Serum inhibin B as a marker for spermatogenesis

Inhibin B generated by Sertoli cells provides negative feedback on FSH secretion. In men, inhibin B seems to be the physiologically important form of inhibin. Serum inhibin B was measured by two-site immunoenzymatic assay in 40 normal men (27 years of age) with sperm concentrations 100 +/- 9.2 x 10(6)/mL, 51 subfertile men (31 years of age) with sperm concentrations 6.8 +/- 0.8 x 10(6)/mL, 16 men with varicocele with sperm concentrations 54.3 +/- 0.8 x 10(6)/mL (31 years of age), men with hypogonadotrophic hypogonadism, men with Klinefelter syndrome, and men with obstructive and non-obstructive azoospermia. In men with normal sperm concentrations (>20 x 10(6) mL) serum inhibin B was 201 +/- 17 pg/mL and FSH 4 +/- 0.5 IU/L. Varicocele patients showed normal sperm concentrations > 20 x 10(6)/mL, normal serum inhibin B (173 +/- 21 pg/mL), and normal FSH levels (4.6 +/- 0.6 IU/L). In patients with sperm concentrations < 20 x 10(6)/mL the inhibin B level was 118 +/- 14 pg/mL and the FSH level was 10 +/- 1.1 IU/L. In all patients, except those with hypogonadotrophic hypogonadism and Klinefelter syndrome. inhibin B and FSH were inversely correlated (r = -.41, p > 0.01). There was a positive correlation between inhibin B and sperm concentrations (r = .34, p < .01). In varicocele men there was a correlation of r = .574, p < .05. Inhibin B may be a marker of exocrine testicular function and may offer an improved diagnosis of testicular dysfunction.     

成年女性年龄相关的促卵泡刺激素和促黄体生成素水平与骨密度关系

目的调查女性年龄相关的血清促卵泡刺激素(FSH)和促黄体生成素(LH)水平及其与骨密度的关系。方法测定699例受试者血清FSH和LH浓度及正位腰椎(AP)、侧位腰椎(LP)、总髋部(T-hip)、远端前臂(DF)骨密度,评价血清FSH和LH与年龄、骨密度的关系。结果FSH和LH从40岁起随增龄而增加,至≥60岁随增龄而下降。绝经前血清FSH和LH的几何平均值(SD)分别为3.94±2.08IU/L和7.51±2.58IU/L,绝经后分别为28.8±1.88IU/L和25.6±1.95IU/L。血清FSH与LH呈高度正相关(r=0.734,P=0.000)。FSH和LH与各部位骨密度呈显著负相关,FSH与骨密度的相关程度(r=-0.597～-0.492)好于LH与骨密度(r=-0.332～-0.452)的相关程度。其中FSH(r=-0.597)和LH(r=-0.452)与腰椎骨密度的负相关性最好。结论成年女性血清FSH和LH随年龄和绝经状态而变化,FSH和LH与骨密度明显相关。血清FSH和LH增加的妇女骨密度下降。     

Modulation of immunoradiometric and bioactive follicle stimulating hormone secretion and clearance in young and elderly men during treatment with tamoxifen or flutamide.

The secretion and clearance of immunoactive and bioactive follicle-stimulating hormone (FSH) in healthy young men (N = 10) and elderly men (N = 7) during blockade of endogenous sex steroid hormones with tamoxifen, an antiestrogen, and flutamide, an antiandrogen, was investigated. To this end, subjects underwent blood sampling basally every 10 minutes for 24 hours, and then received 2 consecutive intravenous pulses of synthetic gonadotropin releasing hormone (GnRH; 10 micrograms and 100 micrograms) every 2 hours. This paradigm was repeated on two subsequent visits, in which subjects received either flutamide HCl, a specific nonsteroidal competitive antagonist of the androgen receptor (750 mg daily for 3 days), or tamoxifen, a selective antagonist of the estrogen receptor (20 mg daily for 9 days). Serum immunoactive FSH concentrations were measured in each sample by immunoradiometric assay (IRMA). Serum bioactive FSH concentrations were determined by an in vitro bioassay (rat granulosa cell aromatase system) on 24-hour serum pools. Deconvolution analysis was used to analyze both the FSH IRMA 24-hour time series and FSH release after GnRH. Comparisons between young and elderly men of the basal state showed significantly increased 24-hour mean serum immunoactive and bioactive FSH concentrations and significantly decreased free testosterone concentrations in elderly men. By deconvolution analysis, elderly men had a significant decrease in FSH secretory burst duration, and an increase in FSH half-life and FSH secretory burst amplitude compared with younger men. In response to sex steroid receptor blockade in young men, there was a significant increase in mean serum bioactive FSH concentrations during antiandrogen treatment, but not during antiestrogen treatment.(ABSTRACT TRUNCATED AT 250 WORDS)     

