LHRH兴奋试验早期鉴别诊断青少年的体质性青春发育延迟和男性低促性腺激素性功能低减的价值

目的　以LHRH兴奋试验鉴别诊断体质性青春发育延迟 (constitu tionaldelayedpuberty ,CDP)和男性低促性腺激素性性功能低减 (hypogonadotropichypogonadism ,HH)。 方法　所有患者试验时均处于生殖发育第Ⅰ期 ,试验时给患者静脉注射LHRH 10 0 μg ,分别于 -15、0、15、3 0、45、60、90及 12 0min取血 3毫升 ,用放免法测定血清黄体生成素 (LH)和促卵泡激素 (FSH )水平。此后患者在门诊每 3～ 2 4个月随诊一次 ,一直追查到 18岁以后即至确诊有无正常青春发育后为止。根据其青春发育情况将患者分为青春发育正常组 (n =3 4) ,CDP组 (n =16)及HH组 (n =3 1)。 3组患者接受LHRH兴奋试验的年龄分别为 ( 10 .2± 0 .9)岁 ( 9～ 14岁 ) ,( 16.0± 1.0 )岁 ( 14～ 18岁 )和 ( 17.1± 1.4)岁 ( 16～ 2 2岁 )。结果　正常组 ,CDP组和HH组血清LH基础值和达峰时间均无差异 ,而血清LH峰值 ,血清LH峰值与基础值间的差值即血清LH增加值 ,血清LH增加倍数及血清LH曲线下面积 (AUCLH) ,正常组均明显高于CDP组和HH组 (P均 <0 .0 0 1) ,CDP组也明显高于HH组 (P均 <0 .0 0 1)。在 3组受试者中 ,分别绘制血清LH峰值、LH增加值对LHRH兴奋试验的工作特性曲线 (ROC) ,根据ROC可以确定以下两指标的切点 :血清LH峰值 8IU/L ,血清LH增     

支气管哮喘患者肺功能与转化生长因子β1关系的研究

目的 观察哮喘患者急性发作期、缓解期的肺功能和血清转化生长因子β1(TGF-β1))的变化,探讨其临床意义.方法 对55例支气管哮喘急性发作期和50例缓解期患者作常规肺通气功能检测,同时用酶联免疫吸附试验(ELISA)测定其血清TGF-β1水平,并设30例健康者作为对照组.结果 哮喘急性发作期、缓解期血清TGF-β1水平均低于对照组,有统计学差异(P＜0.01,P＜0.05),其中急性发作期血清TGF-β1水平明显低于缓解期和对照组(P＜0.01);急性发作期肺功能指标FEV1%、FEV1/FVC明显低于缓解期和对照组(P＜0.01),FEF50、FEF75在急性发作期与缓解期比较差异无统计学意义(P＞0.05);TGF-β1与FEV1%、FEV1/FVC、FEF50、FEF75呈显著正相关(P＜0.01).结论 血清TGF-β1降低与肺功能减退和哮喘发作有直接关系,提示TGF-β1是反映气道炎症程度的可靠指标.反映小气道功能的FEF50、FEF75在急性发作期与缓解期变化不大,缓解期患者仍存在小气道功能异常,提示缓解期气道炎症持续存在.     

老年慢性支气管炎患者血清细胞因子检测的意义

目的　探讨白细胞介素 2 (IL 2 )、IL 6、IL 8和肿瘤坏死因子 α(TNF α)在慢性支气管炎发病机制中的作用。　 方法 　采用放射免疫法 (RIA)检测 3 0例慢性支气管炎患者急性发作期和临床缓解期血清IL 2、IL 6,IL 8及TNF α水平 ,并以 3 0例健康人血清中IL 2、IL 6、IL 8及TNF α水平作为对照。　 结果 　 3 0例慢性支气管炎患者急性发作期血清IL 6、IL 8、TNF α显著高于缓解期 (P <0 0 1) ,而缓解期血清IL 6、IL 8、TNF α与对照组相比仍然有差异 (P <0 0 1) ;IL 2浓度在发作期和缓解期均低于对照组 (P <0 0 5 ) ,但发作期和缓解期比较差异无显著性。慢性支气管炎患者急性发作期和临床缓解期血清IL 6与IL 8,IL 6与TNF α ,IL 8与TNF α水平均呈正相关 (r=0 70 9,0 63 3 ,0 615 ) ,但与IL 2水平无明显相关性。　 结论 　血清IL 2、IL 6、IL 8、TNF α不仅参与了慢性支气管炎急性感染时的发病机制 ,而且在慢性炎症的发展过程中发挥重要作用     

