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作 者:吴效科[1,2] 张祖暄[1,2] 苏延华[1,2]
机构地区:[1]南京军区南京总医院妇产科 [2]南京大学医学院
出 处:《中华妇产科杂志》1998年第3期153-156,共4页Chinese Journal of Obstetrics and Gynecology
摘 要:目的探讨多囊卵巢综合征(PCOS)患者垂体-卵巢、垂体-肾上腺、垂体-甲状腺轴功能的改变与其病理生理的关系。方法对黄体生成素(LH)/卵泡刺激素(FSH)≥3的15例Ⅰ型组患者、LH/FSH<3的15例Ⅱ型组患者和20例对照组妇女,以促黄体生成素释放激素(LRH,100μg)、促肾上腺皮质激素(ACTH,250μg)和促甲状腺激素释放激素(TRH,500μg),分别兴奋垂体-卵巢、垂体-肾上腺皮质、垂体-甲状腺轴,观察3组相应靶腺体内分泌指标的变化。结果LRH兴奋试验后,LH反应浓度是Ⅰ型组>Ⅱ型组>对照组,但两个患者组的血睾酮(T)水平均呈上升曲线,且程度相似;ACTH兴奋试验后,两个患者组的皮质醇、硫酸脱氢表雄酮和T的反应浓度显著高于对照组,尤以Ⅱ型组明显;TRH兴奋试验后,两个患者组的促甲状腺激素和泌乳素的反应浓度均高于对照组,但Ⅰ型组的游离甲状腺素的反应浓度于2小时点低于另外两组。结论PCOS患者的雄激素过多,Ⅰ型组与LH有关,Ⅱ型组还与胰岛素有关。肾上腺皮质功能亢进加剧了其雄激素过多和胰岛素抵抗现象。PCOS患者存在亚临床甲状腺功能低下现象。? Objective To assess the role of the functional states of pituitaryovary, adrenal and thyroid axes in the pathophysiology of polycystic ovarian syndrome (PCOS). Methods The stimulation tests of abovementioned three endocrine axes by luteinizing hormone releasing hormone (LRH, 100 μg), adrenocorticotrophin (ACTH, 250 μg) and thyroid releasing hormoune (TRH, 500 μg), respectively, were performed in each subjects of two PCOS groups [luteinizing hormone/follicle stimulating hormone (LH/FSH)≥3, Group 1, n=15; LH/FSH<3, Group 2, n=15] and the control (n=20). Endocrine indices of corresponding target glands were evaluated by radioimmunoassay (RIA). Results After LRH administration, the amplitude of LH responses in three groups were as follows: Group 1>Group 2>control while mean testosterone levels were elevated to a similar extent in two PCOS groups and remained unchanged in the control. Following ACTH stimulation, PCOS subjects, especially of Group 2 with obvious insulin resistance, showed higher responses of cortisol, dehydroepiandrosterone sulfate and testosterone as compared with the controls. However, during TRH testing, exaggerated thyroidstimulating hormone and prolactin responses in two PCOS groups and blunted free thyroxine response at two hour point in Group 1 were observed, as compared with the control. Conclusion It appears that ovarian androgen excess in women with PCOS is mainly LHdependent in Group 1 and insulindependent in Group 2. Enhanced adrenal activity may contribute to both hyperandrogenism and insulin resistance in this syndrome, and subclinical hypothyroidism may exist in affected subjects, especially of Group 1.【
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