial were sustained during the open-label extension, Dr. Porter said. 

For those randomized to vehicle, there was a substantial response of 56.3% for AN50 during the randomized portion of the study, but catchup in the vehicle group to those on active therapy occurred rapidly over the open-label extension. By the end of 32 weeks, the score among the crossover patients slightly exceeded that of those on continuous therapy (88.5% vs 81.0%).

AN75 responses at week 32 were 66.7% and 61.5% in the continuous arm and crossover arm, respectively. The proportion of patients reaching an AN90 or AN100 response, meaning clear or almost clear, were 19% and 38.5%, in continuous treatment and crossover arms, respectively.

One of the secondary endpoints was the HS Clinical Response 50, indicating at least a 50% reduction in the AN count with no increase in abscesses or draining fistulae. At 32 weeks, the proportions of patients who met this endpoint were 81.0% and 88.5% in the continuous treatment and crossover arms, respectively. 

The mean reduction in International HS Severity Scoring System scores from baseline were 4.1 and 4.5 in the continuous treatment and crossover arms, respectively. 
 

Patients in the Study Mostly Women, 42% Black Individuals

Most (94%) of the participants were women; about 45% and 42% were White and Black individuals, respectively. Most of the remaining patients were Asian individuals. The median age at entry was 29 years, and the mean body mass index was approximately 34 kg/m2. A substantial proportion of patients had systemic comorbidities, according to Dr. Porter, who noted that about 25% had anxiety, depression, or both.

“This phenotype — a high proportion of women with nodules but no draining tunnels and a substantial number of comorbidities — is one we often see in patients with mild HS,” Dr. Porter said.

The safety and tolerability profile of ruxolitinib cream was quite good, according to Dr. Porter, who noted that there were fewer treatment-related adverse events in the open-label extension. Overall, the number of treatment-related adverse events (3.6%), including application site reactions leading to discontinuation (1.8%) was low. 

Although there is a growing list of therapies now approved for HS, Dr. Porter emphasized that all have been developed for moderate to severe disease. She suggested that there is a sizable group of patients with mild disease for whom such therapies as biologics might not be warranted even if symptom relief is needed.

Given this unmet need, she said phase 3 trials are warranted to confirm the benefits and the safety of a topical therapy that can be used as needed to control intermittent HS flares.

Asked to comment, the lead author of a recently published review article on the “evolving treatment landscape” of HS, James G. Krueger, MD, professor in clinical investigation at Rockefeller University, New York City, agreed that there is an unmet need for effective and safe therapies in milder HS.

“I agree with the premise,” said Dr. Krueger, indicating that phase 3 data will be essential to confirm the promise of this approach. Dr. Krueger, who did not hear the results presented at the EADV meeting, listed several JAK inhibitors in his review that have shown promising efficacy as oral agents and support JAK signaling as a target of HS treatment. 

Topical ruxolitinib (Opzelura) is currently approved in the United States for treating nonsegmental vitiligo in patients aged ≥ 12 years and for mild to moderate atopic dermatitis in patients aged ≥ 12 years. In Europe, it is approved for treatment of nonsegmental vitiligo with facial involvement in patients aged ≥ 12 years. 

Dr. Porter reported no potential conflicts of interest. Dr. Krueger reported financial relationships with more than 25 pharmaceutical companies not including Incyte, which is developing ruxolitinib cream.

A version of this article appeared on Medscape.com.

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— Following the report of results from a randomized trial in which a topically applied Janus kinase (JAK) inhibitor was highly active in patients with mild to moderate hidradenitis suppurativa (HS), an open-label extension showed that 16 more weeks of treatment on as-needed basis provided complete or near complete clearance of lesions in up to 38.5% of patients.

“Ruxolitinib cream may be a novel approach to address an unmet medical need in the treatment of milder HS for which there are no currently approved treatments,” reported Martina L. Porter, MD, assistant professor of dermatology, Harvard Medical School, and Beth Israel Deaconess Medical Center, both in Boston, Massachusetts.

In the earlier 16-week, double-blind, randomized period of this phase 2b study, 69 adults with mild to moderate HS were randomized to 1.5% ruxolitinib cream or vehicle, applied twice daily for 16 weeks. The new results are from the open-label extension period, where those on the vehicle were crossed over to topical ruxolitinib and treatment was continued for another 16 weeks.
 

Over 80% Meet Primary Endpoint at 32 Weeks

Entry criteria for the study included Hurley stage I or II HS with no draining tunnels. Hurley stage III patients were not eligible. Patients had to have an abscess or inflammatory nodule (AN) count of 3 lesions concentrated in a single anatomic area or up to 10 lesions if disseminated. The median AN count of those enrolled was 5.4. 

In the randomized portion of the study and in the open-label extension, the recommendation for application was to apply the medication to nodules and a 1-cm area of surrounding skin. As-needed treatment was only recommended in the extension portion of the study and rescue medication was not allowed.

The goal of the open-label extension was to evaluate how long the improvements were sustained, according to Dr. Porter, who presented the results at the 2024 European Academy of Dermatology and Venereology (EADV) meeting.

The primary endpoints of AN50, signaling at least a 50% reduction in AN count from baseline, among those initially randomized to ruxolitinib cream climbed slightly from 79.2% at the end of 16 weeks to 81.0% at the end of 32 weeks.

This shows that the benefits recorded in the randomized phase of the trial were sustained during the open-label extension, Dr. Porter said. 

For those randomized to vehicle, there was a substantial response of 56.3% for AN50 during the randomized portion of the study, but catchup in the vehicle group to those on active therapy occurred rapidly over the open-label extension. By the end of 32 weeks, the score among the crossover patients slightly exceeded that of those on continuous therapy (88.5% vs 81.0%).

AN75 responses at week 32 were 66.7% and 61.5% in the continuous arm and crossover arm, respectively. The proportion of patients reaching an AN90 or AN100 response, meaning clear or almost clear, were 19% and 38.5%, in continuous treatment and crossover arms, respectively.

One of the secondary endpoints was the HS Clinical Response 50, indicating at least a 50% reduction in the AN count with no increase in abscesses or draining fistulae. At 32 weeks, the proportions of patients who met this endpoint were 81.0% and 88.5% in the continuous treatment and crossover arms, respectively. 

The mean reduction in International HS Severity Scoring System scores from baseline were 4.1 and 4.5 in the continuous treatment and crossover arms, respectively. 
 

Patients in the Study Mostly Women, 42% Black Individuals

Most (94%) of the participants were women; about 45% and 42% were White and Black individuals, respectively. Most of the remaining patients were Asian individuals. The median age at entry was 29 years, and the mean body mass index was approximately 34 kg/m2. A substantial proportion of patients had systemic comorbidities, according to Dr. Porter, who noted that about 25% had anxiety, depression, or both.

“This phenotype — a high proportion of women with nodules but no draining tunnels and a substantial number of comorbidities — is one we often see in patients with mild HS,” Dr. Porter said.

The safety and tolerability profile of ruxolitinib cream was quite good, according to Dr. Porter, who noted that there were fewer treatment-related adverse events in the open-label extension. Overall, the number of treatment-related adverse events (3.6%), including application site reactions leading to discontinuation (1.8%) was low. 

Although there is a growing list of therapies now approved for HS, Dr. Porter emphasized that all have been developed for moderate to severe disease. She suggested that there is a sizable group of patients with mild disease for whom such therapies as biologics might not be warranted even if symptom relief is needed.

Given this unmet need, she said phase 3 trials are warranted to confirm the benefits and the safety of a topical therapy that can be used as needed to control intermittent HS flares.

Asked to comment, the lead author of a recently published review article on the “evolving treatment landscape” of HS, James G. Krueger, MD, professor in clinical investigation at Rockefeller University, New York City, agreed that there is an unmet need for effective and safe therapies in milder HS.

“I agree with the premise,” said Dr. Krueger, indicating that phase 3 data will be essential to confirm the promise of this approach. Dr. Krueger, who did not hear the results presented at the EADV meeting, listed several JAK inhibitors in his review that have shown promising efficacy as oral agents and support JAK signaling as a target of HS treatment. 

Topical ruxolitinib (Opzelura) is currently approved in the United States for treating nonsegmental vitiligo in patients aged ≥ 12 years and for mild to moderate atopic dermatitis in patients aged ≥ 12 years. In Europe, it is approved for treatment of nonsegmental vitiligo with facial involvement in patients aged ≥ 12 years. 

Dr. Porter reported no potential conflicts of interest. Dr. Krueger reported financial relationships with more than 25 pharmaceutical companies not including Incyte, which is developing ruxolitinib cream.

A version of this article appeared on Medscape.com.

 

— Following the report of results from a randomized trial in which a topically applied Janus kinase (JAK) inhibitor was highly active in patients with mild to moderate hidradenitis suppurativa (HS), an open-label extension showed that 16 more weeks of treatment on as-needed basis provided complete or near complete clearance of lesions in up to 38.5% of patients.

“Ruxolitinib cream may be a novel approach to address an unmet medical need in the treatment of milder HS for which there are no currently approved treatments,” reported Martina L. Porter, MD, assistant professor of dermatology, Harvard Medical School, and Beth Israel Deaconess Medical Center, both in Boston, Massachusetts.

In the earlier 16-week, double-blind, randomized period of this phase 2b study, 69 adults with mild to moderate HS were randomized to 1.5% ruxolitinib cream or vehicle, applied twice daily for 16 weeks. The new results are from the open-label extension period, where those on the vehicle were crossed over to topical ruxolitinib and treatment was continued for another 16 weeks.
 

Over 80% Meet Primary Endpoint at 32 Weeks

Entry criteria for the study included Hurley stage I or II HS with no draining tunnels. Hurley stage III patients were not eligible. Patients had to have an abscess or inflammatory nodule (AN) count of 3 lesions concentrated in a single anatomic area or up to 10 lesions if disseminated. The median AN count of those enrolled was 5.4. 

In the randomized portion of the study and in the open-label extension, the recommendation for application was to apply the medication to nodules and a 1-cm area of surrounding skin. As-needed treatment was only recommended in the extension portion of the study and rescue medication was not allowed.

The goal of the open-label extension was to evaluate how long the improvements were sustained, according to Dr. Porter, who presented the results at the 2024 European Academy of Dermatology and Venereology (EADV) meeting.

The primary endpoints of AN50, signaling at least a 50% reduction in AN count from baseline, among those initially randomized to ruxolitinib cream climbed slightly from 79.2% at the end of 16 weeks to 81.0% at the end of 32 weeks.

This shows that the benefits recorded in the randomized phase of the trial were sustained during the open-label extension, Dr. Porter said. 

For those randomized to vehicle, there was a substantial response of 56.3% for AN50 during the randomized portion of the study, but catchup in the vehicle group to those on active therapy occurred rapidly over the open-label extension. By the end of 32 weeks, the score among the crossover patients slightly exceeded that of those on continuous therapy (88.5% vs 81.0%).

AN75 responses at week 32 were 66.7% and 61.5% in the continuous arm and crossover arm, respectively. The proportion of patients reaching an AN90 or AN100 response, meaning clear or almost clear, were 19% and 38.5%, in continuous treatment and crossover arms, respectively.

One of the secondary endpoints was the HS Clinical Response 50, indicating at least a 50% reduction in the AN count with no increase in abscesses or draining fistulae. At 32 weeks, the proportions of patients who met this endpoint were 81.0% and 88.5% in the continuous treatment and crossover arms, respectively. 

The mean reduction in International HS Severity Scoring System scores from baseline were 4.1 and 4.5 in the continuous treatment and crossover arms, respectively. 
 

Patients in the Study Mostly Women, 42% Black Individuals

Most (94%) of the participants were women; about 45% and 42% were White and Black individuals, respectively. Most of the remaining patients were Asian individuals. The median age at entry was 29 years, and the mean body mass index was approximately 34 kg/m2. A substantial proportion of patients had systemic comorbidities, according to Dr. Porter, who noted that about 25% had anxiety, depression, or both.

“This phenotype — a high proportion of women with nodules but no draining tunnels and a substantial number of comorbidities — is one we often see in patients with mild HS,” Dr. Porter said.

The safety and tolerability profile of ruxolitinib cream was quite good, according to Dr. Porter, who noted that there were fewer treatment-related adverse events in the open-label extension. Overall, the number of treatment-related adverse events (3.6%), including application site reactions leading to discontinuation (1.8%) was low. 

Although there is a growing list of therapies now approved for HS, Dr. Porter emphasized that all have been developed for moderate to severe disease. She suggested that there is a sizable group of patients with mild disease for whom such therapies as biologics might not be warranted even if symptom relief is needed.

Given this unmet need, she said phase 3 trials are warranted to confirm the benefits and the safety of a topical therapy that can be used as needed to control intermittent HS flares.

Asked to comment, the lead author of a recently published review article on the “evolving treatment landscape” of HS, James G. Krueger, MD, professor in clinical investigation at Rockefeller University, New York City, agreed that there is an unmet need for effective and safe therapies in milder HS.

“I agree with the premise,” said Dr. Krueger, indicating that phase 3 data will be essential to confirm the promise of this approach. Dr. Krueger, who did not hear the results presented at the EADV meeting, listed several JAK inhibitors in his review that have shown promising efficacy as oral agents and support JAK signaling as a target of HS treatment. 

Topical ruxolitinib (Opzelura) is currently approved in the United States for treating nonsegmental vitiligo in patients aged ≥ 12 years and for mild to moderate atopic dermatitis in patients aged ≥ 12 years. In Europe, it is approved for treatment of nonsegmental vitiligo with facial involvement in patients aged ≥ 12 years. 

Dr. Porter reported no potential conflicts of interest. Dr. Krueger reported financial relationships with more than 25 pharmaceutical companies not including Incyte, which is developing ruxolitinib cream.

A version of this article appeared on Medscape.com.

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PCPs Play a Key Role in Managing and Preventing the Atopic March in Children

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Changed
Wed, 10/16/2024 - 10:26

Primary care physicians (PCPs) play a key role in treating young patients as they progress through the “atopic march” from atopic dermatitis through food allergy, asthma, and allergic rhinitis. They can also help prevent the process from starting.

“The PCP is usually the first clinician a family with concerns about atopic conditions sees, unless they first visit urgent care or an emergency department after an allergic reaction to food. Either way, families rely on their PCP for ongoing guidance,” said Terri F. Brown-Whitehorn, MD, attending physician in the Division of Allergy and Immunology at the Center for Pediatric Eosinophilic Disorders and the Integrative Health Program at Children’s Hospital of Philadelphia.

“The most important thing PCPs can do is know that the atopic march exists, how it progresses over time, and what signs and symptoms to look for,” she told this news organization.
 

