Atopic Dermatitis

To improve patient care and outcomes, leading dermatologists offered their recommendations on products for sensitive skin. Consideration must be given to:

• Avène Cicalfate Restorative Skin Cream
  Pierre Fabre Dermo-Cosmetique USA
  “Sucralfate for speeding up skin repair and the soothing thermal spring waters found in this product make it perfect postprocedure for immediately cooling and calming the skin.”—Jeannette Graf, MD, New York, New York

• Cetaphil RestoraDerm Eczema Calming Body Moisturizer
  Galderma Laboratories, LP
  “This product is formulated for atopic skin. I personally use it on my face as a moisturizer during the cold New York City winter.”—Anthony M. Rossi, MD, New York, New York

• Vanicream
  Pharmaceutical Specialties, Inc
  “I recommend Vanicream brand products to patients with sensitive skin or eczema. These products are fragrance free and have minimal ingredients.”— Gary Goldenberg, MD, New York, New York

Cutis invites readers to send us their recommendations. Athlete's foot treatments, cleansing devices, redness-reducing products, and face scrubs will be featured in upcoming editions of Cosmetic Corner. Please e-mail your recommendation(s) to the Editorial Office.

Disclaimer: Opinions expressed herein do not necessarily reflect those of Cutis or Frontline Medical Communications Inc. and shall not be used for product endorsement purposes. Any reference made to a specific commercial product does not indicate or imply that Cutis or Frontline Medical Communications Inc. endorses, recommends, or favors the product mentioned. No guarantee is given to the effects of recommended products.

To improve patient care and outcomes, leading dermatologists offered their recommendations on products for sensitive skin. Consideration must be given to:

• Avène Cicalfate Restorative Skin Cream
  Pierre Fabre Dermo-Cosmetique USA
  “Sucralfate for speeding up skin repair and the soothing thermal spring waters found in this product make it perfect postprocedure for immediately cooling and calming the skin.”—Jeannette Graf, MD, New York, New York

• Cetaphil RestoraDerm Eczema Calming Body Moisturizer
  Galderma Laboratories, LP
  “This product is formulated for atopic skin. I personally use it on my face as a moisturizer during the cold New York City winter.”—Anthony M. Rossi, MD, New York, New York

• Vanicream
  Pharmaceutical Specialties, Inc
  “I recommend Vanicream brand products to patients with sensitive skin or eczema. These products are fragrance free and have minimal ingredients.”— Gary Goldenberg, MD, New York, New York

Cutis invites readers to send us their recommendations. Athlete's foot treatments, cleansing devices, redness-reducing products, and face scrubs will be featured in upcoming editions of Cosmetic Corner. Please e-mail your recommendation(s) to the Editorial Office.

Disclaimer: Opinions expressed herein do not necessarily reflect those of Cutis or Frontline Medical Communications Inc. and shall not be used for product endorsement purposes. Any reference made to a specific commercial product does not indicate or imply that Cutis or Frontline Medical Communications Inc. endorses, recommends, or favors the product mentioned. No guarantee is given to the effects of recommended products.

To improve patient care and outcomes, leading dermatologists offered their recommendations on products for sensitive skin. Consideration must be given to:

• Avène Cicalfate Restorative Skin Cream
  Pierre Fabre Dermo-Cosmetique USA
  “Sucralfate for speeding up skin repair and the soothing thermal spring waters found in this product make it perfect postprocedure for immediately cooling and calming the skin.”—Jeannette Graf, MD, New York, New York

• Cetaphil RestoraDerm Eczema Calming Body Moisturizer
  Galderma Laboratories, LP
  “This product is formulated for atopic skin. I personally use it on my face as a moisturizer during the cold New York City winter.”—Anthony M. Rossi, MD, New York, New York

• Vanicream
  Pharmaceutical Specialties, Inc
  “I recommend Vanicream brand products to patients with sensitive skin or eczema. These products are fragrance free and have minimal ingredients.”— Gary Goldenberg, MD, New York, New York

Cutis invites readers to send us their recommendations. Athlete's foot treatments, cleansing devices, redness-reducing products, and face scrubs will be featured in upcoming editions of Cosmetic Corner. Please e-mail your recommendation(s) to the Editorial Office.

Disclaimer: Opinions expressed herein do not necessarily reflect those of Cutis or Frontline Medical Communications Inc. and shall not be used for product endorsement purposes. Any reference made to a specific commercial product does not indicate or imply that Cutis or Frontline Medical Communications Inc. endorses, recommends, or favors the product mentioned. No guarantee is given to the effects of recommended products.

PORTLAND – Short-term daily oral supplementation with 5000 IU of vitamin D₃ was safe and significantly outperformed placebo for lessening the signs and symptoms of atopic dermatitis (AD), according to the results of a randomized, double-blind trial of 65 patients with moderate to severe disease.

At week 12, average improvements on the Scoring Atopic Dermatitis (SCORAD) index (standard deviation, 11.1 points) were 21.2 points in the vitamin D₃ group and 13.9 points (standard deviation, 12.3 points) in the placebo group (P = .02), Karen Sanchez-Armendariz, MD, reported at the annual meeting of the Society for Investigative Dermatology. “Vitamin D₃ should be considered a valuable adjuvant in the treatment of AD, especially in patients with relapses,” she said.

Past studies have reported an inverse relationship between 25(OH)D (vitamin D) serum levels and the severity of AD, noted Dr. Sanchez-Armendariz, who is with the National Autonomous University of Mexico in Mexico City. This finding makes sense, as vitamin D₃ induces the topical production of antimicrobial peptides, which have direct antimicrobial activity and induce a host response characterized by cytokine release, chemotaxis, inflammation, angiogenesis, and re-epithelialization, she added.

Consequently, 25(OH)D deficiency has been posited as a culprit in the pathophysiology of AD. However, scientific and endocrine societies have published differing recommendations about safe and optimal doses for vitamin D₃ supplementation, while experts have noted that 5000 IU per day is needed to achieve an increase of 10 ng 25(OH)D per mL serum (J Am Board Fam Med. 2014 Jul-Aug;27[4]:495-509).

For the study, therefore, Dr. Sanchez-Armendariz and her associates evaluated this dose as adjuvant therapy in patients with moderate to severe AD despite topical hydrocortisone aceponate, soap substitute, and emollient. Patients continued this usual care and received either a cellulose capsule placebo or 5000 IU oral vitamin D₃ per day. Based on previously recommended cutoff values, the researchers considered serum 25(OH)D levels sufficient if they exceeded 30 ng per mL, insufficient if they were between 20 and 30 ng per mL, and deficient if they were less than 20 ng per mL (J Bone Miner Res. 2011 Mar;26[3]:455-7).

At baseline, the placebo and intervention groups resembled each other in terms of baseline levels of 25(OH)D, calcium, and phosphorus, pruritus, and scores on SCORAD and the six-area Total Body Severity Assessment. A total of 59% of patients had insufficient serum 25(OH)D, and 39% were deficient.

Patients in both groups improved on the Total Body Severity Assessment, but the extent of improvement did not statistically differ between groups, Dr. Sanchez-Armendariz reported. Supplementation did significantly increase serum 25(OH)D levels, which at week 12 averaged 58.3 ng per mL (SD, 18.5 ng per mL), compared with 22.2 (SD, 7.6 ng per mL) with placebo (P less than .001).