血清抑制素B对非阻塞性无精子症睾丸精子存在的预测价值

目的:探讨血清抑制素B(INHB)对非阻塞性无精子症(NOA)患者睾丸精子存在与否的预测价值。方法:分别对40例NOA、20例阻塞性无精子症(OA)及10例正常生育男性以双抗体夹心ELISA法测定其血清INHB水平。并用化学发光法检测了上述研究对象的卵泡刺激素(FSH)水平。结果:NOA患者的血清FSH[(21.34±12.15)IU/L]明显高于OA组和正常生育男性组[(3.94±1.52)IU/L和(4.27±2.84 IU/L],而血清INHB水平[(53.15±58.74)ng/L]明显低于后两者[(162.49±78.38)ng/L和(228.49±110.68)ng/L]。正常生育男性与OA组患者的血清INHB水平差异无显著性(P>0.05)。NOA患者血清INHB水平与其睾丸精子抽吸(TESE)的结果有相关性(r=0.528,P<0.01)。TESE获得精子者血清INHB水平[(90.31±72.18)ng/L]显著高于TESE无精子者[(19.54±20.38)ng/L,P<0.01];而两者的血清FSH差异无显著性(P>0.05)。结论:血清INHB可作为预测TESE的参考指标。血清INHB的测定有望替代睾丸活检确定睾丸精子的存在与否。     

Deconvolution analysis of bioassayable LH secretion and half-life in men with idiopathic oligoasthenospermia

To further investigate the nature of neuroendocrine disturbances of the hypothalamo-pituitary-gonadal axis in idiopathic male infertility, we studied 12 infertile men with oligoasthenozoospermia and 13 euspermic controls, matched for age and body mass index, by blood withdrawal at 10-min intervals for 8 h to analyse pulsatile release of bioactive LH (b-LH). The rat interstitial cell testosterone (RICT) bioassay was used in conjunction with a recently validated multiparameter deconvolution algorithm, to estimate the endogenous half-life of b-LH, its secretory burst frequency, amplitude, duration and mass. Oligoasthenospermic men exhibited significant ( p < 0.05) alterations within the LH axis; namely: (1) a prolonged half-life of b-LH (92 min in euspermic men, 127 min in oligoasthenospermic men); (2) a reduced b-LH secretory burst amplitude (2.2 ± 1.2 IU/l/min in euspermic men, 1.7 ± 0.8 IU/l/min in oligoasthenospermic men); (3) a lower bioactive/immunoactive (b/i) ratio for LH secretory burst amplitude (14 in euspermic men, 4 in oligoasthenospermic men); (4) a reduced b/i ratio in the mass of LH secreted per burst (5.4 in euspermic men, 4.1 in oligoasthenospermic men) and (5) decreased coordinate release of b-LH and testosterone in infertile men, as assessed by cross-correlation analysis. These disturbances differ from the neuroendocrine dysregulation described in other states of male hypogonadotrophism.     