The Atopic March

The atopic march describes the progression of allergic diseases in a child over time, with atopic dermatitis and food allergy in infancy tending to be followed by allergic rhinitis and asthma into later childhood and adulthood.

Although the pathophysiology of the inflammation that precedes atopic dermatitis is unclear, two main hypotheses have been proposed. The first suggests a primary immune dysfunction leads to immunoglobulin E (IgE) sensitization, allergic inflammation, and a secondary disturbance of the epithelial barrier; the second starts with a primary defect in the epithelial barrier that leads to secondary immunologic dysregulation and results in inflammation.

Genetics, infection, hygiene, extreme climate, food allergens, probiotics, aeroallergens, and tobacco smoke are thought to play roles in atopic dermatitis. An estimated 10%-12% of children and 1% of adults in the United States have been reported to have the condition, and the prevalence appears to be increasing. An estimated 85% of cases occur during the first year of life and 95% before the age of 5 years.

“Atopy often, though not always, runs in families, so PCPs should inquire about the history of atopic dermatitis, IgE-mediated food allergies, allergic rhinitis, and asthma in the patient’s siblings, parents, and grandparents,” Brown-Whitehorn said.
 

Key Educators

PCPs treat the full gamut of atopic conditions and are key educators on ways families can help mitigate their children’s atopic march or stop it before it begins, said Gerald Bell Lee, MD, an allergist and immunologist at Children’s Healthcare of Atlanta and an associate professor in the Division of Allergy and Immunology at Emory University School of Medicine, Atlanta.

“Most parents who bring their infants with eczema to the PCP assume their child ate something that caused their rash. But the relationship between atopic dermatitis, a type of eczema, and food allergy is more complicated,” he added.

Lee said PCPs should explain to their patients what atopic dermatitis is, how it starts and progresses, and how families can help prevent the condition by, for example, introducing allergenic foods to infants at around 4-6 months of age.
 

Atopic Dermatitis

PCPs should inform parents and other caregivers to wash their hands before moisturizing their child, take care not to contaminate the moisturizer, and bathe their child only when the child is dirty.

“Soap removes protective natural skin oils and increases moisture loss, and exposure to soap and bathing is a main contributor to eczema,” said Lee. “Dry skin loses its protective barrier, allowing outside agents to penetrate and be identified by the immune system.”

“According to one hypothesis, parents may eat food, not wash their hands afterwards, then moisturize their baby. This unhygienic practice spreads food proteins from the adult’s meal, and possibly from contaminants present in the moisturizer, all over the baby’s body,” he added.

Lee said he and his colleagues discourage overbathing babies to minimize the risk for skin injury that begins the atopic march: “New parents are inundated with infant skincare messaging and products. But we need to weigh societal pressures against practicality and ask, ‘Is the child’s skin actually dirty?’ ”

Atopic dermatitis tends to appear on the extensor surfaces, face, and scalp in infants and around arm and leg creases in toddlers and older children. Severe forms of the condition can be more widely distributed on the body, said Aarti P. Pandya, MD, medical director of the Food Allergy Center at Children’s Mercy Kansas City and clinical assistant professor of pediatrics at the University of Missouri-Kansas City School of Medicine, Kansas City, Missouri.
 

Avoid Triggers, Minimize Flares

Triggers of eczema are varied and common. To help minimize flares, PCPs can encourage caregivers to avoid products with fragrances or dyes, minimize the use of soaps, and completely rinse laundry detergent from clothing and household items. “Advise them to keep fingernails short and control dander, pollen, mold, household chemicals, and tobacco smoke, as well as the child’s stress and anxiety, which can also be a trigger,” Lee said.

“Skin infections from organisms such as staph, herpes, or coxsackie can also exacerbate symptoms,” Brown-Whitehorn added. “PCPs can educate caregivers to avoid all known triggers and give them an ‘action plan’ to carry out when skin flares.”
 

Food Allergies

Parents may be unaware food allergens can travel far beyond the plate, Lee said. Researchers vacuuming household bedding, carpets, furniture, and other surfaces have detected unnoticeably tiny quantities of allergenic food proteins in ordinary house dust. Touching this dust appears to provide the main exposure to those allergens.

“According to the dual exposure to allergen hypothesis, an infant’s tolerance to antigens occurs through high-dose exposure by mouth, and allergic sensitization occurs through low-dose exposure through the skin,” he said. “As young as four to six months of age, even before eating solid food, a child develops eczema, has a leaky skin barrier, comes in contact with food, and develops a food allergy.”

IgE-mediated food allergies can begin at any age. “Symptoms occur when a food is ingested and the patient develops symptoms including but not limited to urticariaangioedema, pruritus, flushing, vomiting, diarrhea, coughing, wheezing, difficulty breathing, presyncope, or syncope,” Pandya noted.

In the case of eosinophilic esophagitis, which may also be part of the atopic march, infants and toddlers often have challenging-to-treat symptoms of reflux, while school-age children have reflux and abdominal pain, and adolescents and adults may experience difficulty swallowing and impactions of food or pills, Brown-Whitehorn said.

To differentiate between food allergy and contact dermatitis, Lee suggested providers ask, “ ’Is the rash hives? If yes, is the rash generalized or in a limited area?’ Then consider the statistical probabilities. Skin problems after milk, egg, wheat, soy, peanut, tree nut, fish, shellfish, or sesame are likely due to IgE-mediated food allergy, but after ketchup or strawberry are probably from skin contact.”
 

 

 

Allergic Rhinitis and Asthma

“For asthma, ask about frequency of night cough and symptoms with exercise, laughing, or crying. For allergic rhinitis, look for runny nose, itchy eyes, or sneezing,” Brown-Whitehorn said.

Testing and Monitoring

Assessing the extent of eczema with the Eczema Area and Severity Index or the SCORing Atopic Dermatitis index takes time but may be necessary to obtain insurance coverage for treatments such as biologics.

Avoid ordering IgE food panels, which can result in false positives that can lead to loss of tolerance and nutritional deficiencies; psychological harm from bullying, anxiety, and decreased quality of life; and higher food and healthcare costs, Pandya said.

Treatments
Caregivers may be wary about treatments, and all the three experts this news organization spoke with stressed the importance of educating caregivers about how treatments work and what to expect from them.

“Early and aggressive atopic dermatitis treatment could prevent sensitization to food or aeroallergens, which could help prevent additional atopic diseases, including those on the atopic march,” Pandya said. “Topical steroids are considered first line at any age. Topical phosphodiesterase inhibitors are approved at 3 months of age and above. Topical calcineurin inhibitors are approved at 2 years of age and above. Wet wrap therapy and bleach baths can be effective. Other options include biologic therapy, allergen immunotherapy, and UV therapy.”

Epinephrine auto-injectors can counteract food reactions. For allergic rhinitis, non-sedating antihistamines, steroidal nasal sprays, and nasal antihistamines help. Asthma treatments include various inhaled medications,” Brown-Whitehorn added.
 

When to Refer to Specialists

Involving an allergist, dermatologist, pulmonologist, or ear nose throat specialist to the patient’s care team is advisable in more challenging cases.

If a child is younger than 3 months and has moderate to severe atopic dermatitis, an underlying immune defect may be to blame, so an allergy and immunology assessment is warranted, Brown-Whitehorn said. “An allergist can help any child who has recurrent coughing or wheezing avoid the emergency room or hospitalization.”

“In pediatrics, we always try to find the medication, regimen, and avoidance strategies that use the least treatment to provide the best care for each patient,” Brown-Whitehorn added. “Children eat, play, learn, and sleep, and every stage of the atopic march affects each of these activities. As clinicians, we need to be sure that we are helping children make the best of all these activities.”

Brown-Whitehorn reported financial relationships with DBV Technologies and Regeneron Pharmaceuticals. Lee reported financial relationships with Novartis. Pandya reported financial relationships with DBV Technologies, Thermo Fisher Scientific, and Sanofi.
 

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

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Primary care physicians (PCPs) play a key role in treating young patients as they progress through the “atopic march” from atopic dermatitis through food allergy, asthma, and allergic rhinitis. They can also help prevent the process from starting.

“The PCP is usually the first clinician a family with concerns about atopic conditions sees, unless they first visit urgent care or an emergency department after an allergic reaction to food. Either way, families rely on their PCP for ongoing guidance,” said Terri F. Brown-Whitehorn, MD, attending physician in the Division of Allergy and Immunology at the Center for Pediatric Eosinophilic Disorders and the Integrative Health Program at Children’s Hospital of Philadelphia.

“The most important thing PCPs can do is know that the atopic march exists, how it progresses over time, and what signs and symptoms to look for,” she told this news organization.
 

The Atopic March

The atopic march describes the progression of allergic diseases in a child over time, with atopic dermatitis and food allergy in infancy tending to be followed by allergic rhinitis and asthma into later childhood and adulthood.

Although the pathophysiology of the inflammation that precedes atopic dermatitis is unclear, two main hypotheses have been proposed. The first suggests a primary immune dysfunction leads to immunoglobulin E (IgE) sensitization, allergic inflammation, and a secondary disturbance of the epithelial barrier; the second starts with a primary defect in the epithelial barrier that leads to secondary immunologic dysregulation and results in inflammation.

Genetics, infection, hygiene, extreme climate, food allergens, probiotics, aeroallergens, and tobacco smoke are thought to play roles in atopic dermatitis. An estimated 10%-12% of children and 1% of adults in the United States have been reported to have the condition, and the prevalence appears to be increasing. An estimated 85% of cases occur during the first year of life and 95% before the age of 5 years.

“Atopy often, though not always, runs in families, so PCPs should inquire about the history of atopic dermatitis, IgE-mediated food allergies, allergic rhinitis, and asthma in the patient’s siblings, parents, and grandparents,” Brown-Whitehorn said.
 

Key Educators

PCPs treat the full gamut of atopic conditions and are key educators on ways families can help mitigate their children’s atopic march or stop it before it begins, said Gerald Bell Lee, MD, an allergist and immunologist at Children’s Healthcare of Atlanta and an associate professor in the Division of Allergy and Immunology at Emory University School of Medicine, Atlanta.

“Most parents who bring their infants with eczema to the PCP assume their child ate something that caused their rash. But the relationship between atopic dermatitis, a type of eczema, and food allergy is more complicated,” he added.

Lee said PCPs should explain to their patients what atopic dermatitis is, how it starts and progresses, and how families can help prevent the condition by, for example, introducing allergenic foods to infants at around 4-6 months of age.
 

Atopic Dermatitis

PCPs should inform parents and other caregivers to wash their hands before moisturizing their child, take care not to contaminate the moisturizer, and bathe their child only when the child is dirty.

“Soap removes protective natural skin oils and increases moisture loss, and exposure to soap and bathing is a main contributor to eczema,” said Lee. “Dry skin loses its protective barrier, allowing outside agents to penetrate and be identified by the immune system.”

“According to one hypothesis, parents may eat food, not wash their hands afterwards, then moisturize their baby. This unhygienic practice spreads food proteins from the adult’s meal, and possibly from contaminants present in the moisturizer, all over the baby’s body,” he added.

Lee said he and his colleagues discourage overbathing babies to minimize the risk for skin injury that begins the atopic march: “New parents are inundated with infant skincare messaging and products. But we need to weigh societal pressures against practicality and ask, ‘Is the child’s skin actually dirty?’ ”

Atopic dermatitis tends to appear on the extensor surfaces, face, and scalp in infants and around arm and leg creases in toddlers and older children. Severe forms of the condition can be more widely distributed on the body, said Aarti P. Pandya, MD, medical director of the Food Allergy Center at Children’s Mercy Kansas City and clinical assistant professor of pediatrics at the University of Missouri-Kansas City School of Medicine, Kansas City, Missouri.
 

Avoid Triggers, Minimize Flares

Triggers of eczema are varied and common. To help minimize flares, PCPs can encourage caregivers to avoid products with fragrances or dyes, minimize the use of soaps, and completely rinse laundry detergent from clothing and household items. “Advise them to keep fingernails short and control dander, pollen, mold, household chemicals, and tobacco smoke, as well as the child’s stress and anxiety, which can also be a trigger,” Lee said.

“Skin infections from organisms such as staph, herpes, or coxsackie can also exacerbate symptoms,” Brown-Whitehorn added. “PCPs can educate caregivers to avoid all known triggers and give them an ‘action plan’ to carry out when skin flares.”
 

Food Allergies

Parents may be unaware food allergens can travel far beyond the plate, Lee said. Researchers vacuuming household bedding, carpets, furniture, and other surfaces have detected unnoticeably tiny quantities of allergenic food proteins in ordinary house dust. Touching this dust appears to provide the main exposure to those allergens.

“According to the dual exposure to allergen hypothesis, an infant’s tolerance to antigens occurs through high-dose exposure by mouth, and allergic sensitization occurs through low-dose exposure through the skin,” he said. “As young as four to six months of age, even before eating solid food, a child develops eczema, has a leaky skin barrier, comes in contact with food, and develops a food allergy.”

IgE-mediated food allergies can begin at any age. “Symptoms occur when a food is ingested and the patient develops symptoms including but not limited to urticariaangioedema, pruritus, flushing, vomiting, diarrhea, coughing, wheezing, difficulty breathing, presyncope, or syncope,” Pandya noted.

In the case of eosinophilic esophagitis, which may also be part of the atopic march, infants and toddlers often have challenging-to-treat symptoms of reflux, while school-age children have reflux and abdominal pain, and adolescents and adults may experience difficulty swallowing and impactions of food or pills, Brown-Whitehorn said.

To differentiate between food allergy and contact dermatitis, Lee suggested providers ask, “ ’Is the rash hives? If yes, is the rash generalized or in a limited area?’ Then consider the statistical probabilities. Skin problems after milk, egg, wheat, soy, peanut, tree nut, fish, shellfish, or sesame are likely due to IgE-mediated food allergy, but after ketchup or strawberry are probably from skin contact.”
 

 

 

Allergic Rhinitis and Asthma

“For asthma, ask about frequency of night cough and symptoms with exercise, laughing, or crying. For allergic rhinitis, look for runny nose, itchy eyes, or sneezing,” Brown-Whitehorn said.

Testing and Monitoring

Assessing the extent of eczema with the Eczema Area and Severity Index or the SCORing Atopic Dermatitis index takes time but may be necessary to obtain insurance coverage for treatments such as biologics.

Avoid ordering IgE food panels, which can result in false positives that can lead to loss of tolerance and nutritional deficiencies; psychological harm from bullying, anxiety, and decreased quality of life; and higher food and healthcare costs, Pandya said.

Treatments
Caregivers may be wary about treatments, and all the three experts this news organization spoke with stressed the importance of educating caregivers about how treatments work and what to expect from them.

