Laredo Quesada J M, Jara Sánchez C, Benítez Rodríguez J, Fernández Gundín M J, Vargas Castrillón E, Muñoz González J J, Llerena Ruiz A, Cobaleda Polo J, Pérez-Manga G
Departamento de Medicina, Universidad Complutense de Madrid.
An Med Interna. 1991 Feb;8(2):66-8.
The acetylation phenotype was determined, by means of sulfamethazine measurement, in 87 patients (83 male) with confirmed bronchogenic carcinoma and in 93 healthy control patients (41 male) of equal ages. 48 patients and 54 controls were classified as being "slow acetylators" (Ch2 n.s.) When the persons were individually analysed by phenotype, it was confirmed that the patients showed a significantly lower rate of acetylated sulfamethazine than the control group (p less than 0.02), owing to the poor acetylation of patients with small-cell lung cancer. This difference should be confirmed by more detailed pharmacokinetic studies before regarding it as a possible interference of paraneoplasic type. The polymorphism acetylator cannot be considered a genetic marker related to the risk of having lung cancer.
通过磺胺二甲嘧啶测定，对87例确诊为支气管源性肺癌的患者（83例男性）和93例年龄相仿的健康对照者（41例男性）进行乙酰化表型测定。48例患者和54例对照者被归类为“慢乙酰化者”（χ²无显著性差异）。当按表型对个体进行分析时，证实患者组乙酰化磺胺二甲嘧啶的比率显著低于对照组（p<0.02），原因是小细胞肺癌患者乙酰化能力较差。在将此差异视为可能的副肿瘤类型干扰之前，应通过更详细的药代动力学研究加以证实。乙酰化多态性不能被视为与患肺癌风险相关的遗传标记。
