Atopic Dermatitis

WASHINGTON — The most significant justification for proactive topical steroid therapy administered between atopic dermatitis flares is that "normal-looking" skin is not really normal, said Dr. Andreas Wollenberg.

"It doesn't follow our dermatological tradition to treat skin that doesn't look diseased," Dr. Wollenberg said during a debate session at the annual meeting of the American Academy of Allergy, Asthma, and Immunology. But even when symptoms temporarily subside, "there is a barrier defect in the normal-looking skin. There is an infiltration of inflammatory cells in the normal looking skin. And there is an alteration of the dendritic cells in the normal looking skin."

Administering therapy proactively, as opposed to only upon flaring, increases a patient's sense of control over the disease. "From the patient's point of view, it's the patient who rules the disease, and not the disease who rules the patient," he said. "Our patients love proactive therapy."

Proactive treatment also can decrease the number of flares, as well as flare duration and severity, compared with as-needed therapy, said Dr. Wollenberg, of the Department of Dermatology and Allergy, Ludwig-Maximilians-Universität, Munich. He recently completed a study showing that tacrolimus 0.1% ointment given twice weekly "significantly reduced the number of [disease exacerbations or DE] requiring substantial therapeutic intervention … the percentage of DE treatment days … and increased the time to first DE," (Allergy 2008;63:742-50).

In a rebuttal, Dr. Mark Boguniewicz of the National Jewish Medical and Research Center in Denver, cautioned that "before we accept a new paradigm like this we need to consider a few things. A critical appraisal of the current data would be useful."

"Should we ignore practice guidelines, practice parameters, consensus statements, package inserts, and the [Food and Drug Administration] boxed warnings, and can we afford to?" he asked. "And what do the adherence studies tell us?

"Does it make sense to apply topic medications to normal-appearing skin in a disease where most of our patients outgrow the problem early on?"

He also pointed out that the effects of long-term corticosteroids on unaffected skin are not known.

Both presenters disclosed financial and consulting relationships to multiple pharmaceutical companies.

WASHINGTON — The most significant justification for proactive topical steroid therapy administered between atopic dermatitis flares is that "normal-looking" skin is not really normal, said Dr. Andreas Wollenberg.

"It doesn't follow our dermatological tradition to treat skin that doesn't look diseased," Dr. Wollenberg said during a debate session at the annual meeting of the American Academy of Allergy, Asthma, and Immunology. But even when symptoms temporarily subside, "there is a barrier defect in the normal-looking skin. There is an infiltration of inflammatory cells in the normal looking skin. And there is an alteration of the dendritic cells in the normal looking skin."

Administering therapy proactively, as opposed to only upon flaring, increases a patient's sense of control over the disease. "From the patient's point of view, it's the patient who rules the disease, and not the disease who rules the patient," he said. "Our patients love proactive therapy."

Proactive treatment also can decrease the number of flares, as well as flare duration and severity, compared with as-needed therapy, said Dr. Wollenberg, of the Department of Dermatology and Allergy, Ludwig-Maximilians-Universität, Munich. He recently completed a study showing that tacrolimus 0.1% ointment given twice weekly "significantly reduced the number of [disease exacerbations or DE] requiring substantial therapeutic intervention … the percentage of DE treatment days … and increased the time to first DE," (Allergy 2008;63:742-50).

In a rebuttal, Dr. Mark Boguniewicz of the National Jewish Medical and Research Center in Denver, cautioned that "before we accept a new paradigm like this we need to consider a few things. A critical appraisal of the current data would be useful."

"Should we ignore practice guidelines, practice parameters, consensus statements, package inserts, and the [Food and Drug Administration] boxed warnings, and can we afford to?" he asked. "And what do the adherence studies tell us?

"Does it make sense to apply topic medications to normal-appearing skin in a disease where most of our patients outgrow the problem early on?"

He also pointed out that the effects of long-term corticosteroids on unaffected skin are not known.

Both presenters disclosed financial and consulting relationships to multiple pharmaceutical companies.

WASHINGTON — The most significant justification for proactive topical steroid therapy administered between atopic dermatitis flares is that "normal-looking" skin is not really normal, said Dr. Andreas Wollenberg.

"It doesn't follow our dermatological tradition to treat skin that doesn't look diseased," Dr. Wollenberg said during a debate session at the annual meeting of the American Academy of Allergy, Asthma, and Immunology. But even when symptoms temporarily subside, "there is a barrier defect in the normal-looking skin. There is an infiltration of inflammatory cells in the normal looking skin. And there is an alteration of the dendritic cells in the normal looking skin."

Administering therapy proactively, as opposed to only upon flaring, increases a patient's sense of control over the disease. "From the patient's point of view, it's the patient who rules the disease, and not the disease who rules the patient," he said. "Our patients love proactive therapy."

Proactive treatment also can decrease the number of flares, as well as flare duration and severity, compared with as-needed therapy, said Dr. Wollenberg, of the Department of Dermatology and Allergy, Ludwig-Maximilians-Universität, Munich. He recently completed a study showing that tacrolimus 0.1% ointment given twice weekly "significantly reduced the number of [disease exacerbations or DE] requiring substantial therapeutic intervention … the percentage of DE treatment days … and increased the time to first DE," (Allergy 2008;63:742-50).

In a rebuttal, Dr. Mark Boguniewicz of the National Jewish Medical and Research Center in Denver, cautioned that "before we accept a new paradigm like this we need to consider a few things. A critical appraisal of the current data would be useful."

"Should we ignore practice guidelines, practice parameters, consensus statements, package inserts, and the [Food and Drug Administration] boxed warnings, and can we afford to?" he asked. "And what do the adherence studies tell us?

"Does it make sense to apply topic medications to normal-appearing skin in a disease where most of our patients outgrow the problem early on?"

He also pointed out that the effects of long-term corticosteroids on unaffected skin are not known.

Both presenters disclosed financial and consulting relationships to multiple pharmaceutical companies.

WASHINGTON — Allergies to peanuts, eggs, and dust mites significantly increase the risk of persistent atopic dermatitis, study results showed.

