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。     

男性Grave''s病患者垂体促性腺激素和性激素分泌的变化

目的　探讨高甲状腺激素对男性垂体促性腺激素和性激素分泌的影响。方法　对15例初诊男性Grave’s病患者分别在治疗前和治疗后 8～ 13个月进行促性腺激素释放激素(GnRH)兴奋试验 ,观察垂体促性腺激素黄体生成素 (LH)、卵泡刺激素 (FSH )和泌乳素 (PRL)和性激素 [睾酮 (T)和雌二醇 (E2 ) ]水平及对GnRH刺激的反应 ,计算曲线下面积 ,同时测定性激素结合球蛋白 (SHBG)水平 ,并以 9名正常人作为对照组 ,进行比较。结果　Grave’s病患者LH和FSH水平显著高于对照组 (P <0 .0 5或P <0 .0 1) ,对GnRH刺激反应也增强 ;T和SHBG升高 ,PRL和E2无明显变化 ,E2 /T则明显低于对照组水平 (P <0 .0 5 )。甲状腺激素和T与SHBG呈显著正相关 (P<0 .0 1)。经过治疗 ,甲状腺功能恢复正常后上述异常指标均恢复至正常水平。结论　高甲状腺激素时垂体促性腺激素细胞分泌和储备功能增强 ,而这种改变是可逆的。     

男性肝病肝损害程度对血清性激素水平的影响

[目的]探讨男性慢性肝炎、肝硬化、慢加急肝衰竭患者的肝损害程度对血清性激素的影响。[方法]收集男性肝病患者84例,其中肝炎肝硬化患者42例,慢性肝炎患者32例,慢加急及亚急性肝衰竭患者10例;同期入选相同年龄段健康体检男性人群42例为对照组。采用放射免疫法检测外周血清雌二醇(estradiol,E2)、卵泡刺激素(follicle-stimulating hormone,FSH)、促黄体生成素(luteotropic hormone,LH)、催乳素(prolactin,PRL)、黄体酮(progesterone,PROG)、睾酮(testosterone,TSTO)和硫酸去氢表雄酮(dehydroepiandrosterone sulfate,DHEA-SO4)7种性激素水平,观察患者的性激素水平特点。[结果]慢性肝炎者PRL水平显著高于对照组(t=2.804,P=0.015)。E2、PRL水平随着肝功能恶化而递增,而DHEA-SO4水平则在肝硬化者下降,肝衰竭者升高,在分级不同的肝硬化患者比较中差异有统计学意义,Spearman相关分析显示,E2、PRL与肝功能Child-Pugh分级呈正相关性(r=0.572,0.550;P=0.003,0.004),而FSH、LH、PROG、TSTO和DHEA-SO4水平与肝功能Child-Pugh分级无关。[结论]PRL是反映早期肝损害的敏感指标,同时PRL和E2也是反映肝硬化肝功能损害程度的可靠指标,与肝功能Child-Pugh分级具有一定的正相关性;肝衰竭患者E2、PRL、DHEA-SO4水平明显高于肝硬化者和健康人。     

男性系统性红斑狼疮患者性激素变化的分析研究

目的:探讨男性系统性红斑狼疮(SLE)患者性激素指标睾酮(T)、泌乳素(PRL)、雌二醇(E2)、黄体生成素(LH)、卵泡刺激素(FSH)、孕酮(Pro)及其相关比值与病情的关系。方法:采用美国ARCHITECT i2000SR化学发光分析仪测定69例男性SLE患者(检测组)和41例健康者(对照组)的性激素6项指标。结果:与对照组比较,SLE组T水平显著降低(P0.05),PRL、E2、LH水平显著升高(P0.05),FSH、Pro差异无统计学意义(P0.05);T正常、PRL、E2、LH升高及PRL、E2、LH正常、T降低2组结果相关比值T/PRL、T/E2、T/LH均显著降低(P0.05)。SLE活动期PRL水平明显高于稳定期,差异有统计学意义(P0.05);活动期T、E2、LH、FSH、Pro水平与稳定期差异无统计学意义(P0.05)。结论:T、PRL、E2、LH水平及其相关比值与男性SLE病情密切相关,对评估SLE活动性评价有一定意义。     

