Atopic Dermatitis

Trixéra Sélectiose Emollient Cream and other products in the Trixéra Sélectiose product line are available in 400-mL sizes to provide better value. The emollient cream is designed to improve four symptoms of atopic skin: hypersensitivity, irritation, dehydration, and a reduced skin barrier. The cream may be used daily or alternately with Trixéra Selectiose Emollient Balm. The cream is formulated to help relieve dry, intolerant skin, especially during the fall and winter months, by reinforcing the skin's protective barrier. Regular use of the cream may help relieve itching and sensitivity, as well as reduce the time between atopic flares. This product is appropriate for adults, children, and infants.

Avène

www.aveneusa.com

Trixéra Sélectiose Emollient Cream and other products in the Trixéra Sélectiose product line are available in 400-mL sizes to provide better value. The emollient cream is designed to improve four symptoms of atopic skin: hypersensitivity, irritation, dehydration, and a reduced skin barrier. The cream may be used daily or alternately with Trixéra Selectiose Emollient Balm. The cream is formulated to help relieve dry, intolerant skin, especially during the fall and winter months, by reinforcing the skin's protective barrier. Regular use of the cream may help relieve itching and sensitivity, as well as reduce the time between atopic flares. This product is appropriate for adults, children, and infants.

Avène

www.aveneusa.com

Trixéra Sélectiose Emollient Cream and other products in the Trixéra Sélectiose product line are available in 400-mL sizes to provide better value. The emollient cream is designed to improve four symptoms of atopic skin: hypersensitivity, irritation, dehydration, and a reduced skin barrier. The cream may be used daily or alternately with Trixéra Selectiose Emollient Balm. The cream is formulated to help relieve dry, intolerant skin, especially during the fall and winter months, by reinforcing the skin's protective barrier. Regular use of the cream may help relieve itching and sensitivity, as well as reduce the time between atopic flares. This product is appropriate for adults, children, and infants.

Avène

www.aveneusa.com

BERLIN — Atopic dermatitis is strongly and independently associated with attention-deficit/hyperactivity disorder, three large German studies suggest.

If the relationship is causal—and that's an unsettled issue—then atopic dermatitis would explain roughly 10% of all cases of ADHD, Dr. Jochen Schmitt estimated at the annual congress of the European Academy of Dermatology and Venereology.

Atopic dermatitis is the most common chronic inflammatory disorder in childhood, and ADHD is the most common psychiatric diagnosis. The nature of the relationship is a classic chicken-versus-egg question, he said.

“As dermatologists, we first think that eczema causes sleeping problems, and this then would maybe cause ADHD. But a close friend of mine who is a psychiatrist says, no, ADHD causes psychologic distress and this distress is an exacerbating factor for eczema,” explained Dr. Schmitt, a dermatologist at Carl Gustav Carus Technical University in Dresden, Germany.

“It's also possible that this is a syndrome: that eczema, ADHD, and sleeping problems are parts of one syndrome with another third or fourth underlying cause. And it's even possible that all these things are true: that eczema triggers ADHD and vice versa and that sleeping problems could play a crucial role,” he continued.

Dr. Schmitt first became interested in the relationship between atopic dermatitis and ADHD after learning of a Dutch group's hypothesis that some cases of ADHD are an allergic hypersensitivity disorder (Pediatr. Allergy Immunol. 2009;20:107–12).

Dr. Schmitt and his coinvestigators reviewed a German administrative health care database containing complete information on the outpatient care of 600,000 residents of Saxony. They identified 1,436 subjects aged 6–17 years with atopic dermatitis and randomly selected an equal number of age- and gender-matched controls. In a multivariate logistic regression analysis, the investigators showed that a diagnosis of atopic dermatitis was independently associated with a 1.47-fold increased likelihood of prevalent ADHD (JAMA 2009;301:724–6).

“The recent JAMA study and prior studies show a very interesting association that may display another profound effect of atopic dermatitis on affected individuals,” Dr. Lawrence F. Eichenfield said in an interview. “The epidemiologic information is intriguing.”

“One question is whether the diagnostic label of ADHD is specific enough; in this study the ICD-10 diagnosis of hyperkinetic disorder was generally used, which includes impaired attention and overactivity, implying restlessness,” commented Dr. Eichenfield, chief of pediatric and adolescent dermatology at Rady Children's Hospital, San Diego. “Is this all secondary to sleep disturbance and pruritus? We hope to see further studies that look at AD symptom severity as a variable and further work to help us to understand this association,” he said.

Dr. Schmitt and his coinvestigators also reviewed a second cross-sectional study, KIGGS—a population-based nationwide German survey including 13,318 youths aged 3–17 years, of whom 1,952 had atopic dermatitis and 653 had ADHD. After adjustment for potential confounders, including parental smoking, breastfeeding, perinatal health problems, and atopic comorbidity, individuals with atopic dermatitis were 1.54-fold more likely to carry a diagnosis of ADHD than those without atopic dermatitis.

Among the 6,484 children aged 3–11 years, Dr. Schmitt and colleagues found that those with atopic dermatitis and parent-reported sleep problems had a highly significant 2.67-fold increased likelihood of ADHD, compared with children without atopic dermatitis. But atopic dermatitis patients without sleep problems did not have a significantly increased rate of ADHD (J. Epidemiol. Community Health 2009 [doi:10.1136/jech.2009.093534]).

To move beyond the limitations imposed by cross-sectional data, Dr. Schmitt and his coworkers turned to the German Infant Nutritional Intervention Study (GINI-Plus), a 3,000-patient multicenter prospective investigation into environmental and genetic influences on the development of allergies.

In an analysis of GINI-Plus data, the investigators found that physician-diagnosed atopic dermatitis during infancy was an independent risk factor for mental health problems at age 10 years.

“Most interestingly, even those children who only had eczema during the first 2 years of life and cleared afterwards had an increased risk of mental health problems at age 10,” Dr. Schmitt said.

He and his colleagues plan to examine the relationship between severity of atopic dermatitis and ADHD risk. If the association between eczema and ADHD indeed proves to be causal, then effective treatment of the dermatologic disorder would have exciting potential as a strategy for the prevention of ADHD, he noted.

Dr. Schmitt disclosed having no financial conflicts of interest.

The GINI-Plus study is funded by the German Federal Ministry of Education and Research.

It's “possible that this is a syndrome: that eczema, ADHD, and sleeping problems are parts of one syndrome with another third or fourth underlying cause,” said Dr. Jochen Schmitt.

Source Courtesy Dr. Jochen Schmitt

'Studies show a very interesting association that may display another profound effect of atopic dermatitis.'

Source Dr. Eichenfield

BERLIN — Atopic dermatitis is strongly and independently associated with attention-deficit/hyperactivity disorder, three large German studies suggest.

If the relationship is causal—and that's an unsettled issue—then atopic dermatitis would explain roughly 10% of all cases of ADHD, Dr. Jochen Schmitt estimated at the annual congress of the European Academy of Dermatology and Venereology.

Atopic dermatitis is the most common chronic inflammatory disorder in childhood, and ADHD is the most common psychiatric diagnosis. The nature of the relationship is a classic chicken-versus-egg question, he said.

“As dermatologists, we first think that eczema causes sleeping problems, and this then would maybe cause ADHD. But a close friend of mine who is a psychiatrist says, no, ADHD causes psychologic distress and this distress is an exacerbating factor for eczema,” explained Dr. Schmitt, a dermatologist at Carl Gustav Carus Technical University in Dresden, Germany.

“It's also possible that this is a syndrome: that eczema, ADHD, and sleeping problems are parts of one syndrome with another third or fourth underlying cause. And it's even possible that all these things are true: that eczema triggers ADHD and vice versa and that sleeping problems could play a crucial role,” he continued.

Dr. Schmitt first became interested in the relationship between atopic dermatitis and ADHD after learning of a Dutch group's hypothesis that some cases of ADHD are an allergic hypersensitivity disorder (Pediatr. Allergy Immunol. 2009;20:107–12).

Dr. Schmitt and his coinvestigators reviewed a German administrative health care database containing complete information on the outpatient care of 600,000 residents of Saxony. They identified 1,436 subjects aged 6–17 years with atopic dermatitis and randomly selected an equal number of age- and gender-matched controls. In a multivariate logistic regression analysis, the investigators showed that a diagnosis of atopic dermatitis was independently associated with a 1.47-fold increased likelihood of prevalent ADHD (JAMA 2009;301:724–6).

“The recent JAMA study and prior studies show a very interesting association that may display another profound effect of atopic dermatitis on affected individuals,” Dr. Lawrence F. Eichenfield said in an interview. “The epidemiologic information is intriguing.”

“One question is whether the diagnostic label of ADHD is specific enough; in this study the ICD-10 diagnosis of hyperkinetic disorder was generally used, which includes impaired attention and overactivity, implying restlessness,” commented Dr. Eichenfield, chief of pediatric and adolescent dermatology at Rady Children's Hospital, San Diego. “Is this all secondary to sleep disturbance and pruritus? We hope to see further studies that look at AD symptom severity as a variable and further work to help us to understand this association,” he said.

Dr. Schmitt and his coinvestigators also reviewed a second cross-sectional study, KIGGS—a population-based nationwide German survey including 13,318 youths aged 3–17 years, of whom 1,952 had atopic dermatitis and 653 had ADHD. After adjustment for potential confounders, including parental smoking, breastfeeding, perinatal health problems, and atopic comorbidity, individuals with atopic dermatitis were 1.54-fold more likely to carry a diagnosis of ADHD than those without atopic dermatitis.

Among the 6,484 children aged 3–11 years, Dr. Schmitt and colleagues found that those with atopic dermatitis and parent-reported sleep problems had a highly significant 2.67-fold increased likelihood of ADHD, compared with children without atopic dermatitis. But atopic dermatitis patients without sleep problems did not have a significantly increased rate of ADHD (J. Epidemiol. Community Health 2009 [doi:10.1136/jech.2009.093534]).

To move beyond the limitations imposed by cross-sectional data, Dr. Schmitt and his coworkers turned to the German Infant Nutritional Intervention Study (GINI-Plus), a 3,000-patient multicenter prospective investigation into environmental and genetic influences on the development of allergies.

In an analysis of GINI-Plus data, the investigators found that physician-diagnosed atopic dermatitis during infancy was an independent risk factor for mental health problems at age 10 years.

“Most interestingly, even those children who only had eczema during the first 2 years of life and cleared afterwards had an increased risk of mental health problems at age 10,” Dr. Schmitt said.

