大量证据表明,异喹胍型羟化代谢与异烟肼型乙酰化代谢的人群多态分布具有遗传决定性。因此,根据不同个体对不同类型药物进行羟化或乙酰化代谢能力的遗传差异,可将人群分为强代谢者(EM)与弱代谢者(PM)或快乙酰化者(RA)与慢乙酰化者(SA)。其中,PM或SA表现为常染色体隐性遗传特征。迄今,要确定某型药物代谢的表型,在方法学上要求受试者服用某种工具药,然后计算其尿样的代谢比率,最后根据代谢比率的频数分布图或临界值(antimode)判断其表型。 There is ample evidence that genetic polymorphism in the population of isoquinidine-type hydroxylated and isoniazidacetylated metabolites is hereditary. Therefore, the population can be divided into strong metabolizer (EM) and weak metabolizer (PM) or fast acetylator (RA) and slow acetyl (RA) according to the genetic difference of hydroxylation or acetylation metabolism of different types of drugs by different individuals. (SA). Among them, PM or SA showed autosomal recessive genetic characteristics. To date, to determine the phenotype of a certain type of drug metabolism, the methodology requires the subject to take a tool and then calculate the metabolic rate of the urine sample. Finally, the frequency distribution of the metabolic rate or the antimode Its phenotype.