PEDIATRICS Vol. 101 No. 3 March 1998, p. e8
Received Aug 18, 1997; accepted Nov 18, 1997.
,
, §,
, §, and
From the * Department of Pediatrics, University of Geneva,
Geneva, Switzerland; the Departments of
Pediatrics and
§ Dermatology, Johns Hopkins University School of Medicine, Baltimore,
Maryland; and the
Department of Pediatrics, The Mount Sinai School
of Medicine, New York, New York.
Objective. There is a growing body of clinical and laboratory evidence to support the notion that food allergy plays a role in the pathogenesis of atopic dermatitis (AD). However, the incidence of IgE-mediated food allergy in children with AD is not well established.
Design. A prospective study to determine the prevalence of IgE-mediated food hypersensitivity among patients referred to a university-based dermatologist for evaluation of AD.
Setting. University hospital pediatric dermatology clinic.
Patients. A total of 63 patients with AD were recruited (35 male; 32 white, 24 African-American, 7 Asian).
Methods. Patients were assigned an AD symptom score
(SCORAD) and were screened for food-specific serum IgE antibodies to
six foods (milk, egg, wheat, soy, peanut, fish) known to be the most allergenic in children. The levels of food-specific serum IgE were
determined by the CAP System fluoroscein-enzyme immunoassay (CAP);
patients with a value
0.7 kIUa/L were invited for an additional allergy evaluation. Those with CAP values below the cutoff were considered not food allergic. Patients were considered to be allergic if they met one of the following criteria for at least one food: 1)
reaction on food challenge; 2) CAP value more than the 95% confidence
interval predictive for a reaction; 3) convincing history of an acute
significant (hives, respiratory symptoms) reaction after the isolated
ingestion of a food to which there was a positive CAP or prick skin
test.
Results. A total of 63 patients (median age, 2.8 years; median SCORAD, 41.1) were recruited; 22 had negative CAP values (without a significant difference in age or SCORAD score, compared with the 41 with positive specific IgE values). Further allergy evaluation was offered to the 41 remaining patients; 10 were lost to follow-up and 31 were evaluated further. Of these, 19 underwent a total of 50 food challenges (36 double-blind, placebo-controlled, and 14 open), with 11 patients experiencing 18 positive challenges (94% with skin reactions). Additionally, 6 patients had a convincing history with a predictive level of IgE; 5 had a convincing history with positive, indeterminate levels of IgE; and 1 had predictive levels of IgE (to egg and peanut) without a history of an acute reaction. Overall, 23/63 (37%; 95% confidence interval, 25% to 50%) had clinically significant IgE-mediated food hypersensitivity without a significant difference in age or symptom score between those with or without food allergy.
Conclusions. Approximately one third of children with refractory, moderate-severe AD have IgE-mediated clinical reactivity to food proteins. The prevalence of food allergy in this population is significantly higher than that in the general population, and an evaluation for food allergy should be considered in these patients.
Key words: atopic dermatitis (eczema), food allergy, IgE-mediated, prevalence, hypersensitivity.
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