He and his colleagues plan to examine the relationship between severity of atopic dermatitis and ADHD risk. If the association between eczema and ADHD indeed proves to be causal, then effective treatment of the dermatologic disorder would have exciting potential as a strategy for the prevention of ADHD, he noted.

Dr. Schmitt disclosed having no financial conflicts of interest.

The GINI-Plus study is funded by the German Federal Ministry of Education and Research.

It's “possible that this is a syndrome: that eczema, ADHD, and sleeping problems are parts of one syndrome with another third or fourth underlying cause,” said Dr. Jochen Schmitt.

Source Courtesy Dr. Jochen Schmitt

'Studies show a very interesting association that may display another profound effect of atopic dermatitis.'

Source Dr. Eichenfield

BERLIN — Atopic dermatitis is strongly and independently associated with attention-deficit/hyperactivity disorder, three large German studies suggest.

If the relationship is causal—and that's an unsettled issue—then atopic dermatitis would explain roughly 10% of all cases of ADHD, Dr. Jochen Schmitt estimated at the annual congress of the European Academy of Dermatology and Venereology.

Atopic dermatitis is the most common chronic inflammatory disorder in childhood, and ADHD is the most common psychiatric diagnosis. The nature of the relationship is a classic chicken-versus-egg question, he said.

“As dermatologists, we first think that eczema causes sleeping problems, and this then would maybe cause ADHD. But a close friend of mine who is a psychiatrist says, no, ADHD causes psychologic distress and this distress is an exacerbating factor for eczema,” explained Dr. Schmitt, a dermatologist at Carl Gustav Carus Technical University in Dresden, Germany.

“It's also possible that this is a syndrome: that eczema, ADHD, and sleeping problems are parts of one syndrome with another third or fourth underlying cause. And it's even possible that all these things are true: that eczema triggers ADHD and vice versa and that sleeping problems could play a crucial role,” he continued.

Dr. Schmitt first became interested in the relationship between atopic dermatitis and ADHD after learning of a Dutch group's hypothesis that some cases of ADHD are an allergic hypersensitivity disorder (Pediatr. Allergy Immunol. 2009;20:107–12).

Dr. Schmitt and his coinvestigators reviewed a German administrative health care database containing complete information on the outpatient care of 600,000 residents of Saxony. They identified 1,436 subjects aged 6–17 years with atopic dermatitis and randomly selected an equal number of age- and gender-matched controls. In a multivariate logistic regression analysis, the investigators showed that a diagnosis of atopic dermatitis was independently associated with a 1.47-fold increased likelihood of prevalent ADHD (JAMA 2009;301:724–6).

“The recent JAMA study and prior studies show a very interesting association that may display another profound effect of atopic dermatitis on affected individuals,” Dr. Lawrence F. Eichenfield said in an interview. “The epidemiologic information is intriguing.”

“One question is whether the diagnostic label of ADHD is specific enough; in this study the ICD-10 diagnosis of hyperkinetic disorder was generally used, which includes impaired attention and overactivity, implying restlessness,” commented Dr. Eichenfield, chief of pediatric and adolescent dermatology at Rady Children's Hospital, San Diego. “Is this all secondary to sleep disturbance and pruritus? We hope to see further studies that look at AD symptom severity as a variable and further work to help us to understand this association,” he said.

Dr. Schmitt and his coinvestigators also reviewed a second cross-sectional study, KIGGS—a population-based nationwide German survey including 13,318 youths aged 3–17 years, of whom 1,952 had atopic dermatitis and 653 had ADHD. After adjustment for potential confounders, including parental smoking, breastfeeding, perinatal health problems, and atopic comorbidity, individuals with atopic dermatitis were 1.54-fold more likely to carry a diagnosis of ADHD than those without atopic dermatitis.

Among the 6,484 children aged 3–11 years, Dr. Schmitt and colleagues found that those with atopic dermatitis and parent-reported sleep problems had a highly significant 2.67-fold increased likelihood of ADHD, compared with children without atopic dermatitis. But atopic dermatitis patients without sleep problems did not have a significantly increased rate of ADHD (J. Epidemiol. Community Health 2009 [doi:10.1136/jech.2009.093534]).

To move beyond the limitations imposed by cross-sectional data, Dr. Schmitt and his coworkers turned to the German Infant Nutritional Intervention Study (GINI-Plus), a 3,000-patient multicenter prospective investigation into environmental and genetic influences on the development of allergies.

In an analysis of GINI-Plus data, the investigators found that physician-diagnosed atopic dermatitis during infancy was an independent risk factor for mental health problems at age 10 years.

“Most interestingly, even those children who only had eczema during the first 2 years of life and cleared afterwards had an increased risk of mental health problems at age 10,” Dr. Schmitt said.

He and his colleagues plan to examine the relationship between severity of atopic dermatitis and ADHD risk. If the association between eczema and ADHD indeed proves to be causal, then effective treatment of the dermatologic disorder would have exciting potential as a strategy for the prevention of ADHD, he noted.

Dr. Schmitt disclosed having no financial conflicts of interest.

The GINI-Plus study is funded by the German Federal Ministry of Education and Research.

It's “possible that this is a syndrome: that eczema, ADHD, and sleeping problems are parts of one syndrome with another third or fourth underlying cause,” said Dr. Jochen Schmitt.

Source Courtesy Dr. Jochen Schmitt

'Studies show a very interesting association that may display another profound effect of atopic dermatitis.'

Source Dr. Eichenfield

Heparin-induced skin lesions are fairly common among patients receiving heparin for treatment or prophylaxis, especially among women, and those who are overweight or who have taken the drug for more than 9 days, a new study has determined.

Prior research had suggested that many cases were caused by heparin-induced thrombocytopenia. The study by Dr. Marc Schindewolf and colleagues contradicts those data: A delayed-type hypersensitivity reaction caused the lesions in all 24 of the cases they observed (CMAJ 2009 Sept. 28 [doi:10.1503/cmaj.081729

Dr. Schindewolf of the Hospital of the Johann Wolfgang Goethe University in Frankfurt, Germany, and his coauthors also postulated that heparin-induced skin lesions are probably much more common than currently believed. Their observed incidence of 7.5% far exceeded their expected findings of 2%, which were based on prior clinical observations. “During the study we were surprised by the high number of patients with [lesions],” they wrote. “For most of the patients, the diagnosis was made because of our study. Therefore, it is tempting to speculate that many cases of heparin-induced skin lesions are undiagnosed.”

The study comprised 320 patients enrolled over a 12-month period, all of whom were taking some form of heparin as treatment or prophylaxis. The patients' mean age was 61 years; the median duration of heparin use was 9 days, but it ranged from 7 to 1,095 days. Most (60%) were taking enoxaparin; 31% were taking nadroparin. The remainder was taking other forms of heparin.

In all, 24 patients developed heparin-induced skin lesions. Most of the cases were small eczema-like plaques at the injection site. A few patients had generalized itchy erythematous plaques. In 23 patients, a delayed-type hypersensitivity response was the confirmed cause. One patient refused to consent to a punch biopsy or allergologic testing. Although all of these patients were screened for immune-mediated heparin-induced thrombocytopenia, it was detected in only one patient.

Compared with those who did not develop lesions, more of those who did were women (71% vs. 45%), had a higher body mass index (30 kg/m

The lesions should be viewed as a symptom requiring an investigation of some underlying etiology, they wrote: “We recommend obtaining a punch biopsy; comparing platelet counts before, during, and after therapy; and performing appropriate laboratory investigations to exclude heparin-induced thrombocytopenia.”

The authors reported having no financial conflicts with regard to the study.

Heparin-induced skin lesions are fairly common among patients receiving heparin for treatment or prophylaxis, especially among women, and those who are overweight or who have taken the drug for more than 9 days, a new study has determined.

Prior research had suggested that many cases were caused by heparin-induced thrombocytopenia. The study by Dr. Marc Schindewolf and colleagues contradicts those data: A delayed-type hypersensitivity reaction caused the lesions in all 24 of the cases they observed (CMAJ 2009 Sept. 28 [doi:10.1503/cmaj.081729

Dr. Schindewolf of the Hospital of the Johann Wolfgang Goethe University in Frankfurt, Germany, and his coauthors also postulated that heparin-induced skin lesions are probably much more common than currently believed. Their observed incidence of 7.5% far exceeded their expected findings of 2%, which were based on prior clinical observations. “During the study we were surprised by the high number of patients with [lesions],” they wrote. “For most of the patients, the diagnosis was made because of our study. Therefore, it is tempting to speculate that many cases of heparin-induced skin lesions are undiagnosed.”

The study comprised 320 patients enrolled over a 12-month period, all of whom were taking some form of heparin as treatment or prophylaxis. The patients' mean age was 61 years; the median duration of heparin use was 9 days, but it ranged from 7 to 1,095 days. Most (60%) were taking enoxaparin; 31% were taking nadroparin. The remainder was taking other forms of heparin.

In all, 24 patients developed heparin-induced skin lesions. Most of the cases were small eczema-like plaques at the injection site. A few patients had generalized itchy erythematous plaques. In 23 patients, a delayed-type hypersensitivity response was the confirmed cause. One patient refused to consent to a punch biopsy or allergologic testing. Although all of these patients were screened for immune-mediated heparin-induced thrombocytopenia, it was detected in only one patient.

Compared with those who did not develop lesions, more of those who did were women (71% vs. 45%), had a higher body mass index (30 kg/m

The lesions should be viewed as a symptom requiring an investigation of some underlying etiology, they wrote: “We recommend obtaining a punch biopsy; comparing platelet counts before, during, and after therapy; and performing appropriate laboratory investigations to exclude heparin-induced thrombocytopenia.”

The authors reported having no financial conflicts with regard to the study.

Heparin-induced skin lesions are fairly common among patients receiving heparin for treatment or prophylaxis, especially among women, and those who are overweight or who have taken the drug for more than 9 days, a new study has determined.

Prior research had suggested that many cases were caused by heparin-induced thrombocytopenia. The study by Dr. Marc Schindewolf and colleagues contradicts those data: A delayed-type hypersensitivity reaction caused the lesions in all 24 of the cases they observed (CMAJ 2009 Sept. 28 [doi:10.1503/cmaj.081729

Dr. Schindewolf of the Hospital of the Johann Wolfgang Goethe University in Frankfurt, Germany, and his coauthors also postulated that heparin-induced skin lesions are probably much more common than currently believed. Their observed incidence of 7.5% far exceeded their expected findings of 2%, which were based on prior clinical observations. “During the study we were surprised by the high number of patients with [lesions],” they wrote. “For most of the patients, the diagnosis was made because of our study. Therefore, it is tempting to speculate that many cases of heparin-induced skin lesions are undiagnosed.”

