Atopic bronchial asthma (ABA) is most probably caused by an interaction of multiple disease susceptibility genes with poorly identified environmental factors. The number of genes involved in this complex polygenic disorder has not yet been fully determined. The genetic polymorphism of a glutathione-S-transferase (GST) super-gene family was studied. High levels of GSTM10/0 (79%) and GSTT10/0 (58%) genotypes were found in ABA children compared to those in relevant controls (45 and 20%, respectively). Polymorphisms of GSTP1 genes were not found to be associated with asthma. The frequencies of null allele homozygotes for both GST genes (GST1 0/0 and GSTT1 0/0) occur in 49% of asthmatic patients, whereas these genotypes comprise only 12% in the controls. The presence of both GSTM1 and GSTT1 null alleles result in a 7-fold increase of asthma disease risk (OR 7.15; 95% CI = 2.70-18.98). A combination of functionally impaired genotypes of all three GST genes was four times more common in ABA patients compared to the controls (35 and 8%, respectively). Ninety percent of ABA children with atopic dermatitis had a GSTM1 deficiency (0/0) when compared to 57% GSTM10/0 genotypes in the group of ABA children without this complication. The genetic tests for GSTM1 and GSTT1 homozygotes for null alleles (GSTM10/0 and GSTTMI1 0/0) might be useful in the identification of persons at risk for ABA, and might thus be of great practical value for the predictive medicine service.

Key words: atopic bronchial asthma (ABA), GSTM1, GSTT1, GSTP1, genetic polymorphism.