Barletta C, Vagiri D, Scavo D
Policlinico Umberto I, Roma.
Minerva Endocrinol. 1992 Jul-Sep;17(3):107-19.
To investigate whether inappropriate LH secretion in Polycystic Ovary Syndrome (PCO) was related to a reduction of inhibitory opioid control on the GnRH-LH system, 23 women affected by PCO (12 obese, BMI: 37.1 +/- 3.9 and 11 non obese, BMI: 21.5 + 2.4) and 19 fertile women (10 obese, BMI: 38.8 + 1.8 and 9 non obese, BMI: 20.1 + 1.5) were studied. Plasma levels of Beta-Endorphin (B-Ep) in basal condition and LH and FSH serum levels following acute administration of naloxone (0.1 mg/kg e.v.) were evaluated in the PCO and control groups. Moreover, in order to investigate whether the neuroendocrine abnormalities in PCO are a primary hypothalamic defect or secondary to an inappropriate feedback of gonadal steroids, the LH response following Naloxone administration was evaluated again after two months of clomiphene therapy (50 mg p.os ones a day for 5 days). The women affected by PCO had increased LH/FSH ratio, testosterone levels (P < 0.001, P < 0.01) and significantly decreased T/E2 ratio, SHBG levels compared to the normal women (P < 0.01, P < 0.001). B-Ep plasma levels in PCOs OB and PCOs nOB (6.13 + 1.2 Pmol/L, 4.8 + 0.4 Pmol/L) were similar to those observed in obese and non obese control women (7.2 + 2.5 Pmol/L, 4.2 + 1.3 Pmol/L), respectively. In the PCO and control groups naloxone induced a significant increase of FSH and LH levels. Thus the area under the curve of LH and FSH was significant higher after naloxone, than following saline infusion both in PCO (P < 0.01, P < 0.05) and controls (P < 0.001, P < 0.001). However, in PCO the post naloxone FSH increase was similar to that found in fertile women, while the LH increase post naloxone was lower than that observed in controls (50 + 32.4% vs 101.6 + 36.7%; P < 0.01). Particularly in PCO with LH/FSH ratio equal or higher than 3, no significant variation of LH levels was found after naloxone. Moreover the LH increase post naloxone was similar in PCO OB (46 + 19.8%) and in PCO nOB (49.9 + 13.1%), correlated negatively with LH basal levels (P < 0.02), LH/FSH (P < 0.005), E1/E2 (P < 0.005) and was independent of T/E2, BMI and duration of the disease. Following clomiphene treatment, the LH response after naloxone was significantly higher than that observed before treatment (from 9.4 + 4.2 mUI/ml to 16.5 + 3.9 mUI/ml, P < 0.001).(ABSTRACT TRUNCATED AT 400 WORDS)
为研究多囊卵巢综合征（PCO）患者促黄体生成素（LH）分泌异常是否与阿片类物质对促性腺激素释放激素-促黄体生成素（GnRH-LH）系统的抑制性控制减弱有关，对23例PCO患者（12例肥胖，BMI：37.1±3.9；11例非肥胖，BMI：21.5±2.4）和19例可育女性（10例肥胖，BMI：38.8±1.8；9例非肥胖，BMI：20.1±1.5）进行了研究。评估了PCO组和对照组基础状态下的β-内啡肽（B-Ep）血浆水平以及急性注射纳洛酮（0.1mg/kg静脉注射）后LH和FSH的血清水平。此外，为研究PCO患者的神经内分泌异常是原发性下丘脑缺陷还是继发于性腺类固醇的不适当反馈，在克罗米芬治疗两个月后（50mg口服，每日1次，共5天）再次评估纳洛酮给药后的LH反应。与正常女性相比，PCO患者的LH/FSH比值、睾酮水平升高（P<0.001，P<0.01），T/E2比值、性激素结合球蛋白（SHBG）水平显著降低（P<0.01，P<0.001）。肥胖PCO患者（PCOs OB）和非肥胖PCO患者（PCOs nOB）的B-Ep血浆水平分别与肥胖和非肥胖对照女性相似（6.13±1.2Pmol/L，4.8±0.4Pmol/L与7.2±2.5Pmol/L，4.2±1.3Pmol/L）。在PCO组和对照组中，纳洛酮均导致FSH和LH水平显著升高。因此，无论是PCO组（P<0.01，P<0.05）还是对照组（P<0.001，P<0.001），纳洛酮给药后LH和FSH的曲线下面积均显著高于输注生理盐水后。然而，在PCO患者中，纳洛酮给药后FSH的升高与可育女性相似，而纳洛酮给药后LH的升高低于对照组（50±32.4%对101.6±36.7%；P<0.01）。特别是LH/FSH比值等于或高于3的PCO患者，纳洛酮给药后LH水平无显著变化。此外，肥胖PCO患者（46±19.8%）和非肥胖PCO患者（49.9±13.1%）纳洛酮给药后LH的升高相似，与LH基础水平（P<0.02）、LH/FSH（P<0.005）、E1/E2（P<0.005）呈负相关，且与T/E2、BMI和病程无关。克罗米芬治疗后，纳洛酮给药后的LH反应显著高于治疗前（从9.4±4.2mUI/ml升至16.5±3.9mUI/ml，P<0.001）。（摘要截断于400字）