The study comprised 320 patients enrolled over a 12-month period, all of whom were taking some form of heparin as treatment or prophylaxis. The patients' mean age was 61 years; the median duration of heparin use was 9 days, but it ranged from 7 to 1,095 days. Most (60%) were taking enoxaparin; 31% were taking nadroparin. The remainder was taking other forms of heparin.

In all, 24 patients developed heparin-induced skin lesions. Most of the cases were small eczema-like plaques at the injection site. A few patients had generalized itchy erythematous plaques. In 23 patients, a delayed-type hypersensitivity response was the confirmed cause. One patient refused to consent to a punch biopsy or allergologic testing. Although all of these patients were screened for immune-mediated heparin-induced thrombocytopenia, it was detected in only one patient.

Compared with those who did not develop lesions, more of those who did were women (71% vs. 45%), had a higher body mass index (30 kg/m

The lesions should be viewed as a symptom requiring an investigation of some underlying etiology, they wrote: “We recommend obtaining a punch biopsy; comparing platelet counts before, during, and after therapy; and performing appropriate laboratory investigations to exclude heparin-induced thrombocytopenia.”

The authors reported having no financial conflicts with regard to the study.

SAN FRANCISCO — Start simple and use a step-wise approach to treat children with atopic dermatitis, Dr. Sheila Fallon Friedlander recommended.

“Atopic dermatitis matters so much because it can become infected, can impair physical and psychologic function, and has a tremendous effect on family quality of life,” Dr. Friedlander said at a seminar on women's and pediatric dermatology sponsored by Skin Disease Education Foundation.

Using a ladder analogy, start at the bottom with repair of the skin barrier. The next rung is an intervention to short circuit inflammation. Then take care of itching, treat infections, address triggers, and educate patients and their family.

Is the family compliant? “This is extremely important. You need to get family to buy in to a treatment plan that is often complicated,” said Dr. Friedlander of the University of California, San Diego.

Consider the age of the child, severity and duration of disease, and how much body surface area is affected.

Bathing can be beneficial to atopic skin if it hydrates the stratum corneum and removes dirt, scales, and bugs, but breaks in the skin can occur during evaporation, so bathing and moisturizers together are better than either alone, Dr. Friedlander said.

She is a fan of ceramide-based creams for atopic dermatitis. “Ceramides can decrease the amount of steroid you use or perhaps you can use [them] instead of steroids and do as well,” she said.

If barrier repair does not work, the next step of the ladder is short circuiting inflammation. With corticosteroids for atopic dermatitis, use the weakest strength to do the job, blast and taper off, or consider weekend pulses of high potency steroids.

Topical calcineurin inhibitors are another therapeutic option. “There are a lot of data out there, so we know a lot about them,” she said.

Dr. Friedlander's relevant disclosures include being a consultant for Astellas, Graceway Pharmaceuticals, and Novartis. She also receives research support from Astellas, Novartis, Promius Pharma, and SkinMedica. SDEF and this news organization are owned by Elsevier.

SAN FRANCISCO — Start simple and use a step-wise approach to treat children with atopic dermatitis, Dr. Sheila Fallon Friedlander recommended.

“Atopic dermatitis matters so much because it can become infected, can impair physical and psychologic function, and has a tremendous effect on family quality of life,” Dr. Friedlander said at a seminar on women's and pediatric dermatology sponsored by Skin Disease Education Foundation.

Using a ladder analogy, start at the bottom with repair of the skin barrier. The next rung is an intervention to short circuit inflammation. Then take care of itching, treat infections, address triggers, and educate patients and their family.

Is the family compliant? “This is extremely important. You need to get family to buy in to a treatment plan that is often complicated,” said Dr. Friedlander of the University of California, San Diego.

Consider the age of the child, severity and duration of disease, and how much body surface area is affected.

Bathing can be beneficial to atopic skin if it hydrates the stratum corneum and removes dirt, scales, and bugs, but breaks in the skin can occur during evaporation, so bathing and moisturizers together are better than either alone, Dr. Friedlander said.

She is a fan of ceramide-based creams for atopic dermatitis. “Ceramides can decrease the amount of steroid you use or perhaps you can use [them] instead of steroids and do as well,” she said.

If barrier repair does not work, the next step of the ladder is short circuiting inflammation. With corticosteroids for atopic dermatitis, use the weakest strength to do the job, blast and taper off, or consider weekend pulses of high potency steroids.

Topical calcineurin inhibitors are another therapeutic option. “There are a lot of data out there, so we know a lot about them,” she said.

Dr. Friedlander's relevant disclosures include being a consultant for Astellas, Graceway Pharmaceuticals, and Novartis. She also receives research support from Astellas, Novartis, Promius Pharma, and SkinMedica. SDEF and this news organization are owned by Elsevier.

SAN FRANCISCO — Start simple and use a step-wise approach to treat children with atopic dermatitis, Dr. Sheila Fallon Friedlander recommended.

“Atopic dermatitis matters so much because it can become infected, can impair physical and psychologic function, and has a tremendous effect on family quality of life,” Dr. Friedlander said at a seminar on women's and pediatric dermatology sponsored by Skin Disease Education Foundation.

Using a ladder analogy, start at the bottom with repair of the skin barrier. The next rung is an intervention to short circuit inflammation. Then take care of itching, treat infections, address triggers, and educate patients and their family.

Is the family compliant? “This is extremely important. You need to get family to buy in to a treatment plan that is often complicated,” said Dr. Friedlander of the University of California, San Diego.

Consider the age of the child, severity and duration of disease, and how much body surface area is affected.

Bathing can be beneficial to atopic skin if it hydrates the stratum corneum and removes dirt, scales, and bugs, but breaks in the skin can occur during evaporation, so bathing and moisturizers together are better than either alone, Dr. Friedlander said.

She is a fan of ceramide-based creams for atopic dermatitis. “Ceramides can decrease the amount of steroid you use or perhaps you can use [them] instead of steroids and do as well,” she said.

If barrier repair does not work, the next step of the ladder is short circuiting inflammation. With corticosteroids for atopic dermatitis, use the weakest strength to do the job, blast and taper off, or consider weekend pulses of high potency steroids.

Topical calcineurin inhibitors are another therapeutic option. “There are a lot of data out there, so we know a lot about them,” she said.

Dr. Friedlander's relevant disclosures include being a consultant for Astellas, Graceway Pharmaceuticals, and Novartis. She also receives research support from Astellas, Novartis, Promius Pharma, and SkinMedica. SDEF and this news organization are owned by Elsevier.

BUDAPEST, HUNGARY — Mild atopic dermatitis in patients with filaggrin mutations was associated with significantly greater skin barrier dysfunction than in patients with comparable wild-type atopic dermatitis in a comparative laboratory study.

This more pronounced epidermal barrier defect and skin permeability should allow greater penetration of antigens—which then draw an immune response resulting in contact sensitization and irritancy reactions—as well as predisposition to other atopic diseases such as hay fever and asthma, Dr. Sharizan Abdul-Ghaffar said at the annual meeting of the European Society for Dermatological Research.

This hypothesized chain of events was supported by the findings in the lab study of 13 patients with filaggrin-related atopic dermatitis (AD) and 45 controls with similarly mild AD without filaggrin mutations, according to Dr. Abdul-Ghaffar of the University of Edinburgh (Scotland). The subjects with filaggrin-related AD displayed significantly greater baseline transepidermal water loss on uninvolved flexor forearm skin than did controls. Moreover, the number of tape strips required to mechanically break the skin barrier, as signalled by achieving transepidermal water loss in excess of 20 g/m

A 24-hour application of the irritant sodium lauryl sulfate in various concentrations resulted in dose-dependent increased transepidermal water loss in both patient groups. The increases, however, were consistently greater in the patients with filaggrin mutations.

"This certainly suggests that filaggrin-related eczema patients are less able to cope with irritancy and would explain the increased likelihood of developing problems such as irritant hand dermatitis," she said.

Eleven of the 13 (85%) AD patients with filaggrin mutations had hay fever, compared with 22 of 45 (49%) controls, but the prevalence of asthma in the two groups was similar.

In patch testing using the European Standard Series, 3 of 7 (43%) subjects with filaggrin-related AD developed more than five positive reactions, compared with just 1 of 25 (4%) controls with wild-type AD.

"All of these results certainly support an underlying barrier defect in the pathogenesis of filaggrin-related eczema," concluded Dr. Abdul-Ghaffar.

Several audience members said that they would have expected to see even bigger differences in the test results between AD patients with and without filaggrin mutations.

Dr. Abdul-Ghaffar said the explanation may reside in the selection bias deliberately introduced in the study. Filaggrin-related AD is often at the more severe end of the disease spectrum, but to be eligible for this study patients had to have mild AD.

'This certainly suggests that filaggrin-related eczema patients are less able to cope with irritancy.'

Source DR. ABDUL-GHAFFAR

BUDAPEST, HUNGARY — Mild atopic dermatitis in patients with filaggrin mutations was associated with significantly greater skin barrier dysfunction than in patients with comparable wild-type atopic dermatitis in a comparative laboratory study.

This more pronounced epidermal barrier defect and skin permeability should allow greater penetration of antigens—which then draw an immune response resulting in contact sensitization and irritancy reactions—as well as predisposition to other atopic diseases such as hay fever and asthma, Dr. Sharizan Abdul-Ghaffar said at the annual meeting of the European Society for Dermatological Research.

This hypothesized chain of events was supported by the findings in the lab study of 13 patients with filaggrin-related atopic dermatitis (AD) and 45 controls with similarly mild AD without filaggrin mutations, according to Dr. Abdul-Ghaffar of the University of Edinburgh (Scotland). The subjects with filaggrin-related AD displayed significantly greater baseline transepidermal water loss on uninvolved flexor forearm skin than did controls. Moreover, the number of tape strips required to mechanically break the skin barrier, as signalled by achieving transepidermal water loss in excess of 20 g/m

A 24-hour application of the irritant sodium lauryl sulfate in various concentrations resulted in dose-dependent increased transepidermal water loss in both patient groups. The increases, however, were consistently greater in the patients with filaggrin mutations.

"This certainly suggests that filaggrin-related eczema patients are less able to cope with irritancy and would explain the increased likelihood of developing problems such as irritant hand dermatitis," she said.

Eleven of the 13 (85%) AD patients with filaggrin mutations had hay fever, compared with 22 of 45 (49%) controls, but the prevalence of asthma in the two groups was similar.

In patch testing using the European Standard Series, 3 of 7 (43%) subjects with filaggrin-related AD developed more than five positive reactions, compared with just 1 of 25 (4%) controls with wild-type AD.

