Better Atopy Outcome Measures Demanded

RALEIGH, N.C. – Atopic dermatitis is a disease that until now has gone underappreciated by regulatory authorities, the pharmaceutical industry, and the general public, according to thought leaders determined to turn the situation around.

"The first and probably foremost reason atopic dermatitis has been somewhat ignored is that it is perceived as a childhood disease, and that makes development of drugs very, very difficult. First, you have to go through studies in adults and then you have to go through children," Dr. Lisa A. Beck noted during a special plenary session devoted to atopic dermatitis at the conference.

Courtesy Mrs. Emily Boynton, URMC Public Relations Department

Another stumbling block is that researchers haven’t adequately documented the negative effects atopic dermatitis can have on daily life for patients and caregivers. Clinicians who care for atopy patients are aware of it. The outside world is not, observed Dr. Beck, professor of dermatology and medicine at the University of Rochester (N.Y.). Also, better diagnostic criteria for atopic dermatitis are needed. The diagnosis isn’t always as straightforward as in psoriasis, which is "the great comparator in our range of diseases," she said.

A damaging perception that’s particularly entrenched within the regulatory agencies is that atopic dermatitis is not high priority because it lacks serious comorbidities, Dr. Beck continued.

Research Barriers

"That’s something we come up against in atopic dermatitis all the time: the idea that it’s a disease of misery rather than a disease of mortality," agreed Dr. Neil Graham of Regeneron Pharmaceuticals in Tarrytown, N.Y. "However, our view is that human misery is something we should be trying to treat therapeutically, and that this has value both economically and to society. I think we’ve seen this accomplished successfully with psoriasis, which is the template we can use in atopic dermatitis."

Biopharmaceutical companies are interested in applying the psoriasis drug development template to atopic dermatitis. Regeneron is developing a biologic agent that simultaneously blocks interleukins-4 and -13 for the treatment of atopic dermatitis and other diseases whose predominant mechanism involves Th2-driven eosinophilic inflammation, including eosinophilic asthma, chronic sinusitis with nasal polyps, and conjunctival allergic disease. The company wants an agent that can be subcutaneously injected every week or two, noted Dr. Graham.

"We hope eventually to intervene in children and potentially interrupt the atopic march. It will probably take us many years to get there," he said.

Regulatory agencies will almost certainly require that clinical trials involving any biologic agent under development for atopic dermatitis initially be restricted to patients with moderate to severe disease.

That’s a problem, according to Dr. Graham, because the Food and Drug Administration defines the clinical severity of atopic dermatitis using the Investigator’s Global Assessment (IGA) scale: a limited tool that’s not up to the task of capturing the full impact of the disease. Better means of defining the moderate to severely affected patient subset are essential. Also, a standardized, clinically relevant measure of disease severity reduction in response to treatment is needed – something akin to the Psoriasis Area Severity Index (PASI) 50 or -75 as used in psoriasis.

Dr. Eric Simpson agreed that regulatory authorities haven’t devoted sufficient attention to study design requirements or definitions of therapeutic success. For instance, the FDA requires evidence of improvement in the IGA as the bar that must be cleared in order to obtain approval of drugs for atopic dermatitis. Yet the IGA has never been adequately validated, nor has the metric’s definition been standardized. Indeed, the definition changes over time, from one phase-III clinical trial to the next.

"The inter-relater reliability of the IGA is unknown. I think it could be a major issue," said Dr. Simpson of the Oregon Health and Science University, Portland.

He proposed that participants in the SID special session on atopic dermatitis create a position paper recommending better outcome measures to the FDA. "We need to work with the agency to do what’s best for good clinical research," he said.

Identifying Biomarkers

According to Dr. Graham, atopic dermatitis is on the radar of major biotech companies that have biologic agents for psoriasis. They are working to develop biologics for atopic dermatitis, targeting a variety of pathways including interleukins-5, -4, and -13, as well as IgE.

Reliable biomarkers are needed to make drug development in atopic dermatitis go quickly and efficiently. After all, biomarker data are now routinely incorporated into early-phase development of new drugs for psoriasis, and these data are included in support of new drug applications to the FDA. But objective biomarkers have been notably lacking in atopic dermatitis, he noted.

Dr. Emma Guttman-Yassky announced help is at hand. While efforts to identify blood biomarkers have proved deeply disappointing, skin biomarkers are another story. She and her coinvestigators have identified a set of reliable skin biomarkers of therapeutic response in atopic dermatitis patients.