“Early and aggressive atopic dermatitis treatment could prevent sensitization to food or aeroallergens, which could help prevent additional atopic diseases, including those on the atopic march,” Pandya said. “Topical steroids are considered first line at any age. Topical phosphodiesterase inhibitors are approved at 3 months of age and above. Topical calcineurin inhibitors are approved at 2 years of age and above. Wet wrap therapy and bleach baths can be effective. Other options include biologic therapy, allergen immunotherapy, and UV therapy.”

Epinephrine auto-injectors can counteract food reactions. For allergic rhinitis, non-sedating antihistamines, steroidal nasal sprays, and nasal antihistamines help. Asthma treatments include various inhaled medications,” Brown-Whitehorn added.
 

When to Refer to Specialists

Involving an allergist, dermatologist, pulmonologist, or ear nose throat specialist to the patient’s care team is advisable in more challenging cases.

If a child is younger than 3 months and has moderate to severe atopic dermatitis, an underlying immune defect may be to blame, so an allergy and immunology assessment is warranted, Brown-Whitehorn said. “An allergist can help any child who has recurrent coughing or wheezing avoid the emergency room or hospitalization.”

“In pediatrics, we always try to find the medication, regimen, and avoidance strategies that use the least treatment to provide the best care for each patient,” Brown-Whitehorn added. “Children eat, play, learn, and sleep, and every stage of the atopic march affects each of these activities. As clinicians, we need to be sure that we are helping children make the best of all these activities.”

Brown-Whitehorn reported financial relationships with DBV Technologies and Regeneron Pharmaceuticals. Lee reported financial relationships with Novartis. Pandya reported financial relationships with DBV Technologies, Thermo Fisher Scientific, and Sanofi.
 

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

Primary care physicians (PCPs) play a key role in treating young patients as they progress through the “atopic march” from atopic dermatitis through food allergy, asthma, and allergic rhinitis. They can also help prevent the process from starting.

“The PCP is usually the first clinician a family with concerns about atopic conditions sees, unless they first visit urgent care or an emergency department after an allergic reaction to food. Either way, families rely on their PCP for ongoing guidance,” said Terri F. Brown-Whitehorn, MD, attending physician in the Division of Allergy and Immunology at the Center for Pediatric Eosinophilic Disorders and the Integrative Health Program at Children’s Hospital of Philadelphia.

“The most important thing PCPs can do is know that the atopic march exists, how it progresses over time, and what signs and symptoms to look for,” she told this news organization.
 

The Atopic March

The atopic march describes the progression of allergic diseases in a child over time, with atopic dermatitis and food allergy in infancy tending to be followed by allergic rhinitis and asthma into later childhood and adulthood.

Although the pathophysiology of the inflammation that precedes atopic dermatitis is unclear, two main hypotheses have been proposed. The first suggests a primary immune dysfunction leads to immunoglobulin E (IgE) sensitization, allergic inflammation, and a secondary disturbance of the epithelial barrier; the second starts with a primary defect in the epithelial barrier that leads to secondary immunologic dysregulation and results in inflammation.

Genetics, infection, hygiene, extreme climate, food allergens, probiotics, aeroallergens, and tobacco smoke are thought to play roles in atopic dermatitis. An estimated 10%-12% of children and 1% of adults in the United States have been reported to have the condition, and the prevalence appears to be increasing. An estimated 85% of cases occur during the first year of life and 95% before the age of 5 years.

“Atopy often, though not always, runs in families, so PCPs should inquire about the history of atopic dermatitis, IgE-mediated food allergies, allergic rhinitis, and asthma in the patient’s siblings, parents, and grandparents,” Brown-Whitehorn said.
 

Key Educators

PCPs treat the full gamut of atopic conditions and are key educators on ways families can help mitigate their children’s atopic march or stop it before it begins, said Gerald Bell Lee, MD, an allergist and immunologist at Children’s Healthcare of Atlanta and an associate professor in the Division of Allergy and Immunology at Emory University School of Medicine, Atlanta.

“Most parents who bring their infants with eczema to the PCP assume their child ate something that caused their rash. But the relationship between atopic dermatitis, a type of eczema, and food allergy is more complicated,” he added.

Lee said PCPs should explain to their patients what atopic dermatitis is, how it starts and progresses, and how families can help prevent the condition by, for example, introducing allergenic foods to infants at around 4-6 months of age.
 

Atopic Dermatitis

PCPs should inform parents and other caregivers to wash their hands before moisturizing their child, take care not to contaminate the moisturizer, and bathe their child only when the child is dirty.

“Soap removes protective natural skin oils and increases moisture loss, and exposure to soap and bathing is a main contributor to eczema,” said Lee. “Dry skin loses its protective barrier, allowing outside agents to penetrate and be identified by the immune system.”

“According to one hypothesis, parents may eat food, not wash their hands afterwards, then moisturize their baby. This unhygienic practice spreads food proteins from the adult’s meal, and possibly from contaminants present in the moisturizer, all over the baby’s body,” he added.

Lee said he and his colleagues discourage overbathing babies to minimize the risk for skin injury that begins the atopic march: “New parents are inundated with infant skincare messaging and products. But we need to weigh societal pressures against practicality and ask, ‘Is the child’s skin actually dirty?’ ”

Atopic dermatitis tends to appear on the extensor surfaces, face, and scalp in infants and around arm and leg creases in toddlers and older children. Severe forms of the condition can be more widely distributed on the body, said Aarti P. Pandya, MD, medical director of the Food Allergy Center at Children’s Mercy Kansas City and clinical assistant professor of pediatrics at the University of Missouri-Kansas City School of Medicine, Kansas City, Missouri.
 

Avoid Triggers, Minimize Flares

Triggers of eczema are varied and common. To help minimize flares, PCPs can encourage caregivers to avoid products with fragrances or dyes, minimize the use of soaps, and completely rinse laundry detergent from clothing and household items. “Advise them to keep fingernails short and control dander, pollen, mold, household chemicals, and tobacco smoke, as well as the child’s stress and anxiety, which can also be a trigger,” Lee said.

“Skin infections from organisms such as staph, herpes, or coxsackie can also exacerbate symptoms,” Brown-Whitehorn added. “PCPs can educate caregivers to avoid all known triggers and give them an ‘action plan’ to carry out when skin flares.”
 

Food Allergies

Parents may be unaware food allergens can travel far beyond the plate, Lee said. Researchers vacuuming household bedding, carpets, furniture, and other surfaces have detected unnoticeably tiny quantities of allergenic food proteins in ordinary house dust. Touching this dust appears to provide the main exposure to those allergens.

“According to the dual exposure to allergen hypothesis, an infant’s tolerance to antigens occurs through high-dose exposure by mouth, and allergic sensitization occurs through low-dose exposure through the skin,” he said. “As young as four to six months of age, even before eating solid food, a child develops eczema, has a leaky skin barrier, comes in contact with food, and develops a food allergy.”

IgE-mediated food allergies can begin at any age. “Symptoms occur when a food is ingested and the patient develops symptoms including but not limited to urticariaangioedema, pruritus, flushing, vomiting, diarrhea, coughing, wheezing, difficulty breathing, presyncope, or syncope,” Pandya noted.

In the case of eosinophilic esophagitis, which may also be part of the atopic march, infants and toddlers often have challenging-to-treat symptoms of reflux, while school-age children have reflux and abdominal pain, and adolescents and adults may experience difficulty swallowing and impactions of food or pills, Brown-Whitehorn said.

To differentiate between food allergy and contact dermatitis, Lee suggested providers ask, “ ’Is the rash hives? If yes, is the rash generalized or in a limited area?’ Then consider the statistical probabilities. Skin problems after milk, egg, wheat, soy, peanut, tree nut, fish, shellfish, or sesame are likely due to IgE-mediated food allergy, but after ketchup or strawberry are probably from skin contact.”
 

 

 

Allergic Rhinitis and Asthma

“For asthma, ask about frequency of night cough and symptoms with exercise, laughing, or crying. For allergic rhinitis, look for runny nose, itchy eyes, or sneezing,” Brown-Whitehorn said.

Testing and Monitoring

Assessing the extent of eczema with the Eczema Area and Severity Index or the SCORing Atopic Dermatitis index takes time but may be necessary to obtain insurance coverage for treatments such as biologics.

Avoid ordering IgE food panels, which can result in false positives that can lead to loss of tolerance and nutritional deficiencies; psychological harm from bullying, anxiety, and decreased quality of life; and higher food and healthcare costs, Pandya said.

Treatments
Caregivers may be wary about treatments, and all the three experts this news organization spoke with stressed the importance of educating caregivers about how treatments work and what to expect from them.

“Early and aggressive atopic dermatitis treatment could prevent sensitization to food or aeroallergens, which could help prevent additional atopic diseases, including those on the atopic march,” Pandya said. “Topical steroids are considered first line at any age. Topical phosphodiesterase inhibitors are approved at 3 months of age and above. Topical calcineurin inhibitors are approved at 2 years of age and above. Wet wrap therapy and bleach baths can be effective. Other options include biologic therapy, allergen immunotherapy, and UV therapy.”

Epinephrine auto-injectors can counteract food reactions. For allergic rhinitis, non-sedating antihistamines, steroidal nasal sprays, and nasal antihistamines help. Asthma treatments include various inhaled medications,” Brown-Whitehorn added.
 

When to Refer to Specialists

Involving an allergist, dermatologist, pulmonologist, or ear nose throat specialist to the patient’s care team is advisable in more challenging cases.

If a child is younger than 3 months and has moderate to severe atopic dermatitis, an underlying immune defect may be to blame, so an allergy and immunology assessment is warranted, Brown-Whitehorn said. “An allergist can help any child who has recurrent coughing or wheezing avoid the emergency room or hospitalization.”

“In pediatrics, we always try to find the medication, regimen, and avoidance strategies that use the least treatment to provide the best care for each patient,” Brown-Whitehorn added. “Children eat, play, learn, and sleep, and every stage of the atopic march affects each of these activities. As clinicians, we need to be sure that we are helping children make the best of all these activities.”

Brown-Whitehorn reported financial relationships with DBV Technologies and Regeneron Pharmaceuticals. Lee reported financial relationships with Novartis. Pandya reported financial relationships with DBV Technologies, Thermo Fisher Scientific, and Sanofi.
 

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

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Study Evaluates Safety of Benzoyl Peroxide Products for Acne

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Changed
Tue, 10/15/2024 - 09:06

 

Among 111 prescription or over-the-counter products for acne that contain benzoyl peroxide (BPO), 38 (34%) contained benzene levels above the Food and Drug Administration (FDA) limit of 2 ppm, according to results from an analysis that used gas chromatography–mass spectrometry and other methods.

The analysis, which was published in the Journal of Investigative Dermatology and expands on a similar study released more than 6 months ago, also found that encapsulated BPO products break down into benzene at room temperature but that refrigerating them may mitigate this effect.

“Our research provides the first experimental evidence that cold storage can help reduce the rate of benzoyl peroxide breakdown into benzene,” said one of the study authors, Christopher G. Bunick, MD, PhD, associate professor of dermatology at Yale University, New Haven, Connecticut. “Therefore, cold storage throughout the entire supply chain — from manufacturing to patient use — is a reasonable and proportional measure at this time for those continuing to use benzoyl peroxide medicine.” One acne product, the newer prescription triple-combination therapy (adapalene-clindamycin-BPO) “already has a cold shipping process in place; the patient just needs to continue that at home,” he noted.

For the study — which was funded by an independent lab, Valisure — researchers led by Valisure CEO and founder David Light, used gas chromatography-mass spectrometry to detect benzene levels in 111 BPO drug products from major US retailers and selected ion flow tube mass-spectrometry to quantify the release of benzene in real time. Benzene levels ranged from 0.16 ppm to 35.30 ppm, and 38 of the products (34%) had levels above the FDA limit of 2 ppm for drug products. “The results of the products sampled in this study suggest that formulation is likely the strongest contributor to benzene concentrations in BPO drug products that are commercially available, since the magnitude of benzene detected correlates most closely with specific brands or product types within certain brands,” the study authors wrote.

When the researchers tested the stability of a prescription encapsulated BPO drug product at cold (2 °C) and elevated temperature (50 °C), no apparent benzene formation was observed at 2 °C, whereas high levels of benzene formed at 50 °C, “suggesting that encapsulation technology may not stabilize BPO drug products, but cold storage may greatly reduce benzene formation,” they wrote.

In another component of the study, researchers exposed a BP drug product to a UVA/UVB lamp for 2 hours and found detectable benzene through evaporation and substantial benzene formation when exposed to UV light at levels below peak sunlight. The experiment “strongly justifies the package label warnings to avoid sun exposure when using BPO drug products,” the authors wrote. “Further evaluation to determine the influence of sun exposure on BPO drug product degradation and benzene formation is warranted.”

In an interview, John Barbieri, MD, MBA, assistant professor of dermatology at Harvard Medical School and director of the Advanced Acne Therapeutics Clinic at Brigham and Women’s Hospital, Boston, Massachusetts characterized the findings as “an important issue that we should take seriously.” However, “we also must not overreact.” 

BPO is a foundational acne treatment without any clear alternative, he said, pointing out that no evidence currently exists “to support that routine use of benzoyl peroxide–containing products for acne is associated with a meaningful risk of benzene in the blood or an increased risk of cancer.”

And although it is prudent to minimize benzene exposure as much as possible, Barbieri continued, “it is not clear that these levels are a clinically meaningful incremental risk in the setting of an acne cream or wash. There is minimal cutaneous absorption of benzene, and it is uncertain how much benzene aerosolizes with routine use, particularly for washes which are not left on the skin.”

Bunick said that the combined data from this and the study published in March 2024 affected which BPO products he recommends for patients with acne. “I am using exclusively the triple combination therapy (adapalene-clindamycin-benzoyl peroxide) because I know it has the necessary cold supply chain in place to protect the product’s stability. I further encourage patients to place all their benzoyl peroxide–containing products in the refrigerator at home to reduce benzene formation and exposure.”

Bunick reported having served as an investigator and/or a consultant/speaker for many pharmaceutical companies, including as a consultant for Ortho-Dermatologics; but none related to this study. Barbieri reported having no relevant disclosures.

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

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Among 111 prescription or over-the-counter products for acne that contain benzoyl peroxide (BPO), 38 (34%) contained benzene levels above the Food and Drug Administration (FDA) limit of 2 ppm, according to results from an analysis that used gas chromatography–mass spectrometry and other methods.

The analysis, which was published in the Journal of Investigative Dermatology and expands on a similar study released more than 6 months ago, also found that encapsulated BPO products break down into benzene at room temperature but that refrigerating them may mitigate this effect.