性腺功能减退症在BPH患者发病情况及睾酮补充治疗的探讨

目的了解BPH患者的血清性激素水平及各临床参数,以明确其中性腺功能减退患者的比例;探讨血清性激素与BPH的关系,并进一步讨论合并BPH的性腺功能减退患者睾酮补充治疗(TST)的可行性.方法 1999年9月至2001年4月间我研究所收治的BPH患者103例(平均年龄±标准差69.2±6.2岁).检测患者血清总睾酮(T)、游离睾酮(fT)、雌二醇(E2)、卵泡刺激素(FSH)、黄体生成素(LH)和泌乳素(PRL)等激素水平,同时收集相应病例的年龄、病史、体重指数(BMI)、血清PSA水平、前列腺体积、尿流率及I-PSS等临床资料.将血清T水平低于3ng/ml者归为性腺功能减退组,其余为非减退组,比较两组各激素及临床参数的差异.结果本组BPH患者性腺功能减退症30例(占29.7%).两组患者虽然血清T水平有显著性差异(2.75比4.81ng/ml,P＜0.001),但各临床参数以及激素水平无显著性差异.结论本组BPH患者人群中有近1/3的患者有性腺功能减退,但此状态与BPH的临床参数无相关关系.作者认为,合并BPH的性腺功能减退症患者若出现性腺功能减退的症状,在监测尿流率、前列腺体积和血清PSA的前提下可考虑TST,使其血清睾酮水平恢复正常,以改善其生活质量.     

男性青少年肥胖伴乳房发育症对垂体-性腺轴功能影响的研究

测量 4 0例男性青少年肥胖伴乳房发育 ( OGMA)患者 ( OGMA组 )的阴茎长度、睾丸体积 ,判断其性机能状况 ,采用放射免疫分析法测定其血清黄体生成素 ( LH)、卵泡刺激激素 ( FSH)、催乳素( PRL)、总睾酮 ( TT)和雌二醇 ( E2 )水平 ,并分别与 4 0例单纯性肥胖者 (对照 组 )及正常体重者 (对照 组 )进行配对比较 (三组为同身高、同年龄 )。结果 OGMA组阴茎长度及睾丸体积明显小于两对照组( P分别 <0 .0 5、0 .0 1) ,阴茎勃起长度 ( 8.8± 3.5cm)、首次遗精发生率 ( 32 .5% )均明显小于对照 组( 10 .0± 3.8cm、67.5% ) ,P值均 <0 .0 1;血清 TT水平和　 T/ E2 　 OGMA组和对照 组均低于对照 组 ( P<0 .0 5～ 0 .0 1) ,而 L H水平高于对照 组 ( P<0 .0 1) ;OGMA组 FSH和 PRL水平高于两对照组( P<0 .0 5～ 0 .0 1)。提示 OGMA患者性发育滞后 ,垂体 -性腺轴功能紊乱 ,存在原发性性腺机能减退 ;乳房发育及肥胖与性发育滞后密切相关。     