"We believe that these biomarkers represent the molecular fingerprints of the disease and might be key to future development of targeted treatments," said Dr. Guttman-Yassky, director of occupational and contact dermatitis at Mount Sinai Medical Center, New York.

She and her coinvestigators took lesional and nonlesional skin biopsies from 12 atopic dermatitis patients before and after undergoing narrow-band UVB phototherapy three times weekly for 12 weeks, a regimen the patients responded to with a mean 81% reduction in SCORAD index scores. Reversal of epidermal hyperplasia and abnormal keratinocyte differentiation – the histologic hallmarks of atopic dermatitis – was associated with elimination of inflammatory leukocytes and Th2-associated cytokines and chemokines (J. Allergy Clin. Immunol. 2011;128:583-93).

Among the skin biomarkers of atopic dermatitis that reversed with effective therapy were inflammatory dendritic epidermal cells, myeloid and plasmacytoid dendritic cells, CD3+ T cells, and interleukins-4 and -13.

This study, as well as another by Dr. Guttman-Yassky and her colleagues (in press), demonstrated a major role for interleukin-22 in atopic dermatitis. The cytokine was markedly overexpressed in lesional skin, with resultant upregulation of the antimicrobial protein’s S100A7, S100A8, and S100A9. After narrow-band UVB therapy, expression of IL-22 expression was downregulated, as were the IL-22-induced chemokines S100A7-9.

Expression of the three antimicrobial proteins in lesional skin also appears to be useful as a biomarker defining acute disease. Their levels jump within 3 days after onset of acute atopic dermatitis, according to Dr. Guttman-Yassky.

"Are we there yet in terms of biomarkers in atopic dermatitis? That’s the million-dollar question. Regarding biomarker availability, I think yes. We now have biomarkers that are highly informative on the reversal of disease pathology with treatment," she said. "I believe that the next step is clinical trials with specific immune antagonists that incorporate biomarkers of response. I think biomarkers are key if we want to know if new therapies really work. This will enhance early decisions and reduce the cost of developing new treatments."

An important implication of the narrow-band UVB/biomarker study in terms of atopic dermatitis pathogenesis is that the data argue against a fixed genetic phenotype, since the atopic dermatitis epidermal phenotype was shown to be reversed with broad-based immune-targeted phototherapy. Instead, the study results argue in favor of what Dr. Guttman-Yassky called "the inside-out hypothesis" of atopic dermatitis, which postulates that the epidermal abnormalities that define the disease are caused by underlying immune activation.

Her studies were supported by the National Institutes of Health.

HOME Project Seeks Standardization

During the same session, Dr. Hywel C. Williams provided an update on a major international project called Harmonising Outcome Measures for Eczema (HOME). The goal of the HOME project is to develop a consensus on a core set of outcome measures to be used in all atopic dermatitis clinical research. This should make future studies easier to compare, contrast, and synthesize in meta-analyses.

A minimum set of core outcome measures in atopic dermatitis is needed because the situation can be chaotic, noted Dr. Williams, professor of dermatology and director of the Center for Evidence-Based Dermatology at the University of Nottingham (U.K.).

"There are more than 20 named scales for atopic dermatitis, including SCORAD, POEM, SASSAD, ADASI, ADAM, EASI, and the FSSS. Some have been only partly tested. Many have not been tested at all. At international meetings I see people shouting at each other, trying to communicate what the results of their studies mean. Some people are in the SCORAD camp, some are in the SASSAD camp, others are in the EASI camp. How can we possibly communicate? This is a shameful situation which we really have to put right if we are to progress," he said.

The HOME project is modeled after Outcome Measures in Rheumatology, or OMERACT, an international consensus group that meets every 2 years with the goal of raising the quality of rheumatologic research. HOME comprises atopic dermatitis researchers, clinical experts, journal editors, patient advocates, and representatives from the European regulatory agency. The FDA was invited but didn’t attend last year’s HOME meeting in Amsterdam, where working groups were formed to identify the best evidence-based instruments for assessing atopic disease signs, symptoms, flares, quality of life, and treatment efficacy and safety. The HOME group will meet next year in San Diego on April 6-7.

Aside from Dr. Graham, a Regeneron employee, the other speakers in the special session reported receiving research grants from various sources but declared having no conflicts of interest with regard to their presentations.