IL-4、IL-8和IL-10在支气管哮喘和慢性阻塞性肺疾病中的对比研究

目的 比较支气管哮喘和慢性阻塞性肺疾病(COPD)患者外周血IL4、IL-8和IL10的水平.方法 采用双抗体夹心法检测急性加重期和稳定期COPD患者各50例、急性发作期和缓解期哮喘患者各50例及50例健康志愿者血清中IL-4、IL-8、IL-10的水平.结果 两种疾病的急性发作期患者血清IL-4、IL-8水平均显著高于缓解期患者及对照组(P均＜0.05),血清IL-10水平显著低于缓解期患者和对照组(P均＜0.05).哮喘急性发作期患者血清IL-4水平显著高于COPD急性加重期患者(P＜0.05);IL-8和IL-10水平低于COPD急性加重期患者(P＜0.05).哮喘缓解期患者血清IL-10水平低于COPD缓解期患者(P＜0.05).结论 IL-4、IL-8和IL10参与了哮喘和COPD的气道炎症反应,IL4在哮喘的气道炎症形成中起重要的作用,而IL-8和IL-10为COPD的主要炎症因子.     

哮喘患者巨噬细胞MIP-1a在血清中的表达及与病情的关系研究

【】目的：探讨哮喘患者巨噬细胞炎症蛋白-1a(MIP-1a)在血清中的表达以及与病情的关系。方法 选取2015年2月至2016年6月在我院治疗的哮喘患者114例,其中哮喘急性发作期患者76例(急性发作期组),哮喘缓解期患者38例(缓解期组),同时选取健康志愿者100例作为对照,检测各组血清MIP-1a以及第1秒用力呼气容积(FEV1)占预计值百分比。结果 急性发作期组血清MIP-1a为(52.31±7.81)ng/L,明显高于缓解期组和对照组(p＜0.05),而FEV1占预计值为(53.82±16.61)%,明显低于缓解期组和对照组(p＜0.05);缓解期组血清MIP-1a为(24.27±6.10)ng/L,明显高于对照组(p＜0.05),而FEV1占预计值为(71.22±15.54)%,明显低于对照组(p＜0.05);重度急性发作期患者血清MIP-1a为(62.82±8.03)ng/L,明显高于轻度和中度急性发作期患者(p＜0.05),而FEV1占预计值为(45.23±11.42)%,明显低于轻度和中度急性发作期患者(p＜0.05);中度急性发作期患者血清MIP-1a为(50.41±7.22)ng/L,明显高于轻度急性发作期患者(p＜0.05),而FEV1占预计值为(452.16±14.67)%,明显低于轻度急性发作期患者(p＜0.05);急性发作期组患者血清MIP-1a与患者病情呈正相关(rs=0.322,p＜0.05),与FEV1占预计值呈负相关(r=-0.401,p＜0.05)。结论 哮喘患者血清MIP-1a表达升高,尤其急性发作期患者显著升高,其表达水平与患者病情及肺功能有一定关系。     

