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曲安奈德抑制排卵的机制。

The mechanism of ovulation inhibition by triamcinolone acetonide.

作者信息

Cunningham G R, Goldzieher J W, de la Pena A, Oliver M

出版信息

J Clin Endocrinol Metab. 1978 Jan;46(1):8-14. doi: 10.1210/jcem-46-1-8.

DOI:10.1210/jcem-46-1-8
PMID:376542
Abstract

A single dose of 25 mg triamcinolone acetonide, when given on day 1 or 2 of the menstrual cycle, inhibits ovulation. To examine the mechanism of this action, daily determinations of plasm FSH, LH, estrone plus estradiol (E1 + E2), and progestins were performed. Some subjects also received a single dose of LH-RH or hCG on cycle day 15 or clomiphene citrate on days 5-9. Triamcinolone acetonide itself caused variable suppression of plasma estrogens, loss of the mid-cycle gonadotropin surge, and a deficient or absent rise in plasma progestins. Impaired secretion of estrogen did not seem to be due to low gonadotropin levels. FSH and LH responses to LH-RH were adequate in relation to prevailing estrogen levels. Four of six women treated with clomiphene responded with plasma progestin levels which exceed 8 ng/ml. Triamcinolone acetonide seems to affect the hypothalamic-pituitary-ovarian axis mainly by hypothalamic suppression and possibly by a direct effect on the ovary as well.

摘要

在月经周期第1天或第2天给予单剂量25毫克曲安奈德可抑制排卵。为研究此作用机制,每日测定血浆促卵泡生成素(FSH)、促黄体生成素(LH)、雌酮加雌二醇(E1 + E2)和孕激素。部分受试者在周期第15天还接受了单剂量促性腺激素释放激素(LH - RH)或人绒毛膜促性腺激素(hCG),或在第5 - 9天接受了枸橼酸氯米芬治疗。曲安奈德本身导致血浆雌激素的抑制程度不一、中期促性腺激素高峰消失以及血浆孕激素升高不足或未升高。雌激素分泌受损似乎并非由于促性腺激素水平低所致。FSH和LH对LH - RH的反应与当时的雌激素水平相关,是充足的。接受枸橼酸氯米芬治疗的6名女性中有4名的血浆孕激素水平超过8纳克/毫升。曲安奈德似乎主要通过抑制下丘脑,也可能通过对卵巢的直接作用来影响下丘脑 - 垂体 - 卵巢轴。

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The mechanism of ovulation inhibition by triamcinolone acetonide.曲安奈德抑制排卵的机制。
J Clin Endocrinol Metab. 1978 Jan;46(1):8-14. doi: 10.1210/jcem-46-1-8.
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