Pediatric patients with a peanut allergy (OR = 2.9), egg allergy (OR = 2.7), or dust mite allergy (OR = 4.0) were significantly more likely to have persistent atopic dermatitis (AD) than were those without these factors in a study of 177 patients, reported Dr. Ejaz Yousef, chief of pediatric allergy and immunology at the Alfred I. duPont Hospital for Children in Wilmington, Del.

Patients aged 5-18 years were assessed for potential predictors of persistent AD, including race, age at onset, age of solid food introduction, whether the patients were breastfed, smoke exposure, coincident infection, other atopic disease, peripheral eosinophilia, and total IgE level. Predictors were compared with AD remission versus persistence status.

Among the patients, 76% were considered to have persistent disease. No other variables were significantly associated with AD persistence, although there was a trend toward increased risk of persistent disease in those with exposure to tobacco smoke and peripheral eosinophilia, Dr. Yousef said in a poster at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

The findings highlight "the importance of determining the presence of these risk factors in patients with AD, and [of taking] steps to modify those that can be modified" wrote Dr. Yousef.

Dr. Yousef reported having no relevant financial relationships.

WASHINGTON — Allergies to peanuts, eggs, and dust mites significantly increase the risk of persistent atopic dermatitis, study results showed.

Pediatric patients with a peanut allergy (OR = 2.9), egg allergy (OR = 2.7), or dust mite allergy (OR = 4.0) were significantly more likely to have persistent atopic dermatitis (AD) than were those without these factors in a study of 177 patients, reported Dr. Ejaz Yousef, chief of pediatric allergy and immunology at the Alfred I. duPont Hospital for Children in Wilmington, Del.

Patients aged 5-18 years were assessed for potential predictors of persistent AD, including race, age at onset, age of solid food introduction, whether the patients were breastfed, smoke exposure, coincident infection, other atopic disease, peripheral eosinophilia, and total IgE level. Predictors were compared with AD remission versus persistence status.

Among the patients, 76% were considered to have persistent disease. No other variables were significantly associated with AD persistence, although there was a trend toward increased risk of persistent disease in those with exposure to tobacco smoke and peripheral eosinophilia, Dr. Yousef said in a poster at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

The findings highlight "the importance of determining the presence of these risk factors in patients with AD, and [of taking] steps to modify those that can be modified" wrote Dr. Yousef.

Dr. Yousef reported having no relevant financial relationships.

WASHINGTON — Allergies to peanuts, eggs, and dust mites significantly increase the risk of persistent atopic dermatitis, study results showed.

Pediatric patients with a peanut allergy (OR = 2.9), egg allergy (OR = 2.7), or dust mite allergy (OR = 4.0) were significantly more likely to have persistent atopic dermatitis (AD) than were those without these factors in a study of 177 patients, reported Dr. Ejaz Yousef, chief of pediatric allergy and immunology at the Alfred I. duPont Hospital for Children in Wilmington, Del.

Patients aged 5-18 years were assessed for potential predictors of persistent AD, including race, age at onset, age of solid food introduction, whether the patients were breastfed, smoke exposure, coincident infection, other atopic disease, peripheral eosinophilia, and total IgE level. Predictors were compared with AD remission versus persistence status.

Among the patients, 76% were considered to have persistent disease. No other variables were significantly associated with AD persistence, although there was a trend toward increased risk of persistent disease in those with exposure to tobacco smoke and peripheral eosinophilia, Dr. Yousef said in a poster at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

The findings highlight "the importance of determining the presence of these risk factors in patients with AD, and [of taking] steps to modify those that can be modified" wrote Dr. Yousef.

Dr. Yousef reported having no relevant financial relationships.

WASHINGTON — EpiPen prescriptions were more common in U.S. cities at higher latitudes and with lower UVB exposure than more southern cities, suggesting a possible link between vitamin D levels and allergic disorders.

For every increase in latitude degree, the number of prescriptions for the allergy rescue medication (per 1,000 people) increased by 0.6, according to findings presented in a poster at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

"While we think that vitamin D is the most likely explanation, we also understand that these are population data, and that much more work needs to be done before we can say with confidence that low vitamin D causes food allergy," Dr. Carlos A. Camargo said in an interview.

Dr. Camargo, an emergency physician at Massachusetts General Hospital in Boston, and colleagues, looked at the number of EpiPen prescriptions in 38 west-coast cities in 2004. Data were obtained from Wolters Kluwer Health, a Phoenix-based health care information services provider. The cities were in Washington, Oregon, and California.

The data were correlated with average UVB exposure and controlled for 17 demographic characteristics.

In total, there were 151,073 EpiPen prescriptions, accounting for 245,169 pens, or 7.45 EpiPens per 1,000 people.

People in Bellingham, Wash. (latitude 48.76) required the greatest number of EpiPen prescriptions at 15.77 per 1,000 people in the city.

The lowest number of prescriptions (2.11 prescriptions per 1,000 people) was registered in Bakersfield, Calif. (latitude 35.37) which, according to the Bakersfield Convention and Visitor's Bureau, records about 300 days of sunshine annually. Bakersfield receives approximately 50% more UVB over a calendar year than Bellingham.

Although exact annual UVB exposure data per city weren't available, Dr. Camargo said that "The key concept is that, for the west coast of the U.S.A., latitude and UVB exposure are colinear; a higher latitude equals lower UVB." And although Washington is a notoriously rainy state, "It's not the rainy days in Washington that matter, but rather the higher latitude, though rainy/cloudy days don't help."

In their earlier analysis, he and his colleagues found that New England states had the highest levels of EpiPen prescriptions, with 8-12 per 1,000 persons, whereas southern states—including California—had only 3 per 1,000 (J. Clin. Allergy Immunol. 2007;120:131-6).

Dr. Camargo, a faculty member at Harvard Medical School, Boston, and his coauthors reported financial ties to several pharmaceutical companies on diverse topics. None of the investigators has financial ties to the food industry, supplement manufacturers, or the indoor tanning industry.

'While we think that vitamin D is the most likely explanation, we also understand that these are population data.' DR. CAMARGO

WASHINGTON — EpiPen prescriptions were more common in U.S. cities at higher latitudes and with lower UVB exposure than more southern cities, suggesting a possible link between vitamin D levels and allergic disorders.

