Luteinizing hormone-releasing hormone and serum growth hormone in insulin-dependent diabetes.

Growth hormone (GH) responses were studied in 26 insulin-dependent diabetics after the intravenous administration of 100 microgram of synthetic luteinizing hormone-releasing hormone (LH-RH). Although the mean basal GH concentration was significantly higher than that of 20 matched non-diabetic controls, no significant increment occurred after the LH-RH injection. (The controls also showed no rise in GH.) It seems that the GH hypersecretion of insulin-requiring diabetics does not, as is frequently noted in acromegaly, respond to the injection of LH-RH.     

Effect of epidural anesthesia on the function of hormonal regulation in the hypothalamic-pituitary-testicular axis

To evaluate the effects of epidural anesthesia on the hypothalamic-pituitary-testicular axis, we examined the concentrations of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and testosterone (T). The effects of epidural anesthesia on plasma levels of LH, FSH and T were investigated in 8 men aged from 64 to 87 years, suffering from untreated prostate cancer. There were no significant differences in plasma levels of LH, FSH or T between patients under epidural anesthesia and patients under no anesthesia. The effects of epidural anesthesia on plasma levels of LH, FSH and T after LH releasing hormone (LH-RH) administration were studied in 10 men between 65 and 84 years with diagnoses of untreated prostate cancer. Plasma LH and FSH levels increased significantly after LH-RH administration under epidural anesthesia or no anesthesia. Plasma LH and FSH were lower under epidural anesthesia than under no anesthesia. No change in plasma T level was observed after LH-RH administration under epidural anesthesia. We conclude that there is no effect of epidural anesthesia on the hypothalamic-pituitary-testicular axis.     

Clinical and histopathological characteristics of gonadotropin-producing pituitary adenomas

The clinical and histopathological characteristics in six cases of gonadotropin-producing adenoma are presented. Definitive diagnosis was made by the determination of gonadotropin levels in culture medium. Several authors have reported that gonadotropin-producing adenomas are very rare; however, hormonal assay of adenoma cell culture medium may indicate the real incidence of gonadotropin-producing adenomas to be greater than is thought. In reported cases, practically no endocrinological symptoms have been found suggesting increased gonadotropin levels, and basal values of plasma gonadotropins have been reported as only slightly over the normal range. Gonadotropin-producing adenomas may have been misdiagnosed as nonsecreting adenomas. The clinical characteristics of gonadotropin-producing adenomas can be summarized as follows: 1) a tendency for more rapid growth than nonsecreting adenomas; 2) prominent suprasellar extension with marked enhancement on computerized tomography; and 3) diminished response of luteinizing hormone (LH) alone in response to LH-releasing hormone (LH-RH) stimulation, and the ratio of peak follicle-stimulating hormone to peak LH in the LH-RH stimulation test is more frequently over 1:1 in cases of gonadotropin-producing adenoma than in cases of nonsecreting adenoma and craniopharyngioma. Immunoperoxidase staining revealed two kinds of adenoma cells, one intensely and the other faintly stained. Abundant mitochondria and few secretory granules were characteristic electron microscopic features. Oncocytic transformation of adenoma cells was suggested by immunoperoxidase staining and the electron microscopic appearance, and may suppress the elevation of circulating plasma gonadotropin levels. Thus, hormonal assay of adenoma cell culture medium and immunoperoxidase staining are essential for definitive diagnosis of gonadotropin-producing adenomas.     

Clinical and endocrinological studies of the luteinizing hormone-releasing hormone analogue therapy in prostatic cancer patients