小睾丸组织超微结构变化与性激素相关性研究

目的 :探讨小睾丸组织超微结构变化和性激素改变及其相关性。　方法 :对 8例小睾丸病人和 12例健康成人血清进行性激素测定 ,光镜及电镜观察小睾丸组织的超微结构变化。　结果 :小睾丸病人和正常对照组血清性激素FSH、LH、T分别为 (2 1.0 5± 9.15 )IU/Lvs (6 74± 3 5 2 )IU/L、(2 2 .88± 6 .2 5 )IU/Lvs (6 6 0± 1 4 8)IU/L、(0 .30± 0 .0 4 )nmol/Lvs (17 5 5± 9 2 5 )nmol/L ,两者相比差异有显著性 (P <0 .0 1) ;精曲小管直径和管壁厚度分别为 (37.33± 6 .80 )、(10 .30± 1.82 ) μm ,与正常组的 (198 4 6± 2 9 84 )、(2 95± 0 2 0 ) μm相比 ,差异有极显著性 (P <0 .0 1) ;组织超微结构变化显著。　结论 :小睾丸组织精曲小管、生精上皮、支持细胞、界膜、间质细胞及血管均发生严重的病理改变 ,其形成可能与遗传和免疫反应有关     

Peripheral INSL3 concentrations decline with age in a large population of Australian men

The novel peptide hormone insulin-like peptide 3 (INSL3) is a major secretory product of the Leydig cells of the testis, and in adult men is secreted into the blood, giving rise to circulating concentrations ranging from 0.5 to 2.5 ng/mL. We studied a large randomly recruited cohort of 1183 men from South Australia, comparing serum INSL3 concentrations with age, and a variety of endocrine, cognitive and morphological parameters. While INSL3 concentration declines significantly (p < 0.001) and continuously with age from 1.29 +/- 0.47 ng/mL in young men (age 35-44 years) to 0.79 +/- 0.39 ng/mL in the age group 75-80 years, there is no correlation with testosterone or components of the hypothalamo-pituitary-gonadal (HPG) axis, independent of age, nor with any other parameter measured, including thyroid or prostate status and obesity. For men exhibiting normal follicle stimulating hormone (FSH) and high luteinizing hormone (LH) levels, there was a significant inverse correlation with plasma oestradiol. Unilaterally orchidectomized men had INSL3 values intermediate between intact men and anorchid subjects, and showed inverse correlations (p < 0.001) between INSL3 and FSH or LH concentrations, which were independent of age. Taken together, the data show that INSL3 is an independent measure of Leydig cell function (quality and number), which appears to be independent of acute control via the HPG axis. Its decline with age reflects a decline in the properties of the Leydig cell population only, and emphasizes a gonadal component in the age-related decrease in androgen production.     

Hypophyseal-Gonadal Dysfunction in Men with Non-Alcoholic Liver Cirrhosis

Seven males with liver cirrhosis associated with hepatitis and one with schistosomal liver fibrosis were studied for hypophyseal gonadal dysfunction and compared to six age matched controls. Cirrhotics as a group had higher serum 17 beta estradiol levels (22.1 +/- 6.3 vs 7.8 +/- 0.8 pg/ml, p less than 0.05) which did not rise after four days of human chorionic gonadotropin (hCG) stimulation. Conversely, there was an adequate rise in serum testosterone level after hCG stimulation (332.8 +/- 99.7 ng/dl baseline to 887.6 +/- 67.1 ng/dl, p less than 0.01). Compared to the controls, cirrhotics had lower baseline serum follicle stimulating hormone (FSH) (3.6 +/- 1.7 vs. 10.2 +/- 1.5 mIu/ml, p less than 0.02) and higher serum prolactin (13.5 +/- 2.5 vs. 6.8 +/- 1.0 ng/ml, p less than 0.05). Pituitary dynamic function testing in cirrhotics revealed blunted response of luteinizing hormone (LH) and FSH, to luteinizing hormone releasing hormone (LHRH) in four out of eight subjects tested. We conclude that the mechanism of hypogonadism in non-alcoholic cirrhosis is mostly hypogonadotropic in origin rather than primary gonadal injury which is common in alcoholic cirrhosis.     

