Experimental cryptorchidism in the adult mouse: II. A hormonal study

Serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), and testosterone levels and secretory capacity of the in vitro stimulated testis were determined in control and bilateral cryptorchid mice after 7, 14, 21, and 28 days. In a separate study, serum FSH, LH, and testosterone levels were measured in unilateral and bilateral cryptorchid, hemicastrate, and bilaterally castrate adult mice after 28 days of treatment. Serum FSH levels were significantly increased in bilaterally cryptorchid mice compared to controls (0 days) at 7, 14, 21, and 28 days, but serum LH and testosterone levels did not change. At 28 days, the elevated serum FSH levels in the unilateral and bilateral cryptorchid mice were not different than those in hemicastrate mice. However, the FSH levels in bilaterally castrate mice after 28 days were significantly higher than all other groups. Serum LH and testosterone levels were significantly different only in the bilaterally castrate group, compared to control levels. Both the normal and cryptorchid testes of all ages studied were capable of producing equal levels of testosterone in vitro, both basally and with a human chorionic gonadotropin (hCG) dose of 700 mIU/ml (maximum stimulatory dose for both the normal and the 28 day cryptorchid testes). Changes that occur in mice with experimentally induced cryptorchidism are not identical to those seen in the rat. Serum FSH levels increase, but no changes occur in serum LH and testosterone levels. Additionally, a cryptorchid mouse testis is not hyperresponsive to hCG stimulation in vitro.     

Response to acute hCG stimulation and steroidogenic potential of Leydig cell fibroblastic precursors in humans

The process of early testosterone (T) secretion and Leydig cell differentiation in humans was studied to explore the steroidogenic capacity of Leydig cell fibroblastic precursors. Seven cryptorchid boys received hCG prior to orchidopexy. Patients CP, PB, and MR received one injection of 1000 IU; patients JR and GG, three daily injections of 1000 IU, and patients MP and MM, five daily injections of 1000 IU. A testicular biopsy was obtained at the time of operation, 24 hours after the last injection. Serum T (ng/dl) before and after hCG stimulation and testicular T (ng/g) were determined by RIA. A control prepubertal testis (tumoral orchidectomy) was incubated in vitro and showed a time-dependent accumulation of T both in the medium and the testicular tissue. Testosterone released into the medium at 1, 2, and 4 hours was 0.76, 1.43, and 4.03 ng/ml, respectively. Tissue T at 0, 1, 2, and 4 hours was 9, 11, 16, and 24 ng/g, respectively. This indicates synthesis and secretion of T into the medium. Control testes showed abundant fibroblastic precursors with scanty cytoplasm, few organelles, heterochromatic nuclei, and minute nucleoli. No Leydig cells were present. After 1 day of hCG stimulation, numerous fibroblasts were activated, displaying enlarged cytoplasms with increased numbers of organelles, nuclei rich in euchromatin, and bigger nucleoli. No Leydig cells were present. Basal serum testosterone was 58.2 +/- 45.3 ng/dl and 87.3 +/- 42.0 after hCG administration, while testicular T was 974.0 +/- 686.0 ng/g (control prepubertal testicular T is 10-50 ng/g). After 3 days of hCG, activated fibroblasts increased and immature Leydig cells appeared. Basal serum T was 35.5 +/- 7.8 ng/dl and 394.0 +/- 24.0 after hCG stimulation, while testicular T rose to 2797.5 +/- 1222.6 ng/g. After 5 days, mature Leydig cells appeared for the first time. Serum T was 58 +/- 59.3 ng/dl (basal) and 641.5 +/- 390 ng/dl (after hCG); testicular T was 789 ng/g (patient MM did not have a value for testicular T). HCG induced numerous coated pits and endocytic vesicles in activated fibroblasts and young Leydig cells, suggesting receptor aggregation and internalization of hormone-receptor complexes. Peroxidase-antiperoxidase (PAP) localization of T was positive in peritubular fibroblasts and Leydig cells.(ABSTRACT TRUNCATED AT 400 WORDS)     

Testicular endocrine function in patients with prostatic cancer receiving medical castration by long-term administration of LH-RH agonists

Six patients with advanced prostatic cancer who had been treated by long-term administration of LH-RH agonistic preparations (Buserelin or Leupron) were tested for their pituitary-testicular endocrine functions. Serum levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone (T), prolactin (PRL), estradiol (E2) and dihydrotestosterone (DHT) were measured consecutively. In all medically castrated patients, serum levels of LH, FSH, T, DHT and E2 were suppressed and particularly serum T levels were below the castration level of 1.0 ng/ml. On the other hand, serum PRL levels were unchanged after the long-term treatment with the agonists. Serum LH and FSH levels failed to respond to LH-RH stimulation after the treatment, whereas serum T responded to stimulation by human chorionic gonadotropin (hCG) to various degrees. It was remarkable that, in 4 out of 6 medically castrated patients treated up to more than 3 years, serum T response levels above 1.0 ng/ml were noted. It is suggested that testicular endocrine function to secrete T and DHT in patients under treatment with long-term LH-RH agonist administration are still preserved in response to hCG stimulation.     