"All of these results certainly support an underlying barrier defect in the pathogenesis of filaggrin-related eczema," concluded Dr. Abdul-Ghaffar.

Several audience members said that they would have expected to see even bigger differences in the test results between AD patients with and without filaggrin mutations.

Dr. Abdul-Ghaffar said the explanation may reside in the selection bias deliberately introduced in the study. Filaggrin-related AD is often at the more severe end of the disease spectrum, but to be eligible for this study patients had to have mild AD.

'This certainly suggests that filaggrin-related eczema patients are less able to cope with irritancy.'

Source DR. ABDUL-GHAFFAR

BUDAPEST, HUNGARY — Mild atopic dermatitis in patients with filaggrin mutations was associated with significantly greater skin barrier dysfunction than in patients with comparable wild-type atopic dermatitis in a comparative laboratory study.

This more pronounced epidermal barrier defect and skin permeability should allow greater penetration of antigens—which then draw an immune response resulting in contact sensitization and irritancy reactions—as well as predisposition to other atopic diseases such as hay fever and asthma, Dr. Sharizan Abdul-Ghaffar said at the annual meeting of the European Society for Dermatological Research.

This hypothesized chain of events was supported by the findings in the lab study of 13 patients with filaggrin-related atopic dermatitis (AD) and 45 controls with similarly mild AD without filaggrin mutations, according to Dr. Abdul-Ghaffar of the University of Edinburgh (Scotland). The subjects with filaggrin-related AD displayed significantly greater baseline transepidermal water loss on uninvolved flexor forearm skin than did controls. Moreover, the number of tape strips required to mechanically break the skin barrier, as signalled by achieving transepidermal water loss in excess of 20 g/m

A 24-hour application of the irritant sodium lauryl sulfate in various concentrations resulted in dose-dependent increased transepidermal water loss in both patient groups. The increases, however, were consistently greater in the patients with filaggrin mutations.

"This certainly suggests that filaggrin-related eczema patients are less able to cope with irritancy and would explain the increased likelihood of developing problems such as irritant hand dermatitis," she said.

Eleven of the 13 (85%) AD patients with filaggrin mutations had hay fever, compared with 22 of 45 (49%) controls, but the prevalence of asthma in the two groups was similar.

In patch testing using the European Standard Series, 3 of 7 (43%) subjects with filaggrin-related AD developed more than five positive reactions, compared with just 1 of 25 (4%) controls with wild-type AD.

"All of these results certainly support an underlying barrier defect in the pathogenesis of filaggrin-related eczema," concluded Dr. Abdul-Ghaffar.

Several audience members said that they would have expected to see even bigger differences in the test results between AD patients with and without filaggrin mutations.

Dr. Abdul-Ghaffar said the explanation may reside in the selection bias deliberately introduced in the study. Filaggrin-related AD is often at the more severe end of the disease spectrum, but to be eligible for this study patients had to have mild AD.

'This certainly suggests that filaggrin-related eczema patients are less able to cope with irritancy.'

Source DR. ABDUL-GHAFFAR

Budapest, Hungary — The calcineurin inhibitor pimecrolimus exerted more beneficial effects than betamethasone on the disrupted epidermal barrier of atopic dermatitis both structurally and immunologically, according to the results of a small randomized, double-blind study.

The take-away message from this study is that pimecrolimus (Elidel) may be the better option for long-term management of atopic dermatitis, Dr. Jens-Michael Jensen said at the annual congress of the European Society for Dermatological Research.

He reported on 15 atopic dermatitis patients with symmetrical lesions on their upper arms.

The patients were randomized to 3 weeks of twice-daily topical therapy with pimecrolimus 1% on one arm and betamethasone valerate cream 0.1% on the other.

Changes in epidermal barrier function were probed via electron microscopy, immunohistochemical staining, and gene array analysis of protein expression.

Betamethasone resulted in significantly greater clinical improvement and a more pronounced reduction in the epidermal hyperproliferation that is a hallmark of atopic dermatitis.

That being said, the change in epidermal proliferation induced by betamethasone went too far, with suppression to below-normal levels and epidermal thinning, whereas epidermal proliferation in the pimecrolimus-treated lesions was akin to that seen in healthy skin, according to Dr. Jensen.

The treatment-related ultrastructural changes seen through the electron microscope were more favorable with pimecrolimus, as were the changes in expression of genes playing key roles in skin immunologic function, according to Dr. Jensen of the University of Kiel (Germany).

Electron microscopy showed extensive baseline disruption of the lipid bilayers at the stratum granulosum and stratum corneum interface in lesional skin.

The integrity of this lipid bilayer is critical to a well-functioning skin barrier, he explained.

After pimecrolimus therapy, the lipid bilayer architecture became regular and continuous, as in normal skin, while after betamethasone therapy, the lipid bilayer remained irregular and disrupted.

At baseline, lesional skin contained just 9% physiological lamellar bodies, while healthy skin contained 91%.

After treatment with pimecrolimus, 82% of lamellar bodies identified on electron microscopy were categorized as physiological.

In contrast, following betamethasone therapy only 9% of lamellar bodies were categorized as physiological—the same as in untreated atopic dermatitis.

Current thinking is that barrier repair prevents penetration of allergens into the skin, with subsequent immune sensitization and inflammation.

The emerging concept of atopic dermatitis is that barrier disruption is not a secondary event occurring in response to immunologic reaction, but rather is a primary event, he explained.

The expression of psoriasin, a chemotactic protein that plays an important role in fighting off penetration of the skin by Escherichia coli, essentially disappeared after 3 weeks of betamethasone therapy. So did expression of other antimicrobial peptides involved in innate immunity, including human beta-defensin-2 and -3 and RNase 7. The expression of genes controlling for stratum corneum keratin production was suppressed as well.

"This decrease is related to broad downregulation of general protein synthesis by the corticosteroid, which is not what we see with pimecrolimus," Dr. Jensen noted.

The expression of antimicrobial peptides was only mildly to moderately suppressed following pimecrolimus therapy. And the gene expression pattern for keratins became normalized, he said.

Dr. Jensen disclosed that the study was supported by Novartis (manufacturer of Elidel), which provided him with a travel grant.

Budapest, Hungary — The calcineurin inhibitor pimecrolimus exerted more beneficial effects than betamethasone on the disrupted epidermal barrier of atopic dermatitis both structurally and immunologically, according to the results of a small randomized, double-blind study.

The take-away message from this study is that pimecrolimus (Elidel) may be the better option for long-term management of atopic dermatitis, Dr. Jens-Michael Jensen said at the annual congress of the European Society for Dermatological Research.

He reported on 15 atopic dermatitis patients with symmetrical lesions on their upper arms.

The patients were randomized to 3 weeks of twice-daily topical therapy with pimecrolimus 1% on one arm and betamethasone valerate cream 0.1% on the other.

Changes in epidermal barrier function were probed via electron microscopy, immunohistochemical staining, and gene array analysis of protein expression.

Betamethasone resulted in significantly greater clinical improvement and a more pronounced reduction in the epidermal hyperproliferation that is a hallmark of atopic dermatitis.

That being said, the change in epidermal proliferation induced by betamethasone went too far, with suppression to below-normal levels and epidermal thinning, whereas epidermal proliferation in the pimecrolimus-treated lesions was akin to that seen in healthy skin, according to Dr. Jensen.

The treatment-related ultrastructural changes seen through the electron microscope were more favorable with pimecrolimus, as were the changes in expression of genes playing key roles in skin immunologic function, according to Dr. Jensen of the University of Kiel (Germany).

Electron microscopy showed extensive baseline disruption of the lipid bilayers at the stratum granulosum and stratum corneum interface in lesional skin.

The integrity of this lipid bilayer is critical to a well-functioning skin barrier, he explained.

After pimecrolimus therapy, the lipid bilayer architecture became regular and continuous, as in normal skin, while after betamethasone therapy, the lipid bilayer remained irregular and disrupted.

At baseline, lesional skin contained just 9% physiological lamellar bodies, while healthy skin contained 91%.

After treatment with pimecrolimus, 82% of lamellar bodies identified on electron microscopy were categorized as physiological.

In contrast, following betamethasone therapy only 9% of lamellar bodies were categorized as physiological—the same as in untreated atopic dermatitis.

Current thinking is that barrier repair prevents penetration of allergens into the skin, with subsequent immune sensitization and inflammation.

The emerging concept of atopic dermatitis is that barrier disruption is not a secondary event occurring in response to immunologic reaction, but rather is a primary event, he explained.

The expression of psoriasin, a chemotactic protein that plays an important role in fighting off penetration of the skin by Escherichia coli, essentially disappeared after 3 weeks of betamethasone therapy. So did expression of other antimicrobial peptides involved in innate immunity, including human beta-defensin-2 and -3 and RNase 7. The expression of genes controlling for stratum corneum keratin production was suppressed as well.

"This decrease is related to broad downregulation of general protein synthesis by the corticosteroid, which is not what we see with pimecrolimus," Dr. Jensen noted.

The expression of antimicrobial peptides was only mildly to moderately suppressed following pimecrolimus therapy. And the gene expression pattern for keratins became normalized, he said.

Dr. Jensen disclosed that the study was supported by Novartis (manufacturer of Elidel), which provided him with a travel grant.

Budapest, Hungary — The calcineurin inhibitor pimecrolimus exerted more beneficial effects than betamethasone on the disrupted epidermal barrier of atopic dermatitis both structurally and immunologically, according to the results of a small randomized, double-blind study.

The take-away message from this study is that pimecrolimus (Elidel) may be the better option for long-term management of atopic dermatitis, Dr. Jens-Michael Jensen said at the annual congress of the European Society for Dermatological Research.

He reported on 15 atopic dermatitis patients with symmetrical lesions on their upper arms.

The patients were randomized to 3 weeks of twice-daily topical therapy with pimecrolimus 1% on one arm and betamethasone valerate cream 0.1% on the other.

Changes in epidermal barrier function were probed via electron microscopy, immunohistochemical staining, and gene array analysis of protein expression.

Betamethasone resulted in significantly greater clinical improvement and a more pronounced reduction in the epidermal hyperproliferation that is a hallmark of atopic dermatitis.

That being said, the change in epidermal proliferation induced by betamethasone went too far, with suppression to below-normal levels and epidermal thinning, whereas epidermal proliferation in the pimecrolimus-treated lesions was akin to that seen in healthy skin, according to Dr. Jensen.

The treatment-related ultrastructural changes seen through the electron microscope were more favorable with pimecrolimus, as were the changes in expression of genes playing key roles in skin immunologic function, according to Dr. Jensen of the University of Kiel (Germany).

