THURSDAY, July 9, 2009 (HealthDay News) -- A defective gene significantly increases the likelihood of developing such allergic disorders as eczema and asthma, Scottish researchers report.
Reviewing the findings of 24 studies, researchers from the University of Edinburgh concluded that mutations of the filaggrin gene -- which is thought to help maintain an effective skin barrier against the environment -- significantly increase the risk for developing allergic sensitization, atopic eczema, allergic rhinitis and asthma in people with eczema.
The link between atopic eczema and filaggrin gene mutations appeared to be particularly strong, the study found.
"These findings provide strong supporting evidence that, at least in a subset of those with allergic problems, the filaggrin gene defect may be the fundamental predisposing factor not only for the development of eczema but also for initial sensitization and progression of allergic disease," the study authors wrote. "Our findings suggest that filaggrin is a robust biomarker for allergic conditions."
They called for further research to investigate whether filaggrin can be used to identify people at high risk for allergic conditions. Restoring skin barrier function early in life in people with filaggrin defects might help prevent the development of allergic sensitization and stop the development and progression of allergic disorders, the researchers suggested.
The study was to be published online July 10 in BMJ.
In an accompanying editorial, Hugo Van Bever, a professor of pediatric allergy and immunology at National University Singapore, and his colleagues described the finding as an important advance in understanding the genetic basis of allergic disease.
The next step is to determine whether it's possible to distinguish different genotypes of allergy, which could provide a breakthrough in the prevention, diagnosis and treatment of allergies in children, they said.
The American Academy of Allergy, Asthma & Immunology has more about allergies.
SOURCE: BMJ, news release, July 9, 2009
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