RALEIGH, N.C. – Atopic dermatitis is a disease that until now has gone underappreciated by regulatory authorities, the pharmaceutical industry, and the general public, according to thought leaders determined to turn the situation around.

"The first and probably foremost reason atopic dermatitis has been somewhat ignored is that it is perceived as a childhood disease, and that makes development of drugs very, very difficult. First, you have to go through studies in adults and then you have to go through children," Dr. Lisa A. Beck noted during a special plenary session devoted to atopic dermatitis at the conference.

Courtesy Mrs. Emily Boynton, URMC Public Relations Department

Another stumbling block is that researchers haven’t adequately documented the negative effects atopic dermatitis can have on daily life for patients and caregivers. Clinicians who care for atopy patients are aware of it. The outside world is not, observed Dr. Beck, professor of dermatology and medicine at the University of Rochester (N.Y.). Also, better diagnostic criteria for atopic dermatitis are needed. The diagnosis isn’t always as straightforward as in psoriasis, which is "the great comparator in our range of diseases," she said.

A damaging perception that’s particularly entrenched within the regulatory agencies is that atopic dermatitis is not high priority because it lacks serious comorbidities, Dr. Beck continued.

Research Barriers

"That’s something we come up against in atopic dermatitis all the time: the idea that it’s a disease of misery rather than a disease of mortality," agreed Dr. Neil Graham of Regeneron Pharmaceuticals in Tarrytown, N.Y. "However, our view is that human misery is something we should be trying to treat therapeutically, and that this has value both economically and to society. I think we’ve seen this accomplished successfully with psoriasis, which is the template we can use in atopic dermatitis."

Biopharmaceutical companies are interested in applying the psoriasis drug development template to atopic dermatitis. Regeneron is developing a biologic agent that simultaneously blocks interleukins-4 and -13 for the treatment of atopic dermatitis and other diseases whose predominant mechanism involves Th2-driven eosinophilic inflammation, including eosinophilic asthma, chronic sinusitis with nasal polyps, and conjunctival allergic disease. The company wants an agent that can be subcutaneously injected every week or two, noted Dr. Graham.

"We hope eventually to intervene in children and potentially interrupt the atopic march. It will probably take us many years to get there," he said.

Regulatory agencies will almost certainly require that clinical trials involving any biologic agent under development for atopic dermatitis initially be restricted to patients with moderate to severe disease.

That’s a problem, according to Dr. Graham, because the Food and Drug Administration defines the clinical severity of atopic dermatitis using the Investigator’s Global Assessment (IGA) scale: a limited tool that’s not up to the task of capturing the full impact of the disease. Better means of defining the moderate to severely affected patient subset are essential. Also, a standardized, clinically relevant measure of disease severity reduction in response to treatment is needed – something akin to the Psoriasis Area Severity Index (PASI) 50 or -75 as used in psoriasis.

Dr. Eric Simpson agreed that regulatory authorities haven’t devoted sufficient attention to study design requirements or definitions of therapeutic success. For instance, the FDA requires evidence of improvement in the IGA as the bar that must be cleared in order to obtain approval of drugs for atopic dermatitis. Yet the IGA has never been adequately validated, nor has the metric’s definition been standardized. Indeed, the definition changes over time, from one phase-III clinical trial to the next.

"The inter-relater reliability of the IGA is unknown. I think it could be a major issue," said Dr. Simpson of the Oregon Health and Science University, Portland.

He proposed that participants in the SID special session on atopic dermatitis create a position paper recommending better outcome measures to the FDA. "We need to work with the agency to do what’s best for good clinical research," he said.

Identifying Biomarkers

According to Dr. Graham, atopic dermatitis is on the radar of major biotech companies that have biologic agents for psoriasis. They are working to develop biologics for atopic dermatitis, targeting a variety of pathways including interleukins-5, -4, and -13, as well as IgE.

Reliable biomarkers are needed to make drug development in atopic dermatitis go quickly and efficiently. After all, biomarker data are now routinely incorporated into early-phase development of new drugs for psoriasis, and these data are included in support of new drug applications to the FDA. But objective biomarkers have been notably lacking in atopic dermatitis, he noted.

Dr. Emma Guttman-Yassky announced help is at hand. While efforts to identify blood biomarkers have proved deeply disappointing, skin biomarkers are another story. She and her coinvestigators have identified a set of reliable skin biomarkers of therapeutic response in atopic dermatitis patients.