冠心病患者性激素水平失衡的研究

目的 :研究冠心病患者性激素水平的变化。方法 :选择冠心病患者 5 0例 ,用放射免疫法测定血清雌二醇 （E2 ）、孕酮 （P）、促卵泡刺激素 （FSH）、促黄体生成素 （L H）、睾酮 （T）、泌乳素 （PRL）及生长激素 （GH）的变化 ;采用酶法观测空腹总胆固醇 （TC）、甘油三酯 （TG）、高密度脂蛋白 （HDL）及低密度脂蛋白胆固醇 （L DL- C）的变化。结果 :1男性冠心病组与对照组比 E2 、P均升高 （P<0 .0 5 ） ,T水平亦明显下降 （P<0 .0 1） ;女性冠心病组与对照比 ,P水平均显著升高 （P<0 .0 1） ,E2 水平下降 （P<0 .0 5 ）。 2男性冠心病患者 TC,TG,L DL- C均显著高于对照组 （P<0 .0 1） ,HDL 显著低于对照组 （P<0 .0 1） ;女性冠心病患者 TC,TG,L DL- C均高于对照组 （P<0 .0 5 ） ,HDL 低于对照 （P<0 .0 5 ）。结论 :冠心病患者存在血脂代谢异常。但男性与女性冠心病患者的性激素水平失衡存在差异 :男性 E2 ,P升高 ,T降低 ,女性 P升高 ,E2 降低     

严重脓毒症早期性激素水平与器官损伤的相关性及对预后的影响

目的:探讨严重脓毒症患者早期血清性激素水平与器官损伤之间的相关性及对预后的影响。方法:回顾性分析53例男性严重脓毒症患者的临床资料,收集患者72 h内血清睾酮(T)、雌二醇(E2)和催乳素(PRL)水平,并进行Marshall和APACHEⅡ评分,4周后根据存活情况分为存活组和死亡组,另外选择同期20例男性健康体检者作为对照组。结果:存活组32例,死亡组21例;存活组的血清T低于死亡组和对照组(均P0.01),血清E2和PRL水平高于死亡组和对照组(均P0.05),Marshall和APACHEⅡ评分均低于死亡组(均P0.01);死亡组血清E2显著低于对照组(P0.01),血清T和PRL与对照组无显著差异(P0.05),但呈降低趋势;生存组和死亡组Marshall评分与血清T呈正相关(r=0.637),与血清E2和PRL呈负相关(r分别为-0.732和-0.654,均P0.05)。结论:严重脓毒症早期患者血清T、E2和PRL水平与器官功能的损伤程度密切相关,血清高E2、PRL和低T水平可能具有保护器官的作用。     

不同类型慢性乙型肝炎血清HBV DNA基因含量与临床的关系

探讨不同类型慢性乙型肝炎 (慢乙肝 )患者病毒复制水平与肝损害程度的关系。 180例慢乙肝患者血清HBVDNA基因含量采用荧光定量PCR方法检测。血清HBeAg阳性组HBVDNA含量 (10 6 3 5± 1 84)显著高于HBeAg阴性组 (10 4 73± 1 88) (P <0 0 1) ,不同类型慢乙肝组血清HBVDNA含量相比较无显著性差异 (P >0 0 5 )。研究证实 ,血清HBeAg的存在影响HBVDNA的水平变化 ,不同类型慢性乙型肝炎肝损害程度与血清HBVDNA基因含量无明显关系     

老年男性抑郁症患者治疗前后认知功能和性激素水平的变化

目的观察老年男性抑郁症患者治疗前后认知功能和性激素的变化。方法选择老年男性抑郁症患者50例作为抑郁症组、体检中心70岁以上男性健康体检者50例作为对照组。采用化学免疫发光法检测血清雌二醇(E2)、睾酮(T)、促黄体生成素(LH)、促卵泡激素(FSH)、孕酮(P)及泌乳素(PRL)水平。采用数字广度-倒背(DSB)、数字广度-顺背(DSF)、简易智力状态检查量表(MMSE)评估认知功能。结果老年男性抑郁症组患者血清E2和T水平低于对照组(P0.05),两组血清LH、FSH、P、PRL水平比较无统计学差异(P0.05)。老年男性抑郁症组DSB评分、DSF评分和MMSE评分均低于对照组(P0.05)。抑郁症组患者治疗后血清E2和T水平明显高于治疗前(P0.05),治疗前后血清LH、FSH、P和PRL水平比较无统计学差异(P0.05)。抑郁症患者治疗后DSB评分、DSF评分和MMSE评分均高于治疗前(P0.05)。老年男性抑郁症患者DSF评分与血清T和LH呈正相关(P0.05),MMSE评分与血清T呈正相关(P0.05)。结论老年男性抑郁症患者认知功能和血清E2、T水平下降。     

