Pathophysiology of ovarian steroid secretion in polycystic ovary syndrome

被引:12
作者
Barnes, RB [1 ]
机构
[1] Univ Chicago, Dept Obstet & Gynecol, Chicago, IL 60637 USA
来源
SEMINARS IN REPRODUCTIVE ENDOCRINOLOGY | 1997年 / 15卷 / 02期
关键词
polycystic ovary syndrome; ovarian hyperandrogenism; P450c17;
D O I
10.1055/s-2007-1016297
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The ovary in polycystic ovary syndrome (PCOS) produces markedly increased amounts of steroids in response to gonadotropin stimulation. Because FSH secretion is under tight long-loop negative-feedback control and LH is not, hyperandrogenism is the primary clinical manifestation of excess steroid production in PCOS. however, estrogen production by multiple, small follicles may inhibit FSH secretion sufficiently to prevent selection of a single, dominant follicle. Ovarian stimulation testing has suggested that ovarian hyperandrogenism is a result of dysregulation of the androgen producing enzyme P450c17. ACTH stimulation testing is consistent with dysregulation of adrenal P450c17 in about two-thirds of hyperandrogenic women. In most cases dysregulation appears to be due to an intrinsic abnormality of P450c17, or to an abnormality of autocrine/paracrine factors which regulate P450c17. Both LH and insulin hypersecretion are most often a result of the steroid secretory abnormalities. Once present they may amplify the underlying cause of dysregulation of P450c17.
引用
收藏
页码:159 / 168
页数:10
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