Luteinizing hormone pulsatility in men with damage to the germinal epithelium

Bioactive-LH (B-LH) was measured in plasma by in-vitro bioassay and immunoactive-LH (I-LH) by immunoassay at 10 min intervals for 6 h in five men after standard chemotherapy for Hodgkin's disease. Eleven normal men acted as controls. Follicle-stimulating hormone (FSH) was markedly raised in the treated patients (mean +/- SEM; 12.8 +/- 2.8 vs. 2.7 +/- 0.4 IU l-1, P less than 0.006) reflecting damage to the germinal epithelium. Bioactive (27.4 +/- 2.8 vs. 12.9 +/- 1.3 IU l-1) and I-LH (9.6 +/- 2.0 vs. 4.9 +/- 0.4 IU l-1) were elevated (P less than 0.006) in the patient group whilst testosterone levels (24.0 +/- 3.8 vs. 19.6 +/- 2.4 nmol l-1) were normal. The testosterone I-LH ratio, a putative index of Leydig cell dysfunction, was negatively correlated with FSH levels (r = -0.85, P less than 0.02). Bioactive and I-LH pulse peak amplitude were elevated, as were pulse maxima (P less than 0.05). In contrast, B-LH pulse frequency was similar between the patients (2 pulses per 6 h) and controls (median 2, range 1-3 pulses per 6 h) as was the I-LH pulse frequency (median 2, 1-2 pulses per 6 h in both groups). The mean B:I LH ratios were similar (2.94 +/- 0.09 vs. 2.63 +/- 0.14) in both groups, although the inter-pulse B:I ratio was increased (P less than 0.007) in the patient group.(ABSTRACT TRUNCATED AT 250 WORDS)     

24-hour pulsatile and circadian patterns of cortisol secretion in alcoholic men

Pulsatile and circadian patterns of cortisol secretion during acute (3 to 16 days) and chronic (29 to 39 days) abstinence were examined in alcoholic men with no clinical or laboratory evidence of hepatic dysfunction or nutritional deficiencies. Mean and integrated 24-hour serum concentrations of cortisol determined by sampling the blood every 20 minutes over a 24-hour period were increased in six out of 10 alcoholic subjects during acute abstinence when compared with normal controls. Sustained abstinence in seven subjects with follow-up studies caused significant decreases in the mean maximal cortisol peak amplitude (13 +/- 1.0 SEM acutely vs. 10.3 +/- 0.52 micrograms/dl follow-up; P = 0.01), mean 24-hour serum cortisol concentrations (10.9 micrograms/dl +/- 1.2 vs. 8.5 micrograms/dl +/- 0.26; P = 0.047), interpulse valley mean (9.3 micrograms/dl +/- 0.88 vs. 6.5 micrograms/dl +/- 0.34; P = 0.007), and valley nadir (7.9 micrograms/dl +/- 0.69 vs. 5.4 micrograms/dl +/- 0.30; P = 0.0036) concentrations. Cortisol pulse frequency was normal. Although circadian cortisol rhythmicity was maintained in alcoholics, the timing of the circadian acrophase was delayed significantly (P = 0.006) during acute abstinence (1022 [clocktime] +/- 34 min) as compared with normal controls (0743 [clocktime] +/- 34 min), and the amplitude of circadian cortisol rhythms exceeded normal in five of 10 alcoholics. Analysis of data in one alcoholic subject by a new multiparameter deconvolution method demonstrated increases in secretory burst amplitude (0.64 microgram/dl +/- 0.08 SD), mass of cortisol released per burst (9.8 micrograms/dl +/- 1.2 SD), and daily endogenous cortisol production rate (22 mg +/- 2.4 SD) during acute abstinence. These values were statistically different when compared with seven normal controls and the subjects' values during sustained abstinence (P less than 0.02). In conclusion, the results of the present study suggest increased daily production of cortisol as a possible mechanism underlying the elevated serum cortisol concentrations in chronic alcoholics during acute abstinence. This abnormality is shown to be reversible with sustained abstinence from alcohol.     

Specific regulatory actions of dihydrotestosterone and estradiol on the dynamics of FSH secretion and clearance in humans