Relationship between adult dark spermatogonia and secretory capacity of Leydig cells in cryptorchidism

OBJECTIVE: To examine whether hormonal therapy before orchidopexy affects the histology of the testis and to assess the responsiveness of the Leydig cells, as it has been shown that although basal plasma testosterone levels are within the 'normal' range in cryptorchid boys there is an insufficient increase of testosterone after a human chorionic gonadotrophin (hCG) stimulation in approximately 30% of cryptorchid boys. PATIENTS AND METHODS: In all, 55 boys (aged 1-7 years) with a unilateral undescended testis were included in the study and divided into two groups. Group I (32 boys) received hormonal therapy before orchidopexy; 17 boys received a long-acting LHRH analogue (buserelin) administered as a nasal spray in doses of 20 microg/day for 28 days, followed by 1500 IU hCG intramuscularly (i.m.) once a week for 3 weeks, and the remaining 15 received 1500 IU hCG i.m. once a week for 3 weeks. Group II (33 boys) had orchidopexy alone. During orchidopexy biopsies were taken from the undescended and contralateral descended testes of the boys in both groups for histological analyses. Variations in the number of adult dark (Ad) spermatogonia per tubule (Ad/T) were assessed and testosterone levels were measured during the course of the hormonal therapy (before treatment, 14 days after initiation of buserelin administration, 24 h after each hCG injection, and 3 months after cessation of therapy). RESULTS: In group I, 17 boys (53%) had a 'normal' Ad/T after hormonal treatment vs only six (18%) in group II after orchidopexy alone (P = 0.019). In the hormonally treated boys (group I) we compared the testosterone values 24 h after the second injection of hCG (when the response was most pronounced). Those with a normal Ad/T had a mean (sd) testosterone level of 199.5 (97.6) ng/dL vs 99.6 (85) ng/dL in those with an inadequate Ad/T response to hormonal therapy (P < 0.003). CONCLUSION: We have confirmed that there are two subgroups of cryptorchid boys. Patients with a sufficient Leydig cell secretory capacity will have normal testicular histology and Ad spermatogonia count after hormonal treatment. While those with a suboptimal Leydig cell capacity will have a low Ad spermatogonia count and consequently poor prognosis for future fertility, despite successful surgery. As to whether different types and durations of the hormonal therapy in patients with impaired Leydig cell response could lead to improved testicular histology and consequently improved prognosis for future fertility, remains to be answered.     

Effects of hCG stimulation after withdrawal of long-term oestrogen treatment in patients with prostate carcinoma

Testosterone depletion is the keystone for therapy of patients metastic prostatic carcinoma. Our objective was to investigate Leydig cell function and testosterone levels after withdrawal of long-term endocrine treatment in patients with prostatic carcinoma. Thirteen patients with prostatic carcinoma, previously treated with oestrogens for at least 4 y, were stimulated with 5000 IU human chorionic gonadotrophin (hCG). The stimulation was performed 3-6 y after cessation of the oestrogen therapy. Serum concentrations of testosterone, luteinizing hormone (LH) and follicle stimulating hormone (FSH) were measured before and 24 and 48 h after hCG stimulation. Before hCG stimulation all patients had low serum testosterone concentrations (mean 2.0+/-0.2 nmol/l) and 24 and 48 h after hCG stimulation the values had not significantly increased (mean 2.4+/-0.2 and 2.5+/-1.1 nmol/l, respectively). LH and FSH were within or above the normal range before but after hCG stimulation the values significantly increased. In conclusion, the study shows that the Leydig cells were unable to respond to hCG stimulation more than 3 y after cessation of oestrogen therapy. The Leydig cell function seems to be irreversibly impaired by long-term oestrogen treatment.     