Interestingly, at week 12, all patients in the vitamin D₃ group achieved serum 25(OH)D levels of at least 30 ng per mL, as did 41% of patients in the placebo arm. Patients in both groups who achieved this “sufficient” serum 25(OH)D level averaged a nearly 21-point improvement on the SCORAD (SD, 11.1 points), compared with 7.5 points (SD, 9.9 points) among patients who remained deficient, and 17.4 points (SD, 12.7 points) among patients who remained insufficient (P = .004 for difference among groups; P = .02 for difference between sufficient and insufficient groups).

An analysis of variance confirmed this finding, showing that, regardless of treatment group, patients whose final serum 25(OH)D level was at least 20 ng per mL scored an average of 20 points on the SCORAD, compared with 38 points for patients whose 25(OH)D level remained below 20 ng per mL. Patients whose final 25(OH)D level exceeded 20 ng per mL had fivefold greater odds of having a SCORAD below 25 than did patients with lower serum 25(OH)D levels (odds ratio, 5.1; 95% confidence interval, 1.2-22.6; P = .03).

The investigators identified no adverse effects of vitamin D₃ supplementation, Dr. Sanchez-Armendariz said. “Attaining 25(OH)D levels above 20 ng per mL in addition to baseline therapy reduced the SCORAD of patients with moderate to severe atopic dermatitis,” she added. Clinicians should consider vitamin D3 deficiency and supplementation in patients with relapsing or refractory AD, she emphasized.

Dr. Sanchez-Armendariz reported no external funding sources and no conflicts of interest.

PORTLAND – Short-term daily oral supplementation with 5000 IU of vitamin D₃ was safe and significantly outperformed placebo for lessening the signs and symptoms of atopic dermatitis (AD), according to the results of a randomized, double-blind trial of 65 patients with moderate to severe disease.

At week 12, average improvements on the Scoring Atopic Dermatitis (SCORAD) index (standard deviation, 11.1 points) were 21.2 points in the vitamin D₃ group and 13.9 points (standard deviation, 12.3 points) in the placebo group (P = .02), Karen Sanchez-Armendariz, MD, reported at the annual meeting of the Society for Investigative Dermatology. “Vitamin D₃ should be considered a valuable adjuvant in the treatment of AD, especially in patients with relapses,” she said.

Past studies have reported an inverse relationship between 25(OH)D (vitamin D) serum levels and the severity of AD, noted Dr. Sanchez-Armendariz, who is with the National Autonomous University of Mexico in Mexico City. This finding makes sense, as vitamin D₃ induces the topical production of antimicrobial peptides, which have direct antimicrobial activity and induce a host response characterized by cytokine release, chemotaxis, inflammation, angiogenesis, and re-epithelialization, she added.

Consequently, 25(OH)D deficiency has been posited as a culprit in the pathophysiology of AD. However, scientific and endocrine societies have published differing recommendations about safe and optimal doses for vitamin D₃ supplementation, while experts have noted that 5000 IU per day is needed to achieve an increase of 10 ng 25(OH)D per mL serum (J Am Board Fam Med. 2014 Jul-Aug;27[4]:495-509).

For the study, therefore, Dr. Sanchez-Armendariz and her associates evaluated this dose as adjuvant therapy in patients with moderate to severe AD despite topical hydrocortisone aceponate, soap substitute, and emollient. Patients continued this usual care and received either a cellulose capsule placebo or 5000 IU oral vitamin D₃ per day. Based on previously recommended cutoff values, the researchers considered serum 25(OH)D levels sufficient if they exceeded 30 ng per mL, insufficient if they were between 20 and 30 ng per mL, and deficient if they were less than 20 ng per mL (J Bone Miner Res. 2011 Mar;26[3]:455-7).

At baseline, the placebo and intervention groups resembled each other in terms of baseline levels of 25(OH)D, calcium, and phosphorus, pruritus, and scores on SCORAD and the six-area Total Body Severity Assessment. A total of 59% of patients had insufficient serum 25(OH)D, and 39% were deficient.

Patients in both groups improved on the Total Body Severity Assessment, but the extent of improvement did not statistically differ between groups, Dr. Sanchez-Armendariz reported. Supplementation did significantly increase serum 25(OH)D levels, which at week 12 averaged 58.3 ng per mL (SD, 18.5 ng per mL), compared with 22.2 (SD, 7.6 ng per mL) with placebo (P less than .001).

Interestingly, at week 12, all patients in the vitamin D₃ group achieved serum 25(OH)D levels of at least 30 ng per mL, as did 41% of patients in the placebo arm. Patients in both groups who achieved this “sufficient” serum 25(OH)D level averaged a nearly 21-point improvement on the SCORAD (SD, 11.1 points), compared with 7.5 points (SD, 9.9 points) among patients who remained deficient, and 17.4 points (SD, 12.7 points) among patients who remained insufficient (P = .004 for difference among groups; P = .02 for difference between sufficient and insufficient groups).

An analysis of variance confirmed this finding, showing that, regardless of treatment group, patients whose final serum 25(OH)D level was at least 20 ng per mL scored an average of 20 points on the SCORAD, compared with 38 points for patients whose 25(OH)D level remained below 20 ng per mL. Patients whose final 25(OH)D level exceeded 20 ng per mL had fivefold greater odds of having a SCORAD below 25 than did patients with lower serum 25(OH)D levels (odds ratio, 5.1; 95% confidence interval, 1.2-22.6; P = .03).

The investigators identified no adverse effects of vitamin D₃ supplementation, Dr. Sanchez-Armendariz said. “Attaining 25(OH)D levels above 20 ng per mL in addition to baseline therapy reduced the SCORAD of patients with moderate to severe atopic dermatitis,” she added. Clinicians should consider vitamin D3 deficiency and supplementation in patients with relapsing or refractory AD, she emphasized.

Dr. Sanchez-Armendariz reported no external funding sources and no conflicts of interest.

PORTLAND – Short-term daily oral supplementation with 5000 IU of vitamin D₃ was safe and significantly outperformed placebo for lessening the signs and symptoms of atopic dermatitis (AD), according to the results of a randomized, double-blind trial of 65 patients with moderate to severe disease.

At week 12, average improvements on the Scoring Atopic Dermatitis (SCORAD) index (standard deviation, 11.1 points) were 21.2 points in the vitamin D₃ group and 13.9 points (standard deviation, 12.3 points) in the placebo group (P = .02), Karen Sanchez-Armendariz, MD, reported at the annual meeting of the Society for Investigative Dermatology. “Vitamin D₃ should be considered a valuable adjuvant in the treatment of AD, especially in patients with relapses,” she said.

Past studies have reported an inverse relationship between 25(OH)D (vitamin D) serum levels and the severity of AD, noted Dr. Sanchez-Armendariz, who is with the National Autonomous University of Mexico in Mexico City. This finding makes sense, as vitamin D₃ induces the topical production of antimicrobial peptides, which have direct antimicrobial activity and induce a host response characterized by cytokine release, chemotaxis, inflammation, angiogenesis, and re-epithelialization, she added.

Consequently, 25(OH)D deficiency has been posited as a culprit in the pathophysiology of AD. However, scientific and endocrine societies have published differing recommendations about safe and optimal doses for vitamin D₃ supplementation, while experts have noted that 5000 IU per day is needed to achieve an increase of 10 ng 25(OH)D per mL serum (J Am Board Fam Med. 2014 Jul-Aug;27[4]:495-509).