The authors investigated immunoactive and bioactive follicle-stimulating hormone (FSH) secretion and clearance in six healthy young men during steady-state infusions of vehicle (basal, B, 28 hours), dihydrotestosterone (DHT, 4.5 days), or estradiol (4.5 days) accompanied by blood sampling at 10-minute intervals for 28 hours. Serum FSH concentrations were assayed by a two-site immunoradiometric assay (IRMA) and two separate in vitro bioassays (rat granulosa and Sertoli cell systems). FSH measurements included: 24-hour mean serum concentrations (IRMA and bioassay), multiple-parameter deconvolution of 24-hour pulsatile FSH time series and FSH release in response to exogenous gonadotropin-releasing hormone (GnRH) boluses (IRMA) to assess secretion and clearance, and circadian serum FSH concentration rhythms by cosinor analysis (IRMA). We found: 1) a significant decrease in 24-hour mean IRMA FSH concentrations during DHT infusion while both in vitro estimates of FSH bioactivity were unchanged; 2) significant decreases in the mass of IRMA FSH secreted per 24 hours during DHT infusion; 3) significant decreases in the IRMA FSH half-life during estradiol infusion without any change in FSH interpulse interval; 4) no steroidal effects on FSH secretory responses to exogenous GnRH; and 5) abolition of basal circadian FSH rhythms during sex-steroid infusions. Based on these findings, we conclude that steady-state sex-steroid hormone infusions selectively alter IRMA FSH secretion and clearance without affecting IRMA FSH pulse frequency or mean concentrations of bioactive FSH.     

Clinical studies in an adult male patient with "isolated follicle stimulating hormone (FSH) deficiency"

Previous reports concerning isolated follicle stimulating hormone (FSH) deficiency and its possible pathogenesis have been conflicting. Both "normal" and "abnormal" FSH response to luteinizing hormone releasing hormone (LHRH) infusion have been described. We studied a 22-year-old man with normal basal serum testosterone and luteinizing hormone (LH) levels but undetectable levels of serum FSH. His serum LH titers showed one secretory spike during a 40-hour sampling at 20-minute intervals, whereas his serum FSH titers remained undetectable (less than 0.4 IU/l). Infusion of LHRH, 0.2 microgram/minute for 4 hours, induced the expected rise in the serum LH levels, but serum FSH levels remained low and only at one point reached 0.9 IU/l (normal adult male basal range 0.9-10.3 IU/l). The patient received LHRH, 100 micrograms/day, for three days. A second LHRH infusion, 0.2 microgram/minute for 4 hours, induced a normal rise in both the serum LH and FSH titers. The serum sex steroid binding globulin level was 10.3 ng DHT bound/ml (normal adult male level 8.0 +/- 0.3 ng DHT bound/ml). Presence of circulating auto-antibodies to the serum FSH was excluded by determining the binding of [125I] FSH with the patient's serum and comparing it with sera obtained from two normal male adult volunteers. Pituitary function tests were otherwise intact. Presence of a pituitary tumor was excluded by computerized axial tomography and x-ray studies of the pituitary fossa and normal visual fields. Clinically, the patient demonstrated cryptorchidism, hypospadias, surgically repaired omphalocele, and bilateral hearing loss.(ABSTRACT TRUNCATED AT 250 WORDS)     

Inhibin and steroid response to testicular stimulation with pure FSH (Metrodin) in infertile men with unilateral cryptorchidism

Summary. Static measurements of immuno-reactive inhibin have proven of little relevance in the diagnosis of testicular disorders. Dynamic evaluation of the inhibin secretory reserve might detect a specific Sertoli cell defect in a subgroup of infertile men. We compared the response of inhibin and steroids to an intravenous injection of pure FSH (Metrodin, Serono, 300 IU) in 13 infertile men with unilateral cryptorchidism to that in eight normal fertile men. Blood was aspirated before, 24, 48, and 72 h after the FSH injection. Two subgroups of patients with unilateral cryptorchidism were detected: those who responded by secreting inhibin in a pattern similar to normal men (seven patients), and those who responded poorly or not at all (six patients). The presumed cause of this difference is a defect of Sertoli cell reserve function due to a combination of insults to the testes, and not to cryptorchidism itself. The difference in response to FSH cannot be predicted from semen analysis nor from static hormone measurements. Overall, inhibin levels correlated significantly with the serum concentrations of FSH (r = -0.36, P <0.05), testosterone (r = 0.37, P <0.05), and 17-hydroxyprogesterone (r = 0.66, P <0.001).
It is concluded that, in infertile men with unilateral cryptorchidism, stimulation of Sertoli cells by FSH can identify a subgroup of patients with Sertoli cell malfunction involving inhibin synthesis.     