A luteinizing hormone-releasing hormone (LH-RH) analogue was administered for 3 to 32 months to 15 prostatic cancer patients in stage B-D (B:3, C:8, D:4). Intratesticular, intratubular and prostatic androgen levels were measured by radioimmunoassay before and after LH-RH analogue therapy. The measurement of serum prostatic acid phosphatase (PAP) and prostatic specific antigen (PA) levels was also conducted. Thereafter, we assessed the effect of the LH-RH analogue on androgen levels and the relation of prostatic tissue 5 alpha-dihydrotestosterone (DHT) level to the clinical response. The results were as follows: 1) Johnsen's mean germinal epithelium count was significantly decreased from 7.7 +/- 2.1 (mean +/- S.D.) to 4.3 +/- 2.3, and the wall thickness of seminiferous tubules was increased from 5.93 +/- 1.31 to 11.9 +/- 3.64 microns. 2) Plasma testosterone (T), intratesticular and intratubular androgen levels were significantly decreased (plasma T: from 4.40 +/- 1.84 to 0.61 +/- 0.32 ng/ml, intratesticular T: from 335.3 +/- 170.3 to 4.6 +/- 3.8 ng/g.t.w., DHT: from 25.3 +/- 11.7 to 3.7 +/- 2.7 ng/g.t.w., intratubular T: from 50.8 +/- 36.6 to 0.10 +/- 0.99 ng/g.t.w. and DHT: 7.54 +/- 3.20 to 0.63 +/- 0.90 ng/g.t.w.). 3) Crude nuclear DHT levels in prostatic tissue fell from 15.3 +/- 9.3 (N = 8) to 0.37 +/- 0.54 pg/mg protein (N = 3) and the level was non-detectable in 5 of 8 cases. 4) Complete remission was achieved in 1 patient, partial response in 5, objective stable in 8, and objective progression in 1 patient, according to Shimazaki's criteria.(ABSTRACT TRUNCATED AT 250 WORDS)     

Testicular Steroid Response to Continuous and Pulsatile Intravenous Luteinizing Hormone-Releasing Hormone Administration in Normal Men

In 18 healthy normal men Leydig cell response was examined following intravenous luteinizing hormone-releasing hormone (LH-RH) administration under standardized conditions. The same total amount of LH-RH was administered for 3 hours both in a continuous (1 microgram/min; C (1,1)) and in a pulsatile fashion, by giving a 20 micrograms dose at 20 minutes intervals, P (20, 20), and a 60 micrograms dose at 60 minutes intervals, P (60, 60). Following the different modes of LH-RH administration which all caused 3-4 fold elevations of the mean endogenous luteinizing hormone (LH) concentrations and 1.7-2 fold elevations of the mean follicle-stimulating hormone (FSH) serum levels, an overt increase of the mean testosterone (T) levels was noticed up to 1.5 X the baseline value. No difference was observed in the total amount of T release among the investigated groups. The patterns of the T response, however, clearly differed from one another with a rapid increase, during the C (1, 1) and the P (20, 20) LH-RH administration, and a delayed but persistent T increase in the P (60, 60) experiment. The mean 17-hydroxyprogesterone (17-OHP) concentrations demonstrated a similar course to T in the P (60,60) experiment, while significant increases of the oestradiol (E 2) levels were never observed in all three experiments. In view of the comparable LH and FSH increments in response to LH-RH administration in either experiment the differences in T responses may be explained by assuming a direct effect of LH-RH on Leydig cell steroidogenesis in the men.     

Diminished response of ovarian cAMP to luteinizing hormone in experimental uremia

In prepuberal female rats with acute bilateral nephrectomy or chronic subtotal nephrectomy, the increase of ovarian cAMP concentration in response to submaximal doses of luteinizing hormone (LH 10 micrograms) and human chorionic gonadotropine (hCG 2.5 IU) was diminished (CO + 2.5 IU hCG 488 +/- 49 pmoles cAMP/mg protein; NX + 2.5 IU hCG 366 +/- 56. P less than 0.05). The cAMP response to follicle stimulating hormone (FSH) was unchanged. The abnormality was found both after administration of LH in vivo and incubation of ovaries with LH in vitro. Similarly, plasma estradiol concentrations in response to submaximal hCG stimulation were diminished. Basal cAMP concentrations and cAMP concentrations after maximal stimulation were unchanged. The defect was observed both in ovaries of untreated prepuberal rats, of pregnant mare serum (PMS)-treated rats (follicular phase) and PMS/hCG-treated rats (luteal phase). Diminished ovarian cAMP response to LH was observed both in parathyroid intact and in parathyroidectomized rats. Administration of 1,25(OH)2D3 in physiological doses (60 ng/kg) to acutely uremic rats restored diminished ovarian cAMP response to submaximal LH stimulation irrespective of parathyroid status. The effect of 1,25(OH)2D3 could not be reproduced by hypercalcemia resulting from intraperitoneal calcium injection. In vivo administration of indomethacin further diminished ovarian cAMP response in uremic animals and had no effect in control animals. Incubation of ovaries with PGE1 and PGE2 increased basal and stimulated cAMP concentrations and abolished the difference between control and uremic animals. The diminished response of ovarian cAMP content to submaximal doses of hCG was not corrected by bromocriptine (1 mg/kg) despite normalization of hyperprolactinemia. The present study shows diminished ovarian cAMP and plasma estradiol response to LH in experimental uremia. It documents a role of 1,25(OH)2D3 and prostaglandins in the genesis of this abnormality.     

