[The application of gonadotropin in treatment of male central hypogonadism].

OBJECTIVE: To observe the efficacy of human chorionic gonadotrophin (hCG) and hCG plus human menopausal gonadotropin (HMG) for central hypogonadism in male patients. METHODS: 64 men with central hypogonadism were recruited in this study, including 19 patients with Kallmann syndrome, 41 patients with idiopathic hypogonadotrophic hypogonadism (IHH) and 4 patients with hypogonadism after brain surgery. 33 patients were treated with hCG 1500 IU intramuscularly twice a week, whereas 31 patients were treated with intramuscular hCG 1500 IU plus HMG 75 IU twice a week, for at least 6 months. RESULTS: After treatment, all patients felt stronger physically and 42/64 patients developed beard, pubes or armpit hair. The testis volume enlarged significantly [(3.08 +/- 2.44) ml vs (8.92 +/- 5.37) ml, P < 0.001], and serum follicle-stimulating hormone, luteinizing hormone and testosterone concentrations were higher significantly than those before treatment (P < 0.05). 6/64 patients underwent spermatorrhea and 2 patient were found to have spermatogenesis. If judged by the testis volume, 52 patients (81.2%) were effective and 12 patients were ineffective. CONCLUSIONS: For male patients with the central hypogonadism, hCG and hCG plus HMG can promote the pubertal development and maturation of second sex characteristics, as well as enhance the physical strength; in some patients both androgen production and spermatogenesis can be achieved.

[Effect of large-dosage of 5alpha-reductase inhibitors on the spermatogenesis of male rats].

OBJECTIVE: To identify the role of 5alpha-reductase in the spermatogenesis of male rats by studying the effect of two 5alpha-reductase inhibitors, Epristeride and Finasteride, on the spermatogenesis in male Sprague-Dawley (SD) rats. METHODS: Changes in the weight of the testis, serum testosterone and dihydrotestosterone levels, epididymal sperm count, and reproductive function were observed and analyzed after the two 5alpha-reductase inhibitors were administered to male SD rats orally. RESULTS: The experiment showed that in comparison with control animals, both the two 5alpha-reductase inhibitors: 1. suppressed the development of the prostate and reduced the weight of the testis in the experimental groups (P < 0.05); 2. decreased the serum level of dihydrotestosterone and enhanced testosterone; 3. inhibited epididymal sperm count and productive function. CONCLUSION: High dosages of the 5alpha-reductase inhibitor, Epristeride, can suppress the development of the prostate and reduce the weight of the testis, decrease dihydrotestosterone, and inhibit spermatogenesis and productive function in male rats.

[Effect of selective 5alpha-reductase inhibitor or/and testosterone undecanoate on the reproductive function of male rats].

OBJECTIVE: To investigate whether 5alpha-reductase inhibitor and dihydrotestosterone (DHT) play a role in spermatogenesis in male rats. METHODS: Thirty-two male rats were divided into 4 groups (Groups C, T, F and FT). Group C received plant oil injection and oral starch perfusion, Group T testosterone undecanoate (TU, 20 mg/kg) injection and oral starch perfusion, Group F plant oil injection and oral Finasteride perfusion, and Group FT TU (20 mg/kg) injection and oral Finasteride perfusion. Data on serum T and DHT, sperm count, sperm mobility and reproductive function were collected and analysed. RESULTS: (1) 5alpha-reductase inhibitor, Finasteride and TU reduced the weight of the testis and epididymis in the experiment groups compared with the negative control (Group C), but TU increased the weight of the prostate while Finasteride decreased it compared with the positive control (Group T). TU combined with Finasteride could counteract the effect of the weight increase of the prostate, but not that of the testis. (2) Finasteride, or Finasteride combined with TU, reduced the DHT but increased the testosterone level in comparison with the control group. (3) Both Finasteride and TU could inhibit epididymal sperm count and reproductive function compared with the control, but the effect was less significant in Group FT than in Group F. CONCLUSION: High dosages of 5alpha-reductase inhibitor, Finasteride, can suppress male reproductive function, but the inhibiting effect could be counteracted by administration of 5alpha-reductase inhibitor along with TU.

[Effect of androgen on erythropoietin in patients with hypogonadism].