慢性阻塞性肺疾病患者同型半胱氨酸水平变化及意义探讨

目的 探讨慢性阻塞性肺疾病(COPD)患者不同病期血浆同型半胱氨酸、血浆谷胱甘肽(GSH)水平的变化,以了解同型半胱氨酸在COPD患者发生、发展过程中的作用及其临床意义.方法 2006年1月至2008年6月收集46例COPD急性发作期患者(COPD急性发作期组)、45例COPD缓解期患者(COPD缓解期组)及38例健康受试者(健康对照组).测定各组的多项指标:吸烟指数、体质量指数、血浆同型半胱氨酸、血浆GSH、肺功能和动脉血气.结果 ①COPD急性发作期组血浆同型半胱氨酸高于健康对照组和COPD缓解期组,(31.93±26.19) μmol/L vs (10.79±2.32) μmol/L,(21.98±9.13) μmol/L,三组比较差异有统计学意义(F=13.08,P＜0.01).②COPD缓解期组血浆GSH明显低于健康对照组和COPD急性发作期组,(71.72±76.36) mg/L vs (166.38±63.51) mg/L,(145.18±80.41) mg/L,三组比较差异有统计学意义(F=19.11,P＜0.01).③COPD患者不论急性发作期,还是缓解期,血浆同型半胱氨酸与GSH均呈明显负相关(COPD急性发作期:r=0.579,P＜0.01;COPD缓解期:r=-0.721,P＜0.01);COPD急性发作期血浆GSH与第一秒用力呼气容积/用力肺活量呈正相关(r=0.488,P＜0.05).结论 COPD患者存在高同型半胱氨酸血症,血浆同型半胱氨酸参与COPD的氧化应激.     

支气管哮喘肺功能动态变化的特点及意义

目的 深入研究支气管哮喘肺功能的动态改变特点和机制.方法 对50例哮喘患者分别于急性发作期、慢性持续期和缓解期进行肺通气功能、肺容量、体积描记法和脉冲振荡法(IOS)检测.结果 仅DLCO和ITGV在不同分期间差异无统计学意义,余各参数在不同分期问差异均有统计学意义.FVC、FEV1/FVC、FVC/pre、FEV,、FEV1/pre、PEF、PEF/pre、FEF25、FEF50、X5在急性发作期显著低于慢性持续期和缓解期,RV、RV/TLC、Rtot、Fres、Z5、R5、R20、AX在急性发作期显著高于慢性持续期和缓解期,而在慢性持续期和缓解期之间差异无统计学意义.FEV1缓解期较急性发作期的改善值和改善率均显著高于FVC(△FEV1/△FVC＞1).R20的改善值大于R5-R20[△R20/△(R5-R20)＞1],AX的改善率最高.肺容量参数IC、RV和RV/TLC缓解期较急性发作期的改善值与FVC、FEV1、FEV1/FVC、PEF的改善值均显著相关(P＜0.05).IOS各参数改善值与FVC、FEV1、PEF的改善值均显著相关(P＜0.001).结论 哮喘气道阻力的增加以中心气道阻力为主,其治疗反应以流速改善型为主.IOS和肺通气功能、肺容量、体描仪检测具有良好的相关性.IOS在区分气道阻塞的部位和治疗反应类型,哮喘和COPD的鉴别诊断方面有较高的临床价值.     

内皮素等炎性因子与夜间哮喘发生机理的研究

目的　探讨 2 4小时内皮素 1(ET- 1)和粒细胞 -巨噬细胞集落剌激因子 (GM- CSF)的动态变化与哮喘病人夜间加重或发作的关系。方法　检测夜间哮喘病人急性发作期、缓解期和健康对照组血清中 ET- 1和 GM- CSF在 4am(早晨 4时 )与 4pm(下午 4时 )含量的变化及峰值流速 (PEF)变化的相关性。结果　急性发作期患者 ET- 1和 GM- CSF水平在 4am与 4pm均较缓解期和健康对照组显著增高。急性发作期组 4am ET- 1较 4pm明显增高 (P<0 .0 5 ) ,而 4am GM- CSF的水平虽稍高于 4pm,但没有统计学意义。与 ET- 1变化相反 ,峰值流速 (PEF)的变化 4am较 4pm明显降低 (P<0 .0 5 ) ,4pm的 ET- 1增高值与 4pm PEF下降值呈显著负相关 (r=- 0 .7999,P<0 .0 1)。结论　ET- 1和 GM- CSF不但参与哮喘病人急性发作而且 ET- 1夜间增高与夜间肺功能下降密切相关。     