“Our research provides the first experimental evidence that cold storage can help reduce the rate of benzoyl peroxide breakdown into benzene,” said one of the study authors, Christopher G. Bunick, MD, PhD, associate professor of dermatology at Yale University, New Haven, Connecticut. “Therefore, cold storage throughout the entire supply chain — from manufacturing to patient use — is a reasonable and proportional measure at this time for those continuing to use benzoyl peroxide medicine.” One acne product, the newer prescription triple-combination therapy (adapalene-clindamycin-BPO) “already has a cold shipping process in place; the patient just needs to continue that at home,” he noted.

For the study — which was funded by an independent lab, Valisure — researchers led by Valisure CEO and founder David Light, used gas chromatography-mass spectrometry to detect benzene levels in 111 BPO drug products from major US retailers and selected ion flow tube mass-spectrometry to quantify the release of benzene in real time. Benzene levels ranged from 0.16 ppm to 35.30 ppm, and 38 of the products (34%) had levels above the FDA limit of 2 ppm for drug products. “The results of the products sampled in this study suggest that formulation is likely the strongest contributor to benzene concentrations in BPO drug products that are commercially available, since the magnitude of benzene detected correlates most closely with specific brands or product types within certain brands,” the study authors wrote.

When the researchers tested the stability of a prescription encapsulated BPO drug product at cold (2 °C) and elevated temperature (50 °C), no apparent benzene formation was observed at 2 °C, whereas high levels of benzene formed at 50 °C, “suggesting that encapsulation technology may not stabilize BPO drug products, but cold storage may greatly reduce benzene formation,” they wrote.

In another component of the study, researchers exposed a BP drug product to a UVA/UVB lamp for 2 hours and found detectable benzene through evaporation and substantial benzene formation when exposed to UV light at levels below peak sunlight. The experiment “strongly justifies the package label warnings to avoid sun exposure when using BPO drug products,” the authors wrote. “Further evaluation to determine the influence of sun exposure on BPO drug product degradation and benzene formation is warranted.”

In an interview, John Barbieri, MD, MBA, assistant professor of dermatology at Harvard Medical School and director of the Advanced Acne Therapeutics Clinic at Brigham and Women’s Hospital, Boston, Massachusetts characterized the findings as “an important issue that we should take seriously.” However, “we also must not overreact.” 

BPO is a foundational acne treatment without any clear alternative, he said, pointing out that no evidence currently exists “to support that routine use of benzoyl peroxide–containing products for acne is associated with a meaningful risk of benzene in the blood or an increased risk of cancer.”

And although it is prudent to minimize benzene exposure as much as possible, Barbieri continued, “it is not clear that these levels are a clinically meaningful incremental risk in the setting of an acne cream or wash. There is minimal cutaneous absorption of benzene, and it is uncertain how much benzene aerosolizes with routine use, particularly for washes which are not left on the skin.”

Bunick said that the combined data from this and the study published in March 2024 affected which BPO products he recommends for patients with acne. “I am using exclusively the triple combination therapy (adapalene-clindamycin-benzoyl peroxide) because I know it has the necessary cold supply chain in place to protect the product’s stability. I further encourage patients to place all their benzoyl peroxide–containing products in the refrigerator at home to reduce benzene formation and exposure.”

Bunick reported having served as an investigator and/or a consultant/speaker for many pharmaceutical companies, including as a consultant for Ortho-Dermatologics; but none related to this study. Barbieri reported having no relevant disclosures.

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

 

Among 111 prescription or over-the-counter products for acne that contain benzoyl peroxide (BPO), 38 (34%) contained benzene levels above the Food and Drug Administration (FDA) limit of 2 ppm, according to results from an analysis that used gas chromatography–mass spectrometry and other methods.

The analysis, which was published in the Journal of Investigative Dermatology and expands on a similar study released more than 6 months ago, also found that encapsulated BPO products break down into benzene at room temperature but that refrigerating them may mitigate this effect.

“Our research provides the first experimental evidence that cold storage can help reduce the rate of benzoyl peroxide breakdown into benzene,” said one of the study authors, Christopher G. Bunick, MD, PhD, associate professor of dermatology at Yale University, New Haven, Connecticut. “Therefore, cold storage throughout the entire supply chain — from manufacturing to patient use — is a reasonable and proportional measure at this time for those continuing to use benzoyl peroxide medicine.” One acne product, the newer prescription triple-combination therapy (adapalene-clindamycin-BPO) “already has a cold shipping process in place; the patient just needs to continue that at home,” he noted.

For the study — which was funded by an independent lab, Valisure — researchers led by Valisure CEO and founder David Light, used gas chromatography-mass spectrometry to detect benzene levels in 111 BPO drug products from major US retailers and selected ion flow tube mass-spectrometry to quantify the release of benzene in real time. Benzene levels ranged from 0.16 ppm to 35.30 ppm, and 38 of the products (34%) had levels above the FDA limit of 2 ppm for drug products. “The results of the products sampled in this study suggest that formulation is likely the strongest contributor to benzene concentrations in BPO drug products that are commercially available, since the magnitude of benzene detected correlates most closely with specific brands or product types within certain brands,” the study authors wrote.

When the researchers tested the stability of a prescription encapsulated BPO drug product at cold (2 °C) and elevated temperature (50 °C), no apparent benzene formation was observed at 2 °C, whereas high levels of benzene formed at 50 °C, “suggesting that encapsulation technology may not stabilize BPO drug products, but cold storage may greatly reduce benzene formation,” they wrote.

In another component of the study, researchers exposed a BP drug product to a UVA/UVB lamp for 2 hours and found detectable benzene through evaporation and substantial benzene formation when exposed to UV light at levels below peak sunlight. The experiment “strongly justifies the package label warnings to avoid sun exposure when using BPO drug products,” the authors wrote. “Further evaluation to determine the influence of sun exposure on BPO drug product degradation and benzene formation is warranted.”

In an interview, John Barbieri, MD, MBA, assistant professor of dermatology at Harvard Medical School and director of the Advanced Acne Therapeutics Clinic at Brigham and Women’s Hospital, Boston, Massachusetts characterized the findings as “an important issue that we should take seriously.” However, “we also must not overreact.” 

BPO is a foundational acne treatment without any clear alternative, he said, pointing out that no evidence currently exists “to support that routine use of benzoyl peroxide–containing products for acne is associated with a meaningful risk of benzene in the blood or an increased risk of cancer.”

And although it is prudent to minimize benzene exposure as much as possible, Barbieri continued, “it is not clear that these levels are a clinically meaningful incremental risk in the setting of an acne cream or wash. There is minimal cutaneous absorption of benzene, and it is uncertain how much benzene aerosolizes with routine use, particularly for washes which are not left on the skin.”

Bunick said that the combined data from this and the study published in March 2024 affected which BPO products he recommends for patients with acne. “I am using exclusively the triple combination therapy (adapalene-clindamycin-benzoyl peroxide) because I know it has the necessary cold supply chain in place to protect the product’s stability. I further encourage patients to place all their benzoyl peroxide–containing products in the refrigerator at home to reduce benzene formation and exposure.”

Bunick reported having served as an investigator and/or a consultant/speaker for many pharmaceutical companies, including as a consultant for Ortho-Dermatologics; but none related to this study. Barbieri reported having no relevant disclosures.

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

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FROM THE JOURNAL OF INVESTIGATIVE DERMATOLOGY

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A 7-Year-Old Boy Presents With Dark Spots on His Scalp and Areas of Poor Hair Growth

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Given the trichoscopic findings, scrapings from the scaly areas were taken and revealed hyphae, confirming the diagnosis of tinea capitis. A fungal culture identified Trichophyton tonsurans as the causative organism.

Tinea capitis is the most common dermatophyte infection in children. Risk factors include participation in close-contact sports like wrestling or jiu-jitsu, attendance at daycare for younger children, African American hair care practices, pet ownership (particularly cats and rodents), and living in overcrowded conditions.

Diagnosis of tinea capitis requires a thorough clinical history to identify potential risk factors. On physical examination, patchy hair loss with associated scaling should raise suspicion for tinea capitis. Inflammatory signs, such as pustules and swelling, may suggest the presence of a kerion, further supporting the diagnosis. Although some practitioners use Wood’s lamp to help with diagnosis, its utility is limited. It detects fluorescence in Microsporum species (exothrix infections) but not in Trichophyton species (endothrix infections).

Trichoscopy can be a valuable tool when inflammation is minimal, and only hair loss and scaling are observed. Trichoscopic findings suggestive of tinea capitis include comma hairs, corkscrew hairs (as seen in this patient), Morse code-like hairs, zigzag hairs, bent hairs, block hairs, and i-hairs. Other common, though not characteristic, findings include broken hairs, black dots, perifollicular scaling, and diffuse scaling.

KOH (potassium hydroxide) analysis is another useful method for detecting fungal elements, though it does not identify the specific fungus and may not be available in all clinical settings. Mycologic culture remains the gold standard for diagnosing tinea capitis, though results can take 3-4 weeks. Newer diagnostic techniques, such as PCR analysis and MALDI-TOF/MS, offer more rapid identification of the causative organism.

Dr. Matiz
Dr. Catalina Matiz


The differential diagnosis includes:

  • Seborrheic dermatitis, which presents with greasy, yellowish scales and itching, with trichoscopy showing twisted, coiled hairs and yellowish scaling.
  • Psoriasis, which can mimic tinea capitis but presents with well-demarcated red plaques and silvery-white scales. Trichoscopy shows red dots and uniform scaling.
  • Alopecia areata, which causes patchy hair loss without inflammation or scaling, with trichoscopic findings of exclamation mark hairs, black dots, and yellow dots.
  • Trichotillomania, a hair-pulling disorder, which results in irregular patches of hair loss. Trichoscopy shows broken hairs of varying lengths, V-sign hairs, and flame-shaped residues at follicular openings.

Treatment of tinea capitis requires systemic antifungals and topical agents to prevent fungal spore spread. Several treatment guidelines are available from different institutions. Griseofulvin (FDA-approved for patients > 2 years of age) has been widely used, particularly for Microsporum canis infections. However, due to limited availability in many countries, terbinafine (FDA-approved for patients > 4 years of age) is now commonly used as first-line therapy, especially for Trichophyton species. Treatment typically lasts 4-6 weeks, and post-treatment cultures may be recommended to confirm mycologic cure.

Concerns about drug resistance have emerged, particularly for terbinafine-resistant dermatophytes linked to mutations in the squalene epoxidase enzyme. Resistance may be driven by limited antifungal availability and poor adherence to prolonged treatment regimens. While fluconazole and itraconazole are used off-label, growing evidence supports their effectiveness, although one large trial showed suboptimal cure rates with fluconazole.

Though systemic antifungals are generally safe, hepatotoxicity remains a concern, especially in patients with hepatic conditions or other comorbidities. Lab monitoring is advised for patients on prolonged or multiple therapies, or for those with coexisting conditions. The decision to conduct lab monitoring should be discussed with parents, balancing the very low risk of hepatotoxicity in healthy children against their comfort level.

An alternative to systemic therapy is photodynamic therapy (PDT), which has been reported as successful in treating tinea capitis infections, particularly in cases of T. mentagrophytes and M. canis. However, large-scale trials are needed to confirm PDT’s efficacy and safety.

In conclusion, children presenting with hair loss, scaling, and associated dark spots on the scalp should be evaluated for fungal infection. While trichoscopy can aid in diagnosis, fungal culture remains the gold standard for confirmation.
 

Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego.

References

Rudnicka L et al. Hair shafts in trichoscopy: clues for diagnosis of hair and scalp diseases. Dermatol Clin. 2013 Oct;31(4):695-708, x. doi: 10.1016/j.det.2013.06.007.

Gupta AK et al. An update on tinea capitis in children. Pediatr Dermatol. 2024 Aug 7. doi: 10.1111/pde.15708.

Anna Waskiel-Burnat et al. Trichoscopy of tinea capitis: A systematic review. Dermatol Ther (Heidelb). 2020 Feb;10(1):43-52. doi: 10.1007/s13555-019-00350-1.
 

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Given the trichoscopic findings, scrapings from the scaly areas were taken and revealed hyphae, confirming the diagnosis of tinea capitis. A fungal culture identified Trichophyton tonsurans as the causative organism.

Tinea capitis is the most common dermatophyte infection in children. Risk factors include participation in close-contact sports like wrestling or jiu-jitsu, attendance at daycare for younger children, African American hair care practices, pet ownership (particularly cats and rodents), and living in overcrowded conditions.

Diagnosis of tinea capitis requires a thorough clinical history to identify potential risk factors. On physical examination, patchy hair loss with associated scaling should raise suspicion for tinea capitis. Inflammatory signs, such as pustules and swelling, may suggest the presence of a kerion, further supporting the diagnosis. Although some practitioners use Wood’s lamp to help with diagnosis, its utility is limited. It detects fluorescence in Microsporum species (exothrix infections) but not in Trichophyton species (endothrix infections).

Trichoscopy can be a valuable tool when inflammation is minimal, and only hair loss and scaling are observed. Trichoscopic findings suggestive of tinea capitis include comma hairs, corkscrew hairs (as seen in this patient), Morse code-like hairs, zigzag hairs, bent hairs, block hairs, and i-hairs. Other common, though not characteristic, findings include broken hairs, black dots, perifollicular scaling, and diffuse scaling.

KOH (potassium hydroxide) analysis is another useful method for detecting fungal elements, though it does not identify the specific fungus and may not be available in all clinical settings. Mycologic culture remains the gold standard for diagnosing tinea capitis, though results can take 3-4 weeks. Newer diagnostic techniques, such as PCR analysis and MALDI-TOF/MS, offer more rapid identification of the causative organism.

Dr. Matiz
Dr. Catalina Matiz


The differential diagnosis includes:

  • Seborrheic dermatitis, which presents with greasy, yellowish scales and itching, with trichoscopy showing twisted, coiled hairs and yellowish scaling.
  • Psoriasis, which can mimic tinea capitis but presents with well-demarcated red plaques and silvery-white scales. Trichoscopy shows red dots and uniform scaling.
  • Alopecia areata, which causes patchy hair loss without inflammation or scaling, with trichoscopic findings of exclamation mark hairs, black dots, and yellow dots.
  • Trichotillomania, a hair-pulling disorder, which results in irregular patches of hair loss. Trichoscopy shows broken hairs of varying lengths, V-sign hairs, and flame-shaped residues at follicular openings.

Treatment of tinea capitis requires systemic antifungals and topical agents to prevent fungal spore spread. Several treatment guidelines are available from different institutions. Griseofulvin (FDA-approved for patients > 2 years of age) has been widely used, particularly for Microsporum canis infections. However, due to limited availability in many countries, terbinafine (FDA-approved for patients > 4 years of age) is now commonly used as first-line therapy, especially for Trichophyton species. Treatment typically lasts 4-6 weeks, and post-treatment cultures may be recommended to confirm mycologic cure.