Time course of serum testosterone and luteinizing hormone levels after cessation of long-term luteinizing hormone-releasing hormone agonist treatment in patients with prostate cancer

INTRODUCTION: In order to elucidate the influence of hormone-releasing hormone (LH-RH) agonist therapy cessation on pituitary/testicular function and its clinical implications, we investigated prospectively hormonal (luteinizing hormone: LH; testosterone: T) responses in patients with prostate cancer who received long-term LH-RH 10 agonist therapy. PATIENTS AND METHODS: A consecutive 32 patients who had received LH-RH agonist therapy over 24 months were enrolled. As a baseline, T and LH were measured at the time of LH-RH agonist therapy cessation, monthly for 3 months, and subsequently, every 3 months. RESULTS: The median duration of LH-RH agonist therapy was 30 months (24-87 months) with median follow-up duration of 24 months following cessation. All patients had castrated T levels and suppressed LH levels at baseline. Median duration of castrated T levels following cessation was 6 months. Median time to normalization of T levels was 24 months. LH levels returned to normal within 3 months in all cases. Patients who received androgen deprivation therapy for 30 months or longer required a longer time for recovery of T levels. Patients over 65 years of age showed a statistically significant longer time for recovery of T levels (P=0.0167). CONCLUSIONS: Long-term LH-RH agonist therapy has remarkable effects on serum T level that last for a significant time after cessation, a fact that should be applied to the interpretation of both PSA and serum T levels after cessation of androgen deprivation therapy.     

Long-Term, Pulsatile, Low Dose, Subcutaneous Luteinizing Hormone-Releasing Hormone Administration in Men with Idiopathic Oligozoospermia Failure of Therapeutic and Hormonal Response

In four normal men with a history of long standing infertility, severely disturbed sperm qualities (determined in at least three spermiograms), normal serum luteinizing hormone (LH) and follicle stimulating hormone (FSH) levels (measured over a time period of 90 minutes), and lack of evidence of further andrological or other obvious endocrine disorders the effectiveness of luteinizing hormone-releasing hormone (LH-RH) treatment was investigated. LH-RH was administered subcutaneously with a portable, comterized infusion pump (Zyclomat) for 3 months, with administration intervals of 90 minutes and bolus dosages of 5 micrograms (three patients) and 20 micrograms (one patient). Semen qualities during and after LH-RH treatment, as compared to pretreatment values, showed no improvement in volume of ejaculate, number of sperms per milliliter and motility. During or at the end of the treatment period no evident differences were observed in serum LH, FSH and testosterone levels (measured over a 90 minutes period) compared with hormonal values before LH-RH therapy, nor at the low-dose (5 micrograms) neither at the high-dose (20 micrograms) administration schedule. It is concluded that pulsatile subcutaneous LH-RH treatment in normogonadotropic, oligozoospermic men does not seem to improve the therapeutical arsenal.     