For every increase in latitude degree, the number of prescriptions for the allergy rescue medication (per 1,000 people) increased by 0.6, according to findings presented in a poster at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

"While we think that vitamin D is the most likely explanation, we also understand that these are population data, and that much more work needs to be done before we can say with confidence that low vitamin D causes food allergy," Dr. Carlos A. Camargo said in an interview.

Dr. Camargo, an emergency physician at Massachusetts General Hospital in Boston, and colleagues, looked at the number of EpiPen prescriptions in 38 west-coast cities in 2004. Data were obtained from Wolters Kluwer Health, a Phoenix-based health care information services provider. The cities were in Washington, Oregon, and California.

The data were correlated with average UVB exposure and controlled for 17 demographic characteristics.

In total, there were 151,073 EpiPen prescriptions, accounting for 245,169 pens, or 7.45 EpiPens per 1,000 people.

People in Bellingham, Wash. (latitude 48.76) required the greatest number of EpiPen prescriptions at 15.77 per 1,000 people in the city.

The lowest number of prescriptions (2.11 prescriptions per 1,000 people) was registered in Bakersfield, Calif. (latitude 35.37) which, according to the Bakersfield Convention and Visitor's Bureau, records about 300 days of sunshine annually. Bakersfield receives approximately 50% more UVB over a calendar year than Bellingham.

Although exact annual UVB exposure data per city weren't available, Dr. Camargo said that "The key concept is that, for the west coast of the U.S.A., latitude and UVB exposure are colinear; a higher latitude equals lower UVB." And although Washington is a notoriously rainy state, "It's not the rainy days in Washington that matter, but rather the higher latitude, though rainy/cloudy days don't help."

In their earlier analysis, he and his colleagues found that New England states had the highest levels of EpiPen prescriptions, with 8-12 per 1,000 persons, whereas southern states—including California—had only 3 per 1,000 (J. Clin. Allergy Immunol. 2007;120:131-6).

Dr. Camargo, a faculty member at Harvard Medical School, Boston, and his coauthors reported financial ties to several pharmaceutical companies on diverse topics. None of the investigators has financial ties to the food industry, supplement manufacturers, or the indoor tanning industry.

'While we think that vitamin D is the most likely explanation, we also understand that these are population data.' DR. CAMARGO

WASHINGTON — EpiPen prescriptions were more common in U.S. cities at higher latitudes and with lower UVB exposure than more southern cities, suggesting a possible link between vitamin D levels and allergic disorders.

For every increase in latitude degree, the number of prescriptions for the allergy rescue medication (per 1,000 people) increased by 0.6, according to findings presented in a poster at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

"While we think that vitamin D is the most likely explanation, we also understand that these are population data, and that much more work needs to be done before we can say with confidence that low vitamin D causes food allergy," Dr. Carlos A. Camargo said in an interview.

Dr. Camargo, an emergency physician at Massachusetts General Hospital in Boston, and colleagues, looked at the number of EpiPen prescriptions in 38 west-coast cities in 2004. Data were obtained from Wolters Kluwer Health, a Phoenix-based health care information services provider. The cities were in Washington, Oregon, and California.

The data were correlated with average UVB exposure and controlled for 17 demographic characteristics.

In total, there were 151,073 EpiPen prescriptions, accounting for 245,169 pens, or 7.45 EpiPens per 1,000 people.

People in Bellingham, Wash. (latitude 48.76) required the greatest number of EpiPen prescriptions at 15.77 per 1,000 people in the city.

The lowest number of prescriptions (2.11 prescriptions per 1,000 people) was registered in Bakersfield, Calif. (latitude 35.37) which, according to the Bakersfield Convention and Visitor's Bureau, records about 300 days of sunshine annually. Bakersfield receives approximately 50% more UVB over a calendar year than Bellingham.

Although exact annual UVB exposure data per city weren't available, Dr. Camargo said that "The key concept is that, for the west coast of the U.S.A., latitude and UVB exposure are colinear; a higher latitude equals lower UVB." And although Washington is a notoriously rainy state, "It's not the rainy days in Washington that matter, but rather the higher latitude, though rainy/cloudy days don't help."

In their earlier analysis, he and his colleagues found that New England states had the highest levels of EpiPen prescriptions, with 8-12 per 1,000 persons, whereas southern states—including California—had only 3 per 1,000 (J. Clin. Allergy Immunol. 2007;120:131-6).

Dr. Camargo, a faculty member at Harvard Medical School, Boston, and his coauthors reported financial ties to several pharmaceutical companies on diverse topics. None of the investigators has financial ties to the food industry, supplement manufacturers, or the indoor tanning industry.

'While we think that vitamin D is the most likely explanation, we also understand that these are population data.' DR. CAMARGO

SINT MAARTEN, NETHERLANDS ANTILLES — The North American Contact Dermatitis Group removed 5 allergens from its 2007–2008 standard North American patch test tray and replaced them with 10 new substances to test for in 2009–2010.

The group removed imidazolidinyl urea, 2%; dimethylol dimethyl hydantoin, 1%; diazolidinyl urea, 1%; bisphenol F epoxy resin, 0.025%; and triamcinolone acetonide, 1%, Dr. Kathryn A. Zug reported at the Caribbean Dermatology Symposium.

The 10 allergens added are:

▸ Dimethylaminopropylamine (DMAPA), 1%. “You may be hearing more about this allergen. DMAPA is found in body wash, shampoos, and detergents and can cause face, neck, and eyelid dermatitis,” said Dr. Zug, a dermatologist at Dartmouth-Hitchcock Medical Center in Lebanon, N.H. She said she had no relevant disclosures to report.

▸ D-Limonene, 3%.

▸ Shellac, 20%. “This has been described previously for eyelid dermatitis from mascara,” Dr. Zug said.

▸ Majantole, 5%. She described this as “a new, important fragrance allergen” from a synthetic source.

▸ Oleamidopropyl dimethylamine, 0.1%.

▸ Carvone, 5%.

▸ Lavandula angustifolia (lavender) oil, 2%.

▸ Decyl glucoside, 5%. “This plant-derived surfactant is included in more 'natural' products,” Dr. Zug said. “It's an uncommon allergen, but the North American Contact Dermatitis Group is now monitoring it.”

▸ Jasminum officionale oil (Jasminum grandiflorum), 2%.

▸ Mentha piperita (peppermint) oil, 2%.