Study of the direct action of luteinizing hormone-releasing hormone agonists at the testicular level in intact rats treated with an antiluteinizing hormone serum

Is it well known that LHRH agonists can inhibit testicular functions by gonadal desensitization secondary to endogenous LH release and that a direct action at the gonadal level has also been demonstrated. Since an excess of anti-LH serum can be used, as an alternative to hypophysectomy, to neutralize the influence of endogenous LH release, the relative importance of the testis and pituitary gland in the inhibitory effect of a LHRH agonist, [D-Ser-(TBU)6,des-Gly-NH210]LHRH ethylamide (Buserelin), was studied on gonadal gonadotropin receptors in intact adult male rats treated with equine anti-LH or normal horse serum (NHS). A single administration of increasing doses (1-100 ng) of Buserelin leads to a progressive inhibition of testicular LH and PRL receptor levels by 70% and 40%, respectively, in animals injected with NHS. Treatment with the anti-LH serum completely prevents this inhibitory effect of a single dose of the LHRH agonist. After two successive injections of Buserelin in NHS-treated animals, testicular LH receptors are reduced by 70% and 80% with the 100- and 500-ng doses, respectively, while testicular PRL receptors are inhibited by 40-60%. In animals treated with the anti-LH serum, the inhibition of testicular LH receptors is reduced by only 18% (100 ng Buserelin) and 55% (500 ng Buserelin), while the inhibitory effect on PRL receptors is abolished. The present data show that endogenous LH release induced by a single injection of a LHRH agonist plays an essential role in the loss of testicular LH receptors measured 2 days later. Moreover, upon repeated injection of the LHRH agonist, neutralization of endogenous LH release by an anti-LH serum markedly reduces the inhibitory effect of the LHRH agonist on LH receptors, while it completely prevents the effect on PRL receptors, suggesting that the inhibitory effect of the LHRH agonist in the male rat is predominantly due to endogenous LH release rather than to a direct action of the peptide at the testicular level.     

GONADOTROPHIN, THYROTROPHIN AND PROLACTIN RESERVE IN β THALASSAEMIA

Gonadotrophin (Gn), thyrotrophin (TSH) and prolactin (PRL) reserve was evaluated in patients (aged 12-26 years old) with beta thalassaemia. Abnormalities were detected in Gn reserve only. When compared with young adult controls, three of the four female patients and one of the two adult males had markedly impaired Gn responses to LH-releasing hormone (LHRH). Of the five prepubertal males, one had no Gn rise following LHRH, while responses in the other four patients were comparable to those in boys with delayed puberty. Only one adult male had an exaggerated LH response to LHRH. TSH and PRL dynamics were normal. No correlation could be found between the severity of the disturbance in the gonadal axis and the total number of blood transfusions. Our findings correlate best with the severity of the disease process itself.     

Association of sex hormones with hepatic steatosis in men with chronic hepatitis B

BackgroundNo study on the relationship between hepatic steatosis and sex hormone levels in male patients with chronic hepatitis B (CHB) infection has been conducted.AimsWe aimed to investigate the association between serum sex hormones and hepatic steatosis among a cohort of males with CHB.MethodsIn this cross-sectional study, 268 male patients with CHB were enrolled. All participants underwent anthropometric measurement, blood testing, and FibroScan test. Multiple logistic regression analysis was used to investigate the association of serum sex hormones with hepatic steatosis.ResultsWe included 137 males with and 131 without hepatic steatosis in this study. Subjects with serum testosterone (T) levels in the highest tertile had an odds ratio (OR) (95% confidence interval [CI]) of 0.35 (0.18–0.70) (P for trend=0.003); those with serum prolactin (PRL) levels in the highest tertile had an OR (95%CI) of 0.21 (0.10–0.45) (P for trend<0.001); and those with serum estradiol/testosterone (E2/T) in the highest tertile had an OR (95%CI) of 4.02 (1.97–8.20) (P for trend<0.001) for hepatic steatosis.ConclusionLower serum total T and PRL levels and higher total E2/T are independently associated with presence of hepatic steatosis in male patients with CHB.     