The cost-effectiveness of combined androgen blockade with bicalutamide and luteinizing hormone releasing hormone agonist in men with metastatic prostate cancer

PURPOSE: Combined androgen blockade therapy (CAB) has been shown to have a small survival advantage over luteinizing hormone releasing hormone LH-RH agonists (LH-RHa) alone in men with metastatic prostate cancer. The goal of this study was to assess the cost-effectiveness of CAB with bicalutamide and LH-RH agonist therapy to LH-RH agonist therapy alone. MATERIALS AND METHODS: A macro-simulation model was developed to compare the cost-effectiveness of 2 interventions for stage D2 prostate cancer, 1) CAB with bicalutamide 50 mg per day and monthly dosing of an LH-RHa or 2) monthly LH-RH agonist therapy. Cost and outcomes are tabulated in 5 and 10-year time horizons. Model assumptions were taken from the published literature. Appropriate 1-way and multi-way sensitivity analyses were performed. RESULTS: At 5 years, the incremental cost-effectiveness ratio (ICER) for CAB, when compared with LH-RHa monotherapy, was US dollars 33,677 per quality-adjusted life-year. In other words, for every additional quality-adjusted life year that a patient lived because he received CAB, it cost US dollars 33,677. At 10 years the ICER for CAB was US dollars 20,053 (well within the accepted cost-effectiveness threshold). If quality adjustment was not included, the ICER for CAB was even more favorable (US dollars 20,489 at 5 years and US dollars 13,313 at 10 years). The model was most sensitive to the estimates of effectiveness (survival) of LH-RHa therapy alone and CAB therapy. The model was also fairly sensitive to the quality of life effect of having late stage prostate cancer and the cost of bicalutamide. CONCLUSIONS: CAB with bicalutamide is cost-effective when compared with LH-RH monotherapy in men with stage D2 prostate cancer.     

Treatment of cryptorchidism with pulsatile luteinizing hormone-releasing hormone (LH-RH)

This preliminary report describes a new method of treating bilateral cryptorchidism that may modify the need for surgical intervention. Four of five boys (3 1/2, 3 1/2, 7, 11 and 12 1/2 years of age) given hourly subcutaneous pulses of luteinizing hormone-releasing hormone (LH-RH, 10 to 100 micrograms/day, given in a 3-min pulse every hour) showed evidence of testicular descent after 3 to 19 weeks. The battery-operated, programmable syringe driver was well tolerated by the boys, and the daily insertion of the scalp-vein needles was managed at home by their parents.     

A case of Kallmann's syndrome

A 13-year-old boy visited our hospital with the chief complaint of right undescended testis and retardation of secondary sexual characteristics. Central hyposmia and sensorineural hearing loss were found. The plasma levels of luteinizing hormone (LH) and follicle stimulating hormone (FSH) were low and the reaction to LH-releasing hormone (RH) test was poor. After repeated LH-RH tests, a good response in plasma levels of LH and FSH was observed. The diagnosis of Kallmann's syndrome was made from the above findings. The testicular biopsy specimen from him showed immature testis without any developed Leydig or Sertoli cells. To induce secondary sexual characteristics, 2000 I.U. of human chorionic gonadotropin (hCG) was administered to him twice a week for 3 months. The administration of hCG resulted in elevation of plasma testosterone level, swelling of testes, increase of pubic hair and spurt of height.     

Failure to maintain a suppressed level of serum testosterone during long-acting depot luteinizing hormone-releasing hormone agonist therapy in patients with advanced prostate cancer

OBJECTIVES: It was the aim of this study to analyze the failure rates in achieving or maintaining castrate levels of serum testosterone in patients with advanced prostate cancer treated with the 3-month luteinizing hormone-releasing hormone agonist (LH-RH) therapy. METHODS: Total serum testosterone was determined in 234 patients with prostate cancer in a cross-sectional study. A subset of 90 patients submitted to radical prostatectomy was used as the control group (group 1), and 144 patients with advanced prostate cancer under androgen suppression therapy were included in the study group (groups 2 and 3). The study group was divided into 93 patients (group 2) treated with 50 mg daily bicalutamide and LH-RH agonist (maximal androgen blockade, MAB) and 51 patients treated with the LH-RH agonist alone (group 3). Median follow-up after androgen suppression was 42 months. The castrate testosterone level was defined below 50 ng/dl. RESULTS: The mean serum testosterone level was 29.1 ng/dl in patients undergoing MAB (group 2) and 29.5 ng/dl in patients treated with the LH-RH agonist (group 3; p > 0.05). In group 1, the mean serum testosterone was 445.2 ng/dl (p < 0.0001). The rate of patients with a serum testosterone level higher than 50 ng/dl was 10.9% in patients undergoing androgen suppression, 10% in patients with MAB treatment and 12.5% in those with LH-RH agonist therapy (p > 0.05). In group 1, 98.9% of the patients had a serum testosterone level higher than 50 ng/dl. CONCLUSIONS: A small but clinically significant rate of patients under 3-month LH-RH agonist therapy fail to achieve or maintain castrate testosterone serum levels. This finding supports the need of monitoring testicular response during LH-RH agonist therapy.     