贵州省地方性克汀病垂体—性腺系统功能对LHRH兴奋试验的反应

在已经加碘得到控制的碘缺乏性疾病病区,观察了地方性克汀病垂体--性腺系统对促黄体激素释放因子(LHRH)试验的反应。结果:男性克汀病病人组血清黄体生成激素(LH)和卵泡刺激素(FSH)基础值显著高于对照组,但其血清睾酮(T)值则显著低于对照组。静脉注射 LHRH100μg15分钟后,克汀病病人组血清 FSH 反应高于正常人组,LH 反应与正常对照组相似。两组血清 T 值于试验后无显著变化。静脉注射接着静脉滴注 LHRH,克汀病病人组 FSH 反应高于正常人,其 LH 最大增值和反应倍数均低于对照组,正常人组 LH、FSH 呈双相反应,克汀病病人组则无此反应。血清 T,正常人组试验后2-3小时显著升高,克汀病病人组无则显著变化。结果表明克汀病病人不仅有原发性 Leydig 和 Sertoli 细胞功能低下,而且还有垂体促性腺激素储备和再合成功能的减低。     

男性特发性低促性腺激素型性腺功能减退症87例临床分析

目的探讨男性特发性低促性腺激素型性腺功能减退症(idiopathic hypogonadotropic hypogonadism,IHH)临床特点。方法回顾性分析1985年5月至2006年2月解放军总医院收治的87例男性IHH患者临床资料。结果87例IHH患者就诊年龄平均(18.8±4)岁,其中25例伴有嗅觉减退或消失。87例染色体核型为46,XY。检测甲状腺、肾上腺功能正常,黄体生成素(LH)、卵泡刺激素(FSH)、睾酮(T)基础值低,促性腺激素释放激素[戈那瑞林(GnRH)或促黄体生成素释放激素(LHRH)]兴奋试验LH峰值较基础值升高。18例患者LH脉冲分泌呈现多种异常形式,86.2%(75/87)IHH患者骨龄落后于实际年龄,头颅CT或磁共振成像检查排除下丘脑-垂体区占位性器质性病变。结论根据性发育异常患者合并的各种先天异常、病史、体格检查、染色体核型分析、性激素水平、GnRH或LHRH兴奋试验,必要时行LH脉冲分析、骨龄测定、头颅CT或磁共振成像,可进行IHH的诊断与鉴别诊断。     

老年男性肺心病患者睾丸内分泌功能状态

20例老年男性肺心病患者血浆睾酮(T)低下,经HCG兴奋后,重症组血浆T基础值、峰值、峰值上升速率均显著低于正常对照组(P <0.01或<0.05)。轻症组T基础值也明显低于正常对照组,但峰值、峰值净增值、峰值上升速率与正常无明显差异。缓解期基础T值仍低于正常(P <0.05)。实验结果表明,患者睾丸内分泌功能减退以原发性损害为主,同时也存在继发因素以及下丘脑-垂体-性腺轴之间的反馈机制失调。     

藏族男性肝病患者下丘脑-垂体-性腺轴功能的变化及其临床意义

目的　探讨藏族男性肝病患者下丘脑 垂体 性腺轴的变化 ,了解不同类型肝病患者性腺激素水平的变化 ,协助临床对病情和预后的判断。方法　于 1999- 12～ 2 0 0 4 - 0 4在西藏自治区第二人民医院随机选择西藏地区藏族男性肝病患者 93例 ,包括甲型肝炎、乙型肝炎、酒精性肝病、肝硬化及重症肝炎。同时选取西藏地区 19名健康藏族男性作为对照。测定入选者睾酮 (T)、雌二醇 (E2 )、卵泡刺激素 (FSH)、黄体生成素 (LH )、泌乳素(PRL)及促性腺激素释放激素 (LHRH)的水平。资料统计采用双侧 t检测。结果　肝病患者E2 、PRL和LHRH水平与对照组比较均有显著性差异 (P <0 0 1、P <0 0 1、P <0 0 5 )。急性肝炎T、E2 、PRL升高 ,E2 升高 (P <0 0 1、P <0 0 5、P <0 0 1)。出现高雌激素血症和低睾酮血症 :重症肝炎T、FSH、LH、LHRH降低 (P <0 0 1、P<0 0 5、P <0 0 5、P <0 0 1) ,E2 、PRL升高 ,均为P <0 0 1。结论　性激素水平的变化与肝功能受损程度相一致 ,因此临床上测定性激素水平对了解病情、判断预后有着一定的作用。     