Feedback inhibition of gonadotropins by testosterone in men with hypogonadotropic hypogonadism: comparison to the intact pituitary-testicular axis in primary hypogonadism

Men with hypogonadotropic hypogonadism (HH) due to hypothalamic-pituitary disease present with low serum testosterone levels combined with undetectable, low, or normal gonadotropin levels. Treatment consists of testosterone replacement to reverse the symptoms of androgen deficiency. The aim of this study was to examine the dynamics and feedback inhibition of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) in relation to testosterone in 38 men with HH treated with testosterone. Findings were compared with 11 men with primary hypergonadism (PH). Testosterone replacement led to a suppression of FSH levels from 2.8 IU/L at baseline to 1.1 IU/L and to a suppression of LH levels from 2.3 to 0.8 IU/L. There was a linear correlation between levels of FSH and LH (after natural log transformation for both) and testosterone levels in both the HH and PH groups. However, the differences in intercepts and slopes between the groups were significant. To determine whether nonsuppressed FSH or LH during testosterone replacement reduces the probability of eugonadism, as reflected by normal testosterone levels, gonadotropin levels were measured and categorized as low (<0.5 IU/L), medium (0.5-2 IU/L), and high levels (>2 IU/L). The higher FSH or LH levels were found to significantly decrease the chance for achieving eugonadism. In conclusion, in men with HH due to hypothalamic-pituitary disease or injury, the pituitary-testicular hormonal axis maintains its physiological negative feedback between testosterone and gonadotropins. Thus, gonadotropin levels in men with HH might be useful, together with testosterone concentrations, for assessing the adequacy of androgen replacement.     

Differential patterns of inhibin secretion in response to gonadotrophin stimulation in normal men

Inhibin B is produced by the testis, and its constituent alpha and beta B subunits have been localized immunohistochemically to Leydig as well as Sertoli cells in both rodent and human testes. Whether Leydig cells contribute to circulating inhibin B concentrations, however, is uncertain. We have investigated this by selectively stimulating Leydig and Sertoli cells with hCG and FSH, respectively. The study was a randomized crossover trial, investigating responses to 225 IU recombinant FSH or 3000 IU hCG administered s/c 4-6 weeks apart. Ten normal men were recruited to participate. Blood was taken twice before treatment and after 8, 24, 48, 72 and 96 h. Serum was assayed for FSH, LH and testosterone by radioimmunoassay (RIA); inhibin B and pro-alpha C inhibin forms by ELISA. Administration of hCG, but not FSH, caused a rapid increase in blood testosterone levels, which reached a maximum after 72 h (22.2 +/- 2.7-50.1 +/- 4.5 nmol/L, p < 0.001). Inhibin B concentrations in blood were unchanged following either treatment. Conversely, pro-alpha C concentrations increased following both treatments. FSH administration resulted in a gradual increase in pro-alpha C concentrations (369 +/- 18 pg/mL pre-treatment to 453 +/- 33 pg/mL after 96 h, p=0.013). Administration of hCG resulted in a more rapid response, with pro-alpha C concentrations rising from 384 +/- 23 pg/mL pre-treatment to a peak at 48 h of 535 +/- 45 pg/mL (p=0.007). This response was more rapid than that of testosterone. These results demonstrate that adult human Leydig, as well as Sertoli, cells secrete inhibin alpha subunit in response to gonadotrophin stimulation but provide no evidence for the secretion of inhibin B from Leydig cells. The lack of change in inhibin B secretion in response to FSH suggests that more prolonged or intense stimulation of Sertoli cells may be required for secretion of the dimeric form.     