For the study, therefore, Dr. Sanchez-Armendariz and her associates evaluated this dose as adjuvant therapy in patients with moderate to severe AD despite topical hydrocortisone aceponate, soap substitute, and emollient. Patients continued this usual care and received either a cellulose capsule placebo or 5000 IU oral vitamin D₃ per day. Based on previously recommended cutoff values, the researchers considered serum 25(OH)D levels sufficient if they exceeded 30 ng per mL, insufficient if they were between 20 and 30 ng per mL, and deficient if they were less than 20 ng per mL (J Bone Miner Res. 2011 Mar;26[3]:455-7).

At baseline, the placebo and intervention groups resembled each other in terms of baseline levels of 25(OH)D, calcium, and phosphorus, pruritus, and scores on SCORAD and the six-area Total Body Severity Assessment. A total of 59% of patients had insufficient serum 25(OH)D, and 39% were deficient.

Patients in both groups improved on the Total Body Severity Assessment, but the extent of improvement did not statistically differ between groups, Dr. Sanchez-Armendariz reported. Supplementation did significantly increase serum 25(OH)D levels, which at week 12 averaged 58.3 ng per mL (SD, 18.5 ng per mL), compared with 22.2 (SD, 7.6 ng per mL) with placebo (P less than .001).

Interestingly, at week 12, all patients in the vitamin D₃ group achieved serum 25(OH)D levels of at least 30 ng per mL, as did 41% of patients in the placebo arm. Patients in both groups who achieved this “sufficient” serum 25(OH)D level averaged a nearly 21-point improvement on the SCORAD (SD, 11.1 points), compared with 7.5 points (SD, 9.9 points) among patients who remained deficient, and 17.4 points (SD, 12.7 points) among patients who remained insufficient (P = .004 for difference among groups; P = .02 for difference between sufficient and insufficient groups).

An analysis of variance confirmed this finding, showing that, regardless of treatment group, patients whose final serum 25(OH)D level was at least 20 ng per mL scored an average of 20 points on the SCORAD, compared with 38 points for patients whose 25(OH)D level remained below 20 ng per mL. Patients whose final 25(OH)D level exceeded 20 ng per mL had fivefold greater odds of having a SCORAD below 25 than did patients with lower serum 25(OH)D levels (odds ratio, 5.1; 95% confidence interval, 1.2-22.6; P = .03).

The investigators identified no adverse effects of vitamin D₃ supplementation, Dr. Sanchez-Armendariz said. “Attaining 25(OH)D levels above 20 ng per mL in addition to baseline therapy reduced the SCORAD of patients with moderate to severe atopic dermatitis,” she added. Clinicians should consider vitamin D3 deficiency and supplementation in patients with relapsing or refractory AD, she emphasized.

Dr. Sanchez-Armendariz reported no external funding sources and no conflicts of interest.

To the Editor:

Atopic dermatitis (AD) is a common skin condition with an increasing prevalence, affecting up to 20% of children and 3% of adults.^1,2 More than 80% of patients with AD have elevated IgE levels.^3,4 IgE modulates the inflammatory response in AD in several ways including “a biphasic immediate/late phase reaction, allergen presentation by IgE-bearing Langerhans cells, allergen-induced activation of IgE-bearing macrophages, and IgE autoreactivity to human proteins.”⁵ Historically, most therapies have focused on mitigating the allergic symptoms caused by degranulated effector cells, such as antihistamines. However, a new class of biologically engineered medications (eg, anti-IgE [omalizumab]) aim to prevent the initiation of the allergic response.⁶ Variable success has been reported using omalizumab in the treatment of AD, though the majority of studies have shown improvement, especially when used in combination with conventional therapies.^4,5,7-22 Omalizumab dosage is determined by body weight and pretreatment serum total IgE levels and is administered via subcutaneous injections every 2 to 4 weeks.^6,7,23-26 However, the dosing tables are based on asthma therapy, in which serum IgE levels may be much lower than chronic AD,^7,24 and the appropriate dosage in AD patients with markedly elevated IgE is unclear. We report an interesting case of a 57-year-old man with erythroderma from long-standing severe chronic AD that was unresponsive to conventional therapy as well as an associated serum IgE level of 17,183 IU/mL who dramatically improved when omalizumab was added to his treatment regimen.

A 57-year-old man presented with essentially 100% body surface area involvement of AD with erythroderma and pruritus. Severe AD developed at infancy and cleared at 5 years of age; childhood onset of asthma was responsive to theophylline and oral inhalers. He developed recurrent AD and asthma at 38 years of age, which was progressive and developed into severe recalcitrant erythroderma by 50 years of age. His AD was unresponsive to multiple therapies, including topical steroids, antibiotics, tacrolimus, bleach baths, antihistamines, methotrexate (15 mg weekly for 1 year, then 12.5 mg weekly for 6 months), UVB phototherapy, and psoralen plus UVA photochemotherapy. He had minimal improvement with cyclosporine (200 mg daily for 4 weeks) and mycophenolate mofetil (3 g daily), and required systemic steroids for relief. The skin was violaceous and lichenified (Figure, A). Laboratory studies were normal, except for a serum IgE level of 17,183 IU/mL (reference range, <150 IU/mL) and peripheral blood eosinophilia up to 29.8% (reference range, 1%–5%) of the differential. Skin biopsies showed AD progressing to lichen simplex chronicus. Omalizumab was added to the therapeutic regimen at a dose of 375 mg every 2 weeks, with noticeable improvement after 3 months. The patient had approximately 80% to 90% clearing with resolution of erythroderma and pruritus, and only limited residual lichenification (Figure, B). The mycophenolate was tapered slowly, and the patient experienced a mild flare at 1 g daily. He is presently on 1 g of mycophenolate daily and omalizumab (375 mg every 2 weeks) and remains remarkably improved. His IgE level decreased to 11,983 IU/mL.

Omalizumab is a monoclonal IgG1 antibody that specifically binds to the FcεRI domain of serum IgE. It blocks binding to high-affinity receptors on effector cells, primarily mast cells, basophils, macrophages, and dendritic cells; it also decreases free IgE serum levels and downregulates the IgE receptor.^{4,6-10,23-25,27,28} Currently, omalizumab is US Food and Drug Administration approved for moderate to severe persistent asthma in patients 6 years or older with a positive aeroallergen skin test and IgE levels up to 700 IU/mL.^{6,7,23-25,27,28}

However, scattered case reports and small case series have described variable success in the treatment of severe AD that is unresponsive to conventional therapy in patients with markedly elevated serum IgE levels.^4,5,7-22 The majority of patients (approximately 80% of published cases yielded by a PubMed search of articles indexed for MEDLINE using the search terms omalizumab and atopic dermatitis) showed improvement when measured by clinical severity scores and quality of life improvement, especially when used in conjunction with conventional therapy. Possible reasons for reported treatment failure include insufficient dosage, lack of established treatment guidelines for markedly elevated serum IgE levels, severity of disease, or variable response with failure to lower IgE level below a required threshold.^7,9,23,24,27

Krathen and Hsu⁹ reported treatment failure with omalizumab for AD in 3 patients with serum IgE levels ranging from 5440 and 24,400 IU/mL, and one review indicated omalizumab may work best in patients with only moderately elevated serum IgE levels.²¹ However, Toledo et al¹⁸ reported efficacy of low-dose omalizumab for pretreatment IgE levels up to 30,000 IU/mL in 6 of 11 reported cases. The pretreatment serum IgE level is not predictive of response, and lowering the serum IgE level without normalization can be efficacious,^12,23 as in the current case. Serum IgE levels are not used for monitoring therapeutic response or calculating future dosing, given potential increases in serum IgE levels during and after therapy (for up to 12 months) secondary to the formation of anti-IgE:IgE complexes.^6,28 Omalizumab appears most effective when used in combination with conventional therapies. Hopefully ongoing studies will further elucidate the role of omalizumab in recalcitrant AD with elevated serum IgE levels.