The gonadotropin-releasing hormone antagonist abarelix depot versus luteinizing hormone releasing hormone agonists leuprolide or goserelin: initial results of endocrinological and biochemical efficacies in patients with prostate cancer

PURPOSE: We contrasted the endocrinological and biochemical efficacies of abarelix depot, a pure gonadotropin-releasing hormone antagonist, with a prospective concurrent control cohort receiving luteinizing hormone releasing hormone (LH-RH) agonists with or without antiandrogen for treatment of patients with prostate cancer receiving initial hormonal therapy. MATERIALS AND METHODS: In this phase 2 open label study 242 patients with prostate cancer requiring initial hormonal treatment received abarelix depot (209) or LH-RH agonists (33) with or without antiandrogen. A total of 100 mg. abarelix depot was delivered intramuscularly every 28 days with an additional injection on day 15. LH-RH agonists with or without antiandrogen were administered according to the depot formulation used. Endocrine efficacy was measured by the absence of testosterone surge and rapidity of castration onset. The rate of prostate specific antigen decrease was assessed. RESULTS: No patient treated with abarelix depot had testosterone surge during week 1 compared with 82% of those treated with LH-RH agonists. The concomitant administration of antiandrogen had no effect. During the first week of drug administration, in 75% of patients treated with abarelix depot and in 0% of those treated with LH-RH agonist medical castration was achieved. Prostate specific antigen decrease was faster, with no flare or surge in patients treated with abarelix depot. Abarelix depot was well tolerated. CONCLUSIONS: Abarelix depot represents a new class of hormonal therapy, gonadotropin releasing hormone antagonists, that has rapid medical castration and avoids the testosterone surge characteristic of LH-RH agonists.     

Absence of epidermal growth factor receptor gene mutations in patients with hormone refractory prostate cancer not responding to gefitinib

BACKGROUND: Mutations in the tyrosine kinase (TK) domain of the epidermal growth factor receptor (EGFR) gene in human cancers are associated with increased sensitivity to anilinoquinazoline EGFR inhibitors. To our knowledge no data have been reported on EGFR gene mutations in hormone refractory prostate cancer (HRPC). METHODS: Between March 2003 and December 2004, 23 patients with HRPC received 250 mg oral gefitinib daily in addition to antiandrogen plus luteinizing hormone-releasing hormone (LH-RH) analog for at least 2 months or until disease progression. Patients with unresected prostate cancer prospectively underwent trans-rectal biopsy of primary tumor (before starting gefitinib treatment). RESULTS: None of the patients demonstrated PSA or objective response to gefitinib. We sequenced exons 18-21 of the EGFR TK domain from genomic DNA isolated from 8 HRPC patients. No patient showed EGFR TK domain mutations. CONCLUSIONS: Our results show EGFR mutations did not occur in these patients suggesting that gefitinib is unlikely to be effective in patients with tumors not harboring specific EGFR TK domain.     

