Morris R J, Freed C R, Kohler P F
Arthritis Rheum. 1979 Jul;22(7):777-80. doi: 10.1002/art.1780220714.
To ascertain if a genetically determined slow drug acetylation rate is correlated with the development of spontaneous systemic lupus erythematosus (SLE), as it is in drug-induced SLE, acetylation phenotypes of 27 patients with spontaneous SLE were determined after administration of dapsone. Thirty-three percent were slow acetylators, 63% were rapid acetylators, and one was indeterminate, a distribution not significantly different from that expected in control subjects. Among 4 pairs of first-degree relatives, all of whom had spontaneous SLE, 7 of the 8 individuals were rapid acetylators. We conclude that people who are slow acetylators are at no greater risk for developing spontaneous SLE than are rapid acetylators and that the slow acetylation phenotype is not correlated with familial SLE.
为了确定基因决定的药物慢乙酰化率是否与自发性系统性红斑狼疮(SLE)的发生相关,如同在药物性SLE中那样,在给予氨苯砜后测定了27例自发性SLE患者的乙酰化表型。33%为慢乙酰化者,63%为快乙酰化者,1例结果不确定,该分布与健康对照者预期的分布无显著差异。在4对均患有自发性SLE的一级亲属中,8个人中有7个是快乙酰化者。我们得出结论,慢乙酰化者发生自发性SLE的风险并不高于快乙酰化者,并且慢乙酰化表型与家族性SLE无关。