To the Editor:

Atopic dermatitis (AD) is a common skin condition with an increasing prevalence, affecting up to 20% of children and 3% of adults.^1,2 More than 80% of patients with AD have elevated IgE levels.^3,4 IgE modulates the inflammatory response in AD in several ways including “a biphasic immediate/late phase reaction, allergen presentation by IgE-bearing Langerhans cells, allergen-induced activation of IgE-bearing macrophages, and IgE autoreactivity to human proteins.”⁵ Historically, most therapies have focused on mitigating the allergic symptoms caused by degranulated effector cells, such as antihistamines. However, a new class of biologically engineered medications (eg, anti-IgE [omalizumab]) aim to prevent the initiation of the allergic response.⁶ Variable success has been reported using omalizumab in the treatment of AD, though the majority of studies have shown improvement, especially when used in combination with conventional therapies.^4,5,7-22 Omalizumab dosage is determined by body weight and pretreatment serum total IgE levels and is administered via subcutaneous injections every 2 to 4 weeks.^6,7,23-26 However, the dosing tables are based on asthma therapy, in which serum IgE levels may be much lower than chronic AD,^7,24 and the appropriate dosage in AD patients with markedly elevated IgE is unclear. We report an interesting case of a 57-year-old man with erythroderma from long-standing severe chronic AD that was unresponsive to conventional therapy as well as an associated serum IgE level of 17,183 IU/mL who dramatically improved when omalizumab was added to his treatment regimen.

A 57-year-old man presented with essentially 100% body surface area involvement of AD with erythroderma and pruritus. Severe AD developed at infancy and cleared at 5 years of age; childhood onset of asthma was responsive to theophylline and oral inhalers. He developed recurrent AD and asthma at 38 years of age, which was progressive and developed into severe recalcitrant erythroderma by 50 years of age. His AD was unresponsive to multiple therapies, including topical steroids, antibiotics, tacrolimus, bleach baths, antihistamines, methotrexate (15 mg weekly for 1 year, then 12.5 mg weekly for 6 months), UVB phototherapy, and psoralen plus UVA photochemotherapy. He had minimal improvement with cyclosporine (200 mg daily for 4 weeks) and mycophenolate mofetil (3 g daily), and required systemic steroids for relief. The skin was violaceous and lichenified (Figure, A). Laboratory studies were normal, except for a serum IgE level of 17,183 IU/mL (reference range, <150 IU/mL) and peripheral blood eosinophilia up to 29.8% (reference range, 1%–5%) of the differential. Skin biopsies showed AD progressing to lichen simplex chronicus. Omalizumab was added to the therapeutic regimen at a dose of 375 mg every 2 weeks, with noticeable improvement after 3 months. The patient had approximately 80% to 90% clearing with resolution of erythroderma and pruritus, and only limited residual lichenification (Figure, B). The mycophenolate was tapered slowly, and the patient experienced a mild flare at 1 g daily. He is presently on 1 g of mycophenolate daily and omalizumab (375 mg every 2 weeks) and remains remarkably improved. His IgE level decreased to 11,983 IU/mL.

Omalizumab is a monoclonal IgG1 antibody that specifically binds to the FcεRI domain of serum IgE. It blocks binding to high-affinity receptors on effector cells, primarily mast cells, basophils, macrophages, and dendritic cells; it also decreases free IgE serum levels and downregulates the IgE receptor.^{4,6-10,23-25,27,28} Currently, omalizumab is US Food and Drug Administration approved for moderate to severe persistent asthma in patients 6 years or older with a positive aeroallergen skin test and IgE levels up to 700 IU/mL.^{6,7,23-25,27,28}

However, scattered case reports and small case series have described variable success in the treatment of severe AD that is unresponsive to conventional therapy in patients with markedly elevated serum IgE levels.^4,5,7-22 The majority of patients (approximately 80% of published cases yielded by a PubMed search of articles indexed for MEDLINE using the search terms omalizumab and atopic dermatitis) showed improvement when measured by clinical severity scores and quality of life improvement, especially when used in conjunction with conventional therapy. Possible reasons for reported treatment failure include insufficient dosage, lack of established treatment guidelines for markedly elevated serum IgE levels, severity of disease, or variable response with failure to lower IgE level below a required threshold.^7,9,23,24,27

Krathen and Hsu⁹ reported treatment failure with omalizumab for AD in 3 patients with serum IgE levels ranging from 5440 and 24,400 IU/mL, and one review indicated omalizumab may work best in patients with only moderately elevated serum IgE levels.²¹ However, Toledo et al¹⁸ reported efficacy of low-dose omalizumab for pretreatment IgE levels up to 30,000 IU/mL in 6 of 11 reported cases. The pretreatment serum IgE level is not predictive of response, and lowering the serum IgE level without normalization can be efficacious,^12,23 as in the current case. Serum IgE levels are not used for monitoring therapeutic response or calculating future dosing, given potential increases in serum IgE levels during and after therapy (for up to 12 months) secondary to the formation of anti-IgE:IgE complexes.^6,28 Omalizumab appears most effective when used in combination with conventional therapies. Hopefully ongoing studies will further elucidate the role of omalizumab in recalcitrant AD with elevated serum IgE levels.

To the Editor:

Atopic dermatitis (AD) is a common skin condition with an increasing prevalence, affecting up to 20% of children and 3% of adults.^1,2 More than 80% of patients with AD have elevated IgE levels.^3,4 IgE modulates the inflammatory response in AD in several ways including “a biphasic immediate/late phase reaction, allergen presentation by IgE-bearing Langerhans cells, allergen-induced activation of IgE-bearing macrophages, and IgE autoreactivity to human proteins.”⁵ Historically, most therapies have focused on mitigating the allergic symptoms caused by degranulated effector cells, such as antihistamines. However, a new class of biologically engineered medications (eg, anti-IgE [omalizumab]) aim to prevent the initiation of the allergic response.⁶ Variable success has been reported using omalizumab in the treatment of AD, though the majority of studies have shown improvement, especially when used in combination with conventional therapies.^4,5,7-22 Omalizumab dosage is determined by body weight and pretreatment serum total IgE levels and is administered via subcutaneous injections every 2 to 4 weeks.^6,7,23-26 However, the dosing tables are based on asthma therapy, in which serum IgE levels may be much lower than chronic AD,^7,24 and the appropriate dosage in AD patients with markedly elevated IgE is unclear. We report an interesting case of a 57-year-old man with erythroderma from long-standing severe chronic AD that was unresponsive to conventional therapy as well as an associated serum IgE level of 17,183 IU/mL who dramatically improved when omalizumab was added to his treatment regimen.