Electron microscopy showed extensive baseline disruption of the lipid bilayers at the stratum granulosum and stratum corneum interface in lesional skin.

The integrity of this lipid bilayer is critical to a well-functioning skin barrier, he explained.

After pimecrolimus therapy, the lipid bilayer architecture became regular and continuous, as in normal skin, while after betamethasone therapy, the lipid bilayer remained irregular and disrupted.

At baseline, lesional skin contained just 9% physiological lamellar bodies, while healthy skin contained 91%.

After treatment with pimecrolimus, 82% of lamellar bodies identified on electron microscopy were categorized as physiological.

In contrast, following betamethasone therapy only 9% of lamellar bodies were categorized as physiological—the same as in untreated atopic dermatitis.

Current thinking is that barrier repair prevents penetration of allergens into the skin, with subsequent immune sensitization and inflammation.

The emerging concept of atopic dermatitis is that barrier disruption is not a secondary event occurring in response to immunologic reaction, but rather is a primary event, he explained.

The expression of psoriasin, a chemotactic protein that plays an important role in fighting off penetration of the skin by Escherichia coli, essentially disappeared after 3 weeks of betamethasone therapy. So did expression of other antimicrobial peptides involved in innate immunity, including human beta-defensin-2 and -3 and RNase 7. The expression of genes controlling for stratum corneum keratin production was suppressed as well.

"This decrease is related to broad downregulation of general protein synthesis by the corticosteroid, which is not what we see with pimecrolimus," Dr. Jensen noted.

The expression of antimicrobial peptides was only mildly to moderately suppressed following pimecrolimus therapy. And the gene expression pattern for keratins became normalized, he said.

Dr. Jensen disclosed that the study was supported by Novartis (manufacturer of Elidel), which provided him with a travel grant.

Food patch test is reproducible, safe, and specific

My stance is that there is a place for atopy patch testing for food allergy in your practice, for a number of reasons.

First, there is a clinical need for this test: We do not have any other test for non–IgE-mediated food allergies, such as food protein–induced enterocolitis, eosinophilic esophagitis, and potentially atopic dermatitis.

Second, the test is well standardized with respect to how reagents are applied, the time until results are read, and the method of reading. In fact, standardization in these respects is better than that for skin prick testing.

One problem with atopy patch tests—I will concede—is that we don't have standardized reagents, but this is also somewhat of an issue for skin prick tests.

Third, atopy patch testing is highly reproducible, with a reproducibility rate of 94% when it is performed on the back (Acta. Derm. Venereol. 2005;85:147-51). The reproducibility rate is lower, at 69%, when the test is performed on the arms.

Fourth, testing is safe. One study among 503 children given atopy patch tests found that 2.2% experienced contact dermatitis and itching, 1.1% had a reaction to the adhesive tape, and 0.2%—a single child—had a wheezing episode (Clin. Pediatrics 2008;47:602-3).

Fifth, atopy patch testing has good diagnostic performance. If we compare it with skin prick testing for the diagnosis of IgE-mediated food allergies to milk, eggs, wheat, and peanuts, it is more specific, although somewhat less sensitive.

Positive and negative predictive values also favor the atopy patch test in children with eosinophilic esophagitis (J. Allergy Clin. Immunol. 2007;119:509-11).

Finally, both the American College of Allergy, Asthma, and Immunology (ACAAI) and the European Academy of Allergy and Clinical Immunology (EAACI) have recognized a role for atopy patch testing as an adjunctive tool in the diagnosis of food allergy.

So academies from both sides of the ocean agree—atopy patch testing has a place in your practice.

By Jonathan M. Spergel, M.D., Ph.D., associate professor of pediatrics and director of the Food Allergy Center at Children's Hospital of Philadelphia. Dr. Spergel disclosed that he has served as a speaker or consultant for GlaxoSmithKline, AstraZeneca, Schering-Plough, and Nutricia, and has received grant support from Ception and Novartis

The food patch test seldom adds information

We already have several tests that can be used for the diagnosis of food allergy: skin prick tests, serum food-specific IgE levels, and an oral food challenge. So we have to ask if atopy patch testing adds anything.

There are two main scenarios in which physicians may consider using patch testing.

In one scenario, a patient with suspected food allergy has a positive skin prick test result and a positive serum IgE level for the food. The question here is whether the patient is clinically intolerant of the food.

Among children with food-specific IgE, patch testing misses two-thirds of those who are clinically intolerant to the food in an oral challenge (J. Allergy Clin. Immunol. 2006;118:923-9). And adding these results to the results of skin prick testing and food-specific IgE allows only 0.5%-7% of children to forgo an oral food challenge.

In another scenario, a patient has symptoms or a syndrome (such as gastrointestinal symptoms or atopic dermatitis), but has negative skin prick test results and a negative serum IgE level. The question here is whether the food is causing the symptoms or syndrome.

In a study among children and adults with atopic dermatitis in remission who had negative skin prick tests and negative serum food-specific IgE, only 17% had a positive atopy patch test for the respective food (Allergy 2004;59:1318-25).

At the same time, 4%-11% of unselected children in the general population have positive food patch test results (Pediatr. Allergy Immunol. 2008;19:599-604).

Interpretation of atopy patch tests is not always straightforward. Some patients develop the angry back syndrome, which may be mistakenly called a positive result. And 8% of patients overall experience some type of adverse effect (Allergy 2006;61:1377-84).

Finally, the previously mentioned professional organizations recommend use of atopy patch testing for foods in selected cases.

In sum, atopy patch testing has not yet gained a place in the diagnosis of food allergy. It is not superior to skin prick tests or food-specific IgE, and it does not replace a properly indicated and performed oral food challenge.

By Dr. Amal H. Assa'ad, professor of clinical pediatrics and director of the Food Allergy and Eosinophilia Clinic at the Children's Hospital Medical Center in Cincinnati. She disclosed being a consultant to GlaxoSmithKline.

Food patch test is reproducible, safe, and specific

My stance is that there is a place for atopy patch testing for food allergy in your practice, for a number of reasons.

First, there is a clinical need for this test: We do not have any other test for non–IgE-mediated food allergies, such as food protein–induced enterocolitis, eosinophilic esophagitis, and potentially atopic dermatitis.

Second, the test is well standardized with respect to how reagents are applied, the time until results are read, and the method of reading. In fact, standardization in these respects is better than that for skin prick testing.

One problem with atopy patch tests—I will concede—is that we don't have standardized reagents, but this is also somewhat of an issue for skin prick tests.

Third, atopy patch testing is highly reproducible, with a reproducibility rate of 94% when it is performed on the back (Acta. Derm. Venereol. 2005;85:147-51). The reproducibility rate is lower, at 69%, when the test is performed on the arms.

Fourth, testing is safe. One study among 503 children given atopy patch tests found that 2.2% experienced contact dermatitis and itching, 1.1% had a reaction to the adhesive tape, and 0.2%—a single child—had a wheezing episode (Clin. Pediatrics 2008;47:602-3).

Fifth, atopy patch testing has good diagnostic performance. If we compare it with skin prick testing for the diagnosis of IgE-mediated food allergies to milk, eggs, wheat, and peanuts, it is more specific, although somewhat less sensitive.

Positive and negative predictive values also favor the atopy patch test in children with eosinophilic esophagitis (J. Allergy Clin. Immunol. 2007;119:509-11).

Finally, both the American College of Allergy, Asthma, and Immunology (ACAAI) and the European Academy of Allergy and Clinical Immunology (EAACI) have recognized a role for atopy patch testing as an adjunctive tool in the diagnosis of food allergy.

So academies from both sides of the ocean agree—atopy patch testing has a place in your practice.

By Jonathan M. Spergel, M.D., Ph.D., associate professor of pediatrics and director of the Food Allergy Center at Children's Hospital of Philadelphia. Dr. Spergel disclosed that he has served as a speaker or consultant for GlaxoSmithKline, AstraZeneca, Schering-Plough, and Nutricia, and has received grant support from Ception and Novartis

The food patch test seldom adds information

We already have several tests that can be used for the diagnosis of food allergy: skin prick tests, serum food-specific IgE levels, and an oral food challenge. So we have to ask if atopy patch testing adds anything.

There are two main scenarios in which physicians may consider using patch testing.

In one scenario, a patient with suspected food allergy has a positive skin prick test result and a positive serum IgE level for the food. The question here is whether the patient is clinically intolerant of the food.

Among children with food-specific IgE, patch testing misses two-thirds of those who are clinically intolerant to the food in an oral challenge (J. Allergy Clin. Immunol. 2006;118:923-9). And adding these results to the results of skin prick testing and food-specific IgE allows only 0.5%-7% of children to forgo an oral food challenge.

In another scenario, a patient has symptoms or a syndrome (such as gastrointestinal symptoms or atopic dermatitis), but has negative skin prick test results and a negative serum IgE level. The question here is whether the food is causing the symptoms or syndrome.

In a study among children and adults with atopic dermatitis in remission who had negative skin prick tests and negative serum food-specific IgE, only 17% had a positive atopy patch test for the respective food (Allergy 2004;59:1318-25).

At the same time, 4%-11% of unselected children in the general population have positive food patch test results (Pediatr. Allergy Immunol. 2008;19:599-604).

Interpretation of atopy patch tests is not always straightforward. Some patients develop the angry back syndrome, which may be mistakenly called a positive result. And 8% of patients overall experience some type of adverse effect (Allergy 2006;61:1377-84).

Finally, the previously mentioned professional organizations recommend use of atopy patch testing for foods in selected cases.

In sum, atopy patch testing has not yet gained a place in the diagnosis of food allergy. It is not superior to skin prick tests or food-specific IgE, and it does not replace a properly indicated and performed oral food challenge.

By Dr. Amal H. Assa'ad, professor of clinical pediatrics and director of the Food Allergy and Eosinophilia Clinic at the Children's Hospital Medical Center in Cincinnati. She disclosed being a consultant to GlaxoSmithKline.

Food patch test is reproducible, safe, and specific

My stance is that there is a place for atopy patch testing for food allergy in your practice, for a number of reasons.

First, there is a clinical need for this test: We do not have any other test for non–IgE-mediated food allergies, such as food protein–induced enterocolitis, eosinophilic esophagitis, and potentially atopic dermatitis.

Second, the test is well standardized with respect to how reagents are applied, the time until results are read, and the method of reading. In fact, standardization in these respects is better than that for skin prick testing.

One problem with atopy patch tests—I will concede—is that we don't have standardized reagents, but this is also somewhat of an issue for skin prick tests.