Effects of LHRH and long-acting LHRH on serum LH and FSH levels of healthy women

A comparison was made between the stimulatory effects of luteinizing hormone-releasing hormone (LHRH) and long acting luteinizing-releasing hormone (I.a. LHRH) on the gonadotropin secretion of normally menstruating women. The luteinizing hormone (LH) and follicle stimulating hormone (FSH) concentrations were measured by RIA. The synthetic I.a. LHRH was found more potent than the parent hormone in terms of the magnitudes and durations of the LH and FSH responses. There was no close correlation between the initial gonadotropin values and the peak levels in normally menstruating women having basal LH and FSH values within the normal ranges.     

Depression of testosterone secretion in male patients with respiratory failure

To investigate the changes of testosterone (T) secretion under sustained hypoxia, we determined basal levels of urine T, 17 ketosteroid, luteinizing hormone releasing hormone (LHRH), luteinizing hormone (LH), follicle stimulating hormone (FSH) and response to LHRH and HCG (human chorionic gonadotropin) in male patients with respiratory failure. After evaluating blood gas data, we also measured serum T, LH, FSH, plasma progesterone (P) and 17 hydroxyprogesterone (17OH-P). The subjects were divided into 3 groups according to PaO2; Group 1 with a PaO2 under 60 Torr, Group 2 with a PaO2 between 60 Torr and under 70 Torr, Group 3 was an age-matched control group. Urine T and serum T were significantly lower in Group 1 compared with those of Group 3. In the LHRH test, augmented relative responsiveness and delayed peak value in LH secretion were observed in Group 1, compared with those of Group 3. As for the HCG test, no differences were observed among the 3 groups. The ratio of 17OH-P to P, which indicates activity of 17-hydroxylase, was observed to be diminished with increasing degrees of hypoxia. These data suggest that in male patients with respiratory failure there was depression in T secretion as well as 17-hydroxylase activity due to hypothalamic-pituitary hypofunction.     

Naltrexone does not reverse the inhibitory effect of chronic restraint on gonadotropin secretion in the intact male rat.

There is considerable evidence suggesting that endogenous opioids may play an important role in acute stress-induced decreases in luteinizing hormone (LH) release. Studies were undertaken to analyze the role of endogenous opioids in chronic stress-induced decrease in circulating LH and follicle-stimulating hormone (FSH). Chronic restraint (6 h daily over 4 days) evoked a decrease in circulating LH and FSH. Naltrexone treatment, (2 mg/kg three times daily) during the 4 days of restraint, caused an increase in plasma concentrations of LH and FSH, and antagonized the LH suppressory effect of morphine (10 mg/kg) administration. Despite this, naltrexone treatment was ineffective in preventing the inhibitory effect of chronic restraint stress on circulating LH and FSH. Chronic restraint also induced a decrease in hypothalamic LH-releasing hormone (LHRH) content in saline-treated rats. On the contrary, in naltrexone-treated rats, chronic restraint evoked an increase in hypothalamic LHRH content. Thus endogenous opioids and chronic stress seem to act by different mechanisms on the hypothalamic LHRH neuron. In unstressed orchidectomized rats, naltrexone administration did not modify circulating LH, but increased plasma concentrations of LH in acutely restrained rats. These data suggest that endogenous opioids may mediate gonadotropin secretion during acute stress, but not during chronic stress.     

Plasma Gonadotrophins and LHRH Infusions in Anorexia Nervosa

Summary: Plasma gonadotrophins and LHRH infusions in anorexia nervosa. P. J. V. Beumont, Suzanne F. Abraham, W. J. Argall and J. R. Turtle, Aust. N.Z. J. Med., 1978, 8, pp. 509–514.
Nine female patients with anorexia nervosa were studied, three of them at different stages of weight gain. Basal plasma LH (luteinising hormone) was depressed in emaciated patients, but basal plasma FSH (follicle stimulating hormone) was normal. LH was significantly lower in patients who had been amenorrhoeic for less than 24 months than in those whose amenorrhoea was of longer duration.
LH and FSH levels were stimulated by LHRH (luteinizing hormone releasing hormone), infused at a rate of 05 μg/min for four hours. One patient, tested at 60% of standard weight, had no LH response. In all other patients below 70% of standard, the maximal LH response occurred within the first hour of infusion. In patients at higher weights, the LH response was biphasic, and the maximal level was reached during the last hour of the infusion. The FSH response, similarly, approached maximal during the first hour in patients below 70% of standard, but continued to rise throughout the infusion in patients at higher weights. Body weight expressed as a percentage of standard correlated significantly with both phases of the LH response, but not with the FSH response.
Most previous authors have found an association between low body weight and depressed pituitary gonadotrophins in anorexia nervosa. The present findings further elucidate this relationship.     

