绝经后女性脑梗死患者血清性激素结合球蛋白的检测及其意义

目的 探讨血清性激素结合球蛋白（SHBG）在绝经后女性脑梗死患者发病过程中的变化及其意义。方法 采用放免法动态测定30例绝经后女性脑梗死患者及30例健康体检者血清SHBG的水平，分析其与脑梗死的关系。结果 绝经后女性脑梗死患者急性期血清SHBG明显高于恢复期及健康对照组。差异有显著性（均P〈0．01），而恢复期与健康对照组血清SHBG差异无显著性（P〉0．05）。结论 绝经后女性脑梗死患者急性期SHBG增高，而在恢复期恢复正常。这种变化是机体对脑梗死的一种适应性反应，有利于脑梗死的恢复。     

性激素与老年脑梗死关系的初步研究

目的 探讨性激素失衡与老年脑梗死的关系及性激素引起脑梗死可能机制。方法 采用放射免疫测定老年急性脑梗死患者急性期及恢复期之雌二醇 (E2)、睾酮 (T)、孕酮 (Pr)、促卵泡生成素 (FSH)、黄体生成素 (LH)血清水平,将之与对照组进行比较,采用沉淀飘浮酶联法及乙酰丙酮显色法测定,急性脑梗死患者及对照组之血清总胆固醇 (TC)、甘油三脂 (TG)、低密度脂蛋白胆固醇 (LDL-C)、极低密度脂蛋白胆固醇 (VLDL-C)、高密度脂蛋白胆固醇 (HDL-C)及其亚组分 (HDL2-C)、 (HDL3-C)。结果 男性脑梗死患者急性期及恢复期 E2、 E2/T比值明显高于男性对照组,女性脑梗死患者急性期及恢复期 E2明显低于女性对照组, FSH、 LH明显高于对照组,且与 E2呈负相关,男性患者 E2、 E2/T比值与 TC、 LDL-C呈正相关,与 HDL-C、 HDL2-C呈负相关;女性患者 E2与 TC、 LDL-C呈负相关,与 HDL-C、 HDL2-C呈正相关。结论 男性 E2、 E2/T比值水平升高,女性 E2水平降低,可能是引起脑梗死的危险因素之一。它们引起脑梗死的机制之一是影响血脂代谢,从而引起动脉粥样硬化。     

脑外伤患者下丘脑-垂体-性腺轴变化的探讨

目的观察脑外伤患者急性期下丘脑-垂体-性腺轴的变化。方法采用放射免疫法测定血清卵泡刺激素(FSH)、黄体生成素(LH)、泌乳素(PRL)、雌二醇(E2)、黄体酮(T)的水平。结果脑外伤患者急性期血清FSH、LH、PRL、E2、T的水平明显增高。结论脑外伤影响下丘脑-垂体-性腺轴的功能变化。     

性激素检测对继发性闭经患者的诊断价值

目的：探讨性激素六项检测对继发性闭经患者闭经原因的诊断价值。方法对61例继发性闭经患者（闭经组）和30例女性健康体检者（对照组）血清中的促黄体生成素（LH）、卵泡刺激素（FSH）、垂体泌乳素（PRL）、雌二醇（E2）、睾酮（T）以及孕酮（P）等6项激素的水平进行检测和比较。结果61例继发性闭经患者各项性激素水平正常15例,占24.6%,其余46例性激素水平均有不同程度升高或降低;闭经组患者E2、FSH、PRL、LH、T与对照组比较差异有统计学意义（P＜0.05或P＜0.01）,P的差异无统计学意义（P＞0.05）。结论血清性激素六项检查可以有效地对闭经原因进行分析,从而可以进行有效的诊断、治疗及预后分析。     