"We believe that these biomarkers represent the molecular fingerprints of the disease and might be key to future development of targeted treatments," said Dr. Guttman-Yassky, director of occupational and contact dermatitis at Mount Sinai Medical Center, New York.

She and her coinvestigators took lesional and nonlesional skin biopsies from 12 atopic dermatitis patients before and after undergoing narrow-band UVB phototherapy three times weekly for 12 weeks, a regimen the patients responded to with a mean 81% reduction in SCORAD index scores. Reversal of epidermal hyperplasia and abnormal keratinocyte differentiation – the histologic hallmarks of atopic dermatitis – was associated with elimination of inflammatory leukocytes and Th2-associated cytokines and chemokines (J. Allergy Clin. Immunol. 2011;128:583-93).

Among the skin biomarkers of atopic dermatitis that reversed with effective therapy were inflammatory dendritic epidermal cells, myeloid and plasmacytoid dendritic cells, CD3+ T cells, and interleukins-4 and -13.

This study, as well as another by Dr. Guttman-Yassky and her colleagues (in press), demonstrated a major role for interleukin-22 in atopic dermatitis. The cytokine was markedly overexpressed in lesional skin, with resultant upregulation of the antimicrobial protein’s S100A7, S100A8, and S100A9. After narrow-band UVB therapy, expression of IL-22 expression was downregulated, as were the IL-22-induced chemokines S100A7-9.

Expression of the three antimicrobial proteins in lesional skin also appears to be useful as a biomarker defining acute disease. Their levels jump within 3 days after onset of acute atopic dermatitis, according to Dr. Guttman-Yassky.

"Are we there yet in terms of biomarkers in atopic dermatitis? That’s the million-dollar question. Regarding biomarker availability, I think yes. We now have biomarkers that are highly informative on the reversal of disease pathology with treatment," she said. "I believe that the next step is clinical trials with specific immune antagonists that incorporate biomarkers of response. I think biomarkers are key if we want to know if new therapies really work. This will enhance early decisions and reduce the cost of developing new treatments."

An important implication of the narrow-band UVB/biomarker study in terms of atopic dermatitis pathogenesis is that the data argue against a fixed genetic phenotype, since the atopic dermatitis epidermal phenotype was shown to be reversed with broad-based immune-targeted phototherapy. Instead, the study results argue in favor of what Dr. Guttman-Yassky called "the inside-out hypothesis" of atopic dermatitis, which postulates that the epidermal abnormalities that define the disease are caused by underlying immune activation.

Her studies were supported by the National Institutes of Health.

HOME Project Seeks Standardization

During the same session, Dr. Hywel C. Williams provided an update on a major international project called Harmonising Outcome Measures for Eczema (HOME). The goal of the HOME project is to develop a consensus on a core set of outcome measures to be used in all atopic dermatitis clinical research. This should make future studies easier to compare, contrast, and synthesize in meta-analyses.

A minimum set of core outcome measures in atopic dermatitis is needed because the situation can be chaotic, noted Dr. Williams, professor of dermatology and director of the Center for Evidence-Based Dermatology at the University of Nottingham (U.K.).

"There are more than 20 named scales for atopic dermatitis, including SCORAD, POEM, SASSAD, ADASI, ADAM, EASI, and the FSSS. Some have been only partly tested. Many have not been tested at all. At international meetings I see people shouting at each other, trying to communicate what the results of their studies mean. Some people are in the SCORAD camp, some are in the SASSAD camp, others are in the EASI camp. How can we possibly communicate? This is a shameful situation which we really have to put right if we are to progress," he said.

The HOME project is modeled after Outcome Measures in Rheumatology, or OMERACT, an international consensus group that meets every 2 years with the goal of raising the quality of rheumatologic research. HOME comprises atopic dermatitis researchers, clinical experts, journal editors, patient advocates, and representatives from the European regulatory agency. The FDA was invited but didn’t attend last year’s HOME meeting in Amsterdam, where working groups were formed to identify the best evidence-based instruments for assessing atopic disease signs, symptoms, flares, quality of life, and treatment efficacy and safety. The HOME group will meet next year in San Diego on April 6-7.

Aside from Dr. Graham, a Regeneron employee, the other speakers in the special session reported receiving research grants from various sources but declared having no conflicts of interest with regard to their presentations.