Preclinical hypogonadism in genetic hemochromatosis in the early stage of the disease: evidence of hypothalamic dysfunction.

We studied endocrine functions at baseline and after TRH and LHRH stimulation in a group of 7 young male patients with genetic hemochromatosis (HE) without liver damage (i.e. fibrosis and cirrhosis). In five patients endocrine re-evaluations after complete iron depletion was also performed. Mean basal testosterone (T), FSH, LH and PRL were significantly lower than in controls. Serum T increased normally after HCG stimulation. The normal or high increments of LH after LHRH stimulation suggest that secretion capacity of LH was intact and that hypothalamic dysfunction could be responsible for the preclinical gonadal deficiency found in our patients. The response of PRL to TRH indicates that secretion capacity of lactotrophs although present, was decreased and did not improve after phlebotomy therapy. After iron depletion the two patients with the lowest basal T levels showed the highest increments indicating that in the early stages of hypothalamic-pituitary damage gonadal dysfunction is still reversible in HE patients.     

Profile of sex hormones in male patients with systemic lupus erythematosus

OBJECTIVE: To study the profile of sex hormones in male patients with systemic lupus erythematosus (SLE). METHOD: Serum prolactin (PRL), testosterone (T), estradiol (E2), follicle-stimulating hormone (FSII) and luteinizing hormone (LH) levels were obtained from 35 males with SLE and compared with 33 age-matched normal controls. RESULTS: No significant differences in serum T, E2, PRL levels and E2/T ratio were observed between male SLE patients and controls. However, patients with SLE had significantly higher levels of gonadotrophins (FSH, LH). Five (14%) SLE patients, but none of the controls, had both low testosterone and elevated LH. Hypoandrogenic male SLE patients did not have overt features of hypogonadism but had a higher prevalence of central nervous system disease and scrositis than those with normal androgen levels. Discase flares, on the other hand, were not significantly more frequent in these patients. Although PRL or T levels per se did not correlate with disease activity in our patients, the ratio of PRL to T showed a significant correlation with SLEDAI scores (p = 0.42. P = 0.01). CONCLUSIONS: Hypoandrogenism is present in some male patients with SLE and may be relevant in disease pathogenesis. However, whether these hormonal abnormalities are intrinsic to SLE or the consequence of any non-specific chronic disorders cannot be distinguished from the current data. Further studies involving a larger number of subjects and inclusion of other disease controls are needed.     

Reversal of chronic ethanol-induced testosterone suppression in peripubertal male rats by opiate blockade

Teenage drinking continues to be a significant problem in the U.S., as well as abroad. We have previously demonstrated that opiate blockade with naltrexone, a drug currently used in patients to diminish alcohol craving, prevented the fall in serum testosterone seen after acute ethanol (EtOH) exposure in young, peripubertal male rats. To follow-up on this reversal, a series of experiments was performed to determine if naltrexone would also prevent the testosterone suppression caused by chronic EtOH exposure. Peripubertal rats either 45 days old (mid-pubertal) or 55 days old (late pubertal) were fed an EtOH-containing liquid diet or pair-fed control diet for 14 days. Each animal was implanted with either a naltrexone containing or placebo pellet before starting the liquid diet. In each age group, EtOH alone significantly suppressed testosterone, whereas naltrexone prevented this fall, although it had no effect alone. Serum luteinizing hormone was also suppressed by EtOH; however, naltrexone did not abrogate this fall. In the 45-day-old animals, beta-luteinizing hormone mRNA levels rose significantly in the EtOH group, but not when naltrexone was coadministered with EtOH. There was no change in hypothalamic luteinizing hormone releasing hormone (LHRH) mRNA, pro-LHRH, or LHRH in any group at either age. Thus, naltrexone is able to partially prevent the EtOH-induced suppression of gonadal testosterone of young, adolescent male rats. This effect appears to be mediated directly at gonadal level, because hypothalamic and pituitary hormone changes were minor and nonsignificant.     

