Prevention of Allergic Disorders

Abstract

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 postconceptive 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.

Can house dust mite-triggered atopic dermatitis be alleviated using acaricides?

“…HDM are the dominant indoor allergen associated with atopic symptoms. '^ HDM allergens have been purified and specific immunoassays, such as the enzyme-linked immunosorbent assay (ELISA), have been developed and used in epidemiological studies to quantify HDM allergen exposure to humans.^''•^^T he detection of HDM allergen in naturally occurring lesions of AD has led to the hypothesis that IgE-mediated allergic contact sensitivity to HDM allergen plays an important part in the pathogenesis of AD.^^ IgE levels are higher in patients with AD than in controls.R ecent evidence strongly suggests that sensitization to allergens is prone to occur in the first 6-12 months of life.^" Efforts to reduce exposure to HDM allergens can offer quite effective secondary and, perhaps, primary prevention [20][21][22] and could provide an alternative candidate in the treatment of AD to topical and/or systemic medicines (which may have associated adverse sideeffects).^^ Reduction of environmental mites produced clinical improvement in AD.^* In Japan, clean room therapy, which reduces the levels of airborne mites to < 3 mites/m^, improved clinical symptoms of patients with AD due to the elimination of HDM faecal pellets.^Î n practice, people suffering from AD do not have access to clinical clean rooms, even for the suggested 11 h a day.^^ A simple, cheap, effective alternative means of reducing HDM exposure is sought.…”