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Atopic dermatitis is one form of eczema, which begins in early infancy and is characterized by extreme pruritus, chronically relapsing course, and distinctive distribution. Atopic dermatitis is typically the first manifestation of a child prone to develop atopic disease, with 50% of all atopic dermatitis developing in the first year of life and 80% by 5 years of age. Approximately 80% of children with atopic dermatitis develop asthma or allergic rhinitis, with many losing their atopic dermatitis (AD) with the onset of respiratory allergy. The acute rash of AD is typically an erythematous, papulovesicular eruption, frequently with weeping and crusting. It typically progresses to a subacute form marked by erythema and scaling papules, and especially in older patients, to a chronic form characterized by thickened, lichenified skin and fibrous papules.  The distribution of the rash varies with age,  involving the cheeks and extensor surfaces of the arms and legs in infancy, the flexor surfaces in the young child food alergy, hypersensitivity, eczema, exema, alergy



Food hypersensitivity has a pathologic role in many children with atopic dermatitis. To establish the causative association between food hypersensitivity and AD, clinical studies have been performed to address t demonstrate that removal of the causative agent leads to resolution of the disorder; introduction of the causative agent provokes the disorder; and avoidance of the causative agent prevents the disorder. As with other chronic, atopic disorders (e.g., asthma), a variety of factors can trigger eczematous lesions [wheezing in the case of asthma] making food alergy, hypersensitivity, eczema, exema, alergy

The therapeutic effect of removing foods to which children with AD are alergic has been addressed in a number of studies. Atherton et al reported that two thirds of children with AD between the ages of 2 and 8 years showed marked improvement during a double-blind cross-over trial of egg and milk exclusion. The trial was conducted over a 12-week period in the patients' homes. Unfortunately, 45% of the patients enrolled in this study dropped out or were excluded from analysis, environmental factors and other triggers of AD were not controlled for, and a significant order effect was found, all raising some question about the

In a prospective follow-up study of 34 patients with AD, 17 children with food allergy, who were diagnosed with food allergy by double-blind placebo-controlled oral food challenges and placed on an appropriate allergen elimination diet, experienced a marked improvement in their eczematous rash at 1 to 2 years and 3 to 4 years follow-up. These children showed significantly greater improvement than 12 similar AD patients who did not have food allergy and 5 children with food

Several investigators have attempted to provoke eczematous skin changes by challenging patients with AD and suspected food allergy. In their studies of children primarily with suspected food hypersensitivity and respiratory allergy, May and Bock reported that four of seven children with a history of eczematous reactions to foods developed skin rashes within 2 hours of administration of a double-blind, placebo-controlled, oral food challenge (DBPCFC) Using a similar challenge

Allergic reactions to foods were very specific. Although patients frequently had positive skin tests [and RASTs] to several members of a botanical family or animal species, indicating immunologic cross-reactivity, the frequency of patients experiencing symptomatic intra-botanical or intra-species cross-reactivity is variable. Legume cross-reactivity was evaluated in 69 children with AD utilizing prick skin tests, in vitro measurements of specific IgE antibodies (immunodot

Food Positive Challenge Positive History Total %
Egg 178 35 213 57
Milk 96 47 143 38
Peanut 28 82 110 29
Soy 55 4 59 16
Wheat 43 0 43 11

Children with AD and newly diagnosed food hypersensitivity were found to have high spontaneous basophil histamine release (SBHR) from peripheral blood basophils, in vitro, compared with patients with AD and no food allergy and normal controls (mean: 35.1% + 3.9% versus 1.8% + 0.2% versus 2.3% + 0.2%, P < 0.001). When these food-allergic patients were placed on appropriate elimination diets for at least 1 year, good clearing of their eczema was seen and a

A number of investigators have evaluated the effect of excluding dietary allergens on the development of AD in young infants. In the 1930s Grulee and Sanford were first to report a decrease in the incidence of AD in breastfed infants.  Since that time there have been numerous conflicting reports about the relative benefit of breast feeding infants to prevent or delay the onset of atopic disease. The potential benefit of breastfeeding is complicated by transmission of food antigens in maternal breast milk. We evaluated six exclusively breastfed infants (age 2.5 to 6 months) who developed classic infantile AD. Each infant had a positive prick