女性脑梗死患者颈动脉粥样硬化斑块与性激素水平的相关性研究

目的 研究女性脑梗死患者颈动脉粥样硬化斑块与性激素雌二醇（E2）、睾酮（T）水平的相关性。方法 应用彩色多普勒超声仪对86例绝经后女性脑梗死患者颈动脉进行检测，观察颈动脉粥样硬化斑块的发生情况。采用放射免疫法检测脑梗死患者血清E2和T水平。按颈动脉超声检测结果将脑梗死患者分为斑块组和非宛块组。结果 与非斑块组比较，斑块组患者血清E2水平和E2／T显著降低（P〈0．05），T水平增高但差异无显著性（P〉0．05）；与轻度斑块组比较，中、重度斑块组患者血清E2水平和E2／T显著降低（P〈0．05和P〈0．01）。结论 E2水平下降及性激素内环境紊乱与绝经后女性脑梗死患者颈动脉粥样硬化斑块密切相关。     

男性血液透析患者性激素水平的变化

目的观察男性血液透析患者的血清性激素水平的变化。方法观察上海市第一人民医院3组人群:血液透析组、对照组、移植组。记录3组的年龄并测定血清性激素的水平,进行分析。结果血液透析组的血清FSH、LH、PRL、E2、P水平显著高于对照组和移植组,T水平显著低于对照组。血液透析组的血清T水平低于移植组,差异无显著性。对照组和移植组的性激素水平差异无显著性。结论在男性血液透析患者中存在着下丘脑-垂体-性腺轴的紊乱,血清FSH、LH、PRL、P、E2水平的明显增高,血清T水平的明显下降。肾移植可以纠正慢性肾衰竭血液透析患者的性激素水平的紊乱。     

脑梗死患者血清sICAM-1、sVCAM-1水平的变化及意义

目的探讨脑梗死患者血清可溶性细胞间黏附分子-1（sICAM-1）、可溶性血管细胞黏附分子-1（sVCAM-1）水平的变化及临床意义。方法采用双抗体夹心酶联免疫吸附法（ELISA法）测定86例脑梗死[急性期脑梗死（急性期组）患者56例，根据梗死灶的容积大小分为3组：大梗死灶组26例、中等梗死灶组5例和小梗死灶组25例；恢复期脑梗死（恢复期组）患者30例]患者和31例健康体检者血清sICAM-1和sVCAM-1的水平。采用斯堪的那维亚卒中量表（SSS）和美国国立卫生研究院卒中量表（NIHSS）对56例急性期组患者临床神经功能缺损程度进行评分。结果急性期组血清sICAM-1、sVCAM-1水平均显著高于恢复期组（P均〈0.05），急性期组和恢复期组血清sICAM-1、sVCAM-1水平均显著高于对照组（P均〈0．05），急性期脑梗死患者血清sICAM-1、sVCAM-1水平与SSS评分、NIHSS评分、梗死灶容积均无相关性（r=0．139、-0．060、-0．034、0．202、-0．098、-0．026，P均〉0．05）。结论sICAM-1、sVCAM-1可能参与了脑梗死早期的炎症反应及再灌注损伤，而与梗死灶的大小和临床神经功能缺损程度无明显相关性。     

单纯性肥胖儿童性腺激素及胰岛素水平的临床研究

目的 观察单纯性肥胖儿童血清中睾酮（T）、雌二醇（E2）、黄体生成素（LH）、促卵泡激素（FSH）、胰岛素（Ins）水平,为单纯性肥胖儿童的早期干预提供理论依据.方法 选取545例单纯性肥胖儿童和150例正常儿童（对照组）,用罗氏2010型全自动电化学发光仪检测血清中的T、E2、LH、FSH及Ins水平.结果 单纯性肥胖儿童血清中E2 Ins水平明显高于正常对照组（P均＜0.01）,T、LH、FSH明显低于正常对照组（P均＜0.01）;肥胖女童E2水平明显高于肥胖男童（P＜0.01）,T、LH、FSH、Ins水平肥胖男、女童之间差异无统计学意义（P均＞0.05）.结论 单纯性肥胖儿童体内性腺激素、Ins分泌水平相对于正常儿童发生了变化,是肥胖儿童未来糖尿病、心血管疾病、性早熟等的危险因素.     

