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[支气管哮喘患儿谷胱甘肽S-转移酶M1和T1的基因多态性]

[Genetic polymorphism in glutathione S-transferase M1 and T1 in children with bronchial asthma].

作者信息

Vavilin V A, Chasovnikova O B, Liakhovich V V, Gavalov S M, Riabova O A

机构信息

Institute of Molecular Biology and Biophysics Siberian Branch of RAMS, Novosibirsk, Russia.

出版信息

Vopr Med Khim. 2000 Jul-Aug;46(4):388-97.

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.

摘要

对100名哮喘儿童和104名健康儿童的谷胱甘肽S-转移酶μ类和θ类基因纯合缺失率(分别为无效基因型GSTM1“-”和GSTT1“-”)进行了比较。支气管哮喘(BA)患者中GSTM1“-”和GSTT1“-”基因型的频率(52 [符号:见原文] 26%)高于健康儿童(42%和11%)(GSTM1“-”的优势比(OR)=1.48;可信区间:0.82 - 2.67;p = 0.16;GSTT1“-”的OR = 2.69;可信区间:1.2 - 6.11;p = 0.0079)。GSTM1“-”和GSTT1“-”组合的OR为5.12;可信区间:0.55 - 119.5;p = 0.107。我们得出结论,无效基因型与儿童BA易感性相关。被动吸烟(PS)增加了GSTM1“-”基因型儿童患BA的风险,但与GSTT1“-”基因型无关。这些基因型与BA的多价过敏、早期发病和病情严重等临床特征之间的关联进行了评估。在非吸烟(NS)患者组中,未发现单个无效基因型与任何临床特征之间存在统计学上的显著关联。NS患者中无效基因型的组合与BA的早期发病相关(OR = 6.5;可信区间:0.78 - 64.95;p < 0.05),而阳性基因型的组合与多价过敏相关(OR = 7.35;可信区间:1.07 - 63.44;p < 0.05)。在PS患者组中,GSTM1“-”基因型与BA的早期发病相关(OR = 9.0;可信区间:1.02 - 203.3;p < 0.05),GSTT1“-”基因型与病情严重相关(OR = 4.64;可信区间:1.16 - 19.34;p < 0.05)。被动吸烟是携带GSTM1“-”基因型患者BA病情不利发展的危险因素。阳性基因型的组合可使PS患者免受疾病所有不利特征的影响。

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