Atopic Dermatitis, food allergy and dietary interventions. A tale of controversy.

Atopic Dermatitis has long been a controversial entity in regard its relationship to food allergy. Indeed, inter-discipline disparity in the way dermatologists and allergologists perceive the food allergy/atopic dermatitis interplay, hampers the design of concise therapeutic strategies and conveys conflicting messages to the patients. Within this conceptual frame, food exclusion regimes are rendered a contentious option. On the basis of this acknowledgment, we opted to put the emphasis on the discrepant perceptions surrounding such therapeutic regimes and to share our view pertaining to their appropriate implementation.

Hypereosinophilia, hyper-IgE syndrome, and atopic dermatitis in a toddler with food hypersensitivity.

We describe a 20-month-old girl with hypereosinophilia, hyper-immunoglobulin (Ig) E syndrome, and atopic dermatitis. Her peripheral eosinophil count and IgE plasma levels were 2.65 x 10(9)/L and 6702 IU/mL, respectively. Specific IgE levels for a variety of foods and inhalants were high and single-blind food challenges were positive for cow's milk, hen's egg, oat, wheat, and soy. When the patient received an extensively hydrolyzed milk formula, an exclusion diet, and 2 mg/kg of prednisone daily, the atopic dermatitis partially improved. Further improvement was observed with 1 mg/kg of azathioprine daily. Long-term clinical response was satisfactory. We suggest that food hypersensitivity should be ruled out in patients with hypereosinophilia, hyper-IgE syndrome, and atopic dermatitis. Azathioprine may be a good therapeutic alternative for treatment in such cases.

Mast cell quantification in the skin of children with atopic dermatitis: its value in diagnosis and in assessing the effectiveness of therapy.

This study reports on the usefulness of skin mast cell quantification (mast cells(mm2) as a parameter for the diagnosis of atopic dermatitis (AD) and for determining the efficacy of the therapeutic measures employed. Fifteen children with AD of moderate to extreme severity, and which started within the first two years of life, were studied. The therapeutic measures were limited to advice regarding the choice of adequate living conditions and of an appropriate diet in conjunction with the oral administration of hydroxyzine. Before treatment, 11 children with active AD were submitted to biopsies of both affected and non-affected skin. After treatment, in six children who were asymptomatic for at least one month, another biopsy was performed at a site of previous skin disease. A biopsy of a previously affected site was also performed in the other four children with a personal history of AD and who had no symptoms for more than one year. Treatment with hydroxyzine significantly reduced the number of papillar and reticular mast cells/mm3 of affected skin. In children who had been asymptomatic for one month, the number of papillar dermis mast cells/mm3 was greater than in those who had been asymptomatic for 12 months. In both groups of asymptomatic children, the number of mast cells/mm3 of affected skin was greater than in non-affected skin.(ABSTRACT TRUNCATED AT 250 WORDS)

Natural history of food hypersensitivity in children with atopic dermatitis.

Patients with atopic dermatitis and food hypersensitivity who were adhering to an elimination diet underwent repeat double-blind, placebo-controlled oral food challenges annually for follow-up of their food allergy. After 1 year, 19 of 75 patients lost all signs of clinical food hypersensitivity (15 of 45 patients allergic to one food, and 4 of 21 allergic to two foods). Of the individual foods, 38 of 121 no longer elicited symptomatic responses. After 2 years, patients underwent a second rechallenge; 4 of 44 patients tested lost their clinical food hypersensitivity. In 20 patients undergoing a third rechallenge, no food hypersensitivity was lost. Loss rate of food hypersensitivity varied among foods; after 1 year, there was a 26% loss of symptomatic food allergy to five major allergens (egg, milk, soy, wheat, and peanut) compared with a 66% loss rate to other food allergens. Loss of symptomatic allergy was not affected by the patient's age at diagnosis, except with milk allergy, for which older patients were more likely to lose clinical food hypersensitivity (p less than 0.05). Total serum IgE and prick skin tests were not useful for predicting loss of symptomatic food hypersensitivity. There was no significant decrease in skin test wheal size corresponding to loss of clinical food hypersensitivity. Patients developing only skin symptoms during the initial challenge were most likely to lose symptomatic food hypersensitivity.