125例女性甲状腺功能减退症患者血清性激素水平检测及分析

目的研究女性甲状腺功能减退症(简称甲减)患者是否存在性激素水平失衡,观察甲状腺激素变化和性激素变化之间的关系。方法采用放射免疫法测定研究对象的睾酮(T)、雌二醇(E2)、促卵泡生成激素(FSH)、促黄体生成激素(LH)、催乳素(PRL)水平,采用硫酸铵沉淀法测定血清性激素结合球蛋白结合容量(SH-BG-BC)。结果 T、E2、SHBG-BC改变差异有统计学意义(P0.01),而FSH、LH、PRL显著升高,差异有统计学意义(P0.01),女性甲减患者性激素E2下降明显,差异有统计学意义(P0.01)。结论女性甲减患者性激素水平紊乱。     

简化促性腺激素释放激素兴奋试验在女性性早熟症诊断中的意义

【目的】探讨简化促性腺激素释放激素（GnRH）兴奋试验在女性性早熟症诊断中的意义。【方法】采用电化学发光免疫法测定60例性早熟女孩基础血清卵泡刺激素（FSH），黄体生成素（LH），雌二醇（E2）水平及行GnRH刺激试验后，血清FSH，LH水平的变化情况．并进行比较。【结果】真性性早熟患儿的FSH，LH值明显升高，LH峰值均〉12IU／L；LH／FSH〉1；假性性早熟患儿LH，FSH值略升高，LH值均〈12IU／L，LH／FSH〈1。【结论】简化GnRH兴奋试验能够直接观察下丘脑-垂体-性腺轴功能状态，对鉴别真性性早熟和假性性早熟有重要意义。     

不同性别脑梗塞性激素、血脂与脂蛋白亚组分的变化及相关性

目的:探讨性激素失调、血脂与脂蛋白亚组分的变化与脑梗塞的关系。方法:采用放射免疫法测定急性CI患者及健康对照者的血清性激素水平,采用沉淀漂浮酶联法及乙酰丙酮显色法测定血脂与脂蛋白亚组分。结果:男性CI患者E2 显著高于正常对照组(P<0 .0 1) ,E2 / T值也明显高于对照组(P<0 .0 5 ) ,女性CI患者E2 明显低于对照组(P<0 .0 1) ,FSH、L H均明显高于对照组(均P<0 .0 5 ) ;CI组TC、L DL- C明显高于对照组;男性E2 与TC、L DL- C呈正相关(均P<0 .0 5 ) ,与HDL- C、HDL2 - C、HDL3- C呈负相关(均P<0 .0 5 ) ;E2 / T与TC、L DL- C呈正相关(均P<0 .0 5 ) ,与HDL- C、HDL2 - C、HDL3- C负相关(均P<0 .0 5 ) ,女性E2 与TC、L DL- C呈负相关(均P<0 .0 5 ) ;与HDL- C、HDL2 - C呈正相关(均P<0 .0 1)。结论:脑梗塞性患者存在严重的性激素失调及脂质代谢异常,性激素及血脂代谢紊乱参与了脑梗塞的发病机制。     

老年女性动脉粥样硬化性血栓性脑梗死患者性激素及血脂变化的研究

目的：研究老年女性动脉粥样硬化性血栓性脑梗死（ＡＴＣＩ）患者体内性激素与血脂的变化规律。方法：测定４６例老年女性ＡＴＣＩ患者（Ａ组）、４３例老年健康女性（Ｂ组）和４１例正常育龄行经的年轻健康女性（Ｃ组）的血清雌二醇（Ｅ２）、促卵泡刺激素（ＦＳＨ）和促黄体生成素（ＬＨ）;同时测定了血浆总胆固醇（ＴＣ）、甘油三酯（ＴＧ）、低密度脂蛋白胆固醇（ＬＤＬＣ）及高密度脂蛋白胆固醇（ＨＤＬＣ）。结果：Ａ组与Ｂ组、Ｃ组比较显示,Ｅ２、ＨＤＬＣ水平显著降低,ＦＳＨ、ＬＨ、ＴＣ、ＴＧ和ＬＤＬＣ水平则显著增高（Ｐ均＜０．０１）。线性相关分析,Ｅ２与ＦＳＨ、ＬＨ、ＴＣ、ＴＧ、ＬＤＬＣ水平呈显著负相关,而与ＨＤＬＣ水平呈显著正相关。结论：老年女性ＡＴＣＩ患者存在着严重的性激素失调及脂代谢异常,可能为老年女性ＡＴＣＩ患者发病的原因之一     

