[支气管哮喘儿童谷胱甘肽s -转移酶M1和T1基因多态性]。

Voprosy meditsinskoi khimii Pub Date : 2000-07-01
V A Vavilin, O B Chasovnikova, V V Liakhovich, S M Gavalov, O A Riabova
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引用次数: 0

摘要

比较哮喘儿童(n = 100)和健康儿童(n = 104)的谷胱甘肽s转移酶类mu和theta基因纯合缺失率(空基因型分别为GSTM1“-”和GSTT1“-”)。支气管哮喘(BA)患者GSTM1“-”和GSTT1“-”基因型的频率(52 26%)比健康儿童(42和11%)增加(GSTM1“-”的优势比(OR) = 1.48;置信区间:0.82—-2.67;P = 0.16;OR for GSTT1"-" = 2.69;置信区间:1.2—-6.11;P = 0.0079)。GSTM1“-”和GSTT1“-”组合的OR为5,12;置信区间:0.55—-119.5;P = 0.107。我们得出结论,零基因型与儿童对BA的易感性相关。被动吸烟(PS)增加GSTM1“-”基因型儿童BA的风险,但不增加GSTT1“-”基因型儿童BA的风险。这些基因型与BA的临床特点如多价过敏、早期发展和重度病程有关。在非吸烟组(NS)患者中,发现个体零基因型与任何临床特征具有统计学上显著的相关性。NS患者中与BA早期发展相关的零基因型组合(OR = 6.5;置信区间:0.78—-64.95;p < 0.05),阳性基因型合并多价过敏(OR = 7.35;置信区间:1.07—-63.44;P < 0.05)。在PS患者组中,GSTM1“-”基因型与BA的早期发展相关(OR = 9.0;置信区间:1.02—-203.3;p < 0.05), GSTT1“-”基因型与病程重有关(OR = 4.64;置信区间:1.16—-19.34;P < 0.05)。被动吸烟是GSTM1“-”基因型患者不良BA病程的危险因素。正基因型的组合保护PS患者免受疾病的所有不利特性。
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[Genetic polymorphism in glutathione S-transferase M1 and T1 in children with bronchial asthma].

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.

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