Concerns about drug resistance have emerged, particularly for terbinafine-resistant dermatophytes linked to mutations in the squalene epoxidase enzyme. Resistance may be driven by limited antifungal availability and poor adherence to prolonged treatment regimens. While fluconazole and itraconazole are used off-label, growing evidence supports their effectiveness, although one large trial showed suboptimal cure rates with fluconazole.

Though systemic antifungals are generally safe, hepatotoxicity remains a concern, especially in patients with hepatic conditions or other comorbidities. Lab monitoring is advised for patients on prolonged or multiple therapies, or for those with coexisting conditions. The decision to conduct lab monitoring should be discussed with parents, balancing the very low risk of hepatotoxicity in healthy children against their comfort level.

An alternative to systemic therapy is photodynamic therapy (PDT), which has been reported as successful in treating tinea capitis infections, particularly in cases of T. mentagrophytes and M. canis. However, large-scale trials are needed to confirm PDT’s efficacy and safety.

In conclusion, children presenting with hair loss, scaling, and associated dark spots on the scalp should be evaluated for fungal infection. While trichoscopy can aid in diagnosis, fungal culture remains the gold standard for confirmation.
 

Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego.

References

Rudnicka L et al. Hair shafts in trichoscopy: clues for diagnosis of hair and scalp diseases. Dermatol Clin. 2013 Oct;31(4):695-708, x. doi: 10.1016/j.det.2013.06.007.

Gupta AK et al. An update on tinea capitis in children. Pediatr Dermatol. 2024 Aug 7. doi: 10.1111/pde.15708.

Anna Waskiel-Burnat et al. Trichoscopy of tinea capitis: A systematic review. Dermatol Ther (Heidelb). 2020 Feb;10(1):43-52. doi: 10.1007/s13555-019-00350-1.
 

Given the trichoscopic findings, scrapings from the scaly areas were taken and revealed hyphae, confirming the diagnosis of tinea capitis. A fungal culture identified Trichophyton tonsurans as the causative organism.

Tinea capitis is the most common dermatophyte infection in children. Risk factors include participation in close-contact sports like wrestling or jiu-jitsu, attendance at daycare for younger children, African American hair care practices, pet ownership (particularly cats and rodents), and living in overcrowded conditions.

Diagnosis of tinea capitis requires a thorough clinical history to identify potential risk factors. On physical examination, patchy hair loss with associated scaling should raise suspicion for tinea capitis. Inflammatory signs, such as pustules and swelling, may suggest the presence of a kerion, further supporting the diagnosis. Although some practitioners use Wood’s lamp to help with diagnosis, its utility is limited. It detects fluorescence in Microsporum species (exothrix infections) but not in Trichophyton species (endothrix infections).

Trichoscopy can be a valuable tool when inflammation is minimal, and only hair loss and scaling are observed. Trichoscopic findings suggestive of tinea capitis include comma hairs, corkscrew hairs (as seen in this patient), Morse code-like hairs, zigzag hairs, bent hairs, block hairs, and i-hairs. Other common, though not characteristic, findings include broken hairs, black dots, perifollicular scaling, and diffuse scaling.

KOH (potassium hydroxide) analysis is another useful method for detecting fungal elements, though it does not identify the specific fungus and may not be available in all clinical settings. Mycologic culture remains the gold standard for diagnosing tinea capitis, though results can take 3-4 weeks. Newer diagnostic techniques, such as PCR analysis and MALDI-TOF/MS, offer more rapid identification of the causative organism.

Dr. Matiz
Dr. Catalina Matiz


The differential diagnosis includes:

  • Seborrheic dermatitis, which presents with greasy, yellowish scales and itching, with trichoscopy showing twisted, coiled hairs and yellowish scaling.
  • Psoriasis, which can mimic tinea capitis but presents with well-demarcated red plaques and silvery-white scales. Trichoscopy shows red dots and uniform scaling.
  • Alopecia areata, which causes patchy hair loss without inflammation or scaling, with trichoscopic findings of exclamation mark hairs, black dots, and yellow dots.
  • Trichotillomania, a hair-pulling disorder, which results in irregular patches of hair loss. Trichoscopy shows broken hairs of varying lengths, V-sign hairs, and flame-shaped residues at follicular openings.

Treatment of tinea capitis requires systemic antifungals and topical agents to prevent fungal spore spread. Several treatment guidelines are available from different institutions. Griseofulvin (FDA-approved for patients > 2 years of age) has been widely used, particularly for Microsporum canis infections. However, due to limited availability in many countries, terbinafine (FDA-approved for patients > 4 years of age) is now commonly used as first-line therapy, especially for Trichophyton species. Treatment typically lasts 4-6 weeks, and post-treatment cultures may be recommended to confirm mycologic cure.

Concerns about drug resistance have emerged, particularly for terbinafine-resistant dermatophytes linked to mutations in the squalene epoxidase enzyme. Resistance may be driven by limited antifungal availability and poor adherence to prolonged treatment regimens. While fluconazole and itraconazole are used off-label, growing evidence supports their effectiveness, although one large trial showed suboptimal cure rates with fluconazole.

Though systemic antifungals are generally safe, hepatotoxicity remains a concern, especially in patients with hepatic conditions or other comorbidities. Lab monitoring is advised for patients on prolonged or multiple therapies, or for those with coexisting conditions. The decision to conduct lab monitoring should be discussed with parents, balancing the very low risk of hepatotoxicity in healthy children against their comfort level.

An alternative to systemic therapy is photodynamic therapy (PDT), which has been reported as successful in treating tinea capitis infections, particularly in cases of T. mentagrophytes and M. canis. However, large-scale trials are needed to confirm PDT’s efficacy and safety.

In conclusion, children presenting with hair loss, scaling, and associated dark spots on the scalp should be evaluated for fungal infection. While trichoscopy can aid in diagnosis, fungal culture remains the gold standard for confirmation.
 

Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego.

References

Rudnicka L et al. Hair shafts in trichoscopy: clues for diagnosis of hair and scalp diseases. Dermatol Clin. 2013 Oct;31(4):695-708, x. doi: 10.1016/j.det.2013.06.007.

Gupta AK et al. An update on tinea capitis in children. Pediatr Dermatol. 2024 Aug 7. doi: 10.1111/pde.15708.

Anna Waskiel-Burnat et al. Trichoscopy of tinea capitis: A systematic review. Dermatol Ther (Heidelb). 2020 Feb;10(1):43-52. doi: 10.1007/s13555-019-00350-1.
 

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Picture 1
A 7-year-old boy presents to the dermatology clinic with his mother for evaluation of dark spots on his scalp and areas of poor hair growth for several months. He reports occasional itching. He has a history of cradle cap as a baby and has been using over-the-counter antifungal shampoo without any improvement. His mother notes a family history of hair loss in several relatives. The patient enjoys practicing jiu-jitsu. He is otherwise healthy, takes no medications, and is up to date on vaccinations. 
Picture 2
Picture 3
On physical examination, the scalp shows scale with associate brown papules and areas of alopecia (Picture 1). Trichoscopy reveals corkscrew hairs, perifollicular erythema, and black dots (Pictures 2 and 3).

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Pulsed Dye Laser a “Go-To Device” Option for Acne Treatment When Access to 1726-nm Lasers Is Limited

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— Lasers and energy-based treatments alone or in combination with medical therapy may improve outcomes for patients with moderate to severe acne, according to Arielle Kauvar, MD.

At the Controversies and Conversations in Laser and Cosmetic Surgery annual symposium, Kauvar, director of New York Laser & Skin Care, New York City, highlighted several reasons why using lasers for acne is beneficial. “First, we know that topical therapy alone is often ineffective, and antibiotic treatment does not address the cause of acne and can alter the skin and gut microbiome,” she said. “Isotretinoin is highly effective, but there’s an increasing reluctance to use it. Lasers and energy devices are effective in treating acne and may also treat the post-inflammatory hyperpigmentation and scarring associated with it.”

The pathogenesis of acne is multifactorial, she continued, including a disruption of sebaceous gland activity, with overproduction and alteration of sebum and abnormal follicular keratinization. Acne also causes an imbalance of the skin microbiome, local inflammation, and activation of both innate and adaptive immunity.

“Many studies point to the fact that inflammation and immune system activation may actually be the primary event” of acne formation, said Kauvar, who is also a clinical professor of dermatology at New York University, New York City. “This persistent immune activation is also associated with scarring,” she noted. “So, are we off the mark in terms of trying to kill sebaceous glands? Should we be concentrating on anti-inflammatory approaches?” 

AviClear became the first 1726-nm laser cleared by the US Food and Drug Administration (FDA) for the treatment of mild to severe acne vulgaris in 2022, followed a few months later with the FDA clearance of another 1726-nm laser, the Accure Acne Laser System in November 2022. These lasers cause selective photothermolysis of sebaceous glands, but according to Kauvar, “access to these devices is somewhat limited at this time.”

What is available includes her go-to device, the pulsed dye laser (PDL), which has been widely studied and shown in a systematic review and meta-analysis of studies to be effective for acne. The PDL “targets dermal blood vessels facilitating inflammation, upregulates TGF-beta, and inhibits CD4+ T cell-mediated inflammation,” she said. “It can also treat PIH [post-inflammatory hyperpigmentation] and may be helpful in scar prevention.”

In an abstract presented at The American Society for Laser Medicine and Surgery (ASLMS) 2024 annual meeting, Kauvar and colleagues conducted a real-world study of PDL therapy in 15 adult women with recalcitrant acne who were maintained on their medical treatment regimen. Their mean age was 27 years, and they had skin types II-IV; they underwent four monthly PDL treatments with follow-up at 1 and 3 months. At each visit, the researchers took digital photographs and counted inflammatory acne lesions, non-inflammatory acne lesions, and post-inflammatory pigment alteration (PIPA) lesions.

The main outcomes of interest were the investigator global assessment (IGA) scores at the 1- and 3-month follow-up visits. Kauvar and colleagues observed a significant improvement in IGA scores at the 1- and 3-month follow-up visits (P < .05), with an average decrease of 1.8 and 1.6 points in the acne severity scale, respectively, from a baseline score of 3.4. By the 3-month follow-up visits, counts of inflammatory and non-inflammatory lesions decreased significantly (P < .05), and 61% of study participants showed a decrease in the PIPA count. No adverse events occurred. 

Kauvar disclosed that she has conducted research for Candela, Lumenis, and Sofwave, and is an adviser to Acclaro.

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

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— Lasers and energy-based treatments alone or in combination with medical therapy may improve outcomes for patients with moderate to severe acne, according to Arielle Kauvar, MD.

At the Controversies and Conversations in Laser and Cosmetic Surgery annual symposium, Kauvar, director of New York Laser & Skin Care, New York City, highlighted several reasons why using lasers for acne is beneficial. “First, we know that topical therapy alone is often ineffective, and antibiotic treatment does not address the cause of acne and can alter the skin and gut microbiome,” she said. “Isotretinoin is highly effective, but there’s an increasing reluctance to use it. Lasers and energy devices are effective in treating acne and may also treat the post-inflammatory hyperpigmentation and scarring associated with it.”

The pathogenesis of acne is multifactorial, she continued, including a disruption of sebaceous gland activity, with overproduction and alteration of sebum and abnormal follicular keratinization. Acne also causes an imbalance of the skin microbiome, local inflammation, and activation of both innate and adaptive immunity.

“Many studies point to the fact that inflammation and immune system activation may actually be the primary event” of acne formation, said Kauvar, who is also a clinical professor of dermatology at New York University, New York City. “This persistent immune activation is also associated with scarring,” she noted. “So, are we off the mark in terms of trying to kill sebaceous glands? Should we be concentrating on anti-inflammatory approaches?” 

AviClear became the first 1726-nm laser cleared by the US Food and Drug Administration (FDA) for the treatment of mild to severe acne vulgaris in 2022, followed a few months later with the FDA clearance of another 1726-nm laser, the Accure Acne Laser System in November 2022. These lasers cause selective photothermolysis of sebaceous glands, but according to Kauvar, “access to these devices is somewhat limited at this time.”

What is available includes her go-to device, the pulsed dye laser (PDL), which has been widely studied and shown in a systematic review and meta-analysis of studies to be effective for acne. The PDL “targets dermal blood vessels facilitating inflammation, upregulates TGF-beta, and inhibits CD4+ T cell-mediated inflammation,” she said. “It can also treat PIH [post-inflammatory hyperpigmentation] and may be helpful in scar prevention.”

In an abstract presented at The American Society for Laser Medicine and Surgery (ASLMS) 2024 annual meeting, Kauvar and colleagues conducted a real-world study of PDL therapy in 15 adult women with recalcitrant acne who were maintained on their medical treatment regimen. Their mean age was 27 years, and they had skin types II-IV; they underwent four monthly PDL treatments with follow-up at 1 and 3 months. At each visit, the researchers took digital photographs and counted inflammatory acne lesions, non-inflammatory acne lesions, and post-inflammatory pigment alteration (PIPA) lesions.

The main outcomes of interest were the investigator global assessment (IGA) scores at the 1- and 3-month follow-up visits. Kauvar and colleagues observed a significant improvement in IGA scores at the 1- and 3-month follow-up visits (P < .05), with an average decrease of 1.8 and 1.6 points in the acne severity scale, respectively, from a baseline score of 3.4. By the 3-month follow-up visits, counts of inflammatory and non-inflammatory lesions decreased significantly (P < .05), and 61% of study participants showed a decrease in the PIPA count. No adverse events occurred. 

Kauvar disclosed that she has conducted research for Candela, Lumenis, and Sofwave, and is an adviser to Acclaro.

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

— Lasers and energy-based treatments alone or in combination with medical therapy may improve outcomes for patients with moderate to severe acne, according to Arielle Kauvar, MD.

At the Controversies and Conversations in Laser and Cosmetic Surgery annual symposium, Kauvar, director of New York Laser & Skin Care, New York City, highlighted several reasons why using lasers for acne is beneficial. “First, we know that topical therapy alone is often ineffective, and antibiotic treatment does not address the cause of acne and can alter the skin and gut microbiome,” she said. “Isotretinoin is highly effective, but there’s an increasing reluctance to use it. Lasers and energy devices are effective in treating acne and may also treat the post-inflammatory hyperpigmentation and scarring associated with it.”

The pathogenesis of acne is multifactorial, she continued, including a disruption of sebaceous gland activity, with overproduction and alteration of sebum and abnormal follicular keratinization. Acne also causes an imbalance of the skin microbiome, local inflammation, and activation of both innate and adaptive immunity.