An allergen that sounds new, but is not, is Myroxylon pereirae resin. “This is one of our familiar allergens, balsam of Peru,” Dr. Zug said. “What has happened? We've taken a simple name—balsam of Peru—and made it more complicated by adopting the botanical name.”

She added, “Hopefully you will all be familiar with it when you see it on a standard tray.”

In discussing the results of a study of allergies to fragrances, Dr. Zug noted that a Lyral sensitization frequency of 2.3% was reported in a comprehensive study of 26 fragrances patch tested in a total of 21,325 patients in Germany (Contact Derm. 2007;57:1–10). Lyral is a component of fragrances and detergents included in the Fragrance Mix II patch test kit.

“Europeans are very interested in figuring out the frequency of [fragrance] allergies,” Dr. Zug said.

Other fragrances not on the standard series that were associated with stronger or more frequent patch test results in the study included tree moss (2.4%), oak moss (2.0%), hydroxycitronellal (1.3%), isoeugenol (1.1%), and cinnamic aldehyde (1.0%).

Because of studies like this, Dr. Zug said, “we may be able to better hone down which fragrance components our patients are allergic to, rather than just telling them they have a fragrance allergy.”

Products Recommended For Very Sensitive Skin

Creams

Aveeno

Vanicream

Deodorant

Almay

Lotions

Aveeno

DML

Theraplex emollient

Ointments

Hydrolatum

Vaseline petroleum jelly

Shampoos and Conditioners

DHS Clear

Free and Clear

Soaps

All liquid washes

Glycerin soap

Vanicream bar

Aveeno bar

Source: Dr. Zug

SINT MAARTEN, NETHERLANDS ANTILLES — The North American Contact Dermatitis Group removed 5 allergens from its 2007–2008 standard North American patch test tray and replaced them with 10 new substances to test for in 2009–2010.

The group removed imidazolidinyl urea, 2%; dimethylol dimethyl hydantoin, 1%; diazolidinyl urea, 1%; bisphenol F epoxy resin, 0.025%; and triamcinolone acetonide, 1%, Dr. Kathryn A. Zug reported at the Caribbean Dermatology Symposium.

The 10 allergens added are:

▸ Dimethylaminopropylamine (DMAPA), 1%. “You may be hearing more about this allergen. DMAPA is found in body wash, shampoos, and detergents and can cause face, neck, and eyelid dermatitis,” said Dr. Zug, a dermatologist at Dartmouth-Hitchcock Medical Center in Lebanon, N.H. She said she had no relevant disclosures to report.

▸ D-Limonene, 3%.

▸ Shellac, 20%. “This has been described previously for eyelid dermatitis from mascara,” Dr. Zug said.

▸ Majantole, 5%. She described this as “a new, important fragrance allergen” from a synthetic source.

▸ Oleamidopropyl dimethylamine, 0.1%.

▸ Carvone, 5%.

▸ Lavandula angustifolia (lavender) oil, 2%.

▸ Decyl glucoside, 5%. “This plant-derived surfactant is included in more 'natural' products,” Dr. Zug said. “It's an uncommon allergen, but the North American Contact Dermatitis Group is now monitoring it.”

▸ Jasminum officionale oil (Jasminum grandiflorum), 2%.

▸ Mentha piperita (peppermint) oil, 2%.

An allergen that sounds new, but is not, is Myroxylon pereirae resin. “This is one of our familiar allergens, balsam of Peru,” Dr. Zug said. “What has happened? We've taken a simple name—balsam of Peru—and made it more complicated by adopting the botanical name.”

She added, “Hopefully you will all be familiar with it when you see it on a standard tray.”

In discussing the results of a study of allergies to fragrances, Dr. Zug noted that a Lyral sensitization frequency of 2.3% was reported in a comprehensive study of 26 fragrances patch tested in a total of 21,325 patients in Germany (Contact Derm. 2007;57:1–10). Lyral is a component of fragrances and detergents included in the Fragrance Mix II patch test kit.

“Europeans are very interested in figuring out the frequency of [fragrance] allergies,” Dr. Zug said.

Other fragrances not on the standard series that were associated with stronger or more frequent patch test results in the study included tree moss (2.4%), oak moss (2.0%), hydroxycitronellal (1.3%), isoeugenol (1.1%), and cinnamic aldehyde (1.0%).

Because of studies like this, Dr. Zug said, “we may be able to better hone down which fragrance components our patients are allergic to, rather than just telling them they have a fragrance allergy.”

Products Recommended For Very Sensitive Skin

Creams

Aveeno

Vanicream

Deodorant

Almay

Lotions

Aveeno

DML

Theraplex emollient

Ointments

Hydrolatum

Vaseline petroleum jelly

Shampoos and Conditioners

DHS Clear

Free and Clear

Soaps

All liquid washes

Glycerin soap

Vanicream bar

Aveeno bar

Source: Dr. Zug

SINT MAARTEN, NETHERLANDS ANTILLES — The North American Contact Dermatitis Group removed 5 allergens from its 2007–2008 standard North American patch test tray and replaced them with 10 new substances to test for in 2009–2010.

The group removed imidazolidinyl urea, 2%; dimethylol dimethyl hydantoin, 1%; diazolidinyl urea, 1%; bisphenol F epoxy resin, 0.025%; and triamcinolone acetonide, 1%, Dr. Kathryn A. Zug reported at the Caribbean Dermatology Symposium.

The 10 allergens added are:

▸ Dimethylaminopropylamine (DMAPA), 1%. “You may be hearing more about this allergen. DMAPA is found in body wash, shampoos, and detergents and can cause face, neck, and eyelid dermatitis,” said Dr. Zug, a dermatologist at Dartmouth-Hitchcock Medical Center in Lebanon, N.H. She said she had no relevant disclosures to report.

▸ D-Limonene, 3%.

▸ Shellac, 20%. “This has been described previously for eyelid dermatitis from mascara,” Dr. Zug said.

▸ Majantole, 5%. She described this as “a new, important fragrance allergen” from a synthetic source.

▸ Oleamidopropyl dimethylamine, 0.1%.

▸ Carvone, 5%.

▸ Lavandula angustifolia (lavender) oil, 2%.