Third, atopy patch testing is highly reproducible, with a reproducibility rate of 94% when it is performed on the back (Acta. Derm. Venereol. 2005;85:147-51). The reproducibility rate is lower, at 69%, when the test is performed on the arms.

Fourth, testing is safe. One study among 503 children given atopy patch tests found that 2.2% experienced contact dermatitis and itching, 1.1% had a reaction to the adhesive tape, and 0.2%—a single child—had a wheezing episode (Clin. Pediatrics 2008;47:602-3).

Fifth, atopy patch testing has good diagnostic performance. If we compare it with skin prick testing for the diagnosis of IgE-mediated food allergies to milk, eggs, wheat, and peanuts, it is more specific, although somewhat less sensitive.

Positive and negative predictive values also favor the atopy patch test in children with eosinophilic esophagitis (J. Allergy Clin. Immunol. 2007;119:509-11).

Finally, both the American College of Allergy, Asthma, and Immunology (ACAAI) and the European Academy of Allergy and Clinical Immunology (EAACI) have recognized a role for atopy patch testing as an adjunctive tool in the diagnosis of food allergy.

So academies from both sides of the ocean agree—atopy patch testing has a place in your practice.

By Jonathan M. Spergel, M.D., Ph.D., associate professor of pediatrics and director of the Food Allergy Center at Children's Hospital of Philadelphia. Dr. Spergel disclosed that he has served as a speaker or consultant for GlaxoSmithKline, AstraZeneca, Schering-Plough, and Nutricia, and has received grant support from Ception and Novartis

The food patch test seldom adds information

We already have several tests that can be used for the diagnosis of food allergy: skin prick tests, serum food-specific IgE levels, and an oral food challenge. So we have to ask if atopy patch testing adds anything.

There are two main scenarios in which physicians may consider using patch testing.

In one scenario, a patient with suspected food allergy has a positive skin prick test result and a positive serum IgE level for the food. The question here is whether the patient is clinically intolerant of the food.

Among children with food-specific IgE, patch testing misses two-thirds of those who are clinically intolerant to the food in an oral challenge (J. Allergy Clin. Immunol. 2006;118:923-9). And adding these results to the results of skin prick testing and food-specific IgE allows only 0.5%-7% of children to forgo an oral food challenge.

In another scenario, a patient has symptoms or a syndrome (such as gastrointestinal symptoms or atopic dermatitis), but has negative skin prick test results and a negative serum IgE level. The question here is whether the food is causing the symptoms or syndrome.

In a study among children and adults with atopic dermatitis in remission who had negative skin prick tests and negative serum food-specific IgE, only 17% had a positive atopy patch test for the respective food (Allergy 2004;59:1318-25).

At the same time, 4%-11% of unselected children in the general population have positive food patch test results (Pediatr. Allergy Immunol. 2008;19:599-604).

Interpretation of atopy patch tests is not always straightforward. Some patients develop the angry back syndrome, which may be mistakenly called a positive result. And 8% of patients overall experience some type of adverse effect (Allergy 2006;61:1377-84).

Finally, the previously mentioned professional organizations recommend use of atopy patch testing for foods in selected cases.

In sum, atopy patch testing has not yet gained a place in the diagnosis of food allergy. It is not superior to skin prick tests or food-specific IgE, and it does not replace a properly indicated and performed oral food challenge.

By Dr. Amal H. Assa'ad, professor of clinical pediatrics and director of the Food Allergy and Eosinophilia Clinic at the Children's Hospital Medical Center in Cincinnati. She disclosed being a consultant to GlaxoSmithKline.

PRAGUE — Steroid-resistant hand eczema responds almost half the time to treatment with oral alitretinoin, data from randomized clinical trials have shown.

Furthermore, 80% of patients who relapsed after alitretinoin treatment was stopped regained disease control when treated again with the agent, Dr. Uwe Hillen of University Clinic in Essen, Germany, reported at the International Congress of Dermatology.

“Alitretinoin produced improvement in all of the individual signs and symptoms of chronic hand eczema,” said Dr. Hillen. “Patients who relapse after initial treatment can be effectively retreated with alitretinoin, suggesting it is a suitable, intermittent treatment option for the long-term management of this chronic, relapsing disease.”

Hand eczema often evolves into a chronic condition, even with strict avoidance of environmental triggers. Standard therapy is topical corticosteroids, and patients have few alternatives if the combination of emollients and topical steroids doesn't work.

Dr. Hillen summarized data from three phase III clinical trials, the largest involving 1,032 patients enrolled at 111 sites in Europe and Canada. Patients in that trial were randomized to oral alitretinoin 10 mg or 30 mg once daily or placebo for 12 or 24 weeks. All patients were advised to avoid known triggers and irritants. The primary end point was the proportion of patients who had a Physician Global Assessment rating of “clear” or “almost clear” at the end of treatment.

Almost half (48%) of patients treated with 30 mg of alitretinoin had complete responses, as did 28% of patients treated with 10 mg, while just 17% of placebo-treated patients had complete or almost complete responses, Dr. Hillen reported.

The second study, a safety study, involved 249 patients from 37 centers in Europe and Canada. All had chronic hand eczema unresponsive to topical steroids, and received open-label alitretinoin 30 mg daily for as long as 24 weeks. Again, almost half (47%) of patients in the alitretinoin group had complete responses, Dr. Hillen said. When response criteria were expanded to include “mild disease,” the response rate increased to 64%.

The third trial included two groups of patients from the first study: 117 patients who initially responded to alitretinoin but relapsed within 24 weeks, and 243 patients who previously had not responded to initial treatment.

Patients in the relapse group were randomized to receive their initial dose of alitretinoin or placebo. Patients in the second group received open-label alitretinoin 30 mg. Among patients who had relapsed, 80% who were randomized a second time to alitretinoin 30 mg had clear or almost clear hands at the end of the study, compared with 8% of patients receiving placebo. Patients retreated with alitretinoin 10 mg had a response rate of 48%, compared with 10% in patients on placebo.

Topical alitretinoin gel 0.1% is approved for the treatment of cutaneous lesions in patients with AIDS-related Kaposi's sarcoma, but oral alitretinoin is not available.

Dr. Hillen reported no disclosures.

PRAGUE — Steroid-resistant hand eczema responds almost half the time to treatment with oral alitretinoin, data from randomized clinical trials have shown.

Furthermore, 80% of patients who relapsed after alitretinoin treatment was stopped regained disease control when treated again with the agent, Dr. Uwe Hillen of University Clinic in Essen, Germany, reported at the International Congress of Dermatology.

“Alitretinoin produced improvement in all of the individual signs and symptoms of chronic hand eczema,” said Dr. Hillen. “Patients who relapse after initial treatment can be effectively retreated with alitretinoin, suggesting it is a suitable, intermittent treatment option for the long-term management of this chronic, relapsing disease.”

Hand eczema often evolves into a chronic condition, even with strict avoidance of environmental triggers. Standard therapy is topical corticosteroids, and patients have few alternatives if the combination of emollients and topical steroids doesn't work.

Dr. Hillen summarized data from three phase III clinical trials, the largest involving 1,032 patients enrolled at 111 sites in Europe and Canada. Patients in that trial were randomized to oral alitretinoin 10 mg or 30 mg once daily or placebo for 12 or 24 weeks. All patients were advised to avoid known triggers and irritants. The primary end point was the proportion of patients who had a Physician Global Assessment rating of “clear” or “almost clear” at the end of treatment.

Almost half (48%) of patients treated with 30 mg of alitretinoin had complete responses, as did 28% of patients treated with 10 mg, while just 17% of placebo-treated patients had complete or almost complete responses, Dr. Hillen reported.

The second study, a safety study, involved 249 patients from 37 centers in Europe and Canada. All had chronic hand eczema unresponsive to topical steroids, and received open-label alitretinoin 30 mg daily for as long as 24 weeks. Again, almost half (47%) of patients in the alitretinoin group had complete responses, Dr. Hillen said. When response criteria were expanded to include “mild disease,” the response rate increased to 64%.

The third trial included two groups of patients from the first study: 117 patients who initially responded to alitretinoin but relapsed within 24 weeks, and 243 patients who previously had not responded to initial treatment.

Patients in the relapse group were randomized to receive their initial dose of alitretinoin or placebo. Patients in the second group received open-label alitretinoin 30 mg. Among patients who had relapsed, 80% who were randomized a second time to alitretinoin 30 mg had clear or almost clear hands at the end of the study, compared with 8% of patients receiving placebo. Patients retreated with alitretinoin 10 mg had a response rate of 48%, compared with 10% in patients on placebo.

Topical alitretinoin gel 0.1% is approved for the treatment of cutaneous lesions in patients with AIDS-related Kaposi's sarcoma, but oral alitretinoin is not available.

Dr. Hillen reported no disclosures.

PRAGUE — Steroid-resistant hand eczema responds almost half the time to treatment with oral alitretinoin, data from randomized clinical trials have shown.

Furthermore, 80% of patients who relapsed after alitretinoin treatment was stopped regained disease control when treated again with the agent, Dr. Uwe Hillen of University Clinic in Essen, Germany, reported at the International Congress of Dermatology.

“Alitretinoin produced improvement in all of the individual signs and symptoms of chronic hand eczema,” said Dr. Hillen. “Patients who relapse after initial treatment can be effectively retreated with alitretinoin, suggesting it is a suitable, intermittent treatment option for the long-term management of this chronic, relapsing disease.”

Hand eczema often evolves into a chronic condition, even with strict avoidance of environmental triggers. Standard therapy is topical corticosteroids, and patients have few alternatives if the combination of emollients and topical steroids doesn't work.

Dr. Hillen summarized data from three phase III clinical trials, the largest involving 1,032 patients enrolled at 111 sites in Europe and Canada. Patients in that trial were randomized to oral alitretinoin 10 mg or 30 mg once daily or placebo for 12 or 24 weeks. All patients were advised to avoid known triggers and irritants. The primary end point was the proportion of patients who had a Physician Global Assessment rating of “clear” or “almost clear” at the end of treatment.

Almost half (48%) of patients treated with 30 mg of alitretinoin had complete responses, as did 28% of patients treated with 10 mg, while just 17% of placebo-treated patients had complete or almost complete responses, Dr. Hillen reported.

The second study, a safety study, involved 249 patients from 37 centers in Europe and Canada. All had chronic hand eczema unresponsive to topical steroids, and received open-label alitretinoin 30 mg daily for as long as 24 weeks. Again, almost half (47%) of patients in the alitretinoin group had complete responses, Dr. Hillen said. When response criteria were expanded to include “mild disease,” the response rate increased to 64%.