The effect of hCG-treatment on in vitro metabolism of progesterone by the human undescended pre-pubertal testis

Testicular biopsies from 8 pre-pubertal boys aged 3 1/2-11 years, with undescended testes, were incubated in vitro with [3H]progesterone (P). All boys had been treated with human chorionic gonadotrophin (hCG) during the 5 weeks prior to surgery. Four boys were operated within 4 days of the last injection and the remaining 4 at 12 days, 14 days, 6 months and 12 months, respectively, after hormone treatment. Significant steroid metabolic activity was demonstrated in all cases. Biopsies taken a short time after hCG-treatment (1-4 days), when blood testosterone levels were high, exhibited a high capacity for metabolizing progesterone in vitro with a low ratio of formed 20 alpha-dihydro-progesterone (20 alpha-DH-P) to 17 alpha-hydroxyprogesterone (17 alpha-OH-P), when compared to biopsies removed from subjects 12-14 days after cessation of treatment. In the latter cases and in biopsies taken at longer intervals after hormone treatment, the metabolic activity and the 20 alpha-DH-P/17 alpha-OH-P ratio had returned to levels characteristic of untreated pre-pubertal cryptorchid testes. These findings indicate that the use of hCG to provoke descent of the malpositioned testes does not result in long-lasting stimulation of steroidogenic function.     

Effect of an antiestrogen on the testicular response to acute and chronic administration of hCG in normal and hypogonadotropic hypogonadic men: tamoxifen and testicular response to hCG

The effect of the antiestrogen tamoxifen (Tx) on the acute and chronic hCG administration was evaluated in patients with hypogonadotropic hypogonadism (HH) and in normal men. An hCG test (5000 IU hCG) was performed before, after two months of hCG administration (2000 IU hCG three times weekly) and after two months of hCG + Tx (2000 IU hCG three times weekly plus 20 mg/day of tamoxifen). Blood samples were obtained before and following 24 and 72 h of every test to determine T, E, 17OHP and SHBG. T increased only in HH with both treatments (X +/- SEM: Basal: 97.9 +/- 19.7; hCG: 237.7 +/- 43.2; hCG +/- Tx: 204.7 +/- 10.7 ng/100 ml). 17OHP rose with hCG alone, but not with hCG + Tx in both groups. E, SHBG and 17OHP/T ratio did not change after treatments. hCG tests: E increased 24 h following hCG administration in every test. The ratio 17OHP/T rose at 24 h in the first and second test but in the third test it did not change. These results support the role of E in the acute hCG-induced Leydig cell desensitization. However, the association of Tx does not improve T serum levels, suggesting that E might not be the unique factor involved in the mechanisms for testicular desensitization.     

同种肾上腺移植治疗Addison病15年回顾(附九例报告)

目的 观察同种肾上腺移植治疗Addison病的远期效果。方法 对9例行同种肾上腺移植术成功的病例进行长期随访，15年后进行疗效评估。结果 7例移植肾上腺存活，其中6例肾上腺生化指标正常，维持正常生活；2例移植肾上腺失活，且生化指标低于正常，长期靠泼尼松维持。结论 同种肾上腺移植术治疗Addison病远期效果良好。     

严重烧伤后下丘脑-垂体-肾上腺皮质轴激素改变的临床观察

目的 动态观察严重烧伤患下丘脑—垂体—肾上腺皮质轴激素水平的变化，为临床治疗和预后提供理论依据。方法 选择50例严重烧伤患，用放射免疫法分别测定其伤后不同时间血浆总皮质醇(GC)、促肾上腺皮质激素(AUH)、醛固酮(ALD0)和尿17—羟皮质类固醇(17—OH)、尿17-酮类固醇(17—KS)的含量，以各项指标的正常值为对照，结合所得数据进行统计学分析。结果 严重烧伤后，患激素水平均显升高，出现休克期和感染期两个高峰；6周后大部分激素水平低于正常值；患死亡前激素水平极低，而创面愈合则逐渐趋于正常。结论 严重烧伤后，下丘脑—垂体—肾上腺皮质轴激素水平呈持续性上升；休克和感染是烧伤后机体应激反应的两个主要因素；如激素含量骤然下降至正常水平以下，表明肾上腺皮质功能已处于衰竭状态，死亡率极高。     