Impaired estrogen-induced negative feedback on gonadotropin secretion in patients with gonadotropin-secreting and nonfunctioning pituitary adenomas

BACKGROUND: Several in vitro studies suggest that gonadotropin-secreting pituitary adenomas (Gn-omas) and non functioning pituitary adenomas (NFPA) originate from gonadotroph cells. Patients with Gn-oma and NFPA frequently show abnormal gonadotropin response to TRH. The aim of the study was to investigate whether the estrogen-induced negative feedback is operating in either patients with Gn-oma or NFPA. MATERIALS AND METHODS: Serum gonadotropin levels were evaluated at 24 h after ethinylestradiol administration (1 mg per os; EE2 test) in seven patients with a diagnosis of Gn-oma, based on the presence of high follicle-stimulating hormone (FSH) and/or lutenising hormone (LH) levels with normal or high levels of sex steroids, in 22 patients with NFPA with normal or low levels of gonadotropin and sex steroids, and 30 sex- and age-matched healthy subjects. A normal response to EE2 test was arbitrarily defined as a serum LH and FSH decrease of at least 40 and 30% below basal levels. RESULTS: Among patients with Gn-oma, only one had a normal FSH inhibition and another, a normal LH inhibition. Among the 22 patients with NFPA, the EE2 test caused a normal FSH or LH reduction in 10 and 15, respectively, while a normal reduction of both FSH and LH was observed in nine. CONCLUSIONS: The study demonstrates that estrogen-induced negative feedback of gonadotropin secretion is disrupted in almost all patients with Gn-oma and in half of those with NFPA. This defective feedback is reminiscent of the resistance to thyroid hormones and glucocorticoids observed in patients with thyroid-stimulating hormone- (TSH-) and adrenocorticotropic hormone- (ACTH-)secreting adenomas, respectively.     

子宫内膜癌患者胰岛素及性激素水平的临床研究

目的探讨子宫内膜癌患者与体内性激素及胰岛素水平变化的相关性。方法随机抽取妇科经病理确诊并收治住院的125例子宫内膜癌患者作为研究组,另选择92例正常妇女作为对照组。采用酶联免疫法检测观察组和对照组胰岛素(INS)、血清孕酮(P)、雌激素(E2)、黄体生成素(LH)、促卵泡生成素(FSH)、睾酮(T)及泌乳素(PRL)水平,并根据两组绝经前和绝经后分别进行统计分析。结果较之对照组,绝经前研究组妇女INS、E2、LH水平升高明显,差异具有统计学意义(P<0.05),P水平明显降低,具统计学差异(P<0.05)。而PRL、FSH水平无显著性差异(P>0.05);绝经后研究组妇女INS、E2、LHS水平显著升高,具有统计学差异(P<0.05),FSH水平则降低明显,差异具有统计学意义(P<0.05),而P、PRL、T水平无显著性差异(P>0.05)。结论绝经前后子宫内膜癌患者均存在INS、E和LH水平异常,而绝经前后患者PRL水平无相关改变。     

女性胆结石患者垂体—性腺轴激素变化的研究

本文采用放射免疫法测定了62例女性胆囊结石和15例女性肝胆管结石患者血清 FSH、LH和血浆 E_2、P、T 的含量.并与42例正常妇女对照分析。实验结果表明育龄女性胆囊结石患者 E_2含量明显升高(P<0.01),T 含量显著减少(P<0.05),绝经后胆囊结石患者 T 含量明显减少(P<0.01),P 含量显著升高(P<0.01),育龄女性和绝经后胆囊结石患者 E_2/T 比值与对照组相比均有显著性差异(P<0.01),育龄女性肝胆管结石患者卵泡期 E_2、T 及 E_2/T 比值有显著性差异。提示女性胆结石患者存在明显的垂体一性腺轴激素合成或代谢的异常。     