The third trial included two groups of patients from the first study: 117 patients who initially responded to alitretinoin but relapsed within 24 weeks, and 243 patients who previously had not responded to initial treatment.

Patients in the relapse group were randomized to receive their initial dose of alitretinoin or placebo. Patients in the second group received open-label alitretinoin 30 mg. Among patients who had relapsed, 80% who were randomized a second time to alitretinoin 30 mg had clear or almost clear hands at the end of the study, compared with 8% of patients receiving placebo. Patients retreated with alitretinoin 10 mg had a response rate of 48%, compared with 10% in patients on placebo.

Topical alitretinoin gel 0.1% is approved for the treatment of cutaneous lesions in patients with AIDS-related Kaposi's sarcoma, but oral alitretinoin is not available.

Dr. Hillen reported no disclosures.

PHILADELPHIA — Community-associated methicillin-resistant Staphylococcus aureus skin infections occur significantly less often among children with atopic dermatitis than among other outpatients with skin and soft tissue infections, based on a retrospective study of 78 children.

Children with atopic dermatitis (AD) and Staphylococcus aureus skin infections had a relatively low incidence (14%) of methicillin resistance, much lower than the rate noted (45.5%) in other outpatient services during the same period, Dr. Catalina Matiz and her colleagues wrote in a poster presented at the annual meeting of the Society for Pediatric Dermatology.

Dr. Matiz, a postdoctoral fellow at Rady Children's Hospital in San Diego, and her coinvestigators conducted a retrospective chart review of 78 children with super-infected AD seen at the Rady pediatric and adolescent dermatology clinic between June 2007 and June 2008. The children had a positive skin culture for S. aureus.

They compared these data with all skin and soft tissue infection outpatient samples sent to the hospital's microbiology lab during the same period, and also with those sent during January 2000 through January 2001 (excluding samples from the dermatology clinic).

The CA-MRSA rate for samples from outpatient services from 2000-2001 was 4% (192 S. aureus-positive cultures). The outpatient services' rates increase from 2000-2001 to 2007-2008, highlight the sharp increase in CA-MRSA over the last several years, Dr. Matiz noted.

The rate of community-associated methicillin-sensitive S. aureus among patients with AD was 86%. In comparison, the CA-MSSA rate for other outpatient services during the same period was 55%. The CA-MSSA rate for outpatient services from 2000-2001 was 96%.

Interestingly, the investigators found that prior history of hospitalization, eczema severity, age, gender and prior antibiotic treatment had no impact on risk of methicillin resistance or sensitivity in these patients.

For the patients with AD, positive S. aureus cultures were most common among patients aged 1-4 years (26%), followed by those aged 5-9 years (24%), and those less than a year (23%).

The double diffusion test (D-test)—which is used to assess inducible resistance to clindamycin—was performed for 576 of the CA-MRSA samples from the hospital's lab in 2008. In all, 2% were positive for clindamycin-inducible resistance. However, none of the D-tests performed on cultures from patients with AD were positive. D-tests were performed for six of nine cultures that showed erythromycin resistance among patients with AD.

The findings are striking. “It's absolutely counterintuitive because if you think of patients with AD as being more at risk for infection, you would think that at the very least they would have the same rate as that occurring in the regular population,” said Dr. Sheila Fallon Friedlander, a study coauthor and a professor of pediatrics and medicine at the University of California, San Diego.

Based on conversations with colleagues, other pediatric dermatologists seem to be seeing similar patterns, said Dr. Friedlander. The researchers are not sure why these children have fewer CA-MRSA infections, though they have a couple of ideas.

It may be that “because these kids are colonized already so much of the time with regular S. aureus, that it may exert sort of a protective effect against CA-MRSA,” Dr. Friedlander said.

In addition, patients with AD tend to present more often with multiple lesions. “That may also play a role in this. It may be that our atopic patients are presenting with secondarily-infected lesions that are distinct from the abscesses and the folliculitis that we are seeing in the community,” she noted.

The findings “have informed the way that I prescribe medications for my patients,” she said. The results suggest that more standard antibiotic drugs with fewer side effects—like cephalosporins—can be used first, especially while waiting for culture results. This could not only reduce costs but also save patients from more serious side effects of antibiotics used for resistant pathogens.

In addition, it would help to reduce selection of more resistant bacteria. “It [could protect] our bigger gun drugs—reserving them for when you really need them,” said Dr. Friedlander, who added that it is important to factor in local demographics about CA-MRSA infection when deciding on a treatment.

Dr. Friedlander pointed out that while the findings are very interesting, this is a small study. “I think it's an interesting first step,” she said. Further prospective studies, looking at both CA-MRSA colonization and infection rates in children with AD, will be important to confirm these results.

In a separate study also presented at the meeting, Canadian researchers found a MRSA colonization rate of 0.5% among 200 pediatric patients with AD, and a S. aureus colonization rate of 61%.

The researchers collected a total of 400 swabs from the nares and open areas/folds of ADpatients (aged 1 month-18 years) with intact skin. Severity of AD was assessed using the an AD severity score, said Dr. Alexandra Balma-Mena, a resident at the Hospital for Sick Children in Toronto. A score of 0-12 was considered mild disease, a score of 13-18 was considered moderate, and a score of 19-25 was considered severe.

More of the patients were male (57%); the average age was 5 years. Most patients had mild disease (66%), followed by moderate (30%), and severe (4%).

Dr. Sheila Fallon Friedlander (left) and Dr. Catalina Matiz found that children with atopic dermatitis and S. aureus had a relatively lower incidence of methicillin resistance.

Source Courtesy Rady Children's Hospital in San Diego

PHILADELPHIA — Community-associated methicillin-resistant Staphylococcus aureus skin infections occur significantly less often among children with atopic dermatitis than among other outpatients with skin and soft tissue infections, based on a retrospective study of 78 children.

Children with atopic dermatitis (AD) and Staphylococcus aureus skin infections had a relatively low incidence (14%) of methicillin resistance, much lower than the rate noted (45.5%) in other outpatient services during the same period, Dr. Catalina Matiz and her colleagues wrote in a poster presented at the annual meeting of the Society for Pediatric Dermatology.

Dr. Matiz, a postdoctoral fellow at Rady Children's Hospital in San Diego, and her coinvestigators conducted a retrospective chart review of 78 children with super-infected AD seen at the Rady pediatric and adolescent dermatology clinic between June 2007 and June 2008. The children had a positive skin culture for S. aureus.

They compared these data with all skin and soft tissue infection outpatient samples sent to the hospital's microbiology lab during the same period, and also with those sent during January 2000 through January 2001 (excluding samples from the dermatology clinic).

The CA-MRSA rate for samples from outpatient services from 2000-2001 was 4% (192 S. aureus-positive cultures). The outpatient services' rates increase from 2000-2001 to 2007-2008, highlight the sharp increase in CA-MRSA over the last several years, Dr. Matiz noted.

The rate of community-associated methicillin-sensitive S. aureus among patients with AD was 86%. In comparison, the CA-MSSA rate for other outpatient services during the same period was 55%. The CA-MSSA rate for outpatient services from 2000-2001 was 96%.

Interestingly, the investigators found that prior history of hospitalization, eczema severity, age, gender and prior antibiotic treatment had no impact on risk of methicillin resistance or sensitivity in these patients.

For the patients with AD, positive S. aureus cultures were most common among patients aged 1-4 years (26%), followed by those aged 5-9 years (24%), and those less than a year (23%).

The double diffusion test (D-test)—which is used to assess inducible resistance to clindamycin—was performed for 576 of the CA-MRSA samples from the hospital's lab in 2008. In all, 2% were positive for clindamycin-inducible resistance. However, none of the D-tests performed on cultures from patients with AD were positive. D-tests were performed for six of nine cultures that showed erythromycin resistance among patients with AD.

The findings are striking. “It's absolutely counterintuitive because if you think of patients with AD as being more at risk for infection, you would think that at the very least they would have the same rate as that occurring in the regular population,” said Dr. Sheila Fallon Friedlander, a study coauthor and a professor of pediatrics and medicine at the University of California, San Diego.

Based on conversations with colleagues, other pediatric dermatologists seem to be seeing similar patterns, said Dr. Friedlander. The researchers are not sure why these children have fewer CA-MRSA infections, though they have a couple of ideas.

It may be that “because these kids are colonized already so much of the time with regular S. aureus, that it may exert sort of a protective effect against CA-MRSA,” Dr. Friedlander said.

In addition, patients with AD tend to present more often with multiple lesions. “That may also play a role in this. It may be that our atopic patients are presenting with secondarily-infected lesions that are distinct from the abscesses and the folliculitis that we are seeing in the community,” she noted.

The findings “have informed the way that I prescribe medications for my patients,” she said. The results suggest that more standard antibiotic drugs with fewer side effects—like cephalosporins—can be used first, especially while waiting for culture results. This could not only reduce costs but also save patients from more serious side effects of antibiotics used for resistant pathogens.

In addition, it would help to reduce selection of more resistant bacteria. “It [could protect] our bigger gun drugs—reserving them for when you really need them,” said Dr. Friedlander, who added that it is important to factor in local demographics about CA-MRSA infection when deciding on a treatment.

Dr. Friedlander pointed out that while the findings are very interesting, this is a small study. “I think it's an interesting first step,” she said. Further prospective studies, looking at both CA-MRSA colonization and infection rates in children with AD, will be important to confirm these results.

In a separate study also presented at the meeting, Canadian researchers found a MRSA colonization rate of 0.5% among 200 pediatric patients with AD, and a S. aureus colonization rate of 61%.

The researchers collected a total of 400 swabs from the nares and open areas/folds of ADpatients (aged 1 month-18 years) with intact skin. Severity of AD was assessed using the an AD severity score, said Dr. Alexandra Balma-Mena, a resident at the Hospital for Sick Children in Toronto. A score of 0-12 was considered mild disease, a score of 13-18 was considered moderate, and a score of 19-25 was considered severe.

More of the patients were male (57%); the average age was 5 years. Most patients had mild disease (66%), followed by moderate (30%), and severe (4%).

Dr. Sheila Fallon Friedlander (left) and Dr. Catalina Matiz found that children with atopic dermatitis and S. aureus had a relatively lower incidence of methicillin resistance.

Source Courtesy Rady Children's Hospital in San Diego

PHILADELPHIA — Community-associated methicillin-resistant Staphylococcus aureus skin infections occur significantly less often among children with atopic dermatitis than among other outpatients with skin and soft tissue infections, based on a retrospective study of 78 children.

