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首页> 外文期刊>Pharmacogenetics >Prospective evaluation of detoxification pathways as markers of cutaneous adverse reactions to sulphonamides in AIDS.
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Prospective evaluation of detoxification pathways as markers of cutaneous adverse reactions to sulphonamides in AIDS.

机译：排毒途径的前瞻性评估，作为艾滋病中磺胺类药物皮肤不良反应的标志。

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The use of sulphonamides is complicated by a high rate of cutaneous reactions in AIDS. Metabolic risk factors have been suspected for these reactions. We conducted a prospective study to evaluate whether glutathione S-transferase M1 null genotype, glutathione deficiency and acetylator status as risk factors. To explain the high frequency of slow acetylator phenotype in AIDS patients, we compared N-acetyltransferase-2 phenotype and genotype in this population. AIDS patients treated with sulphonamides for Pneumocystis carinii pneumonia or toxoplasmosis were followed up for cutaneous reactions. Glutathione S-transferase genotyping, glutathione level determination, N-acetyltransferase-2 genotyping and phenotyping were performed. One hundred and thirty-six AIDS patients were studied. Glutathione S-transferase M1 and T1 null genotypes, intracellular glutathione level, slow acetylator genotype and phenotype were not risk factors for cutaneous sulphonamides reactions. The association of glutathione S-transferase M1 null genotype and the slow acetylator one was a risk factor [Fisher's exact test, odds ratio (OR) = 2.6, 95% confidence interval (CI) = 1.2-5.9; P = 0.02]. A discordance between acetylator genotype and phenotype was found in 35% of patients. This frequency was significantly higher than the 6-7% expected (Fisher's exact test: OR = 7.5, 95% CI = 4.2-13.4; P < 0.0001). Suspected metabolic risk factors for sulphonamides cutaneous reactions were not confirmed prospectively. However, the association of glutathione S-transferase M1 null genotype and the slow acetylator one appeared to increase the risk of reactions. We clearly showed that the acetylation phenotype measured by caffeine probe could be modified by the disease.
机译：艾滋病中高比例的皮肤反应使磺酰胺的使用变得复杂。已怀疑这些反应有代谢危险因素。我们进行了一项前瞻性研究，以评估是否将谷胱甘肽S-转移酶M1基因型无效，谷胱甘肽缺乏和乙酰化状态作为危险因素。为了解释艾滋病患者中慢乙酰化酶表型的高频率，我们比较了该人群的N-乙酰转移酶-2表型和基因型。接受磺胺类药物治疗卡氏肺孢子虫肺炎或弓形虫病的艾滋病患者，应进行皮肤反应。进行了谷胱甘肽S-转移酶基因分型，谷胱甘肽水平测定，N-乙酰基转移酶-2基因分型和表型分析。研究了136名艾滋病患者。谷胱甘肽S-转移酶M1和T1无效基因型，细胞内谷胱甘肽水平，慢乙酰化基因型和表型不是皮肤磺酰胺反应的危险因素。谷胱甘肽S-转移酶M1无效基因型和慢乙酰化酶1的相关性是一个危险因素[Fisher's精确检验，比值比（OR）= 2.6，95％置信区间（CI）= 1.2-5.9; P = 0.02]。在35％的患者中发现乙酰化基因型和表型不一致。该频率显着高于预期的6-7％（费舍尔的精确检验：OR = 7.5，95％CI = 4.2-13.4; P <0.0001）。前瞻性未确认磺胺类药物皮肤反应的可疑代谢危险因素。然而，谷胱甘肽S-转移酶M1无效基因型和慢乙酰化酶一的关联似乎增加了反应的风险。我们清楚地表明，通过咖啡因探针测得的乙酰化表型可被该疾病改变。

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