绝经后女性心脏X综合征患者性激素与β-内啡肽的相关性

目的：研究性激素、β-内啡肽在绝经后女性心脏X综合征（CSX）患者中的关系。方法选取绝经后女性CSX的患者55例及健康无症状绝经后女性57名。所有入选者应用ELISA法测定性激素[包括雌二醇、孕酮、促黄体生成素（LH）、促卵泡刺激素（FSH）、睾酮]和β-内啡肽水平。结果与对照组相比,CSX患者血清雌二醇及血浆β-内啡肽水平均显著减低（P＜0.05）;血清FSH、LH浓度明显升高（P＜0.05）;雌二醇/睾酮比值明显降低（P＜0.05）;孕酮、睾酮有升高趋势,但两组比较差异无统计学意义。线性相关分析显示,CSX患者血清雌二醇与β-内啡肽呈正相关（P＜0.05）;LH与β-内啡肽呈负相关（P＜0.05）;雌二醇/睾酮比值、FSH与β-内啡肽均无明显相关性。多元线性回归显示,雌二醇、LH与β-内啡肽密切相关（P＜0.05）。结论绝经后女性CSX患者雌激素缺乏引起LH升高,可能通过抑制β-内啡肽的释放,导致其疼痛敏感性增高。     

绝经后女性冠心病患者性激素水平与胰岛素抵抗的相关性

目的:探讨绝经后女性冠心病患者性激素水平的变化及与胰岛素抵抗(IR)的关系。方法:检测30例绝经后女性冠心痛患者和30例正常对照组的血清雌二醇(E2)、睾酮(T)、孕酮(P)、促卵泡激素(FSH)、促黄体生成素(LH),水平和空腹血糖(FPG)、葡萄糖耐量试验2 h血糖(2 h PG),空腹胰岛素(FIN),计算胰岛素敏感指数(ISI)及E2/T值,用t检验,并将冠心病患者E2、E2/T与血糖、FIN、ISI作线性相关分析。结果:与对照组比较,绝经后女性冠心病患者E2、ISI显著降低(P<0.01);FPG、2 h PG、FIN显著增高(P<0.05);T、P、FSH、LH无显著差异(P>0.05)。相关分析表明,E2、E2/T与FIN呈显著负相关而与ISI呈显著正相关(P<0.05)。结论:提示绝经后女性高胰岛素血症和IR与雌激素水平降低、E/T比例失调有关,它们共同参与绝经后女性冠心病的发生和发展。     

Characterization of the inappropriate gonadotropin secretion in polycystic ovary syndrome.

To evaluate gonadotropin release in polycystic ovary syndrome (PCO), one or more of the following hypothalamic-pituitary function tests were performed on 24 patients with the syndrome. These tests included (a) the pulsatile pattern and day-to-day fluctuation of gonadotropin release; (b) effects of exogenous estrogen and antiestrogen (clomiphene) administration on gonadotropin release; and (c) pituitary responsiveness to maximal (150 mug) and submaximal (10 mug) luteinizing hormone-releasing factor (LRF) injections. In 10 of the 14 patients sampled frequently (15 min) for 6 h, luteinizing hormone (LH) levels were elevated above the concentration seen in normal cycling women (except the LH surge). These high LH concentrations appeared to be maintained by and temporally related to the presence of exaggerated pulsatile LH release, either in the form of enhanced amplitude or increased frequency. In all subjects, levels of follicle-stimulating hormone (FSH) were low or low normal, and a pulsatile pattern was not discernible. In four patients, daily sampling revealed marked day-to-day fluctuation of LH but not FSH. That the elevated LH levels were not related to a defect in the negative-feedback effect of estrogen was suggested by the appropriate fall of LH in four patients given an acute intravenous infusion of 17beta-estradiol. This infusion had no effect on FSH levels. In addition, clomiphene elicited rises of both LH and FSH that were comparable to the ones observed in normal women given the same treatment. The clomiphene study also suggested that the positive-feed-back mechanism of estrogen on LH release was intact when the preovulatory rises of 17beta-estradiol induced appropriate LH surges. The elevated LH levels appeared to be related to a heightened pituitary responsiveness to the LRF. This was found in the 11 and 2 patients given maximal (150 mug) and submaximal (10 mug) doses of LRF, respectively. The augmented pituitary sensitivity for LH release correlated with the basal levels of both estrone (P less than 0.025) and 17beta-estradiol (P less than 0.02). The net increase in FSH was significantly greater (P less than 0.001) in the PCO patients than the normal women with maximal doses of LRF. With the smaller dose study none of the injections had a discernible effect on FSH concentrations in either subject. The disparity between LH and FSH secretion could be explained by the preferential inhibitory action of estrogen on FSH release, coupled with a relative insensitivity of FSH release. These data indicate that in these PCO patients the abnormalities of the hypothalamic-pituitary regulation of gonadotropin secretion was not an inherent defect but represented a functional derangement consequent to inappropriate estrogen feedback, which led to a vicious cycle of chronic anovulation and inappropriate gonadotropin secretion.     