“Many studies point to the fact that inflammation and immune system activation may actually be the primary event” of acne formation, said Kauvar, who is also a clinical professor of dermatology at New York University, New York City. “This persistent immune activation is also associated with scarring,” she noted. “So, are we off the mark in terms of trying to kill sebaceous glands? Should we be concentrating on anti-inflammatory approaches?” 

AviClear became the first 1726-nm laser cleared by the US Food and Drug Administration (FDA) for the treatment of mild to severe acne vulgaris in 2022, followed a few months later with the FDA clearance of another 1726-nm laser, the Accure Acne Laser System in November 2022. These lasers cause selective photothermolysis of sebaceous glands, but according to Kauvar, “access to these devices is somewhat limited at this time.”

What is available includes her go-to device, the pulsed dye laser (PDL), which has been widely studied and shown in a systematic review and meta-analysis of studies to be effective for acne. The PDL “targets dermal blood vessels facilitating inflammation, upregulates TGF-beta, and inhibits CD4+ T cell-mediated inflammation,” she said. “It can also treat PIH [post-inflammatory hyperpigmentation] and may be helpful in scar prevention.”

In an abstract presented at The American Society for Laser Medicine and Surgery (ASLMS) 2024 annual meeting, Kauvar and colleagues conducted a real-world study of PDL therapy in 15 adult women with recalcitrant acne who were maintained on their medical treatment regimen. Their mean age was 27 years, and they had skin types II-IV; they underwent four monthly PDL treatments with follow-up at 1 and 3 months. At each visit, the researchers took digital photographs and counted inflammatory acne lesions, non-inflammatory acne lesions, and post-inflammatory pigment alteration (PIPA) lesions.

The main outcomes of interest were the investigator global assessment (IGA) scores at the 1- and 3-month follow-up visits. Kauvar and colleagues observed a significant improvement in IGA scores at the 1- and 3-month follow-up visits (P < .05), with an average decrease of 1.8 and 1.6 points in the acne severity scale, respectively, from a baseline score of 3.4. By the 3-month follow-up visits, counts of inflammatory and non-inflammatory lesions decreased significantly (P < .05), and 61% of study participants showed a decrease in the PIPA count. No adverse events occurred. 

Kauvar disclosed that she has conducted research for Candela, Lumenis, and Sofwave, and is an adviser to Acclaro.

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

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Mycosis Fungoides: Measured Approach Key to Treatment

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— When patients of Aaron Mangold, MD, first learn they have mycosis fungoides (MF), the most common form of primary cutaneous T-cell lymphoma (CTCL), some are concerned about whether the diagnosis means a shortened life expectancy.

“In most cases, mycosis fungoides will not shorten one’s life, but it can cause significant symptoms,” Dr. Mangold, codirector of the multidisciplinary cutaneous lymphoma clinic at Mayo Clinic, Scottsdale, Arizona, said at the annual meeting of the Pacific Dermatologic Association. “For early-stage disease, I think of it more like diabetes; this is really a chronic disease” that unlikely will be fatal but may be associated with increased morbidity as the disease progresses, and “the overall goal of therapy should be disease control to increase quality of life.”

courtesy Dr. Aaron Mangold
Dr. Aaron Mangold

Patient- and lymphoma-specific factors drive the choice of therapy. The focus for patients with early-stage disease, Dr. Mangold said, is to treat comorbidities and symptoms, such as itch or skin pain, maximize their quality of life, and consider the potential for associated toxicities of therapy as the disease progresses. Start with the least toxic, targeted, nonimmunosuppressive therapy, “then work toward more toxic immunosuppressive therapies,” he advised. “Use toxic agents just long enough to control the disease, then transition to a maintenance regimen with less toxic immunosuppressive agents.”
 

When Close Follow-Up Is Advised

According to unpublished data from PROCLIPI (the Prospective Cutaneous Lymphoma International Prognostic Index) study presented at the fifth World Congress of Cutaneous Lymphomas earlier in 2024, the following factors warrant consideration for close follow-up and more aggressive treatment: Nodal enlargement greater than 15 mm, age over 60 years, presence of plaques, and large-cell transformation in skin. “These are some of the stigmata in early disease that might guide you toward referring” a patient to a CTCL expert, Dr. Mangold said. (Consensus-based recommendations on the management of MF in children were published in August of 2024.)

According to Dr. Mangold, topical/skin-directed therapies are best for early-stage disease or in combination with systemic therapies in advanced disease. For early-stage disease, one of his preferred options is daily application of a skin moisturizer plus a topical corticosteroid such as clobetasol, halobetasol, or augmented betamethasone, then evaluating the response at 3 months. “This is a cheap option, and we see response rates as high as 90%,” he said. “I don’t often see steroid atrophy when treating patients with active MF. There’s a tendency to think, ‘I don’t want to overtreat.’ I think you can be aggressive. If you look in the literature, people typically pulse twice daily for a couple of weeks with a 1-week break.”

Mechlorethamine, a topical alkylating gel approved in 2013 for the treatment of early-stage MF, is an option when patients fail to respond to topical steroids, prefer to avoid steroids, or have thick, plaque-like disease. With mechlorethamine, it is important to “start slow and be patient,” Dr. Mangold said. “Real-world data shows that it takes 12-18 months to get a good response. Counsel patients that they are likely to get a rash, and that the risk of rash is dose dependent.”

Other treatment options to consider include imiquimod, which can be used for single refractory spots. He typically recommends application 5 days per week with titration up to daily if tolerated for up to 3 months. “Treat until you get a brisk immune response,” he said. “We’ve seen patients with durable, long-term responses.”
 

 

 

UVB Phototherapy Effective

For patients with stage IB disease, topical therapies are less practical and may be focused on refractory areas of disease. Narrow-band UVB phototherapy is the most practical and cost-effective treatment, Dr. Mangold said. Earlier-stage patch disease responds to phototherapy in up to 80% of cases, while plaque-stage disease responds in up to half of cases. “More frequent use of phototherapy may decrease time to clearance, but overall response is similar.”

Dr. Mangold recommends phototherapy 2-3 days per week, titrating up to a maximal response dose, and maintaining that dose for about 3 months. Maintenance involves tapering the phototherapy dose to a minimal dose with continued response. “The goal is to prevent relapse,” he said.

For patients with MF of stage IIB and higher, he considers total skin electron beam therapy, an oral retinoid with phototherapy, systemic agents, and focal radiation with systemic treatment. One of his go-to systemic options is bexarotene, which he uses for early-stage disease refractory to treatment or for less aggressive advanced disease. “We typically use a low dose ... and about half of patients respond,” Dr. Mangold said. The time to response is about 6 months. Bexarotene causes elevated lipids and low thyroid function, so he initiates patients on fenofibrate and levothyroxine at baseline.

Another systemic option is brentuximab vedotin, a monoclonal antibody that targets cells with CD30 expression, which is typically administered in a specialty center every 3 weeks for up to 16 cycles. “In practice, we often use six to eight cycles to avoid neuropathy,” he said. “It’s a good debulking agent, the time to response is 6-9 weeks, and it has a sustained response of 60%.” Neuropathy can occur with treatment, but improves over time.

Other systemic options for MF include romidepsin, mogamulizumab, and extracorporeal photopheresis used in erythrodermic disease.
 

Radiation An Option in Some Cases

Dr. Mangold noted that low doses of radiation therapy can effectively treat MF lesions in as little as one dose. “We can use it as a cure for a single spot or to temporarily treat the disease while other therapies are being started,” he said. Long-term side effects need to be considered when using radiation. “The more radiation, the more side effects.”

Dr. Mangold disclosed that he is an investigator for Sun Pharmaceutical, Solagenix, Elorac, miRagen, Kyowa Kirin, the National Clinical Trials Network, and CRISPR Therapeutics. He has also received consulting fees/honoraria from Kirin and Solagenix.

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

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— When patients of Aaron Mangold, MD, first learn they have mycosis fungoides (MF), the most common form of primary cutaneous T-cell lymphoma (CTCL), some are concerned about whether the diagnosis means a shortened life expectancy.

“In most cases, mycosis fungoides will not shorten one’s life, but it can cause significant symptoms,” Dr. Mangold, codirector of the multidisciplinary cutaneous lymphoma clinic at Mayo Clinic, Scottsdale, Arizona, said at the annual meeting of the Pacific Dermatologic Association. “For early-stage disease, I think of it more like diabetes; this is really a chronic disease” that unlikely will be fatal but may be associated with increased morbidity as the disease progresses, and “the overall goal of therapy should be disease control to increase quality of life.”

courtesy Dr. Aaron Mangold
Dr. Aaron Mangold

Patient- and lymphoma-specific factors drive the choice of therapy. The focus for patients with early-stage disease, Dr. Mangold said, is to treat comorbidities and symptoms, such as itch or skin pain, maximize their quality of life, and consider the potential for associated toxicities of therapy as the disease progresses. Start with the least toxic, targeted, nonimmunosuppressive therapy, “then work toward more toxic immunosuppressive therapies,” he advised. “Use toxic agents just long enough to control the disease, then transition to a maintenance regimen with less toxic immunosuppressive agents.”
 

When Close Follow-Up Is Advised

According to unpublished data from PROCLIPI (the Prospective Cutaneous Lymphoma International Prognostic Index) study presented at the fifth World Congress of Cutaneous Lymphomas earlier in 2024, the following factors warrant consideration for close follow-up and more aggressive treatment: Nodal enlargement greater than 15 mm, age over 60 years, presence of plaques, and large-cell transformation in skin. “These are some of the stigmata in early disease that might guide you toward referring” a patient to a CTCL expert, Dr. Mangold said. (Consensus-based recommendations on the management of MF in children were published in August of 2024.)

According to Dr. Mangold, topical/skin-directed therapies are best for early-stage disease or in combination with systemic therapies in advanced disease. For early-stage disease, one of his preferred options is daily application of a skin moisturizer plus a topical corticosteroid such as clobetasol, halobetasol, or augmented betamethasone, then evaluating the response at 3 months. “This is a cheap option, and we see response rates as high as 90%,” he said. “I don’t often see steroid atrophy when treating patients with active MF. There’s a tendency to think, ‘I don’t want to overtreat.’ I think you can be aggressive. If you look in the literature, people typically pulse twice daily for a couple of weeks with a 1-week break.”

Mechlorethamine, a topical alkylating gel approved in 2013 for the treatment of early-stage MF, is an option when patients fail to respond to topical steroids, prefer to avoid steroids, or have thick, plaque-like disease. With mechlorethamine, it is important to “start slow and be patient,” Dr. Mangold said. “Real-world data shows that it takes 12-18 months to get a good response. Counsel patients that they are likely to get a rash, and that the risk of rash is dose dependent.”

Other treatment options to consider include imiquimod, which can be used for single refractory spots. He typically recommends application 5 days per week with titration up to daily if tolerated for up to 3 months. “Treat until you get a brisk immune response,” he said. “We’ve seen patients with durable, long-term responses.”
 

 

 

UVB Phototherapy Effective

For patients with stage IB disease, topical therapies are less practical and may be focused on refractory areas of disease. Narrow-band UVB phototherapy is the most practical and cost-effective treatment, Dr. Mangold said. Earlier-stage patch disease responds to phototherapy in up to 80% of cases, while plaque-stage disease responds in up to half of cases. “More frequent use of phototherapy may decrease time to clearance, but overall response is similar.”

Dr. Mangold recommends phototherapy 2-3 days per week, titrating up to a maximal response dose, and maintaining that dose for about 3 months. Maintenance involves tapering the phototherapy dose to a minimal dose with continued response. “The goal is to prevent relapse,” he said.

For patients with MF of stage IIB and higher, he considers total skin electron beam therapy, an oral retinoid with phototherapy, systemic agents, and focal radiation with systemic treatment. One of his go-to systemic options is bexarotene, which he uses for early-stage disease refractory to treatment or for less aggressive advanced disease. “We typically use a low dose ... and about half of patients respond,” Dr. Mangold said. The time to response is about 6 months. Bexarotene causes elevated lipids and low thyroid function, so he initiates patients on fenofibrate and levothyroxine at baseline.

Another systemic option is brentuximab vedotin, a monoclonal antibody that targets cells with CD30 expression, which is typically administered in a specialty center every 3 weeks for up to 16 cycles. “In practice, we often use six to eight cycles to avoid neuropathy,” he said. “It’s a good debulking agent, the time to response is 6-9 weeks, and it has a sustained response of 60%.” Neuropathy can occur with treatment, but improves over time.

Other systemic options for MF include romidepsin, mogamulizumab, and extracorporeal photopheresis used in erythrodermic disease.
 

Radiation An Option in Some Cases

Dr. Mangold noted that low doses of radiation therapy can effectively treat MF lesions in as little as one dose. “We can use it as a cure for a single spot or to temporarily treat the disease while other therapies are being started,” he said. Long-term side effects need to be considered when using radiation. “The more radiation, the more side effects.”

Dr. Mangold disclosed that he is an investigator for Sun Pharmaceutical, Solagenix, Elorac, miRagen, Kyowa Kirin, the National Clinical Trials Network, and CRISPR Therapeutics. He has also received consulting fees/honoraria from Kirin and Solagenix.

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

— When patients of Aaron Mangold, MD, first learn they have mycosis fungoides (MF), the most common form of primary cutaneous T-cell lymphoma (CTCL), some are concerned about whether the diagnosis means a shortened life expectancy.

“In most cases, mycosis fungoides will not shorten one’s life, but it can cause significant symptoms,” Dr. Mangold, codirector of the multidisciplinary cutaneous lymphoma clinic at Mayo Clinic, Scottsdale, Arizona, said at the annual meeting of the Pacific Dermatologic Association. “For early-stage disease, I think of it more like diabetes; this is really a chronic disease” that unlikely will be fatal but may be associated with increased morbidity as the disease progresses, and “the overall goal of therapy should be disease control to increase quality of life.”

courtesy Dr. Aaron Mangold
Dr. Aaron Mangold

Patient- and lymphoma-specific factors drive the choice of therapy. The focus for patients with early-stage disease, Dr. Mangold said, is to treat comorbidities and symptoms, such as itch or skin pain, maximize their quality of life, and consider the potential for associated toxicities of therapy as the disease progresses. Start with the least toxic, targeted, nonimmunosuppressive therapy, “then work toward more toxic immunosuppressive therapies,” he advised. “Use toxic agents just long enough to control the disease, then transition to a maintenance regimen with less toxic immunosuppressive agents.”
 

When Close Follow-Up Is Advised

According to unpublished data from PROCLIPI (the Prospective Cutaneous Lymphoma International Prognostic Index) study presented at the fifth World Congress of Cutaneous Lymphomas earlier in 2024, the following factors warrant consideration for close follow-up and more aggressive treatment: Nodal enlargement greater than 15 mm, age over 60 years, presence of plaques, and large-cell transformation in skin. “These are some of the stigmata in early disease that might guide you toward referring” a patient to a CTCL expert, Dr. Mangold said. (Consensus-based recommendations on the management of MF in children were published in August of 2024.)