抗FSH自身抗体对大鼠睾丸生精功能影响的初步研究

目的:建立抗FSH自身抗体大鼠模型,同时研究抗FSH自身抗体对雄性大鼠生精功能的影响。方法:30只SD大鼠(21d龄),随机分为实验组、对照组,各15只。合成大鼠FSHβ亚基上一段特异性氨基酸序列(18肽),将合成多肽与钥孔戚血蓝素(keyholelimpethemocyanin,KLH)偶联,免疫SD大鼠,作为实验组。对照组大鼠用KLH免疫。初次免疫之后,每隔2周加强免疫1次,共7次,于第3次加强免疫后1周(即,免疫第49d)眼眶取血测定血清抗体效价,之后每隔两周测一次抗体效价,至实验结束。并于免疫第77d、91d和105d时,分别处死实验组和对照组大鼠各5只,用光镜和电镜观察大鼠睾丸生精小管结构和附睾精子结构的变化,计数附睾尾精子数量及肿胀精子百分率,并用ELISA法检测大鼠血清T水平。结果:免疫第49d后,实验组大鼠血清抗18肽-KLH抗体效价为1∶200,免疫第63d后,抗体效价达到1∶400,之后抗体效价一直维持在1∶400。免疫第91d后,实验组大鼠附睾尾肿胀精子百分率显著低于对照组(60.4±6.23vs50.60±3.05,P<0.05);免疫第105d后,实验组大鼠生精小管内生精细胞数量及管腔内精子数量均减少,且附睾尾精子数量(46.08±6.56vs32.53±3.41)和肿胀精子百分率(60.60±5.86vs48.60±3.85)均显著低于对照组(P<0.05),而血清T水平显著高于对照组(P<0.05)。结论:抗FSH自身抗体可能会引起睾丸生精障碍。     

Effect of the embolization of completely unpurified islets on portal vein pressure and hepatic biochemistry in clinical practice

Here we report on the impact of completely unpurified islet transplantation on the portal vein pressure (PVP) and the hepatic biochemistry in the peritransplant period and on follow-up. Type I diabetic patients underwent simultaneous kidney and islet transplantation. Islets were not purified from the acinar tissue to prevent loss of endocrine mass. Each patient received a mean 521,846 +/- 201,539.4 islet equivalents (7812.1 islet equivalents/kg/recipient). Immunosuppression and peritransplant medication were given according to the Giessen protocol. The islets were injected into the left hepatic lobe through the umbilical vein. PVP was recorded at time 0 and every 5 min throughout cell infusion. Liver function was assessed daily for the first 10 days, and on follow-up. Basal, peak, and final PVP were 12 +/- 3.8, 25.1 +/- 7.9, and 19.5 +/- 6.2 mmHg, respectively (basal vs. final, p < 0.05). Bilirubin, alkaline phosphatase, prothrombin time, and APTT stayed within normal range. Peak aspartate aminotransferase (AST), alanine aminotransferase (ALT), and serum amylase were 109.4 +/- 61.2 IU/L (basal vs. peak, not significant), 79.5 +/- 56.9 IU/L (basal vs. peak, not significant), and 887.5 +/- 153.6 IU/L (basal vs. peak, p = 0.02), respectively. In all cases AST, ALT, and amylase normalized within 6 days posttransplant and remained so on follow-up (longest control, 33 months posttransplant). Although the intrahepatic infusion of unpurified pancreatic islets affects both the portal vein pressure and the hepatic biochemical profile, this effect is transient and does not compromise the safety of the procedure.     

Intratesticular testosterone concentrations comparable with serum levels are not sufficient to maintain normal sperm production in men receiving a hormonal contraceptive regimen

Intratesticular testosterone (ITT) is thought to play a key role in the control of spermatogenesis in man but is rarely measured. The purposes of this study were 1) to examine the relationship between intratesticular fluid and serum testosterone (T) at baseline and during treatment with a contraceptive regimen known to suppress spermatogenesis and 2) to measure intratesticular fluid androgenic bioactivity. Seven men received 6 months of T enanthate (TE) 100 mg weekly intramuscularly plus levonorgestrel (LNG) 62.5 or 31.25 microg orally daily. Testicular fluid was obtained by percutaneous aspiration at baseline and during month 6. Mean luteinizing hormone (LH) was suppressed 98% from 3.79 +/- 0.80 IU/L at baseline to 0.08 +/- 0.03 IU/L. Mean follicle stimulating hormone (FSH) was suppressed 97%, from 3.29 +/- 0.67 IU/L to 0.10 +/- 0.03 IU/L. Mean serum T levels were similar before (22.8 +/- 1.9 nmol/L) and during treatment (28.7 +/- 2.0 nmol/L) (P = .12). ITT (822 +/- 136 nmol/L) was approximately 40x higher than serum T (P < .001) at baseline. ITT was suppressed 98% during treatment to 13.1 +/- 4.5 nmol/L, a level similar to baseline serum T (P = .08) but significantly lower than on-treatment serum T (P = .01). At baseline, intratesticular fluid androgenic bioactivity (583 +/- 145 nmol/L) was 70% of the ITT concentration measured by radioimmunoassay. Intratesticular androgenic bioactivity was suppressed 93% to 40 +/- 22 nmol/L (P < .01) during treatment, but was 3x higher than ITT (13.1 +/- 4.5 nmol/L). Sperm counts declined from 65 +/- 15 million/mL to 1.3 +/- 1.3 million/mL. In summary, TE plus LNG dramatically suppressed ITT (98%) and intratesticular androgenic bioactivity (93%) to levels approximating those in serum. ITT levels comparable with serum T were insufficient to support normal spermatogenesis. Intratesticular androgenic bioactivity was higher than ITT during treatment, suggesting that other androgens may be prevalent in the low-ITT environment.     