The influence of age on Leydig cell function in patients with varicocele

In a large group of patients with varicocele (n = 108, mean age: 30.9 years) Leydig cell function was investigated by determining the plasma levels of gonadotrophins under basal conditions and after GnRH stimulation, and by measuring the plasma levels of 17-OH-progesterone (17-OH-P), testosterone (T), dihydrotestosterone (DHT) and oestradiol (E2). There was a significant positive correlation between age and the peak plasma LH values after GnRH stimulation (n = 48, r = 41, P less than 0.01). Conversely, an inverse correlation was observed between age and the basal plasma levels of 17-OH-P (n = 56, r = 0.47, P less than 0.01) and T (n = 108, r = 0.27, P less than 0.01). In normals controls of the same age range (n = 46, mean age: 30 years) such correlations were absent. In patients with varicocele, the 17-OH-P/T ratio was increased significantly in peripheral plasma under basal conditions (P less than 0.01) and after hCG stimulation (P less than 0.05), and a similar increase was found in spermatic venous blood. This suggests that in varicocele patients there is some enzymatic impairment involving the last steps of T biosynthesis. In order to verify the influence of ologozoospermia on plasma steroid levels we divided the patients into 2 groups according to sperm count (more than or less than 10 X 10(6)/ml). Three analyses of variance were then carried out between these 2 groups of patients: 1) analysis of peripheral plasma T levels; 2) analysis of peripheral plasma levels of 17-OH-P and 3) spermatic vein levels of these 2 steroids. However, none of these analyses revealed any significant difference between the 2 groups of patients. When we re-grouped the patients according to age (15-30 and 30-45 years) the same analyses of variance revealed significant differences. These results therefore suggest that the duration of idiopathic varicocele per se influences Leydig cell activity.     

Effects of chronic neuroleptic therapy on human PRL secretion and testicular function

Correlation between secretion of testicular steroids and plasma prolactin (PRL) levels, before and during bromocriptin treatment, was studied in 20 psychiatric patients under neuroleptic therapy for two years or longer. Eleven of them were under additional treatment with antiparkinson drugs (AP group). Plasma PRL, testosterone (T), 5 alpha dihydrotestostérone (DHT), 17 beta-estradiol (E2), 17 alpha OH-progestérone (17 alpha OHP), and dehydroepiandrosterone-sulfate (D-S) were measured by specific RIA both at basal level and in response to testicular stimulation by hCG. Mean basal PRL levels were normal in the patients under neuroleptic treatment along (Ne group), and slightly elevated in the AP group. In the Ne group, an unexpected, significant increase occurred in mean plasma PRL during the hCG stimulation, before bromocriptine treatment. Mean basal steroid levels were normal in both groups. The testicular responses to hCG, as reflected by the T, E2, 17 alpha OHP, and DHT mean plasma levels, were within the normal ranges in the AP group; in the Ne group, however, T and DHT displayed a subnormal mean increase, while E2 and 17 alpha OHP responses were within the normal range. These results suggest that some modifications of the enzymatic activity for testicular steroidogenesis could be induced in the patients under neuroleptic treatment alone. Moreover, a significant reverse correlation was found between PRL and T basal in both group; this correlation disappeared during the bromocriptine treatment.     

Effect of unilateral cryptorchidism on the intertubular tissue of the adult rat testis: evidence for intracellular changes within the Leydig cells

Adult male rats were made unilaterally cryptorchid for 1, 2 or 4 weeks, and the morphological response of the Leydig cells was then studied using morphometric assessment of total Leydig cell volume and number per testis in abdominal and scrotal testes. Serum hormone levels were measured and the steroidogenic properties of isolated Leydig cells were evaluated by in-vitro stimulation with hCG and interstitial fluid (IF) obtained from normal rat testes. Total Leydig cell volume and number per testis were not altered in abdominal vs scrotal testes, although the volume of the abdominal testis was 46, 29 and 21%, respectively, of the volume of the contralateral scrotal testis after 1, 2 and 4 weeks. This reduction was accompanied by significant (P less than 0.05) elevation of the serum levels of FSH and LH, although serum testosterone levels were unchanged from the normal range. Despite the lack of quantitative alterations in Leydig cell morphology, hCG- and IF-stimulated testosterone production was significantly (P less than 0.01) greater by abdominal Leydig cells when compared with scrotal Leydig cells derived from the same animals. Ultrastructural examination of Leydig cells in situ suggested an increase in volumetric density of mitochondria in abdominal Leydig cells. Together with the enhanced steroidogenic responses of these cells, these findings suggest that disruption of spermatogenesis in the cryptorchid testis is accompanied by intracellular activation of Leydig cells. Since these effects were not exhibited by Leydig cells from the scrotal testis it is concluded that local factors within the cryptorchid testis are responsible, at least in part, for regulation of Leydig cell activity.     

