Nakamura G
Nihon Sanka Fujinka Gakkai Zasshi. 1981 Oct;33(10):1757-66.
In order to investigate the steroidogenesis of dysfunctional ovaries, adrenal suppression and ovarian stimulation tests were performed on 32 patients with ovulatory defect and 3 volunteers with normal menstrual cycles. The protocol of this study was as follows; 3 mg of dexamethasone (DXM) was given daily for 11 days. From 5th day of DXM, 225 IU of human menopausal gonadotropin (hMG) was injected for 3 days, followed by 5,000 IU of human chorionic gonadotropin (hCG). Serum estrone (E1), estradiol (E2), androstenedione (A), dehydroepiandrosterone (DHA), testosterone (T) and dihydrotestosterone (DHT) were measured by radioimmunoassay. In the patients with polycystic ovaries (PCO) which was confirmed under laparotomy and biopsy, serum E2 levels were markedly elevated by hMG stimulation. The E1 levels were similarly elevated by hMG stimulation and increased further by hCG stimulation. The A levels were significantly high (p less than 0.05), and increased remarkably by hCG. The T levels were very high. And they decreased to 2/3 of the basal level following DXM administration, and they increased again by hCG stimulation. Similar secretion patterns of these steroids in PCO patients were also seen in controls and in some patients with moderately atrophic ovaries (MA). THe secretion pattern of DHA suggested that DHA was also secreted from the PCO, normal ovary and MA ovary. From these results it is presumed that excessive production of androgens is not specific in PCO, but it is the result of continuous intrinsic LH stimulation.
为了研究功能失调卵巢的类固醇生成,对32例排卵缺陷患者和3例月经周期正常的志愿者进行了肾上腺抑制和卵巢刺激试验。本研究方案如下:每天给予3毫克地塞米松(DXM),持续11天。从DXM治疗的第5天起,注射225国际单位的人绝经期促性腺激素(hMG),持续3天,随后注射5000国际单位的人绒毛膜促性腺激素(hCG)。通过放射免疫分析法测定血清雌酮(E1)、雌二醇(E2)、雄烯二酮(A)、脱氢表雄酮(DHA)、睾酮(T)和双氢睾酮(DHT)。在经剖腹手术和活检确诊为多囊卵巢(PCO)的患者中,hMG刺激后血清E2水平显著升高。hMG刺激后E1水平同样升高,hCG刺激后进一步升高。A水平显著升高(p小于0.05),hCG刺激后显著增加。T水平非常高。给予DXM后,T水平降至基础水平的2/3,hCG刺激后又再次升高。在对照组和一些中度萎缩卵巢(MA)患者中也观察到PCO患者这些类固醇的类似分泌模式。DHA的分泌模式表明,DHA也由PCO、正常卵巢和MA卵巢分泌。从这些结果推测,雄激素的过量产生在PCO中并非特异性的,而是持续的内源性促黄体生成素(LH)刺激的结果。