▸ Decyl glucoside, 5%. “This plant-derived surfactant is included in more 'natural' products,” Dr. Zug said. “It's an uncommon allergen, but the North American Contact Dermatitis Group is now monitoring it.”

▸ Jasminum officionale oil (Jasminum grandiflorum), 2%.

▸ Mentha piperita (peppermint) oil, 2%.

An allergen that sounds new, but is not, is Myroxylon pereirae resin. “This is one of our familiar allergens, balsam of Peru,” Dr. Zug said. “What has happened? We've taken a simple name—balsam of Peru—and made it more complicated by adopting the botanical name.”

She added, “Hopefully you will all be familiar with it when you see it on a standard tray.”

In discussing the results of a study of allergies to fragrances, Dr. Zug noted that a Lyral sensitization frequency of 2.3% was reported in a comprehensive study of 26 fragrances patch tested in a total of 21,325 patients in Germany (Contact Derm. 2007;57:1–10). Lyral is a component of fragrances and detergents included in the Fragrance Mix II patch test kit.

“Europeans are very interested in figuring out the frequency of [fragrance] allergies,” Dr. Zug said.

Other fragrances not on the standard series that were associated with stronger or more frequent patch test results in the study included tree moss (2.4%), oak moss (2.0%), hydroxycitronellal (1.3%), isoeugenol (1.1%), and cinnamic aldehyde (1.0%).

Because of studies like this, Dr. Zug said, “we may be able to better hone down which fragrance components our patients are allergic to, rather than just telling them they have a fragrance allergy.”

Products Recommended For Very Sensitive Skin

Creams

Aveeno

Vanicream

Deodorant

Almay

Lotions

Aveeno

DML

Theraplex emollient

Ointments

Hydrolatum

Vaseline petroleum jelly

Shampoos and Conditioners

DHS Clear

Free and Clear

Soaps

All liquid washes

Glycerin soap

Vanicream bar

Aveeno bar

Source: Dr. Zug

ELSEVIER GLOBAL MEDICAL NEWS

ELSEVIER GLOBAL MEDICAL NEWS

ELSEVIER GLOBAL MEDICAL NEWS

LAS VEGAS — Most experts in psychodermatology long ago abandoned the psychoanalytic theory of atopic eczema, characterized in 1940 by Dr. Franz Alexander as an outgrowth of a child's emotional angst at being unable to express anger and hostility arising from maternal rejection.

Still, increasing evidence points to a psychoneuroimmunologic "setup" for atopic dermatitis (AD), if not an eczema personality profile, asserts Dr. Torello M. Lotti, professor and chair of dermatology at the University of Florence, Italy.

Dr. Lotti and other researchers have hypothesized that an interconnection between genetic and environmental factors may predispose a patient to allergic inflammation, which may then cascade in a vulnerable individual into a long-lasting diminished capacity for appropriate protective reactivity within the hypothalamus-pituitary-adrenal (HPA) axis.

Certain responses to experimental conditions point to notable differences in the psycho-neuroendocrine-immune function of people with atopic dermatitis and other inflammatory allergic diseases, Dr. Lotti said during a seminar on dermatology sponsored by Skin Disease Education Foundation.

He cited numerous studies:

▸ Diurnal plasma cortisol (stress marker) variations in AD patients were found to rise and fall with atopy-relevant inflammatory parameters, with associated waxing and waning of allergic symptom severity (J. Clin. Invest. 1992;90:596–603).

▸ AD-like symptoms were actually precipitated in healthy volunteers after treatment with the glucocorticoid receptor antagonist RU 486 (J. Clin. Endocrinol. Metab 1990;71:1474–80).

▸ When exposed to experimental stressor conditions (asking volunteers to speak and do mental arithmetic tasks in front of an audience), eosinophil counts and IgE levels rose significantly in atopic eczema sufferers, but not in healthy volunteers (J. Neuroimmunol. 2002;129:161–7).

▸ Finally, epidemiologic evidence appears to bolster the argument that stress—either exerted by outside events or exquisitely experienced by a vulnerable personality—contributes to the cycle of events perpetuating atopic dermatitis, he said.

A severe shock or emotional event has been found to precede the onset or aggravation of AD in patients in early dermatologic studies, which also tracks with his clinical experience, he noted. An increasing prevalence of AD in children in the Western World may be symptomatic of the more highly-stressed, pressured environments in which they live.

In Dr. Lotti's view, a "biochemical setup" for atopic dermatitis activates not only stress (influencing the sympathetic nervous system and immune response), but also behavior and personality.

An appropriate approach, he said, is to utilize treatments that impact psychological symptoms of distress as well as physiologic symptoms such as pruritus.

He favors doxepin (10 mg at bedtime) or amitriptyline (starting at a dose of 50 mg/day) over antihistamines for "the itch of atopic dermatitis," which he said "is not a regular itch."

Direct acknowledgement of the psychological contributors to atopic dermatitis facilitates "liaison consultations," in which Dr. Lotti sees patients sometimes in the same room at the same time as do psychologists or psychiatrists.

Dr. Lotti disclosed receiving grant or research support or speakers bureau contributions from Merck-Serono, Wyeth, Abbott, and Schering-Plough.

SDEF and SKIN & ALLERGY NEWS are wholly owned subsidiaries of Elsevier.

LAS VEGAS — Most experts in psychodermatology long ago abandoned the psychoanalytic theory of atopic eczema, characterized in 1940 by Dr. Franz Alexander as an outgrowth of a child's emotional angst at being unable to express anger and hostility arising from maternal rejection.

Still, increasing evidence points to a psychoneuroimmunologic "setup" for atopic dermatitis (AD), if not an eczema personality profile, asserts Dr. Torello M. Lotti, professor and chair of dermatology at the University of Florence, Italy.

Dr. Lotti and other researchers have hypothesized that an interconnection between genetic and environmental factors may predispose a patient to allergic inflammation, which may then cascade in a vulnerable individual into a long-lasting diminished capacity for appropriate protective reactivity within the hypothalamus-pituitary-adrenal (HPA) axis.

Certain responses to experimental conditions point to notable differences in the psycho-neuroendocrine-immune function of people with atopic dermatitis and other inflammatory allergic diseases, Dr. Lotti said during a seminar on dermatology sponsored by Skin Disease Education Foundation.

