GENETIC POLYMORPHISM IN GLUTATHIONE S-TRANSFERASES M1 AND T1 IN CHILDREN WITH BRONCHIAL ASTHMA

Abstract Asthmatic (n = 100) and health (n = 104) children were compared for rates of homozygous deletions of the glutathione S-transferase class mu and theta genes (null genotypes, GSTM1"-" and GSTT1"-", respectively). The frequency of GSTM1"-" and GSTT1"-" genotypes in patients with bronchial asthma (BA) (52 [symbol: see text] 26%) were increased compared to healthy children (42 and 11%) (odds ratio (OR) for GSTM1"-" = 1.48; CI: 0.82-2.67; p = 0.16; OR for GSTT1"-" = 2.69; CI: 1.2-6.11; p = 0.0079). OR for GSTM1"-" and GSTT1"-"-combination was 5,12; CI: 0.55-119.5; p = 0.107. We conclude that null-genotypes are associated with susceptibility to BA in children. Passive smoking (PS) increased risk of BA for children with GSTM1"-" genotype, but not with GSTT1"-" genotype. The association of these genotypes was estimated with such clinical peculiarities of BA as polyvalent allergy, early development and heavy course. In the group of nonsmoking (NS) patients was found the statistically in significant association of individual null genotypes with any clinical peculiarities. Combination of null-genotypes in NS patients associated with early development of BA (OR = 6.5; CI: 0.78-64.95; p < 0.05), and combination of plus genotypes--with polyvalent allergy (OR = 7.35; CI: 1.07-63.44; p < 0.05). In the group of PS patients GSTM1"-" genotype was associated with early development of BA (OR = 9.0; CI: 1.02-203.3; p < 0.05) and GSTT1"-" genotype--with heavy course of disease (OR = 4.64; CI: 1.16-19.34; p < 0.05). Passive smoking was the risk factor for the unfavourable course of BA for the patients carrying GSTM1"-" genotype. Combination of plus genotypes protected PS patients from all unfavorable peculiarities of disease.