OBJECTIVES: To observe the change of erythropoietin (EPO) in patients of hypogonadism who received androgen replacement treatment and explore the mechanism of androgen-induced increase of red blood cells and haemoglobin. METHODS: Eight patients with Klinefelter's syndrome, divided into two groups, received TU intramuscular injections of 500 mg or 1000 mg dose, respectively. After three months, seven patients received the second injection of crossover dose. Testosterone levels in serum were measured with RIA before and after the injections treatment. RBC count, impacted volume of blood cells and haemoglobin concentration were measured before treatment and 4, 8 weeks after treatment. At the same interval, EPO levels were measured with ELISA method. RESULTS: Development of the secondary sex characters was improved in all patients after the TU injection. Serum testosterone levels raised significantly and reached the peak one week after the injections. Effective level of testosterone lasted for over 6 weeks. RBC count, impacted volume of blood cells and haemoglobin increased at different degrees after TU injections, but these changes were not significant in statistic(P < 0.05). The increased levels remained for 8 weeks. EPO levels were elevated significantly (P < 0.01 or 0.05) after the TU injection(Pbat > 0.05). The second injection could still make the EPO level go up. CONCLUSIONS: Androgen replacement treatment can increase the EPO levels in patients of hypogonadism, which is one of the mechanism of RBC production increase.

[Androgen replacement therapy for hypogonadal men].

Male hypogonadism is a group of syndromes in clinic andrology characterized by complete or partial androgen deficiency. It can be divided into primary and secondary hypogonadism. Besides the etiological treatment, androgen replacement therapy should be adopted in all patients of primary hypogonadism and patients of secondary hypogonadism who do not have the need of having a child. For patient's benefits, androgen should be used and selected properly as there are so many androgen preparation at present.

[Continuous measurement of urine beta-FSH excretion in men with hypogonadism].

OBJECTIVES: To measure continuously the urine beta-FSH excretion in the patients with male hypogonadism, and to evaluate the significance of urine beta-FSH when used in the clinical practice and pathophysiological study on male hypogonadism. METHODS: Four health male volunteers (aged 19, 22, 27 and 33 years), four patients with the hypogonadotropic hypogonadism (aged 17, 17, 19 and 24 years) and five patients with idiopathy hypogonadism (hypergonadotropic, aged 16, 16, 17, 20 and 22 years) were asked to collect their morning-first urine samples for 30 to 32 days. One normal men collected his urine samples for 63 days. The urine beta-FSH was assayed with the method of EIA, then corrected by creatinine (Cr) concentration. RESULTS: The urine beta-FSH level of normal men was (1.16 +/- 0.20) micrograms/mg Cr, with the peak variation in their curves, peak level at 2.76 micrograms/mg Cr. The levels of urine beta-FSH of 4 patients with the hypogonadotropic hypogonadism were lower significantly than those of normal men [(0.58 +/- 0.31) (0.93 +/- 0.47) (0.47 +/- 0.33) and (0.60 +/- 0.40) micrograms/mg Cr], without fluctuation in their curves. beta-FSH levels of 5 patients with idiopathy hypogonadism were higher significantly [(3.02 +/- 0.93), (4.36 +/- 1.12), (4.79 +/- 0.78), (4.64 +/- 1.42) and (3.88 +/- 1.42) micrograms/mg Cr], with irregular fluctuation, the highest peak level at 6.83 micrograms/mg Cr. The second sexual characteristics of hypogonadal patients were poor and serum testosterone levels low. CONCLUSIONS: The urine beta-FSH level raised with irregular fluctuation in patients with idiopathy hypogonadism, while lowed without any fluctuation in patients with the hypogonadism. These findings suggested that the urine beta-FSH excretion was useful for the clinically classified diagnoses and pathophysiological study on male hypogonadism, and for observing the treatment reaction of androgen replacement.

[Effect of MPA and MPA + TU on the rat spermatogenesis and sexual hormones].

OBJECTIVES: To investigate the effect of administration of MPA with/without TU on serum sexual hormones and spermatogenesis of male rats. METHODS: Twenty rats had been classified into four groups. Each group received injection of saline(group A) or MPA(37.5 or 75 mg/kg) (group B or group C, respectively) or MPA (75 mg/kg) + TU (25 mg/kg) (group D) every month during three months. Data from serum sexual hormones (FSH, LH, T), sperm counting and motility had been collected and analysed. RESULTS: Spermatogenesis of rats undergoing administration of MPA with or without TU had been suppressed. Serum FSH and LH of group B, C, D declined, and so did serum T of group D. Testis of rats of group D atrophied and sperm counting of group D decreased remarkably compared with group B and C. But there was no statistics difference of the sexual hormone level among group B, C and D. CONCLUSIONS: Administration of MPA alone could suppress the levels of FSH and LH and block the spermatogenesis of male rats. MPA combined with TU could offer stronger suppression on spermatogenesis. Mechanism of the suppression on spermatogenesis of MPA + TU is not only limited in the feed-back of gonadotropin, but there maybe exist a direct suppression on testis.