雄性Akt2基因缺失小鼠生殖表型研究

目的通过对雄性Akt2基因敲除纯合子小鼠（Akt2-／-）及野生型小鼠（Akt2＋／＋）基础指标、血清糖脂及性激素水平的评估，探讨Akt2基因缺失对糖脂代谢及睾丸功能的影响。方法雄性Akt2＋／＋及Akt2-／-小鼠各15只，行口眼糖耐量（OGTT）实验（2mg／kg），予动力学实验，将纯合子和野生型小鼠分别随机分为2组，空白组和刺激组，刺激组予人绒毛膜促性腺激素（hCG）刺激4h，空白组予等体积的生理盐水刺激4h，检测各组小鼠体重、体内脂肪重量、血脂、空腹胰岛素及生殖激素水平。结果Akt2-／-小鼠同Akt2＋／＋小鼠相比，餐后随机血糖、0h、1h血糖均显著升高（P〈0．05）；睾丸重量显著增加（P〈0．01）。性激素检测发现Akt2-／-小鼠血清雄烯二酮（A2）（P〈0．01）和睾酮（T）（P〈0．05）显著升高；hCG刺激后，Akt2-／-与Akt2＋／＋小鼠的17-羟孕酮（17-OHP）、A2和T均显著升高，但Akt2＋／＋小鼠的T升高更明显。结论Akt2基因不仅影响糖代谢，同时影响睾丸功能，说明胰岛素调节糖代谢的关键信号分子可能对睾丸生殖功能同样具有重要的调节作用。hCG刺激后，同Akt2＋／＋小鼠相比，Akt2-／-小鼠A2和T升高的幅度较小，说明Akt2基因缺失使雄激素合成亢进，但降低了睾丸对hCG的敏感性。     

Influence of hCG treatment on the metabolism of progesterone and pregnenolone in vitro by the human undescended prepubertal testis

Testicular biopsies were taken from 56 prepubertal and pubertal boys, aged 3-17 years, with undescended testes. The biopsies were incubated in vitro with 3H-progesterone or 3H-pregnenolone. Fifteen of the boys had been treated with human chorionic gonadotrophin (hCG) prior to operation. Nine boys were operated on within 1 week of the last injection of hCG while the others were operated on between 12 days and 2 years after hCG treatment. In non-treated prepubertal boys very small amounts of substrate were converted by means of the enzymes 3 beta-hydroxysteroid-dehydrogenase and 17 alpha-hydroxylase and virtually no testosterone was produced. Immediately after treatment with hCG there was a large increase in the conversion of substrate by 17 alpha-hydroxylase and 3 beta-hydroxysteroid-dehydrogenase. Considerable amounts of testosterone were formed, especially from pregnenolone, while smaller amounts were formed from progesterone. This suggests that testosterone production occurred primarily via the delta 5 pathway, at least beyond the 17 alpha-hydroxylase-step. Within 2 weeks of the last hCG injection, steroidogenic activity had decreased towards levels similar to those found in prepubertal testis from untreated boys. These observations indicate that hCG treatment of boys with undescended testes does not result in irreversible or even long-lasting stimulation of their steroidogenic function.     

Endocrine profile in patients with Klinefelter's syndrome

Twenty-seven patients with Klinefelter's Syndrome, aged 19-38 years were divided according to the basal testosterone (T) levels into sub-eugonadal (less than or equal to 3 ng/ml) and eugonadal (greater than 3ng/ml) groups. The pretreatment T level was 3.21 +/- 1.59 ng/ml. The LH and FSH levels, 14.54 +/- 6.68 mIU/ml and 21.51 +/- 10.74 mIU/ml respectively, were above the upper eugonadal range. Short-term hCG treatment stimulated T production significantly and a further increase was observed following long-term hCG treatment. In patients with sub-eugonadal levels of basal T, a greater relative increment of the T level was observed following the hCG stimulation but not in the absolute T increase. Thus, the assumption that in Klinefelter's patients, the low basal T levels and the relative refractoriness to hCG stimulation are secondary to chronic exposure to elevated LH levels, could not be supported. Higher FSH levels were associated with elevated plasma T levels (p less than 0.025). No such association was established with the LH.     