Serum prolactin and luteinizing hormone levels and the activities of hypothalamic monoamine oxidase A and B and phenylethanolamine-N-methyl transferase are changed during sexual maturation in male rats treated neonatally with melatonin

Male rat pups were given a single dose of melatonin on day 5 of age. On days 30, 45, and 60, prolactin (PRL), luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone (T) were measured in serum and monoamine oxidase A (MAO A) activity, monoamine oxidase B (MAO B), and phenylethanolamine-N-methyl transferase (PNMT) activity were measured in the hypothalamus. Melatonin administration increased serum PRL levels at all ages studied. Serum LH levels were decreased in the melatonin treated group on day 30, but levels were elevated on days 45 and 60 of age as compared to controls. LH response to luteinizing hormone-releasing hormone (LHRH) only increased in melatonin treated animals at 30 days of age. Serum T levels decreased with melatonin treatment at 30 days of age, but increased on days 45 and 60 of age. T response to human chorionic gonadotropin (hCG) was blunted by melatonin treatment at 30 days of life. Hypothalamic MAO A activity increased, after neonatal melatonin administration, at 30 and 45 days of age and decreased at 60 days of life. Early neonatal melatonin administration increased MAO B and PNMT activities on day 45. These findings suggest that neonatal melatonin administration induces an earlier sexual maturation in male rats, possibly related to PRL, LH, MAO, and PNMT increases.     

老年男性性病患者临床与性激素水平的检测与分析

目的　探讨老年男性性病患者的临床特点及性激素水平。方法　对 6 3例老年男性性病患者的临床资料进行分析 ,同时采用放射免疫分析法对老年男性性病患者 4种性激素 (雌二醇、睾酮、促黄体生成素、促卵泡激素 )水平进行了检测。结果　 6 3例老年男性性病患者的传染途径主要为性接触传染 ,4种性病中 ,早期梅毒占第 1位 ,尖锐湿疣占第 2位 ,同时老年男性性病患者中亦存在≥ 2种性病混合感染。老年男性性病患者睾酮水平与正常对照组相比 ,差异有显著的统计学意义 (P <0 0 5 )。结论　老年男性性病患者以早期梅毒占第 1位 ,同时存在多样化及混合感染 ,性激素中睾酮水平的变化可能与老年性行为的改变有关。     

Pituitary and gonadal response to LH releasing hormone administration in the female and male cheetah

Luteinizing hormone releasing hormone (LHRH, 50 micrograms) or saline was administered (i.m.) to adult female and male cheetahs under anaesthesia to evaluate pituitary and gonadal response. Serum LH levels did not fluctuate over a 120-min sampling period in saline-treated animals. Serum LH concentrations were raised (P less than 0.05) in both female and male cheetahs after LHRH injection, the temporal response being similar to previously reported results in unanaesthetized, domestic carnivores. The magnitude of the LHRH-induced LH response was sex-dependent. Over a 120-min post-injection period both saline control and LHRH-induced LH levels were about twofold greater in males than females. Although LHRH had no acute influence on ovarian oestradiol-17 beta production in the female, serum testosterone levels were raised (P less than 0.05) in male cheetahs by 60 min after treatment. This study (1) provides introductory endocrine information on the cheetah, an endangered species, and (2) indicates that exogenous LHRH is effective in acutely altering pituitary (female) and pituitary/gonadal (male) function in an anaesthetized, non-domestic felid.