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Natural history of IgE antibodies in children at risk for atopy
Background:
The relationship between atopic diseases and high serum IgE levels has been emphasized since the mid-sixties, when IgE antibodies were discovered. A number of environmental factors, such as the type of feeding, passive smoking, viral infections, early mold, house dust mite and pet fur exposure modulate IgE synthesis and affect the development of atopic diseases.
Objective:
The aim of the present study was to investigate the natural history of total and specific IgE antibodies in babies at risk for atopy, enrolled in a prospective study for the prevention of atopic disease, and follow-up from birth to 4 years of age.
Methods:
One hundred seventy-four babies (90 boys and 84 girls) at risk for atopy were enrolled in this study. At the last follow-up the children had a median age of 52 months (range 43 to 74 months), dietary and environmental manipulations for the prevention of atopic diseases were recommended. All the infants were examined at the ages of 1, 3, 6, 9, and 12 months and twice each year subsequently when detailed histories were taken and signs and symptoms of atopic disease were sought. Total and specific IgE to cow milk, egg, soy, wheat, and Dermatophagoides pteronyssinus (Dpt) were measured at 6 and 12 months of life and then every year.
Results:
During the first 24 months of life, the number of children with specific IgE to foods (n = 30) was significantly higher in comparison to the number of children with specific IgE to Dpt (n = 12) (P = .0006). Cow milk and egg were the most common offending foods. The number of children with IgE to cow milk (n = 14) was significantly higher than that with IgE to soy (n = 9) (P = .0011). Total serum IgE levels were significantly higher in the group of children who developed atopic disease in comparison with the group that did not (P < .01).
Conclusion:
Dietary and environmental measures may influence the IgE response in atopy-prone children, thus confirming the role of environmental factors in the modulation of the phenotypic expression of atopy.