Testicular steroids in spermatic and peripheral veins after single injection of hCG in patients with varicocele

To determine the function of Leydig cells in patients with varicocele, hCG-stimulated levels of progesterone (Prog), 17 alpha-Hydroxy-4-pregnene-3,20-dione (17OHP), 4-Androstene-3,17-dione (A-dione), testosterone (T), and estradiol-17 beta (E2) in both spermatic and peripheral veins were measured. Seventy-two patients with idiopathic varicocele were divided into four groups: patients in group 1 were untreated, whereas patients in groups 2, 3, and 4 were given a single i.m. injection of 10,000 IU hCG 24 h, 96 h, and 168 h before surgery, respectively. In the spermatic and peripheral veins, levels of Prog, 17OHP, and E2 showed peaks at 24 h, whereas levels of A-dione and T showed peaks at 96 h. Significant increases in the ratios of spermatic veins 17OHP to A-dione and 17OHP to T, and a significant decrease in the ratio of T to E2, was found 24 h following hCG treatment. These results demonstrate that, following hCG injection, there is a transient inhibition of testicular C17-20-lyase activity, probably mediated by E2, even in subfertile males with varicocele.     

醋酸棉酚对男子垂体－性腺轴功能的影响

报道２２例长期停服棉酚男子性激素的水平及其对ＬＨＲＨ和ｈＣＧ刺激的反应。２２例中，１１例生精功能未恢复者（无精子症组）的ＦＳＨ和ＬＨ基础值及其对ＬＨＲＨ刺激反应均显著高于正常对照组（１１例），而睾酮（Ｔ）基础值和Ｔ／ＬＨ比值及Ｔ对ｈＣＧ刺激反应显著低于正常对照组。生精功能恢复组（１１例）的ＦＳＨ基础值及其对ＬＨＲＨ刺激在应均显著高于正常对照组。但是，ＬＨ和Ｔ基础值及其对ＬＨＲＨ和ｈＣＧ刺激反应，二者差异不显著。这些结果说明，不适当的棉酚治疗所引起的永久无精子症者，全睾丸细胞受到严重损害，垂体－睾丸轴系功能调节发生紊乱；而适量的棉酚所引起的暂时无精子症，生精功能恢复以后，睾丸内分泌一般均正常     

The time-response and magnitude of HCG-induced vascular changes are different in scrotal and abdominal testes

Adult unilaterally cryptorchid rats were injected with 50 IU human chorionic gonadotrophin (hCG). At 4, 8, 24 and 72 h after treatment, testicular vascular permeability was studied by injecting colloidal carbon intravenously. The number of blood vessel profiles labelled with carbon was increased by hCG in both types of testes, but the response was more sustained in abdominal than in scrotal testes. The number of polymorphonuclear leucocytes (PMNs) accumulating in testicular blood vessels and migrating into the interstitial space in response to hCG treatment was also measured. The volume density of intravascular and interstitial PMNs was increased in both types of testes but the peak response was larger in scrotal than in abdominal testes. PMN accumulation and vascular leakage were apparently correlated in the scrotal but not in the abdominal testes.
Testicular interstitial fluid (IF) was collected from intact and unilaterally cryptorchid adult rats. The IF was diluted with sterile buffer and injected intracutaneously in test animals. The vascular permeability response was assessed by measuring the leakage of Evans blue into the injection sites. IF from scrotal and abdominal testes increased vascular permeability in the skin. The response was rapid and transient. IF collected from rats given hCG 24 h earlier did not increase vascular permeability. The vascular permeability response to IF was reduced slightly in neutrophil-depleted animals. The inflammation mediator present in IF cannot explain the kinetics and magnitude of the hCG-induced changes in vascular premeability in intact or unilaterally cryptorchid rats.     

Adrenal Androgens and their Effect on Human Semen Quality

The purpose of this study was to elucidate the relationship between the sperm quality (concentration, motility, vitality and morphology) and elevated 17-ketosteroids (17KS) and their metabolites; Androsterone (A). Etiocholanolone (E), Dehydroepiandrosterone (D) and Pregnanediol (P₂). 162 men with normally fractionated urinary 17KS but with different degrees of sperm quality were evaluated. Statistical analysis did not reveal any correlation between sperm quality and levels of the metabolites. The same evaluation was performed on 36 men with elevated abnormal fractionated urinary 17KS metabolites. Here too, no correlation could be indicated. Eight men with pathological fractionated metabolites underwent adrenal gland stimulation by the ACTH test and suppression by dexamethasone concomitant with stimulation by hCG. All the 8 men responded normally. 4 men with abnormal urinary metabolites were treated with dexamethasone (0.5 mg/day) for 3 months. Sperm quality and urinary metabolites were checked during every month of treatment. No improvement in sperm quality was observed, although adrenal function was suppressed. However, 2 wives of the treated men conceived during treatment.
No correlation could be established between the metabolites of androgens in the urine, sperm quality and male fertility.     

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.