The mechanism of ovulation inhibition by triamcinolone acetonide.
The mechanism of ovulation inhibition by triamcinolone acetonide.
复制标题
曲安奈德抑制排卵的机制。
DOI：
10.1210/jcem-46-1-8
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发表时间：
1978
期刊：
影响因子：
--
通讯作者：
M. Oliver
中科院分区：
文献类型：
--
作者：
G. Cunningham;J. Goldzieher;A. de la Peña;M. Oliver
在月经周期的第1天或第2天单次给予25 mg曲安奈德，可抑制排卵。为了研究这种作用的机制，每天测定血浆FSH、LH、雌酮+雌二醇（E1 + E2）和孕激素。一些受试者还在周期第15天接受单次剂量的LH-RH或hCG或在第5-9天接受克罗米芬。曲安奈德本身引起血浆雌激素的可变抑制，周期中期促性腺激素峰的丧失，以及血浆孕激素升高不足或不升高。雌激素分泌受损似乎不是由于低促性腺激素水平。FSH和LH对LH-RH的反应与当时的雌激素水平有关。用克罗米酚治疗的6名妇女中有4名的血浆白蛋白水平超过8 ng/ml。曲安奈德似乎主要通过下丘脑抑制作用影响下丘脑-垂体-卵巢轴，也可能通过对卵巢的直接作用。
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.