Children with atopic dermatitis (AD) and Staphylococcus aureus skin infections had a relatively low incidence (14%) of methicillin resistance, much lower than the rate noted (45.5%) in other outpatient services during the same period, Dr. Catalina Matiz and her colleagues wrote in a poster presented at the annual meeting of the Society for Pediatric Dermatology.

Dr. Matiz, a postdoctoral fellow at Rady Children's Hospital in San Diego, and her coinvestigators conducted a retrospective chart review of 78 children with super-infected AD seen at the Rady pediatric and adolescent dermatology clinic between June 2007 and June 2008. The children had a positive skin culture for S. aureus.

They compared these data with all skin and soft tissue infection outpatient samples sent to the hospital's microbiology lab during the same period, and also with those sent during January 2000 through January 2001 (excluding samples from the dermatology clinic).

The CA-MRSA rate for samples from outpatient services from 2000-2001 was 4% (192 S. aureus-positive cultures). The outpatient services' rates increase from 2000-2001 to 2007-2008, highlight the sharp increase in CA-MRSA over the last several years, Dr. Matiz noted.

The rate of community-associated methicillin-sensitive S. aureus among patients with AD was 86%. In comparison, the CA-MSSA rate for other outpatient services during the same period was 55%. The CA-MSSA rate for outpatient services from 2000-2001 was 96%.

Interestingly, the investigators found that prior history of hospitalization, eczema severity, age, gender and prior antibiotic treatment had no impact on risk of methicillin resistance or sensitivity in these patients.

For the patients with AD, positive S. aureus cultures were most common among patients aged 1-4 years (26%), followed by those aged 5-9 years (24%), and those less than a year (23%).

The double diffusion test (D-test)—which is used to assess inducible resistance to clindamycin—was performed for 576 of the CA-MRSA samples from the hospital's lab in 2008. In all, 2% were positive for clindamycin-inducible resistance. However, none of the D-tests performed on cultures from patients with AD were positive. D-tests were performed for six of nine cultures that showed erythromycin resistance among patients with AD.

The findings are striking. “It's absolutely counterintuitive because if you think of patients with AD as being more at risk for infection, you would think that at the very least they would have the same rate as that occurring in the regular population,” said Dr. Sheila Fallon Friedlander, a study coauthor and a professor of pediatrics and medicine at the University of California, San Diego.

Based on conversations with colleagues, other pediatric dermatologists seem to be seeing similar patterns, said Dr. Friedlander. The researchers are not sure why these children have fewer CA-MRSA infections, though they have a couple of ideas.

It may be that “because these kids are colonized already so much of the time with regular S. aureus, that it may exert sort of a protective effect against CA-MRSA,” Dr. Friedlander said.

In addition, patients with AD tend to present more often with multiple lesions. “That may also play a role in this. It may be that our atopic patients are presenting with secondarily-infected lesions that are distinct from the abscesses and the folliculitis that we are seeing in the community,” she noted.

The findings “have informed the way that I prescribe medications for my patients,” she said. The results suggest that more standard antibiotic drugs with fewer side effects—like cephalosporins—can be used first, especially while waiting for culture results. This could not only reduce costs but also save patients from more serious side effects of antibiotics used for resistant pathogens.

In addition, it would help to reduce selection of more resistant bacteria. “It [could protect] our bigger gun drugs—reserving them for when you really need them,” said Dr. Friedlander, who added that it is important to factor in local demographics about CA-MRSA infection when deciding on a treatment.

Dr. Friedlander pointed out that while the findings are very interesting, this is a small study. “I think it's an interesting first step,” she said. Further prospective studies, looking at both CA-MRSA colonization and infection rates in children with AD, will be important to confirm these results.

In a separate study also presented at the meeting, Canadian researchers found a MRSA colonization rate of 0.5% among 200 pediatric patients with AD, and a S. aureus colonization rate of 61%.

The researchers collected a total of 400 swabs from the nares and open areas/folds of ADpatients (aged 1 month-18 years) with intact skin. Severity of AD was assessed using the an AD severity score, said Dr. Alexandra Balma-Mena, a resident at the Hospital for Sick Children in Toronto. A score of 0-12 was considered mild disease, a score of 13-18 was considered moderate, and a score of 19-25 was considered severe.

More of the patients were male (57%); the average age was 5 years. Most patients had mild disease (66%), followed by moderate (30%), and severe (4%).

Dr. Sheila Fallon Friedlander (left) and Dr. Catalina Matiz found that children with atopic dermatitis and S. aureus had a relatively lower incidence of methicillin resistance.

Source Courtesy Rady Children's Hospital in San Diego

WASHINGTON — A filaggrin mutation appears to confer susceptibility to atopic dermatitis complicated by eczema herpeticum, study results showed.

In a genotyping study, single-locus association tests revealed that filaggrin R501X null mutation is significantly associated with atopic dermatitis (AD) and atopic dermatitis complicated with eczema herpeticum (ADEH) in white and black patients, Kathleen C. Barnes, Ph.D., said in a poster presented at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

"This study of filaggrin polymorphisms suggests the functional R501X mutation, in addition to AD risk, confers an added risk of ADEH, with an estimated effect size of nearly 12 [OR = 11.8] among [white] patients," the researchers wrote. Notably, this is the first study demonstrating an association between filaggrin polymorphisms and the risk of AD and associated traits in blacks, according to Dr. Barnes of the division of allergy and clinical immunology at Johns Hopkins University in Baltimore.

The study included 414 white patients with atopy (165 with AD, 93 with ADEH, and 156 nonatopic controls) and 328 black patients (155 with AD, 21 with ADEH, and 152 nonatopic controls). AD was diagnosed using the U.S. consensus criteria. ADEH was defined as AD with at least one documented episode of eczema herpeticum. Total serum IgE levels were measured and eczema severity was assessed using the eczema area and severity index grading system.

The R501X null mutation was genotyped using the TaqMan allelic discrimination assay. In addition, the 2282del4 mutation was genotyped using an ABI 3700 sequencer. Nine tagging single-nucleotide polymorphisms were genotyped.

The researchers found significant associations between the 2282del4 mutation and AD, with allele frequencies of 10.7% among all AD patients, compared with 5.6% among controls. However, no association was observed when the analysis was limited to the patients with ADEH. Also, no associations were observed between 2282del4 and AD or ADEH among blacks, likely because of the low frequency among healthy controls (less than 1%) and AD patients (6%) and the complete absence among ADEH patients.

"The relationship between this null mutation and disease might be related to an increased propensity to disseminated viral skin infections resulting from skin barrier dysfunction," the researchers speculated.

Dr. Barnes reported having no relevant financial relationships.

WASHINGTON — A filaggrin mutation appears to confer susceptibility to atopic dermatitis complicated by eczema herpeticum, study results showed.

In a genotyping study, single-locus association tests revealed that filaggrin R501X null mutation is significantly associated with atopic dermatitis (AD) and atopic dermatitis complicated with eczema herpeticum (ADEH) in white and black patients, Kathleen C. Barnes, Ph.D., said in a poster presented at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

"This study of filaggrin polymorphisms suggests the functional R501X mutation, in addition to AD risk, confers an added risk of ADEH, with an estimated effect size of nearly 12 [OR = 11.8] among [white] patients," the researchers wrote. Notably, this is the first study demonstrating an association between filaggrin polymorphisms and the risk of AD and associated traits in blacks, according to Dr. Barnes of the division of allergy and clinical immunology at Johns Hopkins University in Baltimore.

The study included 414 white patients with atopy (165 with AD, 93 with ADEH, and 156 nonatopic controls) and 328 black patients (155 with AD, 21 with ADEH, and 152 nonatopic controls). AD was diagnosed using the U.S. consensus criteria. ADEH was defined as AD with at least one documented episode of eczema herpeticum. Total serum IgE levels were measured and eczema severity was assessed using the eczema area and severity index grading system.

The R501X null mutation was genotyped using the TaqMan allelic discrimination assay. In addition, the 2282del4 mutation was genotyped using an ABI 3700 sequencer. Nine tagging single-nucleotide polymorphisms were genotyped.

The researchers found significant associations between the 2282del4 mutation and AD, with allele frequencies of 10.7% among all AD patients, compared with 5.6% among controls. However, no association was observed when the analysis was limited to the patients with ADEH. Also, no associations were observed between 2282del4 and AD or ADEH among blacks, likely because of the low frequency among healthy controls (less than 1%) and AD patients (6%) and the complete absence among ADEH patients.

"The relationship between this null mutation and disease might be related to an increased propensity to disseminated viral skin infections resulting from skin barrier dysfunction," the researchers speculated.

Dr. Barnes reported having no relevant financial relationships.

WASHINGTON — A filaggrin mutation appears to confer susceptibility to atopic dermatitis complicated by eczema herpeticum, study results showed.

In a genotyping study, single-locus association tests revealed that filaggrin R501X null mutation is significantly associated with atopic dermatitis (AD) and atopic dermatitis complicated with eczema herpeticum (ADEH) in white and black patients, Kathleen C. Barnes, Ph.D., said in a poster presented at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

"This study of filaggrin polymorphisms suggests the functional R501X mutation, in addition to AD risk, confers an added risk of ADEH, with an estimated effect size of nearly 12 [OR = 11.8] among [white] patients," the researchers wrote. Notably, this is the first study demonstrating an association between filaggrin polymorphisms and the risk of AD and associated traits in blacks, according to Dr. Barnes of the division of allergy and clinical immunology at Johns Hopkins University in Baltimore.

The study included 414 white patients with atopy (165 with AD, 93 with ADEH, and 156 nonatopic controls) and 328 black patients (155 with AD, 21 with ADEH, and 152 nonatopic controls). AD was diagnosed using the U.S. consensus criteria. ADEH was defined as AD with at least one documented episode of eczema herpeticum. Total serum IgE levels were measured and eczema severity was assessed using the eczema area and severity index grading system.

The R501X null mutation was genotyped using the TaqMan allelic discrimination assay. In addition, the 2282del4 mutation was genotyped using an ABI 3700 sequencer. Nine tagging single-nucleotide polymorphisms were genotyped.

The researchers found significant associations between the 2282del4 mutation and AD, with allele frequencies of 10.7% among all AD patients, compared with 5.6% among controls. However, no association was observed when the analysis was limited to the patients with ADEH. Also, no associations were observed between 2282del4 and AD or ADEH among blacks, likely because of the low frequency among healthy controls (less than 1%) and AD patients (6%) and the complete absence among ADEH patients.

"The relationship between this null mutation and disease might be related to an increased propensity to disseminated viral skin infections resulting from skin barrier dysfunction," the researchers speculated.

Dr. Barnes reported having no relevant financial relationships.