慢性肺原性心脏病左心功能的临床研究

目的：探讨慢性肺原性心脏病（以下简称肺心病）左心功能的变化。方法：采用二维及脉冲多普勒超声心动图测定慢性肺心病患者的左心功能，并与健康人及阻塞性肺气肿患者进行对照。结果：肺心病右心衰竭组患者的射血分数、每搏输出量、心输出量、心脏指数及快速充盈期与心房收缩期二尖瓣口血流比值均有下降，与正常对照组、慢性支气管炎肺气肿组及肺心病右心功能代偿组比较，上述各项指标均有显著差异，Ｐ分别＜０．０１、＜０．０１和＜０．０５。结论：肺心病右心衰竭患者可合并左心功能受损。     

重症慢性肺心病患者甲状腺激素水平观察

目的观察慢性肺心病急性加重期患者血清甲状腺激素变化,并探讨其临床意义。方法用放免法测定48例慢性肺心病急性加重期患者(试验组)及45例同期收治的慢性阻塞性肺疾病(COPD)患者(对照组)血清甲状腺激素(T3,T4,FT3,FT4)及促甲状腺素(TSH)水平,并进行比较。结果肺心病组血清T3,T4,FT3均明显低与对照组(P<0.01),FT4轻度下降,但差异无显著性(P>0.05),TSH水平两组比较差异无显著性(P>0.05)。结论慢性肺心病患者血清甲状腺激素水平的变化对肺心病急性加重期病情判断及其预后估计具有一定临床参考价值。     

Inhibitory effect of central LHRH on LH secretion in the ovariectomized ewe

The role of central luteinizing hormone releasing hormone (LHRH) in the control of pulsatile LHRH and luteinizing hormone (LH) secretion was investigated in ovariectomized adult ewes. Injection of LHRH (2.1-21 pmol) into the third cerebral ventricle caused a delayed but sustained inhibition of LH secretion. Pulse frequency, pulse amplitude and mean LH levels were reduced significantly when compared with the responses to the control injection of saline (50 microliters). The inhibitory effect of centrally administered LHRH was not accompanied by a reduction in the pituitary responsiveness to intravenous LHRH. In contrast to the effect on LH, plasma levels of follicle-stimulating hormone (FSH) and prolactin were unaffected by central LHRH. The inhibitory action of LHRH was antagonized by prior injection of an LHRH antagonist ([N-Ac-D-Nal(2)1, D-p-Cl-Phe2, D-Trp3, D-hArg (Et2)6, D-Ala10] LHRH, 69 pmol) into the third ventricle. Central injection of the LHRH antagonist alone (at the same concentration) did not influence any characteristic of pulsatile LH secretion. In conclusion, these data indicate that exogenous administration of LHRH into the brain exerts a dose-related and receptor-mediated inhibition of LHRH pulse generator activity. However, the physiological significance of endogenous LHRH in the regulation of the LHRH pulse generator remains unresolved.     

Changes in hypothalamic-pituitary-gonadal function in male patients with acute attack of chronic cor pulmonale

Contents of serum luteinizing hormone, follicle-stimulating hormone, and plasma testosterone and estradiol in 50 male patients with acute attack of chronic cor pulmonale and in 26 healthy men were determined using the method of radioimmunoassay, and the response of pituitary gonadotropins to luteinizing hormone-releasing hormone (LHR) was measured. Analysis of the results suggested that there are greatly disturbances of hypothalamic-pituitary-gonadal function in male patients with acute attack of chronic cor pulmonale, and that hypoxemia is an important factor leading to this disorder.