RALEIGH, N.C. – Atopic dermatitis is a disease that until now has gone underappreciated by regulatory authorities, the pharmaceutical industry, and the general public, according to thought leaders determined to turn the situation around.

"The first and probably foremost reason atopic dermatitis has been somewhat ignored is that it is perceived as a childhood disease, and that makes development of drugs very, very difficult. First, you have to go through studies in adults and then you have to go through children," Dr. Lisa A. Beck noted during a special plenary session devoted to atopic dermatitis at the conference.

Courtesy Mrs. Emily Boynton, URMC Public Relations Department

Another stumbling block is that researchers haven’t adequately documented the negative effects atopic dermatitis can have on daily life for patients and caregivers. Clinicians who care for atopy patients are aware of it. The outside world is not, observed Dr. Beck, professor of dermatology and medicine at the University of Rochester (N.Y.). Also, better diagnostic criteria for atopic dermatitis are needed. The diagnosis isn’t always as straightforward as in psoriasis, which is "the great comparator in our range of diseases," she said.

A damaging perception that’s particularly entrenched within the regulatory agencies is that atopic dermatitis is not high priority because it lacks serious comorbidities, Dr. Beck continued.

Research Barriers

"That’s something we come up against in atopic dermatitis all the time: the idea that it’s a disease of misery rather than a disease of mortality," agreed Dr. Neil Graham of Regeneron Pharmaceuticals in Tarrytown, N.Y. "However, our view is that human misery is something we should be trying to treat therapeutically, and that this has value both economically and to society. I think we’ve seen this accomplished successfully with psoriasis, which is the template we can use in atopic dermatitis."

Biopharmaceutical companies are interested in applying the psoriasis drug development template to atopic dermatitis. Regeneron is developing a biologic agent that simultaneously blocks interleukins-4 and -13 for the treatment of atopic dermatitis and other diseases whose predominant mechanism involves Th2-driven eosinophilic inflammation, including eosinophilic asthma, chronic sinusitis with nasal polyps, and conjunctival allergic disease. The company wants an agent that can be subcutaneously injected every week or two, noted Dr. Graham.

"We hope eventually to intervene in children and potentially interrupt the atopic march. It will probably take us many years to get there," he said.

Regulatory agencies will almost certainly require that clinical trials involving any biologic agent under development for atopic dermatitis initially be restricted to patients with moderate to severe disease.

That’s a problem, according to Dr. Graham, because the Food and Drug Administration defines the clinical severity of atopic dermatitis using the Investigator’s Global Assessment (IGA) scale: a limited tool that’s not up to the task of capturing the full impact of the disease. Better means of defining the moderate to severely affected patient subset are essential. Also, a standardized, clinically relevant measure of disease severity reduction in response to treatment is needed – something akin to the Psoriasis Area Severity Index (PASI) 50 or -75 as used in psoriasis.

Dr. Eric Simpson agreed that regulatory authorities haven’t devoted sufficient attention to study design requirements or definitions of therapeutic success. For instance, the FDA requires evidence of improvement in the IGA as the bar that must be cleared in order to obtain approval of drugs for atopic dermatitis. Yet the IGA has never been adequately validated, nor has the metric’s definition been standardized. Indeed, the definition changes over time, from one phase-III clinical trial to the next.

"The inter-relater reliability of the IGA is unknown. I think it could be a major issue," said Dr. Simpson of the Oregon Health and Science University, Portland.

He proposed that participants in the SID special session on atopic dermatitis create a position paper recommending better outcome measures to the FDA. "We need to work with the agency to do what’s best for good clinical research," he said.

Identifying Biomarkers

According to Dr. Graham, atopic dermatitis is on the radar of major biotech companies that have biologic agents for psoriasis. They are working to develop biologics for atopic dermatitis, targeting a variety of pathways including interleukins-5, -4, and -13, as well as IgE.

Reliable biomarkers are needed to make drug development in atopic dermatitis go quickly and efficiently. After all, biomarker data are now routinely incorporated into early-phase development of new drugs for psoriasis, and these data are included in support of new drug applications to the FDA. But objective biomarkers have been notably lacking in atopic dermatitis, he noted.

Dr. Emma Guttman-Yassky announced help is at hand. While efforts to identify blood biomarkers have proved deeply disappointing, skin biomarkers are another story. She and her coinvestigators have identified a set of reliable skin biomarkers of therapeutic response in atopic dermatitis patients.

