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Background: Asthma is an inflammatory airways disease caused by an interaction between susceptibility genes and a diverse group of environmental factors. The GSTP1 Ile105Val polymorphism has been associated with asthma in several studies.
Objective: To examine the hypothesis that polymorphism in the GSTP1 locus is associated with asthma and related phenotypes in a population of subjects stratified by airway obstruction as well as atopic status (IgE level and history).
Methods: Fifty patients with bronchial asthma and fifty normal control subjects were enrolled in this study and were subjected to asthma questionnaire, spirometric studies, conventional polymerase chain reaction (PCR) with enzyme digestion to determine GSTP1 genotype, serum immunoglobulin E (IgE) measurement and eosinophilic count.
Results: The genotype distributions for GSTP1 gene polymorphism in bronchial asthma subjects and controls showed no significant difference. Both patients and controls were found to be in Hardy-Weinberg equilibrium. Presence of the Val/Val genotype did not confer a decreased risk for developing bronchial asthma (odd ratio (OR) = 0.34, 95% confidence interval (CI) = 0.06–1.91, P =0.0331). There was no significant relationship between GSTP1 genotypes and the severity of asthma. In addition, the frequency of GSTP1 genotypes distribution achieved no significance when assessed according to degree of airway obstruction or control of asthma. No associations between the GSTP1 genotypes and atopic status or IgE level were identified.
Conclusion: The present study does not support a substantial role of GSTP1 gene polymorphism in the development of asthma. However, large studies with accurate measurement of the environmental exposure are needed in order to reach adequate power to detect gene-environment interactions and other genes involved in the antioxidant pathway.