He cited numerous studies:

▸ Diurnal plasma cortisol (stress marker) variations in AD patients were found to rise and fall with atopy-relevant inflammatory parameters, with associated waxing and waning of allergic symptom severity (J. Clin. Invest. 1992;90:596–603).

▸ AD-like symptoms were actually precipitated in healthy volunteers after treatment with the glucocorticoid receptor antagonist RU 486 (J. Clin. Endocrinol. Metab 1990;71:1474–80).

▸ When exposed to experimental stressor conditions (asking volunteers to speak and do mental arithmetic tasks in front of an audience), eosinophil counts and IgE levels rose significantly in atopic eczema sufferers, but not in healthy volunteers (J. Neuroimmunol. 2002;129:161–7).

▸ Finally, epidemiologic evidence appears to bolster the argument that stress—either exerted by outside events or exquisitely experienced by a vulnerable personality—contributes to the cycle of events perpetuating atopic dermatitis, he said.

A severe shock or emotional event has been found to precede the onset or aggravation of AD in patients in early dermatologic studies, which also tracks with his clinical experience, he noted. An increasing prevalence of AD in children in the Western World may be symptomatic of the more highly-stressed, pressured environments in which they live.

In Dr. Lotti's view, a "biochemical setup" for atopic dermatitis activates not only stress (influencing the sympathetic nervous system and immune response), but also behavior and personality.

An appropriate approach, he said, is to utilize treatments that impact psychological symptoms of distress as well as physiologic symptoms such as pruritus.

He favors doxepin (10 mg at bedtime) or amitriptyline (starting at a dose of 50 mg/day) over antihistamines for "the itch of atopic dermatitis," which he said "is not a regular itch."

Direct acknowledgement of the psychological contributors to atopic dermatitis facilitates "liaison consultations," in which Dr. Lotti sees patients sometimes in the same room at the same time as do psychologists or psychiatrists.

Dr. Lotti disclosed receiving grant or research support or speakers bureau contributions from Merck-Serono, Wyeth, Abbott, and Schering-Plough.

SDEF and SKIN & ALLERGY NEWS are wholly owned subsidiaries of Elsevier.

LAS VEGAS — Most experts in psychodermatology long ago abandoned the psychoanalytic theory of atopic eczema, characterized in 1940 by Dr. Franz Alexander as an outgrowth of a child's emotional angst at being unable to express anger and hostility arising from maternal rejection.

Still, increasing evidence points to a psychoneuroimmunologic "setup" for atopic dermatitis (AD), if not an eczema personality profile, asserts Dr. Torello M. Lotti, professor and chair of dermatology at the University of Florence, Italy.

Dr. Lotti and other researchers have hypothesized that an interconnection between genetic and environmental factors may predispose a patient to allergic inflammation, which may then cascade in a vulnerable individual into a long-lasting diminished capacity for appropriate protective reactivity within the hypothalamus-pituitary-adrenal (HPA) axis.

Certain responses to experimental conditions point to notable differences in the psycho-neuroendocrine-immune function of people with atopic dermatitis and other inflammatory allergic diseases, Dr. Lotti said during a seminar on dermatology sponsored by Skin Disease Education Foundation.

He cited numerous studies:

▸ Diurnal plasma cortisol (stress marker) variations in AD patients were found to rise and fall with atopy-relevant inflammatory parameters, with associated waxing and waning of allergic symptom severity (J. Clin. Invest. 1992;90:596–603).

▸ AD-like symptoms were actually precipitated in healthy volunteers after treatment with the glucocorticoid receptor antagonist RU 486 (J. Clin. Endocrinol. Metab 1990;71:1474–80).

▸ When exposed to experimental stressor conditions (asking volunteers to speak and do mental arithmetic tasks in front of an audience), eosinophil counts and IgE levels rose significantly in atopic eczema sufferers, but not in healthy volunteers (J. Neuroimmunol. 2002;129:161–7).

▸ Finally, epidemiologic evidence appears to bolster the argument that stress—either exerted by outside events or exquisitely experienced by a vulnerable personality—contributes to the cycle of events perpetuating atopic dermatitis, he said.

A severe shock or emotional event has been found to precede the onset or aggravation of AD in patients in early dermatologic studies, which also tracks with his clinical experience, he noted. An increasing prevalence of AD in children in the Western World may be symptomatic of the more highly-stressed, pressured environments in which they live.

In Dr. Lotti's view, a "biochemical setup" for atopic dermatitis activates not only stress (influencing the sympathetic nervous system and immune response), but also behavior and personality.

An appropriate approach, he said, is to utilize treatments that impact psychological symptoms of distress as well as physiologic symptoms such as pruritus.

He favors doxepin (10 mg at bedtime) or amitriptyline (starting at a dose of 50 mg/day) over antihistamines for "the itch of atopic dermatitis," which he said "is not a regular itch."

Direct acknowledgement of the psychological contributors to atopic dermatitis facilitates "liaison consultations," in which Dr. Lotti sees patients sometimes in the same room at the same time as do psychologists or psychiatrists.

Dr. Lotti disclosed receiving grant or research support or speakers bureau contributions from Merck-Serono, Wyeth, Abbott, and Schering-Plough.

SDEF and SKIN & ALLERGY NEWS are wholly owned subsidiaries of Elsevier.

CHICAGO — Neuroimaging of patients with atopic dermatitis has shown that different areas of the brain are activated in the itch versus scratch cycles.

The findings provide insight into the the role of peripheral and central neural sensitization of nerve fibers in contributing to atopic dermatitis itch. The findings also support the growing interest in drugs that act as antipruritics to reduce central sensitization, Dr. Gil Yosipovitch said.

Using arterial spin labeling-based functional MRI, Dr. Yosipovitch and colleagues at Wake Forest University, Winston-Salem, N.C., showed that the anterior cingulate cortex and dorsolateral prefrontal cortex are highly activated in patients with atopic dermatitis, but are not activated in healthy subjects when itch is induced. The activity in these cortices is also significantly correlated to itch intensity and disease severity scores in atopic dermatitis, according to unpublished data.

Curious about brain processing during scratching, the investigators, in another study, exposed 13 healthy subjects to a scratching stimulus. They found that repetitive scratching activates areas in the brain not activated in itch, most notably the secondary somatosensory cortex (J. Invest. Dermatol. 2008;128:1806–11). They also found significant activity in the cerebellum, which may be involved in coordinating the itch-scratch cycle.