According to Dr. Mangold, topical/skin-directed therapies are best for early-stage disease or in combination with systemic therapies in advanced disease. For early-stage disease, one of his preferred options is daily application of a skin moisturizer plus a topical corticosteroid such as clobetasol, halobetasol, or augmented betamethasone, then evaluating the response at 3 months. “This is a cheap option, and we see response rates as high as 90%,” he said. “I don’t often see steroid atrophy when treating patients with active MF. There’s a tendency to think, ‘I don’t want to overtreat.’ I think you can be aggressive. If you look in the literature, people typically pulse twice daily for a couple of weeks with a 1-week break.”

Mechlorethamine, a topical alkylating gel approved in 2013 for the treatment of early-stage MF, is an option when patients fail to respond to topical steroids, prefer to avoid steroids, or have thick, plaque-like disease. With mechlorethamine, it is important to “start slow and be patient,” Dr. Mangold said. “Real-world data shows that it takes 12-18 months to get a good response. Counsel patients that they are likely to get a rash, and that the risk of rash is dose dependent.”

Other treatment options to consider include imiquimod, which can be used for single refractory spots. He typically recommends application 5 days per week with titration up to daily if tolerated for up to 3 months. “Treat until you get a brisk immune response,” he said. “We’ve seen patients with durable, long-term responses.”
 

 

 

UVB Phototherapy Effective

For patients with stage IB disease, topical therapies are less practical and may be focused on refractory areas of disease. Narrow-band UVB phototherapy is the most practical and cost-effective treatment, Dr. Mangold said. Earlier-stage patch disease responds to phototherapy in up to 80% of cases, while plaque-stage disease responds in up to half of cases. “More frequent use of phototherapy may decrease time to clearance, but overall response is similar.”

Dr. Mangold recommends phototherapy 2-3 days per week, titrating up to a maximal response dose, and maintaining that dose for about 3 months. Maintenance involves tapering the phototherapy dose to a minimal dose with continued response. “The goal is to prevent relapse,” he said.

For patients with MF of stage IIB and higher, he considers total skin electron beam therapy, an oral retinoid with phototherapy, systemic agents, and focal radiation with systemic treatment. One of his go-to systemic options is bexarotene, which he uses for early-stage disease refractory to treatment or for less aggressive advanced disease. “We typically use a low dose ... and about half of patients respond,” Dr. Mangold said. The time to response is about 6 months. Bexarotene causes elevated lipids and low thyroid function, so he initiates patients on fenofibrate and levothyroxine at baseline.

Another systemic option is brentuximab vedotin, a monoclonal antibody that targets cells with CD30 expression, which is typically administered in a specialty center every 3 weeks for up to 16 cycles. “In practice, we often use six to eight cycles to avoid neuropathy,” he said. “It’s a good debulking agent, the time to response is 6-9 weeks, and it has a sustained response of 60%.” Neuropathy can occur with treatment, but improves over time.

Other systemic options for MF include romidepsin, mogamulizumab, and extracorporeal photopheresis used in erythrodermic disease.
 

Radiation An Option in Some Cases

Dr. Mangold noted that low doses of radiation therapy can effectively treat MF lesions in as little as one dose. “We can use it as a cure for a single spot or to temporarily treat the disease while other therapies are being started,” he said. Long-term side effects need to be considered when using radiation. “The more radiation, the more side effects.”

Dr. Mangold disclosed that he is an investigator for Sun Pharmaceutical, Solagenix, Elorac, miRagen, Kyowa Kirin, the National Clinical Trials Network, and CRISPR Therapeutics. He has also received consulting fees/honoraria from Kirin and Solagenix.

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

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Down Syndrome: Several Cutaneous Conditions Common, Study Finds

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Mon, 10/07/2024 - 12:04

 

TOPLINE:

Eczematous dermatitis, folliculitis, and seborrheic dermatitis were the most common skin conditions in patients with Down syndrome (DS) in a 10-year retrospective study.

METHODOLOGY:

  • Researchers conducted a multicenter retrospective study of 1529 patients with DS from eight outpatient dermatology clinics in the United States and Canada between 2011 and 2021.
  • In total, 50.8% of patients were children (0-12 years), 25.2% were adolescents (13-17 years), and 24% were adults (≥ 18 years).
  • The researchers evaluated skin conditions in the patients.

TAKEAWAY:

  • Eczematous dermatitis was the most common diagnosis, affecting 26% of patients, followed by folliculitis (19.3%) and seborrheic dermatitis (15.6%). Dermatophyte infections were diagnosed in 13%.
  • Alopecia areata was the most common autoimmune skin condition, diagnosed in 178 patients (11.6%); 135 (75.8%) were children. Vitiligo was diagnosed in 66 patients (4.3%).
  • The most common cutaneous infections were onychomycosis (5.9%), tinea pedis (5%), and verruca vulgaris/other viral warts (5%).
  • High-risk medication use was reported in 4.3% of patients; acne vulgarishidradenitis suppurativa, and eczematous dermatitis were the most common associated conditions with such medications.

IN PRACTICE:

“Children, adolescents, and adults with DS are most often found to have eczematous, adnexal, and autoimmune skin conditions at outpatient dermatology visits,” the authors wrote. Their findings, they added, “offer valuable insights for clinicians and researchers, aiding in the improved prioritization of screening, diagnosis, and management, as well as facilitating both basic science and clinical research into prevalent skin conditions in individuals with DS.”

SOURCE:

The study was led by Tasya Rakasiwi, of the Department of Dermatology, Dartmouth Health, Manchester, New Hampshire, and was published online in Pediatric Dermatology.

LIMITATIONS:

Over 50% of the patients were children, potentially resulting in bias toward pediatric diagnoses and younger ages of presentation. Race, ethnicity, and sociodemographic factors were not captured, limiting the generalizability of the findings. Medical codes often do not capture disease phenotype or severity, and the manual conversion of International Classification of Diseases (ICD) 9 to ICD-10 codes may introduce potential conversion errors.

DISCLOSURES:

The study was supported by the Pediatric Dermatology Research Alliance. The authors declared no competing interests.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

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TOPLINE:

Eczematous dermatitis, folliculitis, and seborrheic dermatitis were the most common skin conditions in patients with Down syndrome (DS) in a 10-year retrospective study.

METHODOLOGY:

  • Researchers conducted a multicenter retrospective study of 1529 patients with DS from eight outpatient dermatology clinics in the United States and Canada between 2011 and 2021.
  • In total, 50.8% of patients were children (0-12 years), 25.2% were adolescents (13-17 years), and 24% were adults (≥ 18 years).
  • The researchers evaluated skin conditions in the patients.

TAKEAWAY:

  • Eczematous dermatitis was the most common diagnosis, affecting 26% of patients, followed by folliculitis (19.3%) and seborrheic dermatitis (15.6%). Dermatophyte infections were diagnosed in 13%.
  • Alopecia areata was the most common autoimmune skin condition, diagnosed in 178 patients (11.6%); 135 (75.8%) were children. Vitiligo was diagnosed in 66 patients (4.3%).
  • The most common cutaneous infections were onychomycosis (5.9%), tinea pedis (5%), and verruca vulgaris/other viral warts (5%).
  • High-risk medication use was reported in 4.3% of patients; acne vulgarishidradenitis suppurativa, and eczematous dermatitis were the most common associated conditions with such medications.

IN PRACTICE:

“Children, adolescents, and adults with DS are most often found to have eczematous, adnexal, and autoimmune skin conditions at outpatient dermatology visits,” the authors wrote. Their findings, they added, “offer valuable insights for clinicians and researchers, aiding in the improved prioritization of screening, diagnosis, and management, as well as facilitating both basic science and clinical research into prevalent skin conditions in individuals with DS.”

SOURCE:

The study was led by Tasya Rakasiwi, of the Department of Dermatology, Dartmouth Health, Manchester, New Hampshire, and was published online in Pediatric Dermatology.

LIMITATIONS:

Over 50% of the patients were children, potentially resulting in bias toward pediatric diagnoses and younger ages of presentation. Race, ethnicity, and sociodemographic factors were not captured, limiting the generalizability of the findings. Medical codes often do not capture disease phenotype or severity, and the manual conversion of International Classification of Diseases (ICD) 9 to ICD-10 codes may introduce potential conversion errors.

DISCLOSURES:

The study was supported by the Pediatric Dermatology Research Alliance. The authors declared no competing interests.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

 

TOPLINE:

Eczematous dermatitis, folliculitis, and seborrheic dermatitis were the most common skin conditions in patients with Down syndrome (DS) in a 10-year retrospective study.

METHODOLOGY:

  • Researchers conducted a multicenter retrospective study of 1529 patients with DS from eight outpatient dermatology clinics in the United States and Canada between 2011 and 2021.
  • In total, 50.8% of patients were children (0-12 years), 25.2% were adolescents (13-17 years), and 24% were adults (≥ 18 years).
  • The researchers evaluated skin conditions in the patients.

TAKEAWAY:

  • Eczematous dermatitis was the most common diagnosis, affecting 26% of patients, followed by folliculitis (19.3%) and seborrheic dermatitis (15.6%). Dermatophyte infections were diagnosed in 13%.
  • Alopecia areata was the most common autoimmune skin condition, diagnosed in 178 patients (11.6%); 135 (75.8%) were children. Vitiligo was diagnosed in 66 patients (4.3%).
  • The most common cutaneous infections were onychomycosis (5.9%), tinea pedis (5%), and verruca vulgaris/other viral warts (5%).
  • High-risk medication use was reported in 4.3% of patients; acne vulgarishidradenitis suppurativa, and eczematous dermatitis were the most common associated conditions with such medications.

IN PRACTICE:

“Children, adolescents, and adults with DS are most often found to have eczematous, adnexal, and autoimmune skin conditions at outpatient dermatology visits,” the authors wrote. Their findings, they added, “offer valuable insights for clinicians and researchers, aiding in the improved prioritization of screening, diagnosis, and management, as well as facilitating both basic science and clinical research into prevalent skin conditions in individuals with DS.”

SOURCE:

The study was led by Tasya Rakasiwi, of the Department of Dermatology, Dartmouth Health, Manchester, New Hampshire, and was published online in Pediatric Dermatology.

LIMITATIONS:

Over 50% of the patients were children, potentially resulting in bias toward pediatric diagnoses and younger ages of presentation. Race, ethnicity, and sociodemographic factors were not captured, limiting the generalizability of the findings. Medical codes often do not capture disease phenotype or severity, and the manual conversion of International Classification of Diseases (ICD) 9 to ICD-10 codes may introduce potential conversion errors.

DISCLOSURES:

The study was supported by the Pediatric Dermatology Research Alliance. The authors declared no competing interests.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

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Study Supports Efficacy of Home-Based Phototherapy for Psoriasis

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Thu, 10/03/2024 - 11:55

 

TOPLINE:

Home-based phototherapy for plaque and guttate psoriasis is as effective as office-based phototherapy, according to results of the randomized Light Treatment Effectiveness study.

METHODOLOGY:

  • The pragmatic, investigator-initiated, open-label, noninferiority, randomized trial compared the effectiveness of 12 weeks of treatment with narrow-band ultraviolet B phototherapy administered at home (n = 393) vs at the doctor’s office (n = 390).
  • Overall, 783 patients with plaque or guttate psoriasis (mean age, 48 years; 48% women) were enrolled at 42 academic and private clinical dermatology practices in the United States from March 1, 2019, to December 4, 2023, and were followed up through June 2024. At baseline, the mean Physician Global Assessment (PGA) and the mean Dermatology Life Quality Index (DLQI) scores were 2.7 and 12.2, respectively.
  • The two co-primary endpoints were a PGA score ≤ 1 indicating clear or almost clear skin and a DLQI score ≤ 5.

TAKEAWAY:

  • At 12 weeks, a PGA score ≤ 1 was achieved in 32.8% of patients using home-based phototherapy and in 25.6% of those who received office-based phototherapy (P < .001).
  • At 12 weeks, a DLQI score ≤ 5 was achieved in 52.4% and 33.6% of home- and office-treated patients, respectively (P < .001).
  • Similar benefits were seen across all Fitzpatrick skin types.
  • A higher percentage of patients were adherent to home-based (51.4%) vs office-based (15.9%) phototherapy (P < .001).

IN PRACTICE:

“These data support the use of home phototherapy as a first-line treatment option for psoriasis,” and “efforts are needed to make home and office phototherapy more available to patients,” said the study’s lead author.

SOURCE:

Joel M. Gelfand, MD, director of the Psoriasis and Phototherapy Treatment Center at the University of Pennsylvania, Philadelphia, presented the findings at the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis meeting during the annual meeting of the European Academy of Dermatology and Venereology, with simultaneous publication in JAMA Dermatology.

LIMITATIONS:

This was an open-label trial and because of its pragmatic design, outcome data were missing. The cost of the home-based phototherapy equipment used in the study was $6040.88, which was mostly covered by Medicare, but direct costs to patients may have varied depending on their insurance plan.

DISCLOSURES:

The Patient-Centered Outcomes Research Institute funded the study. Daavlin provided and shipped machines for home-based phototherapy to patients at no cost. Dr. Gelfand disclosed serving as a consultant for AbbVie, Artax, Bristol-Myers Squibb, Boehringer Ingelheim, Celldex, and other companies. The full list of author disclosures can be found in the published study.

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

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TOPLINE:

Home-based phototherapy for plaque and guttate psoriasis is as effective as office-based phototherapy, according to results of the randomized Light Treatment Effectiveness study.

METHODOLOGY:

  • The pragmatic, investigator-initiated, open-label, noninferiority, randomized trial compared the effectiveness of 12 weeks of treatment with narrow-band ultraviolet B phototherapy administered at home (n = 393) vs at the doctor’s office (n = 390).
  • Overall, 783 patients with plaque or guttate psoriasis (mean age, 48 years; 48% women) were enrolled at 42 academic and private clinical dermatology practices in the United States from March 1, 2019, to December 4, 2023, and were followed up through June 2024. At baseline, the mean Physician Global Assessment (PGA) and the mean Dermatology Life Quality Index (DLQI) scores were 2.7 and 12.2, respectively.
  • The two co-primary endpoints were a PGA score ≤ 1 indicating clear or almost clear skin and a DLQI score ≤ 5.