Effects of combination therapy with a luteinizing hormone-releasing hormone agonist and chlormadinone acetate on rat prostate weight and plasma testosterone levels

We investigated whether the combination of chlormadinone acetate (CMA) and a luteinizing hormone releasing hormone (LH-RH) agonist, leuprorelin acetate (leuprorelin), more markedly decreased ventral prostate and seminal vesicle weights and plasma sex hormone levels in male rats. Four weeks after administration of 0.28, 0.84 or 2.8 mg/kg of leuprorelin, ventral prostate weights significantly decreased (53.8, 54.4 and 64.1%) and the plasma testosterone levels significantly lowered, but not dose-dependently. After repetitive administrations of 3 and 30 mg/kg/day of CMA, the rates of ventral prostatic atrophy were 37.1 and 65.9%, respectively. Although there was no change in the plasma testosterone level at 3 mg/kg, 30 mg/kg of CMA significantly decreased the level. A combination of leuprorelin (0.28 mg/kg) and CMA (3 or 30 mg/kg) more potently induced ventral prostatic and seminal vesicle atrophy than leuprorelin alone. Furthermore, a combination of leuprorelin and CMA (30 mg/kg) more markedly decreased the plasma testosterone level. According to the pharmacokinetic data for CMA in male rats, the doses of CMA correspond to the clinical dose. These findings suggest that combination therapy with an LH-RH agonist and CMA is more useful than therapy with the agonist alone in the treatment of prostate cancer.     

Gonadal dysfunction after testicular torsion: luteinizing hormone and follicle-stimulating hormone response to gonadotropin releasing hormone

We studied 14 postpubertal patients at an average of 33 months after treatment for testicular torsion. Of these patients 11 had been treated by detorsion and 3 by orchiectomy. Five normal male volunteers of the approximate age of the study group served as controls. The patients treated by detorsion were subdivided into 3 groups based on the degree of atrophy of the detorsed testicle: group 1--no testicular atrophy (5), group 2--25 per cent testicular atrophy (2) and group 3--greater than 90 per cent testicular atrophy (4). Mean duration of torsion was greatest in the orchiectomy group (161 hours) compared to 6, 16 and 29 hours for groups 1, 2 and 3, respectively. The serum luteinizing hormone and follicle-stimulating hormone response to an intravenous bolus of 100 mcg. synthetic gonadotropin releasing hormone was measured in all patients. All groups had a greater mean follicle-stimulating hormone response to gonadotropin releasing hormone stimulation than controls (p less than 0.05). Patients who underwent orchiectomy had the greatest follicle-stimulating hormone response to gonadotropin releasing hormone stimulation. Mean luteinizing hormone response to gonadotropin releasing hormone stimulation was normal in patients without atrophy (group 1) but it was greater than controls in patients who had atrophy (groups 2 and 3) or who underwent orchiectomy (p less than 0.05). Several conclusions could be made from our study. All patient groups treated for torsion had evidence of testicular dysfunction. Patients who underwent orchiectomy displayed more testicular dysfunction than patients who had atrophy after detorsion. Testicular dysfunction after torsion is more likely to involve spermatogenic before Leydig cell function.     

Hypothalamic hamartoma with precocious puberty--a case report

A case of hypothalamic hamartoma with precocious puberty is presented and the literature of reported cases is reviewed. An 8-year-old boy was admitted to our hospital because of precocious puberty and mental retardation. His genital development was Tanner's stage 4 and pubic hair was Tanner's stage 3. Bone age was 11 years. Plain CT showed an isodense mass in the suprasellar cistern which was not enhanced following contrast administration. Metrizamide CT cisternography showed a filling defect in the suprasellar cistern. Endocrinological evaluation revealed high levels of serum luteinizing hormone (LH) and testosterone with a marked response of LH to LH-RH injection. A left frontotemporal craniotomy was performed and the tumor was partially removed. The tumor was gray, firm and well-circumscribed with poor vascularity. Postoperatively, a right oculomotor palsy and transient diabetes insipidus developed. He was discharged ambulatory one month later. Serum LH and testosterone returned to normal and the response of LH to LH-RH injection became normal. Hamartoma was diagnosed on histological examination. Electron micrographic study showed numerous dense granules with approximately 0.1 mu in diameter, in which Judge proved LH-RH by immunofluorescent study in 1977. Our case supports the hypothesis that hypothalamic hamartoma may cause precocious puberty by autonomous secretion of LH-RH and we consider that neurosurgical treatment is recommended.     