What was more striking was a robust deactivation of the anterior cingulate cortex, which is involved in the unpleasant sensation of itch and thus may explain why scratching is so pleasurable, said Dr. Yosipovitch. Furthermore, there was a significant correlation between perceived scratching intensity and bilateral deactivation of the cingulate cortex.

"There is a hypersensitization of the nerve fibers in chronic itch; the nerve fibers are acting wacky," he said. "So when you give a painful stimulus instead of it being perceived as pain, it actually aggravates itch. It's very similar to patients with chronic pain, who when you induce an itchy state, it is perceived as pain.

"Now you can understand why one of my treatments of itch is reduction of central sensitization," he said at the American Academy of Dermatology's Academy 2008 meeting

Drugs targeting this mechanism include selective noradrenergic reuptake inhibitors such as mirtazapine, neuroleptics, and kappa opioids.

Butorphanol is an approved kappa agonist and mu-receptor antagonist analgesic that is available in injectable and intranasal spray formulations, he said. Butorphanol nasal spray is very effective in treating patients with chronic, intractable itch that affects their sleep and quality of life.

"I don't want to send the wrong message that this is a first-line drug for itch, but I'm quite sure we all have these patients and sometimes it's worth a try," he said.

Dr. Yosipovitch also uses 15 mg of mirtazapine (Remeron) at bedtime for intractable itch in patients aged 10 years and older, almost half of whom report a significant improvement in sleep and quality of life. The antidepressant is not addictive, but weight gain can occur.

He suggested that the immunosuppressant azathioprine (Imuran), which is used to prevent kidney transplant rejection and to treat severe rheumatoid arthritis, is underutilized in the United States for atopic dermatitis. He acknowledged concerns about the increased risk of lymphoma associated with azathioprine therapy, but said this is unlikely with short-term use of 1 year or less at a dosage of 1 mg/kg.

In a double-blind, randomized trial conducted in the United Kingdom in 63 patients who had moderate to severe atopic eczema despite having received optimum topical therapy, azathioprine dosed by thiopurine methyltransferase (TPMT) was well tolerated; however, two patients developed drug hypersensitivity (Lancet 2006;367:839–46). At week 12, there was a 37% improvement in mean disease activity with azathioprine, compared with a 20% improvement with placebo. Significant improvements in itch, area of involvement, and quality of life were also observed.

Although the psoriasis biologic therapies—efalizumab, alefacept, and rituximab—are being studied for atopic dermatitis, Dr. Yosipovitch said he is not convinced at this point of their efficacy.

Dr. Yosipovitch, known as "Dr. Itch" to his patients, is fond of the old-fashioned remedy of double-layer wet pajamas in which a moist wet-wrap dressing is covered by a layer of dry pajamas. A Korean study in 10 patients with severe atopic dermatitis confirmed that wet-wrap dressings were associated with clinical improvement and recovery of the epidermal barrier (J. Eur. Acad. Dermatol. Venereol. 2007;21:1360–8).

Dr. Yosipovitch disclosed that he has been on the advisory board of, been a consultant for, or received research grant support from, Acologix Inc., Cara Therapeutics, Taisho Pharmaceutical Co., Stiefel Laboratories Inc., UCB Pharma, Connetics Corp., and the National Eczema Association.

A robust deactivation of the anterior cingulate cortex may explain why scratching is so pleasurable. DR. YOSIPOVITCH

CHICAGO — Neuroimaging of patients with atopic dermatitis has shown that different areas of the brain are activated in the itch versus scratch cycles.

The findings provide insight into the the role of peripheral and central neural sensitization of nerve fibers in contributing to atopic dermatitis itch. The findings also support the growing interest in drugs that act as antipruritics to reduce central sensitization, Dr. Gil Yosipovitch said.

Using arterial spin labeling-based functional MRI, Dr. Yosipovitch and colleagues at Wake Forest University, Winston-Salem, N.C., showed that the anterior cingulate cortex and dorsolateral prefrontal cortex are highly activated in patients with atopic dermatitis, but are not activated in healthy subjects when itch is induced. The activity in these cortices is also significantly correlated to itch intensity and disease severity scores in atopic dermatitis, according to unpublished data.

Curious about brain processing during scratching, the investigators, in another study, exposed 13 healthy subjects to a scratching stimulus. They found that repetitive scratching activates areas in the brain not activated in itch, most notably the secondary somatosensory cortex (J. Invest. Dermatol. 2008;128:1806–11). They also found significant activity in the cerebellum, which may be involved in coordinating the itch-scratch cycle.

What was more striking was a robust deactivation of the anterior cingulate cortex, which is involved in the unpleasant sensation of itch and thus may explain why scratching is so pleasurable, said Dr. Yosipovitch. Furthermore, there was a significant correlation between perceived scratching intensity and bilateral deactivation of the cingulate cortex.

"There is a hypersensitization of the nerve fibers in chronic itch; the nerve fibers are acting wacky," he said. "So when you give a painful stimulus instead of it being perceived as pain, it actually aggravates itch. It's very similar to patients with chronic pain, who when you induce an itchy state, it is perceived as pain.

"Now you can understand why one of my treatments of itch is reduction of central sensitization," he said at the American Academy of Dermatology's Academy 2008 meeting

Drugs targeting this mechanism include selective noradrenergic reuptake inhibitors such as mirtazapine, neuroleptics, and kappa opioids.

Butorphanol is an approved kappa agonist and mu-receptor antagonist analgesic that is available in injectable and intranasal spray formulations, he said. Butorphanol nasal spray is very effective in treating patients with chronic, intractable itch that affects their sleep and quality of life.

"I don't want to send the wrong message that this is a first-line drug for itch, but I'm quite sure we all have these patients and sometimes it's worth a try," he said.

Dr. Yosipovitch also uses 15 mg of mirtazapine (Remeron) at bedtime for intractable itch in patients aged 10 years and older, almost half of whom report a significant improvement in sleep and quality of life. The antidepressant is not addictive, but weight gain can occur.