"We believe that these biomarkers represent the molecular fingerprints of the disease and might be key to future development of targeted treatments," said Dr. Guttman-Yassky, director of occupational and contact dermatitis at Mount Sinai Medical Center, New York.

She and her coinvestigators took lesional and nonlesional skin biopsies from 12 atopic dermatitis patients before and after undergoing narrow-band UVB phototherapy three times weekly for 12 weeks, a regimen the patients responded to with a mean 81% reduction in SCORAD index scores. Reversal of epidermal hyperplasia and abnormal keratinocyte differentiation – the histologic hallmarks of atopic dermatitis – was associated with elimination of inflammatory leukocytes and Th2-associated cytokines and chemokines (J. Allergy Clin. Immunol. 2011;128:583-93).

Among the skin biomarkers of atopic dermatitis that reversed with effective therapy were inflammatory dendritic epidermal cells, myeloid and plasmacytoid dendritic cells, CD3+ T cells, and interleukins-4 and -13.

This study, as well as another by Dr. Guttman-Yassky and her colleagues (in press), demonstrated a major role for interleukin-22 in atopic dermatitis. The cytokine was markedly overexpressed in lesional skin, with resultant upregulation of the antimicrobial protein’s S100A7, S100A8, and S100A9. After narrow-band UVB therapy, expression of IL-22 expression was downregulated, as were the IL-22-induced chemokines S100A7-9.

Expression of the three antimicrobial proteins in lesional skin also appears to be useful as a biomarker defining acute disease. Their levels jump within 3 days after onset of acute atopic dermatitis, according to Dr. Guttman-Yassky.

"Are we there yet in terms of biomarkers in atopic dermatitis? That’s the million-dollar question. Regarding biomarker availability, I think yes. We now have biomarkers that are highly informative on the reversal of disease pathology with treatment," she said. "I believe that the next step is clinical trials with specific immune antagonists that incorporate biomarkers of response. I think biomarkers are key if we want to know if new therapies really work. This will enhance early decisions and reduce the cost of developing new treatments."

An important implication of the narrow-band UVB/biomarker study in terms of atopic dermatitis pathogenesis is that the data argue against a fixed genetic phenotype, since the atopic dermatitis epidermal phenotype was shown to be reversed with broad-based immune-targeted phototherapy. Instead, the study results argue in favor of what Dr. Guttman-Yassky called "the inside-out hypothesis" of atopic dermatitis, which postulates that the epidermal abnormalities that define the disease are caused by underlying immune activation.

Her studies were supported by the National Institutes of Health.

HOME Project Seeks Standardization

During the same session, Dr. Hywel C. Williams provided an update on a major international project called Harmonising Outcome Measures for Eczema (HOME). The goal of the HOME project is to develop a consensus on a core set of outcome measures to be used in all atopic dermatitis clinical research. This should make future studies easier to compare, contrast, and synthesize in meta-analyses.

A minimum set of core outcome measures in atopic dermatitis is needed because the situation can be chaotic, noted Dr. Williams, professor of dermatology and director of the Center for Evidence-Based Dermatology at the University of Nottingham (U.K.).

"There are more than 20 named scales for atopic dermatitis, including SCORAD, POEM, SASSAD, ADASI, ADAM, EASI, and the FSSS. Some have been only partly tested. Many have not been tested at all. At international meetings I see people shouting at each other, trying to communicate what the results of their studies mean. Some people are in the SCORAD camp, some are in the SASSAD camp, others are in the EASI camp. How can we possibly communicate? This is a shameful situation which we really have to put right if we are to progress," he said.

The HOME project is modeled after Outcome Measures in Rheumatology, or OMERACT, an international consensus group that meets every 2 years with the goal of raising the quality of rheumatologic research. HOME comprises atopic dermatitis researchers, clinical experts, journal editors, patient advocates, and representatives from the European regulatory agency. The FDA was invited but didn’t attend last year’s HOME meeting in Amsterdam, where working groups were formed to identify the best evidence-based instruments for assessing atopic disease signs, symptoms, flares, quality of life, and treatment efficacy and safety. The HOME group will meet next year in San Diego on April 6-7.

Aside from Dr. Graham, a Regeneron employee, the other speakers in the special session reported receiving research grants from various sources but declared having no conflicts of interest with regard to their presentations.