A 57-year-old man presented with essentially 100% body surface area involvement of AD with erythroderma and pruritus. Severe AD developed at infancy and cleared at 5 years of age; childhood onset of asthma was responsive to theophylline and oral inhalers. He developed recurrent AD and asthma at 38 years of age, which was progressive and developed into severe recalcitrant erythroderma by 50 years of age. His AD was unresponsive to multiple therapies, including topical steroids, antibiotics, tacrolimus, bleach baths, antihistamines, methotrexate (15 mg weekly for 1 year, then 12.5 mg weekly for 6 months), UVB phototherapy, and psoralen plus UVA photochemotherapy. He had minimal improvement with cyclosporine (200 mg daily for 4 weeks) and mycophenolate mofetil (3 g daily), and required systemic steroids for relief. The skin was violaceous and lichenified (Figure, A). Laboratory studies were normal, except for a serum IgE level of 17,183 IU/mL (reference range, <150 IU/mL) and peripheral blood eosinophilia up to 29.8% (reference range, 1%–5%) of the differential. Skin biopsies showed AD progressing to lichen simplex chronicus. Omalizumab was added to the therapeutic regimen at a dose of 375 mg every 2 weeks, with noticeable improvement after 3 months. The patient had approximately 80% to 90% clearing with resolution of erythroderma and pruritus, and only limited residual lichenification (Figure, B). The mycophenolate was tapered slowly, and the patient experienced a mild flare at 1 g daily. He is presently on 1 g of mycophenolate daily and omalizumab (375 mg every 2 weeks) and remains remarkably improved. His IgE level decreased to 11,983 IU/mL.

Omalizumab is a monoclonal IgG1 antibody that specifically binds to the FcεRI domain of serum IgE. It blocks binding to high-affinity receptors on effector cells, primarily mast cells, basophils, macrophages, and dendritic cells; it also decreases free IgE serum levels and downregulates the IgE receptor.^{4,6-10,23-25,27,28} Currently, omalizumab is US Food and Drug Administration approved for moderate to severe persistent asthma in patients 6 years or older with a positive aeroallergen skin test and IgE levels up to 700 IU/mL.^{6,7,23-25,27,28}

However, scattered case reports and small case series have described variable success in the treatment of severe AD that is unresponsive to conventional therapy in patients with markedly elevated serum IgE levels.^4,5,7-22 The majority of patients (approximately 80% of published cases yielded by a PubMed search of articles indexed for MEDLINE using the search terms omalizumab and atopic dermatitis) showed improvement when measured by clinical severity scores and quality of life improvement, especially when used in conjunction with conventional therapy. Possible reasons for reported treatment failure include insufficient dosage, lack of established treatment guidelines for markedly elevated serum IgE levels, severity of disease, or variable response with failure to lower IgE level below a required threshold.^7,9,23,24,27

Krathen and Hsu⁹ reported treatment failure with omalizumab for AD in 3 patients with serum IgE levels ranging from 5440 and 24,400 IU/mL, and one review indicated omalizumab may work best in patients with only moderately elevated serum IgE levels.²¹ However, Toledo et al¹⁸ reported efficacy of low-dose omalizumab for pretreatment IgE levels up to 30,000 IU/mL in 6 of 11 reported cases. The pretreatment serum IgE level is not predictive of response, and lowering the serum IgE level without normalization can be efficacious,^12,23 as in the current case. Serum IgE levels are not used for monitoring therapeutic response or calculating future dosing, given potential increases in serum IgE levels during and after therapy (for up to 12 months) secondary to the formation of anti-IgE:IgE complexes.^6,28 Omalizumab appears most effective when used in combination with conventional therapies. Hopefully ongoing studies will further elucidate the role of omalizumab in recalcitrant AD with elevated serum IgE levels.

The approval of dupilumab, the first targeted biologic therapy approved in the United States for treatment of atopic dermatitis, provides a welcome, long-awaited alternative to currently available therapies for moderate to severe disease, according to two of the pivotal trial investigators.

In late March, the Food and Drug Administration approved dupilumab, a monoclonal antibody that inhibits signaling of both interleukin-4 and interleukin-13, for the treatment of moderate to severe AD in adults “whose disease is not adequately controlled with topical prescription therapies or when those therapies are not advisable.” It is administered subcutaneously, with an initial 600-mg dose, followed by 300 mg every other week, according to the prescribing information.

Dupilumab (Dupixent) was the second novel treatment approved for AD in less than 4 months – after years of no approvals of new therapies for this indication. In December, crisaborole ointment (Eucrisa) was approved for treatment of mild to moderate AD in patients aged 2 years and older. Crisaborole is a topical phosphodiesterase-4 inhibitor.

Dupilumab’s approval was based on three phase III studies of adults with moderate to severe AD: SOLO-1 and SOLO-2, which evaluated dupilumab as monotherapy, and the CHRONOS study, which compared dupilumab with topical corticosteroids to treatment with topical corticosteroids alone.

At 16 weeks in the SOLO trials, those treated with dupilumab had improvements in signs and symptoms of AD, including pruritus, anxiety and depression, and quality of life, compared with placebo. Almost 40% of those treated with dupilumab met the primary outcome – a score of clear or almost clear on the Investigator’s Global Assessment and a reduction of 2 points or more in that score from baseline – compared with 8%-10% of those on placebo (P less than .001). Injection-site reactions and conjunctivitis were more common among those treated with dupilumab (N Engl J Med. 2016;375:2335-48).

emechcatie@frontlinemedcom.com

The approval of dupilumab, the first targeted biologic therapy approved in the United States for treatment of atopic dermatitis, provides a welcome, long-awaited alternative to currently available therapies for moderate to severe disease, according to two of the pivotal trial investigators.

In late March, the Food and Drug Administration approved dupilumab, a monoclonal antibody that inhibits signaling of both interleukin-4 and interleukin-13, for the treatment of moderate to severe AD in adults “whose disease is not adequately controlled with topical prescription therapies or when those therapies are not advisable.” It is administered subcutaneously, with an initial 600-mg dose, followed by 300 mg every other week, according to the prescribing information.

Dupilumab (Dupixent) was the second novel treatment approved for AD in less than 4 months – after years of no approvals of new therapies for this indication. In December, crisaborole ointment (Eucrisa) was approved for treatment of mild to moderate AD in patients aged 2 years and older. Crisaborole is a topical phosphodiesterase-4 inhibitor.

Dupilumab’s approval was based on three phase III studies of adults with moderate to severe AD: SOLO-1 and SOLO-2, which evaluated dupilumab as monotherapy, and the CHRONOS study, which compared dupilumab with topical corticosteroids to treatment with topical corticosteroids alone.

At 16 weeks in the SOLO trials, those treated with dupilumab had improvements in signs and symptoms of AD, including pruritus, anxiety and depression, and quality of life, compared with placebo. Almost 40% of those treated with dupilumab met the primary outcome – a score of clear or almost clear on the Investigator’s Global Assessment and a reduction of 2 points or more in that score from baseline – compared with 8%-10% of those on placebo (P less than .001). Injection-site reactions and conjunctivitis were more common among those treated with dupilumab (N Engl J Med. 2016;375:2335-48).

emechcatie@frontlinemedcom.com

The approval of dupilumab, the first targeted biologic therapy approved in the United States for treatment of atopic dermatitis, provides a welcome, long-awaited alternative to currently available therapies for moderate to severe disease, according to two of the pivotal trial investigators.

