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近年来,关于遗传变异对药物反应的影响逐渐引起了人们的注意。远在1926年就发现了服用伯氨喹引起溶血的付作用,至50年代初期,侵朝美军为了防治疟疾,广泛服用伯氨喹,发现不少黑人士兵发生溶血性贫血。其后,不断对这一反应的机理进行系统的研究。至50年代中期Carson和Waller分别证实葡萄糖6磷酸脱氢酶(G6PD)缺陷可引起溶血性贫血。现已确认G6PD缺陷是结构基因变异的结果。家系研究证明,本症属于性连锁不完全显性遗传,其等位基因在X染色体上。1952年日本耳鼻喉科医生高原在用过氧化氢(H_2O_2)
In recent years, the impact of genetic variation on the drug response has gradually attracted people’s attention. As early as the early 1950s, the U.S. invasion of North Korea used primaquine extensively to prevent malaria and found that many black soldiers were found to have hemolytic anemia. Since then, the mechanism of this reaction has been systematically studied. By the mid-1950s Carson and Waller confirmed that glucose 6-phosphate dehydrogenase (G6PD) deficiency could cause hemolytic anemia. It has been confirmed that G6PD deficiency is the result of structural gene variation. Pedigree studies have shown that the disease belongs to the sex chain incomplete dominant inheritance, the allele in the X chromosome. In 1952 Japan otolaryngology plateau in the use of hydrogen peroxide (H_2O_2)