Barbieri R L
Department of Obstetrics and Gynecology, State University of New York, Stony Brook 11794.
Curr Opin Obstet Gynecol. 1992 Jun;4(3):372-9.
Mutations in the genes for the insulin receptor, 21-hydroxylase, 11 beta-hydroxylase, and 3 beta-hydroxysteroid dehydrogenase isomerase enzymes are associated with hyperandrogenism. These genetic causes of hyperandrogenism account for less than 10% of all cases. A major goal of future research will be to identify other genetic causes of hyperandrogenism. Evidence continues to accumulate that luteinizing hormone, insulin-like growth factor I, and insulin are major factors regulating ovarian androgen production. Optimal therapy for hyperandrogenism probably includes simultaneous suppression of androgen production and blockade of androgen action.
胰岛素受体、21-羟化酶、11β-羟化酶和3β-羟类固醇脱氢酶异构酶基因的突变与高雄激素血症相关。这些高雄激素血症的遗传病因占所有病例的比例不到10%。未来研究的一个主要目标将是确定高雄激素血症的其他遗传病因。越来越多的证据表明,促黄体生成素、胰岛素样生长因子I和胰岛素是调节卵巢雄激素产生的主要因素。高雄激素血症的最佳治疗可能包括同时抑制雄激素产生和阻断雄激素作用。