In late March, the Food and Drug Administration approved dupilumab, a monoclonal antibody that inhibits signaling of both interleukin-4 and interleukin-13, for the treatment of moderate to severe AD in adults “whose disease is not adequately controlled with topical prescription therapies or when those therapies are not advisable.” It is administered subcutaneously, with an initial 600-mg dose, followed by 300 mg every other week, according to the prescribing information.

Dupilumab (Dupixent) was the second novel treatment approved for AD in less than 4 months – after years of no approvals of new therapies for this indication. In December, crisaborole ointment (Eucrisa) was approved for treatment of mild to moderate AD in patients aged 2 years and older. Crisaborole is a topical phosphodiesterase-4 inhibitor.

Dupilumab’s approval was based on three phase III studies of adults with moderate to severe AD: SOLO-1 and SOLO-2, which evaluated dupilumab as monotherapy, and the CHRONOS study, which compared dupilumab with topical corticosteroids to treatment with topical corticosteroids alone.

At 16 weeks in the SOLO trials, those treated with dupilumab had improvements in signs and symptoms of AD, including pruritus, anxiety and depression, and quality of life, compared with placebo. Almost 40% of those treated with dupilumab met the primary outcome – a score of clear or almost clear on the Investigator’s Global Assessment and a reduction of 2 points or more in that score from baseline – compared with 8%-10% of those on placebo (P less than .001). Injection-site reactions and conjunctivitis were more common among those treated with dupilumab (N Engl J Med. 2016;375:2335-48).

emechcatie@frontlinemedcom.com

Inpatient care for atopic dermatitis in the U.S. totaled almost $128 million between 2002 and 2012, indicating a rising financial burden, according to a study funded by the Agency for Healthcare Research and Quality (AHRQ).

Cost of care averaged $8.3 million per year for adults and $3.3 million per year for children, with per-day costs for adult care increasing from $3,200 in 2002 to $3,783 in 2012 and per-day costs for pediatric care increasing from $2,430 to $2,914 in the same period, according to Shanthi Narla, a doctoral research fellow at Northwestern University, Chicago, and her colleagues (J Invest Dermatol. 2017 Mar 1. doi: 10.1016/j.jid.2017.02.975)

Michail_Petrov-96/Thinkstock

ezimmerman@frontlinemedcom.com

On Twitter @EAZTweets

Inpatient care for atopic dermatitis in the U.S. totaled almost $128 million between 2002 and 2012, indicating a rising financial burden, according to a study funded by the Agency for Healthcare Research and Quality (AHRQ).

Cost of care averaged $8.3 million per year for adults and $3.3 million per year for children, with per-day costs for adult care increasing from $3,200 in 2002 to $3,783 in 2012 and per-day costs for pediatric care increasing from $2,430 to $2,914 in the same period, according to Shanthi Narla, a doctoral research fellow at Northwestern University, Chicago, and her colleagues (J Invest Dermatol. 2017 Mar 1. doi: 10.1016/j.jid.2017.02.975)

Michail_Petrov-96/Thinkstock

ezimmerman@frontlinemedcom.com

On Twitter @EAZTweets

Inpatient care for atopic dermatitis in the U.S. totaled almost $128 million between 2002 and 2012, indicating a rising financial burden, according to a study funded by the Agency for Healthcare Research and Quality (AHRQ).

Cost of care averaged $8.3 million per year for adults and $3.3 million per year for children, with per-day costs for adult care increasing from $3,200 in 2002 to $3,783 in 2012 and per-day costs for pediatric care increasing from $2,430 to $2,914 in the same period, according to Shanthi Narla, a doctoral research fellow at Northwestern University, Chicago, and her colleagues (J Invest Dermatol. 2017 Mar 1. doi: 10.1016/j.jid.2017.02.975)

Michail_Petrov-96/Thinkstock

ezimmerman@frontlinemedcom.com

On Twitter @EAZTweets

ORLANDO – Two drugs that target ion channels in nerves are being used to quiet neurogenic itch.

The powerful anesthetic ketamine and the element strontium have both been formulated into topical compounds that do very well in quelling itches that have been stubbornly resistant to other therapies, Gil Yosipovitch, MD, said at the annual meeting of the American Academy of Dermatology.

msullivan@frontlinemedcom.com

On Twitter @alz_gal

ORLANDO – Two drugs that target ion channels in nerves are being used to quiet neurogenic itch.

The powerful anesthetic ketamine and the element strontium have both been formulated into topical compounds that do very well in quelling itches that have been stubbornly resistant to other therapies, Gil Yosipovitch, MD, said at the annual meeting of the American Academy of Dermatology.

msullivan@frontlinemedcom.com

On Twitter @alz_gal

ORLANDO – Two drugs that target ion channels in nerves are being used to quiet neurogenic itch.

The powerful anesthetic ketamine and the element strontium have both been formulated into topical compounds that do very well in quelling itches that have been stubbornly resistant to other therapies, Gil Yosipovitch, MD, said at the annual meeting of the American Academy of Dermatology.

msullivan@frontlinemedcom.com

On Twitter @alz_gal

Dupilumab, a monoclonal antibody that targets both interleukin-4 and interleukin-13, has been approved for the treatment of moderate to severe atopic dermatitis in adults not adequately controlled with topical prescription therapies or for whom topicals are not appropriate.

The approval marks the first biologic approved for treating AD, according to a March 28 announcement from the Food and Drug Administration.

The FDA approval announcement noted that the safety and efficacy of dupilumab had not been established in patients with asthma. 

Dupilumab currently is being studied for children with AD in phase II studies and is being studied for other indications: eosinophilic esophagitis in phase II studies, and asthma and nasal polyps in phase III studies.

Dupilumab will be marketed as Dupixent by Regeneron.

emechcatie@frontlinemedcom.com

Dupilumab, a monoclonal antibody that targets both interleukin-4 and interleukin-13, has been approved for the treatment of moderate to severe atopic dermatitis in adults not adequately controlled with topical prescription therapies or for whom topicals are not appropriate.

The approval marks the first biologic approved for treating AD, according to a March 28 announcement from the Food and Drug Administration.

The FDA approval announcement noted that the safety and efficacy of dupilumab had not been established in patients with asthma. 

Dupilumab currently is being studied for children with AD in phase II studies and is being studied for other indications: eosinophilic esophagitis in phase II studies, and asthma and nasal polyps in phase III studies.

Dupilumab will be marketed as Dupixent by Regeneron.

emechcatie@frontlinemedcom.com

Dupilumab, a monoclonal antibody that targets both interleukin-4 and interleukin-13, has been approved for the treatment of moderate to severe atopic dermatitis in adults not adequately controlled with topical prescription therapies or for whom topicals are not appropriate.

The approval marks the first biologic approved for treating AD, according to a March 28 announcement from the Food and Drug Administration.

The FDA approval announcement noted that the safety and efficacy of dupilumab had not been established in patients with asthma. 

Dupilumab currently is being studied for children with AD in phase II studies and is being studied for other indications: eosinophilic esophagitis in phase II studies, and asthma and nasal polyps in phase III studies.