TAKEAWAY:

  • At 12 weeks, a PGA score ≤ 1 was achieved in 32.8% of patients using home-based phototherapy and in 25.6% of those who received office-based phototherapy (P < .001).
  • At 12 weeks, a DLQI score ≤ 5 was achieved in 52.4% and 33.6% of home- and office-treated patients, respectively (P < .001).
  • Similar benefits were seen across all Fitzpatrick skin types.
  • A higher percentage of patients were adherent to home-based (51.4%) vs office-based (15.9%) phototherapy (P < .001).

IN PRACTICE:

“These data support the use of home phototherapy as a first-line treatment option for psoriasis,” and “efforts are needed to make home and office phototherapy more available to patients,” said the study’s lead author.

SOURCE:

Joel M. Gelfand, MD, director of the Psoriasis and Phototherapy Treatment Center at the University of Pennsylvania, Philadelphia, presented the findings at the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis meeting during the annual meeting of the European Academy of Dermatology and Venereology, with simultaneous publication in JAMA Dermatology.

LIMITATIONS:

This was an open-label trial and because of its pragmatic design, outcome data were missing. The cost of the home-based phototherapy equipment used in the study was $6040.88, which was mostly covered by Medicare, but direct costs to patients may have varied depending on their insurance plan.

DISCLOSURES:

The Patient-Centered Outcomes Research Institute funded the study. Daavlin provided and shipped machines for home-based phototherapy to patients at no cost. Dr. Gelfand disclosed serving as a consultant for AbbVie, Artax, Bristol-Myers Squibb, Boehringer Ingelheim, Celldex, and other companies. The full list of author disclosures can be found in the published study.

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

 

TOPLINE:

Home-based phototherapy for plaque and guttate psoriasis is as effective as office-based phototherapy, according to results of the randomized Light Treatment Effectiveness study.

METHODOLOGY:

  • The pragmatic, investigator-initiated, open-label, noninferiority, randomized trial compared the effectiveness of 12 weeks of treatment with narrow-band ultraviolet B phototherapy administered at home (n = 393) vs at the doctor’s office (n = 390).
  • Overall, 783 patients with plaque or guttate psoriasis (mean age, 48 years; 48% women) were enrolled at 42 academic and private clinical dermatology practices in the United States from March 1, 2019, to December 4, 2023, and were followed up through June 2024. At baseline, the mean Physician Global Assessment (PGA) and the mean Dermatology Life Quality Index (DLQI) scores were 2.7 and 12.2, respectively.
  • The two co-primary endpoints were a PGA score ≤ 1 indicating clear or almost clear skin and a DLQI score ≤ 5.

TAKEAWAY:

  • At 12 weeks, a PGA score ≤ 1 was achieved in 32.8% of patients using home-based phototherapy and in 25.6% of those who received office-based phototherapy (P < .001).
  • At 12 weeks, a DLQI score ≤ 5 was achieved in 52.4% and 33.6% of home- and office-treated patients, respectively (P < .001).
  • Similar benefits were seen across all Fitzpatrick skin types.
  • A higher percentage of patients were adherent to home-based (51.4%) vs office-based (15.9%) phototherapy (P < .001).

IN PRACTICE:

“These data support the use of home phototherapy as a first-line treatment option for psoriasis,” and “efforts are needed to make home and office phototherapy more available to patients,” said the study’s lead author.

SOURCE:

Joel M. Gelfand, MD, director of the Psoriasis and Phototherapy Treatment Center at the University of Pennsylvania, Philadelphia, presented the findings at the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis meeting during the annual meeting of the European Academy of Dermatology and Venereology, with simultaneous publication in JAMA Dermatology.

LIMITATIONS:

This was an open-label trial and because of its pragmatic design, outcome data were missing. The cost of the home-based phototherapy equipment used in the study was $6040.88, which was mostly covered by Medicare, but direct costs to patients may have varied depending on their insurance plan.

DISCLOSURES:

The Patient-Centered Outcomes Research Institute funded the study. Daavlin provided and shipped machines for home-based phototherapy to patients at no cost. Dr. Gelfand disclosed serving as a consultant for AbbVie, Artax, Bristol-Myers Squibb, Boehringer Ingelheim, Celldex, and other companies. The full list of author disclosures can be found in the published study.

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

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Aspects of the Skin Microbiome Remain Elusive

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Changed
Mon, 09/30/2024 - 13:27

— Although it has been known for several years that more than 1000 species of bacteria from 19 different phyla inhabit the human skin — mainly the superficial epidermis and upper parts of the hair follicles — published studies specifically focusing on the skin microbiome remain limited. 

In one review of the topic, researchers from the National Institutes of Health wrote that the skin is composed of 1.8 million diverse habitats with an abundance of folds, invaginations, and specialized niches that support a wide range of microorganisms. “Many of these microorganisms are harmless and, in some cases, provide vital functions for us to live and they have not evolved over time,” Jill S. Waibel, MD, medical director of the Miami Dermatology and Laser Institute, said at the annual Masters of Aesthetics Symposium. 

Dr. Jill S. Waibel, Miami Dermatology and Laser Institute.
Dr. Jill S. Waibel

“This is complex ecosystem that we don’t really talk about,” she said. “There is wide topographical distribution of bacteria on skin sites. The bacteria we have on our head and neck area is different from that on our feet. There is also a lot of interpersonal variation of the skin microbiome, so one person may have a lot of one type of bacteria and not as much of another.” 
 

A Shield From Foreign Pathogens

At its core, Dr. Waibel continued, the skin microbiome functions as an interface between the human body and the environment, a physical barrier that prevents the invasion of foreign pathogens. The skin also provides a home to commensal microbiota. She likened the skin’s landscape to that of the tundra: “It’s desiccated, has poor nutrients, and it’s very acidic, thus pathogens have a hard time living on it,” she said. “However, our skin microorganisms have adapted to utilize the sparse nutrients available on the skin. That’s why I tell my patients, ‘don’t use a sugar scrub because you’re potentially feeding these bad bacteria.’ ” 

According to more recent research, the skin microbiota in healthy adults remains stable over time, despite environmental perturbations, and they have important roles in educating the innate and adaptive arms of the cutaneous immune system. “Some skin diseases are associated with an altered microbial state: dysbiosis,” said Dr. Waibel, subsection chief of dermatology at Baptist Health South Florida, Miami Beach. “Reversion of this may help prevent or treat the disease.” 

NIH researchers find thousands of new microorganisms living on human skin
Daryl Leja, National Human Genome Research Institute


She cited the following factors that influence the skin microbiome: 

  • Genetics affects the skin microbiome considerably. Individuals with autoimmune predispositions have different microbiota compared with those who don’t.
  • Climate, pollution, and hygiene practices the other influencing factors. “Even clothing can impact the microbiome, by causing the transfer of microorganisms,” she said.
  • Age and hormonal changes (particularly during puberty) and senescence alter the microbial landscape.
  • Systemic health conditions such as diabetes mellitus and irritable bowel disease, as well as cutaneous conditions like psoriasis and atopic dermatitis can also disrupt the skin microbiome.

Ingredients contained in soaps, antibiotics, and cosmetics can also cause skin dysbiosis, Dr. Waibel said. However, the integrity of the skin’s microbiome following dermatological procedures such as excisions, dermabrasion, laser therapy, and other physical procedures is less understood, according to a recent review of the topic. Phototherapy appears to be the most extensively studied, “and shows an increase in microbial diversity post-treatment,” she said. “Light treatments have been found to kill bacteria by inducing DNA damage. More studies need to be performed on specific wavelengths of light used, conditions being treated and individual patient differences.” 

According to the review’s authors, no change in the microbiome was observed in studies of debridement. “That was surprising, as it is a method to remove unhealthy tissue that often contains pathogenic bacteria,” Dr. Waibel said. “The big take-home message is that we need more research.” 

Dr. Waibel disclosed that she has conducted clinical trials for several device and pharmaceutical companies.
 

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

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— Although it has been known for several years that more than 1000 species of bacteria from 19 different phyla inhabit the human skin — mainly the superficial epidermis and upper parts of the hair follicles — published studies specifically focusing on the skin microbiome remain limited. 

In one review of the topic, researchers from the National Institutes of Health wrote that the skin is composed of 1.8 million diverse habitats with an abundance of folds, invaginations, and specialized niches that support a wide range of microorganisms. “Many of these microorganisms are harmless and, in some cases, provide vital functions for us to live and they have not evolved over time,” Jill S. Waibel, MD, medical director of the Miami Dermatology and Laser Institute, said at the annual Masters of Aesthetics Symposium. 

Dr. Jill S. Waibel, Miami Dermatology and Laser Institute.
Dr. Jill S. Waibel

“This is complex ecosystem that we don’t really talk about,” she said. “There is wide topographical distribution of bacteria on skin sites. The bacteria we have on our head and neck area is different from that on our feet. There is also a lot of interpersonal variation of the skin microbiome, so one person may have a lot of one type of bacteria and not as much of another.” 
 

A Shield From Foreign Pathogens

At its core, Dr. Waibel continued, the skin microbiome functions as an interface between the human body and the environment, a physical barrier that prevents the invasion of foreign pathogens. The skin also provides a home to commensal microbiota. She likened the skin’s landscape to that of the tundra: “It’s desiccated, has poor nutrients, and it’s very acidic, thus pathogens have a hard time living on it,” she said. “However, our skin microorganisms have adapted to utilize the sparse nutrients available on the skin. That’s why I tell my patients, ‘don’t use a sugar scrub because you’re potentially feeding these bad bacteria.’ ” 

According to more recent research, the skin microbiota in healthy adults remains stable over time, despite environmental perturbations, and they have important roles in educating the innate and adaptive arms of the cutaneous immune system. “Some skin diseases are associated with an altered microbial state: dysbiosis,” said Dr. Waibel, subsection chief of dermatology at Baptist Health South Florida, Miami Beach. “Reversion of this may help prevent or treat the disease.” 

NIH researchers find thousands of new microorganisms living on human skin
Daryl Leja, National Human Genome Research Institute


She cited the following factors that influence the skin microbiome: 

  • Genetics affects the skin microbiome considerably. Individuals with autoimmune predispositions have different microbiota compared with those who don’t.
  • Climate, pollution, and hygiene practices the other influencing factors. “Even clothing can impact the microbiome, by causing the transfer of microorganisms,” she said.
  • Age and hormonal changes (particularly during puberty) and senescence alter the microbial landscape.
  • Systemic health conditions such as diabetes mellitus and irritable bowel disease, as well as cutaneous conditions like psoriasis and atopic dermatitis can also disrupt the skin microbiome.

Ingredients contained in soaps, antibiotics, and cosmetics can also cause skin dysbiosis, Dr. Waibel said. However, the integrity of the skin’s microbiome following dermatological procedures such as excisions, dermabrasion, laser therapy, and other physical procedures is less understood, according to a recent review of the topic. Phototherapy appears to be the most extensively studied, “and shows an increase in microbial diversity post-treatment,” she said. “Light treatments have been found to kill bacteria by inducing DNA damage. More studies need to be performed on specific wavelengths of light used, conditions being treated and individual patient differences.” 

According to the review’s authors, no change in the microbiome was observed in studies of debridement. “That was surprising, as it is a method to remove unhealthy tissue that often contains pathogenic bacteria,” Dr. Waibel said. “The big take-home message is that we need more research.” 

Dr. Waibel disclosed that she has conducted clinical trials for several device and pharmaceutical companies.
 

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

— Although it has been known for several years that more than 1000 species of bacteria from 19 different phyla inhabit the human skin — mainly the superficial epidermis and upper parts of the hair follicles — published studies specifically focusing on the skin microbiome remain limited. 

In one review of the topic, researchers from the National Institutes of Health wrote that the skin is composed of 1.8 million diverse habitats with an abundance of folds, invaginations, and specialized niches that support a wide range of microorganisms. “Many of these microorganisms are harmless and, in some cases, provide vital functions for us to live and they have not evolved over time,” Jill S. Waibel, MD, medical director of the Miami Dermatology and Laser Institute, said at the annual Masters of Aesthetics Symposium. 

Dr. Jill S. Waibel, Miami Dermatology and Laser Institute.
Dr. Jill S. Waibel

“This is complex ecosystem that we don’t really talk about,” she said. “There is wide topographical distribution of bacteria on skin sites. The bacteria we have on our head and neck area is different from that on our feet. There is also a lot of interpersonal variation of the skin microbiome, so one person may have a lot of one type of bacteria and not as much of another.” 
 

A Shield From Foreign Pathogens

At its core, Dr. Waibel continued, the skin microbiome functions as an interface between the human body and the environment, a physical barrier that prevents the invasion of foreign pathogens. The skin also provides a home to commensal microbiota. She likened the skin’s landscape to that of the tundra: “It’s desiccated, has poor nutrients, and it’s very acidic, thus pathogens have a hard time living on it,” she said. “However, our skin microorganisms have adapted to utilize the sparse nutrients available on the skin. That’s why I tell my patients, ‘don’t use a sugar scrub because you’re potentially feeding these bad bacteria.’ ” 

According to more recent research, the skin microbiota in healthy adults remains stable over time, despite environmental perturbations, and they have important roles in educating the innate and adaptive arms of the cutaneous immune system. “Some skin diseases are associated with an altered microbial state: dysbiosis,” said Dr. Waibel, subsection chief of dermatology at Baptist Health South Florida, Miami Beach. “Reversion of this may help prevent or treat the disease.” 

NIH researchers find thousands of new microorganisms living on human skin
Daryl Leja, National Human Genome Research Institute


She cited the following factors that influence the skin microbiome: 

  • Genetics affects the skin microbiome considerably. Individuals with autoimmune predispositions have different microbiota compared with those who don’t.
  • Climate, pollution, and hygiene practices the other influencing factors. “Even clothing can impact the microbiome, by causing the transfer of microorganisms,” she said.
  • Age and hormonal changes (particularly during puberty) and senescence alter the microbial landscape.
  • Systemic health conditions such as diabetes mellitus and irritable bowel disease, as well as cutaneous conditions like psoriasis and atopic dermatitis can also disrupt the skin microbiome.

Ingredients contained in soaps, antibiotics, and cosmetics can also cause skin dysbiosis, Dr. Waibel said. However, the integrity of the skin’s microbiome following dermatological procedures such as excisions, dermabrasion, laser therapy, and other physical procedures is less understood, according to a recent review of the topic. Phototherapy appears to be the most extensively studied, “and shows an increase in microbial diversity post-treatment,” she said. “Light treatments have been found to kill bacteria by inducing DNA damage. More studies need to be performed on specific wavelengths of light used, conditions being treated and individual patient differences.” 

According to the review’s authors, no change in the microbiome was observed in studies of debridement. “That was surprising, as it is a method to remove unhealthy tissue that often contains pathogenic bacteria,” Dr. Waibel said. “The big take-home message is that we need more research.” 

Dr. Waibel disclosed that she has conducted clinical trials for several device and pharmaceutical companies.
 

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

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