Gonadotropin therapy in males with hypogonadotropic hypogonadism: Factors affecting induction of spermatogenesis after gonadotropin replacement

Sixteen patients with hypogonadotropic hypogonadism received gonadotropin replacement therapy. Two patients treated with HCG alone showed induction of spermatogenesis 2 and 12 months after the start of treatment. Three subjects receiving combination therapy showed sperm appearance 6–28 months after treatment. The patients showing sperm appearance, whose testicular volume was ≥4 ml, showed a higher sperm count and impregnated their partners, although no relationship was found between pretreatment testicular volume and sperm appearance. The response to HCG test correlated with sperm appearance after gonadotropin therapy. Sperm appearance was not observed in any subject except for one who showed no response to luteinizing hormone-releasing hormone (LH-RH) test and none of the patients without response of FSH to LH-RH demonstrated any induction of spermatogenesis. In conclusion, the responses to LH-RH test and possibly to HCG test could predict the induction of spermatogenesis after gonadotropin replacement therapy, and a large testicular volume is associated with post-treatment fertility.     

Seasonal effects on seminal quality, plasma hormone concentrations, and GnRH-induced LH response in fertile and subfertile stallions.

Seasonal effects on hormonal and seminal parameters in subfertile stallions have not been well documented and could provide information that is needed to understand the underlying endocrine mechanisms associated with testicular dysfunction. Such information may be useful in developing diagnostic tools to identify those stallions who are candidates for treatment. This investigation characterizes and compares the effects of season on endocrine function and seminal quality in fertile and subfertile stallions. Eight fertile and six subfertile stallions between the ages of 5 and 18 years were injected intravenously once every hour for 3 hours with either 1 mL saline on the first experimental day or 5 micrograms gonadotropin-releasing hormone in 1 mL saline on the second experimental day during the nonbreeding and breeding season. Heparinized blood samples were collected periodically through a jugular catheter before and after treatment for analysis of luteinizing hormone, follicle-stimulating hormone, testosterone, and estrogen conjugates by radioimmunoassay. Semen samples were collected twice, 1 hour apart, from all stallions in both seasons for analysis of volume, concentration, motility, pH, and morphology. A series of low intravenous doses (5 micrograms) of gonadotropin-releasing hormone induced a significant luteinizing hormone response (P less than 0.05) compared with saline treatment in both fertile and subfertile stallions. Fertile stallions had a twofold higher (P less than 0.05) net increase in plasma luteinizing hormone levels (peak levels minus baseline levels) in the breeding seasons than in the nonbreeding season. The magnitude of the luteinizing hormone response relative to baseline levels in fertile stallions, however, was one-and-one-half times greater (P less than 0.05) in the nonbreeding season than in the breeding season. In contrast, season did not have an effect on the net increase in plasma luteinizing hormone or the magnitude of the luteinizing hormone response relative to baseline levels in subfertile stallions. The net increase in plasma luteinizing hormone was similar between the two groups of stallions in both seasons. The magnitude of luteinizing hormone response relative to baseline levels, however, was lower (P less than 0.05) in subfertile stallions (141 +/- 14%) than in fertile stallions (235 +/- 46%) in the nonbreeding season; the two groups exhibited similar responses in the breeding season. Compared with fertile stallions, subfertile stallions had twofold to fourfold higher (P less than 0.05) plasma levels of gonadotropins and similar testosterone levels. The number of total progressively motile sperm was lower (P less than 0.05) in subfertile stallions in both seasons.(ABSTRACT TRUNCATED AT 400 WORDS)     

The use of synthetic luteinizing hormone-releasing hormone to induce ovulation.

The therapeutic use of synthetic luteinizing hormone-releasing hormone (LH-RH) to induce ovulation has been explored. Three dosage schemes have been compared: a single dose of LH-RH, multiple doses of LH-RH, and LH-RH used in combination with human menopausal gonadotrophins (HMG). The results of these three schemes are presented and compared; the last regimen has proved most successful, with a high pregnancy rate, a low incidence of multiple pregnancy and no evidence of ovarian hyperstimulation.