Dupilumab will be marketed as Dupixent by Regeneron.

emechcatie@frontlinemedcom.com

ORLANDO – Treatment with dupilumab in children and adolescents with moderate to severe atopic dermatitis (AD) reduced severity and pruritus scores from baseline and was well tolerated, in a multicenter, open-label trial of 78 children and adolescents.

Dupilumab’s “powerful ability” to block interleukin-4 and interleukin-13 pathways of inflammation is “especially exciting because AD is even more Th-2 cell driven in children,” said Michael J. Cork, MD, PhD, head of dermatologic research at the University of Sheffield (England), who presented the findings during a late-breaking research session at the annual meeting of the American Academy of Dermatology.

The study assessed the pharmacokinetics, safety, and efficacy of dupilumab and was conducted with 38 children, aged 6-11 years, and 40 adolescents, aged 12-17 years, with moderate to severe AD. All had failed topical corticosteroid therapy. Some of the children (16%) and adolescents (22.5%) had failed at least one systemic therapy.

Both age groups were given either a 2 mg/kg or a 4 mg/kg dose of dupilumab (administered subcutaneously), nothing for 8 weeks, followed by 4 weekly doses of their respective regimens. Mean Eczema Area and Severity Index (EASI) scores at baseline were 31.7 among the adolescents and 35.9 among the children.

At week 12, mean scores in the younger cohort given either 2 mg/kg or 4 mg/kg had improved by 76.2% and 63.4%, respectively, from baseline. In the adolescents, EASI scores at week 12 had improved by a mean of 66.4% in the 2-mg/kg group and 69.7% in the 4-mg/kg group.

Itch also improved “dramatically,” according to Dr. Cork. In the younger children, peak pruritus Numerical Rating Scale scores improved from baseline by a mean of 41.6% in the lower-dose group and 39.6% in the higher-dose group. In the older cohort, pruritus scores improved from baseline by a mean of 30.8% in the lower-dose group and 37.6% in the higher-dose group.

Treatment was well tolerated across the study, and adverse events were “mild, transient, and unrelated,” Dr. Cork said. “I would like to emphasize that these were not related to dupilumab, as they occurred during the period of time after the first dose, in weeks 6 and 7,” he commented. He attributed AD flares experienced in the study to the quick clearance of the drug in the first few weeks.

Dr. Cork reported numerous disclosures, including serving as an adviser, consultant, and investigator for Regeneron, the sponsor of the trial, and Sanofi; the companies developing dupilumab.

wmcknight@frontlinemedcom.com

On Twitter @whitneymcknight

ORLANDO – Treatment with dupilumab in children and adolescents with moderate to severe atopic dermatitis (AD) reduced severity and pruritus scores from baseline and was well tolerated, in a multicenter, open-label trial of 78 children and adolescents.

Dupilumab’s “powerful ability” to block interleukin-4 and interleukin-13 pathways of inflammation is “especially exciting because AD is even more Th-2 cell driven in children,” said Michael J. Cork, MD, PhD, head of dermatologic research at the University of Sheffield (England), who presented the findings during a late-breaking research session at the annual meeting of the American Academy of Dermatology.

The study assessed the pharmacokinetics, safety, and efficacy of dupilumab and was conducted with 38 children, aged 6-11 years, and 40 adolescents, aged 12-17 years, with moderate to severe AD. All had failed topical corticosteroid therapy. Some of the children (16%) and adolescents (22.5%) had failed at least one systemic therapy.

Both age groups were given either a 2 mg/kg or a 4 mg/kg dose of dupilumab (administered subcutaneously), nothing for 8 weeks, followed by 4 weekly doses of their respective regimens. Mean Eczema Area and Severity Index (EASI) scores at baseline were 31.7 among the adolescents and 35.9 among the children.

At week 12, mean scores in the younger cohort given either 2 mg/kg or 4 mg/kg had improved by 76.2% and 63.4%, respectively, from baseline. In the adolescents, EASI scores at week 12 had improved by a mean of 66.4% in the 2-mg/kg group and 69.7% in the 4-mg/kg group.

Itch also improved “dramatically,” according to Dr. Cork. In the younger children, peak pruritus Numerical Rating Scale scores improved from baseline by a mean of 41.6% in the lower-dose group and 39.6% in the higher-dose group. In the older cohort, pruritus scores improved from baseline by a mean of 30.8% in the lower-dose group and 37.6% in the higher-dose group.

Treatment was well tolerated across the study, and adverse events were “mild, transient, and unrelated,” Dr. Cork said. “I would like to emphasize that these were not related to dupilumab, as they occurred during the period of time after the first dose, in weeks 6 and 7,” he commented. He attributed AD flares experienced in the study to the quick clearance of the drug in the first few weeks.

Dr. Cork reported numerous disclosures, including serving as an adviser, consultant, and investigator for Regeneron, the sponsor of the trial, and Sanofi; the companies developing dupilumab.

wmcknight@frontlinemedcom.com

On Twitter @whitneymcknight

ORLANDO – Treatment with dupilumab in children and adolescents with moderate to severe atopic dermatitis (AD) reduced severity and pruritus scores from baseline and was well tolerated, in a multicenter, open-label trial of 78 children and adolescents.

Dupilumab’s “powerful ability” to block interleukin-4 and interleukin-13 pathways of inflammation is “especially exciting because AD is even more Th-2 cell driven in children,” said Michael J. Cork, MD, PhD, head of dermatologic research at the University of Sheffield (England), who presented the findings during a late-breaking research session at the annual meeting of the American Academy of Dermatology.

The study assessed the pharmacokinetics, safety, and efficacy of dupilumab and was conducted with 38 children, aged 6-11 years, and 40 adolescents, aged 12-17 years, with moderate to severe AD. All had failed topical corticosteroid therapy. Some of the children (16%) and adolescents (22.5%) had failed at least one systemic therapy.

Both age groups were given either a 2 mg/kg or a 4 mg/kg dose of dupilumab (administered subcutaneously), nothing for 8 weeks, followed by 4 weekly doses of their respective regimens. Mean Eczema Area and Severity Index (EASI) scores at baseline were 31.7 among the adolescents and 35.9 among the children.

At week 12, mean scores in the younger cohort given either 2 mg/kg or 4 mg/kg had improved by 76.2% and 63.4%, respectively, from baseline. In the adolescents, EASI scores at week 12 had improved by a mean of 66.4% in the 2-mg/kg group and 69.7% in the 4-mg/kg group.

Itch also improved “dramatically,” according to Dr. Cork. In the younger children, peak pruritus Numerical Rating Scale scores improved from baseline by a mean of 41.6% in the lower-dose group and 39.6% in the higher-dose group. In the older cohort, pruritus scores improved from baseline by a mean of 30.8% in the lower-dose group and 37.6% in the higher-dose group.

Treatment was well tolerated across the study, and adverse events were “mild, transient, and unrelated,” Dr. Cork said. “I would like to emphasize that these were not related to dupilumab, as they occurred during the period of time after the first dose, in weeks 6 and 7,” he commented. He attributed AD flares experienced in the study to the quick clearance of the drug in the first few weeks.

Dr. Cork reported numerous disclosures, including serving as an adviser, consultant, and investigator for Regeneron, the sponsor of the trial, and Sanofi; the companies developing dupilumab.

wmcknight@frontlinemedcom.com

On Twitter @whitneymcknight

WAILEA, HAWAII – With the recent approval of crisaborole ointment 2% for the treatment of atopic dermatitis, the question of how to best utilize this novel drug in daily clinical practice was put to two atopic dermatitis experts at the Hawaii Dermatology Seminar sponsored by the Global Academy for Medical Education/Skin Disease Research Foundation.