In a prospective, randomized alergy prevention trial, Zeiger et al compared the benefits of maternal and infant food allergen avoidance on the prevention of allergic disease in infants at high risk for allergic disease. Breastfeeding was encouraged in both prophylaxis and control groups. In the prophylaxis group, mothers eliminated egg, milk, and peanut from their diets, a casein hydrolysate formula was utilized for supplementation or weaning, and solid foods were delayed until 


The double-blind placebo controlled oral food challenge remains the gold standard for diagnosing food hypersensitivity in chronic atopic disorders, such as AD. In the typical office practice, however, a careful history and evidence of food antigen-specific IgE antibodies (prick skin tests, RASTs) may indicate foods that can be eliminated for a 2- to 3-week dietary trial. Symptoms may be recorded in a diary during the trial period. If unequivocal improvement is documented, foods


Once food hypersensitivity is diagnosed, therapy consists of placing the patient on a diet completely eliminating all forms of the offending food allergen. Instructing the patient and family to read food labels to avoid hidden sources of the suspect food and to avoid potential sources of allergen contamination is critical. Hidden food sources may be found as follows:

MILK: Artificial butter flavor, butter, butter fat, buttermilk, casein, caseinates (sodium, calcium, etc.), cheese, cream, cottage cheese, curds, custard, Half & Half, hydrolysates (casein, milk, whey), lactalbumin, lactose, milk (derivatives, protein, solids, malted, condensed, evaporated, dry, whole, low-fat, non-fat, skim), nougat, pudding, rennet casein, sour cream, sour cream solids, sour milk solids, whey (delactosed, demineralized protein concentrate), yogurt. MAY be contained in brown sugar flavoring, natural flavoring, chocholate, caramel flavoring, high protein flour, margarine, Simplesse.
EGG: Egg (white, yolk, dried, powdered, solids), egg substitute, eggnog, globulin, livetin, lysozyme, mayonnaise, meringue, ovalbumin, ovomucin, ovomucoid, Simplesse.
WHEAT: Bread crumbs, bran, cereal extract, cracker meal, enriched flour, farina, gluten, graham flour, high gluten flour, high protein flour, malt, vital gluten, wheat bran, wheat germ, wheat gluten, wheat starch, whole wheat flour, spelt. MAY be contained in gelatinized starch, hydrolyzed vegetable protein, modified food starch, modified starch, natural flavoring, soy sauce, starch, vegetable gum, vegetable starch.
SOY: Hydrolyzed vegetable protein, miso, shoyu sauce, soy (flour, grits, nuts, milk, sprouts), soybean (granules, curd), soy protein (concentrate, isolate), soy sauce, textured vegetable protein (TVP), tofu. MAY be contained in hydrolyzed plant protein, hydrolyzed soy protein, hydrolyzed vegetable protein, natural flavoring, vegetable broth, vegetable gum, vegetable starch.
PEANUT: Cold pressed peanut oil, ground nuts, mixed nuts, Nu-Nuts artificial nuts, peanut, peanut butter, peanut flour. MAY be contained in African, Chinese, Thai, and other ethnic dishes, baked goods (pastries, cookies, and so forth), candy, chili, chocholate candy, egg rolls, hydrolyzed plant protein, hydrolyzed vegetable protein, marzipan, nougat.

A major reason that dietary management fails in food-allergic patients is because of inadequate patient instruction by the treating physician. Helpful information may be obtained from the Food Allergy Network (800-929-4040), a lay organization based in Fairfax, VA. Antihistamines and corticosteroids may modify the 


Approximately one third of children with AD and food allergy will lose (or outgrow) their clinical reactivity to food over 1 to 3 years. Three factors appear to be important in determining the probability of patients losing their clinical reactivity: the food to which the patient is allergic (i.e., patients allergic to peanuts, nuts, fish, and shellfish are not likely to lose their clinical reactivity, whereas those allergic to soy, wheat, milk, and egg are much more likely to develop clinical tolerance);