Relative roles of follicle-stimulating hormone and luteinizing hormone in the control of inhibin secretion in normal men.

The glycoprotein hormone inhibin is produced by the Sertoli cells of the testis under the influence of follicle-stimulating hormone (FSH) and is postulated in turn to inhibit FSH secretion. Luteinizing hormone (LH) is not recognized to have an important role in the control of inhibin secretion in any species. To determine the relative roles of FSH and LH in the control of inhibin secretion in man, we examined the effects of selective FSH and LH replacement on serum inhibin levels in normal men whose endogenous gonadotropins were suppressed by testosterone (T). After a 3-mo control period, nine men received 200 mg T enanthate i.m. weekly for 3-9 mo. During T treatment, serum LH and FSH levels were markedly suppressed and serum inhibin levels fell to 40% of control values. While continuing T, 3-5 mo of treatment with purified hFSH (n = 4) or hLH (n = 4) increased the respective serum gonadotropin level into the upper normal range and significantly increased inhibin levels back to 64 and 55% of control values, respectively. Supraphysiological LH replacement with high doses of human chorionic gonadotropin (n = 3) returned serum inhibin levels to 63% of control values. In no case did inhibin levels return fully to control levels. In conclusion, serum inhibin levels fell during gonadotropin suppression and were partially and approximately equally restored by either FSH or LH treatment. FSH presumably acts directly on the Sertoli cell to increase inhibin secretion whereas LH may act via increases in intratesticular T levels and/or other factor(s).     

Pituitary-testicular responsiveness in male hypogonadotropic hypogonadism

An isolated deficiency of pituitary gonadotropins was demonstrated in six 46 XY males, 22 to 36 years of age, with and without anosmia. Undetectable or low levels of serum follicle-stimulating hormone (FSH) and luteinizing hormone (LH) clearly separated hypogonadotropic from normal adult males. Chronic (8-12 wk) administration of clomiphene citrate caused no increase in serum FSH or LH in gonadotropin-deficient subjects. However, the administration of synthetic luteinizing hormone releasing factor (LRF) resulted in the appearance of serum LH and, to a lesser degree, serum FSH in three subjects tested. While levels of plasma testosterone were significantly lower in gonadotropin-deficient subjects, plasma androstenedione and dehydroepiandrosterone were in a range similar to that of age-matched normal men. Treatment with human chorionic gonadotropin (HCG) increased levels of plasma testosterone to normal adult male values in all gonadotropin-deficient subjects. Cessation of treatment with HCG resulted in the return of plasma testosterone to low, pretreatment levels. That HCG therapy with resultant normal levels of plasma testosterone may somehow stimulate endogenous gonadotropin secretion in gonadotropin-deficient subjects was not evident. The adult male levels of serum FSH and LH after LRF, and plasma testosterone after HCG, confirm pituitary and Leydig cell responsiveness in these subjects.