Prevention of Allergic Disorders
William R. Solomon MD1
1 Professor of Internal Medicine, Chief of the Division of Allergy, The University of Michigan Medical Center, Ann Arbor, MI.
Allergic disease produces substantial pediatric morbidity and individual dysfunction, making its mechanisms an appropriate target for clarification and preventive strategies. Disease expression seems to reflect a constellation of determinants that controls IgE production variably, affects specific function of target organs, and determines exposure to putative allergens. Bases for the two former factors are being defined rapidly and appear to be controlled genetically. Therefore, although stronger eugenic motivation will be required to exploit even present information for effective prevention, parental phenotypes can provide a rough indication of post-conceptive risk.
Despite many divergent data, current evidence fails to support the value of gestational strategies undertaken to prevent allergic disease in the newborn; however, this risk apparently may be reduced by avoiding postnatal allergens. The protection afforded seems to be allergen-specific rather than somehow serving to abate "the allergic tendency." Evidence increasingly is persuasive that sensitization to pollens, foods, and possibly other agents is prone to occur in the first 6 to 12 months of life. Strategies that exclude potent food allergens from the diets of high-risk infants appear to reduce the occurrence of atopic dermatitis, but seem far less able to influence respiratory symptoms. Efforts to limit exposure to potent inhalant allergens (eg, dust mites, animal "danders") are now also feasible and offer quite effective secondary and, perhaps, primary prevention. Trials of these strategies and clarification of other domestic contaminant effects on child health offer "homely" but valid and potentially useful approaches to reducing the impact of allergic disease.