Effects of testosterone and venesection on spinal and peripheral bone mineral in six hypogonadal men with hemochromatosis

To measure the effect of testosterone replacement and venesection on spinal and peripheral bone mineral we prospectively studied six hypogonadal men and six eugonadal men with idiopathic hemochromatosis for 24 months. Venesections were performed every week on all patients, and intramuscular injections of testosterone were administered every 3 weeks to the hypogonadal men only. Bone mineral was measured by quantitative computed tomography in the spine and by single-photon absorptiometry in the forearm. During the 24 month period of observation serum testosterone concentrations and serum ferritin levels became normal. In the hypogonadal men mean lumbar spine bone mineral increased by 13.1 +/- 4.9% (95% CI, 0.5-25.6) and mean forearm bone mineral increased by 4.7 +/- 3.8% (95% CI, -5.1 to 14.6). In contrast in the eugonadal men treated over the same period, mean lumbar spine bone mineral decreased by 3.5 +/- 2.8% (95% CI, -10.9 to 3.8, P less than 0.01) and mean forearm bone mineral remained virtually unchanged (0.07 +/- 0.9%; 95% CI, -1.7 to 3.1, P less than 0.05). These data suggest that bone mineral increases in the lumbar spine and in the forearm in hypogonadal men with hemochromatosis treated by testosterone replacement and venesection.     

特发性无、少精子症病人精浆中性激素水平的测定及意义

目的 :通过测定特发性无、少精子症病人精浆中的性激素水平 ,比较分析精浆性激素与无、少精子症的关系。　方法 :特发性无、少精子症男性各 5 0例 ,正常对照 5 0例。精液常规分析判断精子密度 ,化学发光技术测定精浆性激素水平。　结果 :特发性无、少精子症组黄体生成素 (LH)分别为 (5 .19± 0 .6 7)IU/L和 (4.77± 0 .6 8)IU/L ,与正常组 (2 .19± 0 .2 2 )IU/L相比 ,特发性无精子症组差异有极显著性 (P <0 .0 1) ,特发性少精子症组与正常组相比差异有显著性 (P <0 .0 5 ) ;卵泡刺激素 (FSH)分别为 (1.90± 0 .79)IU/L和 (2 .2 7± 0 .2 5 )IU/L ,与正常组 (1.6 1± 0 .14)IU/L相比 ,差异均有显著性 (P <0 .0 5 ) ;泌乳素 (PRL)分别为 (6 .2 5± 0 .34 )ng/ml和 (6 .33±0 .5 1)ng/ml,与正常组 (6 .36± 0 .32 )ng/ml相比差异均无显著性 (P >0 .0 5 ) ;睾酮 (T)分别为 (1.5 1± 0 .12 )ng/ml和 (1.6 8± 0 .71)ng/ml,与正常组 (1.83± 0 .0 9)ng/ml相比 ,特发性无精子症组差异有显著性 (P <0 .0 5 ) ,特发性少精子症组差异无显著性 (P >0 .0 5 ) ;T/LH的比值分别为 0 .2 9± 0 .0 4和 0 .35± 0 .0 9,与对照组 0 .84± 0 .2 0相比 ,差异均有显著性 (P <0 .0 5 )。　结论 :特发性无、少精子症病人 ,精浆