Two of these experts, Lawrence F. Eichenfield, MD, and Wynnis L. Tom, MD, have garnered extensive clinical trials experience with crisaborole (Eucrisa), which, in December 2016, became the first prescription drug approved by the Food and Drug Administration for atopic dermatitis (AD) in more than 10 years. The topical phosphodiesterase-4 inhibitor is indicated for twice-daily treatment of patients aged 2 years and older with mild to moderate AD.

bjancin@frontlinemedcom.com

WAILEA, HAWAII – With the recent approval of crisaborole ointment 2% for the treatment of atopic dermatitis, the question of how to best utilize this novel drug in daily clinical practice was put to two atopic dermatitis experts at the Hawaii Dermatology Seminar sponsored by the Global Academy for Medical Education/Skin Disease Research Foundation.

Two of these experts, Lawrence F. Eichenfield, MD, and Wynnis L. Tom, MD, have garnered extensive clinical trials experience with crisaborole (Eucrisa), which, in December 2016, became the first prescription drug approved by the Food and Drug Administration for atopic dermatitis (AD) in more than 10 years. The topical phosphodiesterase-4 inhibitor is indicated for twice-daily treatment of patients aged 2 years and older with mild to moderate AD.

bjancin@frontlinemedcom.com

WAILEA, HAWAII – With the recent approval of crisaborole ointment 2% for the treatment of atopic dermatitis, the question of how to best utilize this novel drug in daily clinical practice was put to two atopic dermatitis experts at the Hawaii Dermatology Seminar sponsored by the Global Academy for Medical Education/Skin Disease Research Foundation.

Two of these experts, Lawrence F. Eichenfield, MD, and Wynnis L. Tom, MD, have garnered extensive clinical trials experience with crisaborole (Eucrisa), which, in December 2016, became the first prescription drug approved by the Food and Drug Administration for atopic dermatitis (AD) in more than 10 years. The topical phosphodiesterase-4 inhibitor is indicated for twice-daily treatment of patients aged 2 years and older with mild to moderate AD.

bjancin@frontlinemedcom.com

ATLANTA – Obese females who live in urban settings are significantly more likely to develop atopic diseases, compared with their male counterparts, results from a single-center study showed.

“Some research has shown that obese girls are much more likely to be atopic, but many of them only look at one disease alone, such as atopic dermatitis or food allergies,” lead study author Sairaman Nagarajan, MD, MPH, said in an interview at the annual meeting of the American Academy of Allergy, Asthma, and Immunology. “Most of the studies are in asthma.”

Doug Brunk/Frontline Medical News

The mean age of patients was 9 years, 23% were obese, and 55% were male. The researchers observed no differences in laboratory biomarkers nor in the prevalence of individual/or cumulative atopic disease in obese children, compared with controls. When stratified by gender, obese females had a significantly higher mean atopic disease score, compared with controls (4.00 vs. 2.62, respectively; P less than .001), while males had a significantly lower mean atopic disease score, compared with controls (3 vs. 3.42; P less than .001). Regression models yielded similar results; obese females had a significantly higher mean atopic disease score, compared with controls (by a mean elevation of 1.37 points; P less than .005), while males had a significantly lower mean atopic disease score (by a mean decline of -0.42 points; P less than .006). “From this we can say that female gender is a positive risk factor for atopy, and urban obese females may be particularly likely to benefit from lifestyle modification therapy like exercise and diet in controlling weight, and thereby allergies,” Dr. Nagarajan said.

He noted that it remains unclear whether the findings would apply to children who live in nonurban settings. “It’s difficult to say because there are some variables which are unique to urban minority populations like the housing that they live in and the kind of stores they buy food from,” he said.

Dr. Nagarajan reported having no financial disclosures.

dbrunk@frontlinemedcom.com

ATLANTA – Obese females who live in urban settings are significantly more likely to develop atopic diseases, compared with their male counterparts, results from a single-center study showed.

“Some research has shown that obese girls are much more likely to be atopic, but many of them only look at one disease alone, such as atopic dermatitis or food allergies,” lead study author Sairaman Nagarajan, MD, MPH, said in an interview at the annual meeting of the American Academy of Allergy, Asthma, and Immunology. “Most of the studies are in asthma.”

Doug Brunk/Frontline Medical News

The mean age of patients was 9 years, 23% were obese, and 55% were male. The researchers observed no differences in laboratory biomarkers nor in the prevalence of individual/or cumulative atopic disease in obese children, compared with controls. When stratified by gender, obese females had a significantly higher mean atopic disease score, compared with controls (4.00 vs. 2.62, respectively; P less than .001), while males had a significantly lower mean atopic disease score, compared with controls (3 vs. 3.42; P less than .001). Regression models yielded similar results; obese females had a significantly higher mean atopic disease score, compared with controls (by a mean elevation of 1.37 points; P less than .005), while males had a significantly lower mean atopic disease score (by a mean decline of -0.42 points; P less than .006). “From this we can say that female gender is a positive risk factor for atopy, and urban obese females may be particularly likely to benefit from lifestyle modification therapy like exercise and diet in controlling weight, and thereby allergies,” Dr. Nagarajan said.

He noted that it remains unclear whether the findings would apply to children who live in nonurban settings. “It’s difficult to say because there are some variables which are unique to urban minority populations like the housing that they live in and the kind of stores they buy food from,” he said.

Dr. Nagarajan reported having no financial disclosures.

dbrunk@frontlinemedcom.com

ATLANTA – Obese females who live in urban settings are significantly more likely to develop atopic diseases, compared with their male counterparts, results from a single-center study showed.

“Some research has shown that obese girls are much more likely to be atopic, but many of them only look at one disease alone, such as atopic dermatitis or food allergies,” lead study author Sairaman Nagarajan, MD, MPH, said in an interview at the annual meeting of the American Academy of Allergy, Asthma, and Immunology. “Most of the studies are in asthma.”

Doug Brunk/Frontline Medical News

The mean age of patients was 9 years, 23% were obese, and 55% were male. The researchers observed no differences in laboratory biomarkers nor in the prevalence of individual/or cumulative atopic disease in obese children, compared with controls. When stratified by gender, obese females had a significantly higher mean atopic disease score, compared with controls (4.00 vs. 2.62, respectively; P less than .001), while males had a significantly lower mean atopic disease score, compared with controls (3 vs. 3.42; P less than .001). Regression models yielded similar results; obese females had a significantly higher mean atopic disease score, compared with controls (by a mean elevation of 1.37 points; P less than .005), while males had a significantly lower mean atopic disease score (by a mean decline of -0.42 points; P less than .006). “From this we can say that female gender is a positive risk factor for atopy, and urban obese females may be particularly likely to benefit from lifestyle modification therapy like exercise and diet in controlling weight, and thereby allergies,” Dr. Nagarajan said.

He noted that it remains unclear whether the findings would apply to children who live in nonurban settings. “It’s difficult to say because there are some variables which are unique to urban minority populations like the housing that they live in and the kind of stores they buy food from,” he said.

Dr. Nagarajan reported having no financial disclosures.

dbrunk@frontlinemedcom.com