He suggested that the immunosuppressant azathioprine (Imuran), which is used to prevent kidney transplant rejection and to treat severe rheumatoid arthritis, is underutilized in the United States for atopic dermatitis. He acknowledged concerns about the increased risk of lymphoma associated with azathioprine therapy, but said this is unlikely with short-term use of 1 year or less at a dosage of 1 mg/kg.

In a double-blind, randomized trial conducted in the United Kingdom in 63 patients who had moderate to severe atopic eczema despite having received optimum topical therapy, azathioprine dosed by thiopurine methyltransferase (TPMT) was well tolerated; however, two patients developed drug hypersensitivity (Lancet 2006;367:839–46). At week 12, there was a 37% improvement in mean disease activity with azathioprine, compared with a 20% improvement with placebo. Significant improvements in itch, area of involvement, and quality of life were also observed.

Although the psoriasis biologic therapies—efalizumab, alefacept, and rituximab—are being studied for atopic dermatitis, Dr. Yosipovitch said he is not convinced at this point of their efficacy.

Dr. Yosipovitch, known as "Dr. Itch" to his patients, is fond of the old-fashioned remedy of double-layer wet pajamas in which a moist wet-wrap dressing is covered by a layer of dry pajamas. A Korean study in 10 patients with severe atopic dermatitis confirmed that wet-wrap dressings were associated with clinical improvement and recovery of the epidermal barrier (J. Eur. Acad. Dermatol. Venereol. 2007;21:1360–8).

Dr. Yosipovitch disclosed that he has been on the advisory board of, been a consultant for, or received research grant support from, Acologix Inc., Cara Therapeutics, Taisho Pharmaceutical Co., Stiefel Laboratories Inc., UCB Pharma, Connetics Corp., and the National Eczema Association.

A robust deactivation of the anterior cingulate cortex may explain why scratching is so pleasurable. DR. YOSIPOVITCH

CHICAGO — Neuroimaging of patients with atopic dermatitis has shown that different areas of the brain are activated in the itch versus scratch cycles.

The findings provide insight into the the role of peripheral and central neural sensitization of nerve fibers in contributing to atopic dermatitis itch. The findings also support the growing interest in drugs that act as antipruritics to reduce central sensitization, Dr. Gil Yosipovitch said.

Using arterial spin labeling-based functional MRI, Dr. Yosipovitch and colleagues at Wake Forest University, Winston-Salem, N.C., showed that the anterior cingulate cortex and dorsolateral prefrontal cortex are highly activated in patients with atopic dermatitis, but are not activated in healthy subjects when itch is induced. The activity in these cortices is also significantly correlated to itch intensity and disease severity scores in atopic dermatitis, according to unpublished data.

Curious about brain processing during scratching, the investigators, in another study, exposed 13 healthy subjects to a scratching stimulus. They found that repetitive scratching activates areas in the brain not activated in itch, most notably the secondary somatosensory cortex (J. Invest. Dermatol. 2008;128:1806–11). They also found significant activity in the cerebellum, which may be involved in coordinating the itch-scratch cycle.

What was more striking was a robust deactivation of the anterior cingulate cortex, which is involved in the unpleasant sensation of itch and thus may explain why scratching is so pleasurable, said Dr. Yosipovitch. Furthermore, there was a significant correlation between perceived scratching intensity and bilateral deactivation of the cingulate cortex.

"There is a hypersensitization of the nerve fibers in chronic itch; the nerve fibers are acting wacky," he said. "So when you give a painful stimulus instead of it being perceived as pain, it actually aggravates itch. It's very similar to patients with chronic pain, who when you induce an itchy state, it is perceived as pain.

"Now you can understand why one of my treatments of itch is reduction of central sensitization," he said at the American Academy of Dermatology's Academy 2008 meeting

Drugs targeting this mechanism include selective noradrenergic reuptake inhibitors such as mirtazapine, neuroleptics, and kappa opioids.

Butorphanol is an approved kappa agonist and mu-receptor antagonist analgesic that is available in injectable and intranasal spray formulations, he said. Butorphanol nasal spray is very effective in treating patients with chronic, intractable itch that affects their sleep and quality of life.

"I don't want to send the wrong message that this is a first-line drug for itch, but I'm quite sure we all have these patients and sometimes it's worth a try," he said.

Dr. Yosipovitch also uses 15 mg of mirtazapine (Remeron) at bedtime for intractable itch in patients aged 10 years and older, almost half of whom report a significant improvement in sleep and quality of life. The antidepressant is not addictive, but weight gain can occur.

He suggested that the immunosuppressant azathioprine (Imuran), which is used to prevent kidney transplant rejection and to treat severe rheumatoid arthritis, is underutilized in the United States for atopic dermatitis. He acknowledged concerns about the increased risk of lymphoma associated with azathioprine therapy, but said this is unlikely with short-term use of 1 year or less at a dosage of 1 mg/kg.

In a double-blind, randomized trial conducted in the United Kingdom in 63 patients who had moderate to severe atopic eczema despite having received optimum topical therapy, azathioprine dosed by thiopurine methyltransferase (TPMT) was well tolerated; however, two patients developed drug hypersensitivity (Lancet 2006;367:839–46). At week 12, there was a 37% improvement in mean disease activity with azathioprine, compared with a 20% improvement with placebo. Significant improvements in itch, area of involvement, and quality of life were also observed.

Although the psoriasis biologic therapies—efalizumab, alefacept, and rituximab—are being studied for atopic dermatitis, Dr. Yosipovitch said he is not convinced at this point of their efficacy.

Dr. Yosipovitch, known as "Dr. Itch" to his patients, is fond of the old-fashioned remedy of double-layer wet pajamas in which a moist wet-wrap dressing is covered by a layer of dry pajamas. A Korean study in 10 patients with severe atopic dermatitis confirmed that wet-wrap dressings were associated with clinical improvement and recovery of the epidermal barrier (J. Eur. Acad. Dermatol. Venereol. 2007;21:1360–8).

Dr. Yosipovitch disclosed that he has been on the advisory board of, been a consultant for, or received research grant support from, Acologix Inc., Cara Therapeutics, Taisho Pharmaceutical Co., Stiefel Laboratories Inc., UCB Pharma, Connetics Corp., and the National Eczema Association.

A robust deactivation of the anterior cingulate cortex may explain why scratching is so pleasurable. DR. YOSIPOVITCH