Long term effect of vasectomy on pituitary-gonadal axis.
Explore the source record for details and available documents.
SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
A 36-year-old male complaining of impotence was examined. He was a genotypic male. Phenotypically, he exhibited signs of long-standing estrogen excess, such as feminine body build, gynecomastia, and varicose veins. His testes were soft and borderline small, and his prostate was small and soft. However, he had a normal-sized penis, normal male hair distribution, normal sense of smell, and normal intelligence. The laboratory data were compatible with mild hypogonadotropic hypogonadism. Serum estradiol (E2) levels were consistently elevated. The patient had azoospermia and a decreased semen volume. Inappropriately low levels of luteinizing hormone and follicle-stimulating hormone responded normally to gonadotropin-releasing hormone and clomiphene citrate. Levels of both testosterone (T) and E2 increased dramatically after prolonged clomiphene medication and in response to human chorionic gonadotropin. There was no change in either T or E2 levels in response to manipulations of the pituitary-adrenal axis. It is concluded that the elevated E2 level was responsible for suppression of gonadotropins which, in turn, caused mild hypogonadism and sterility in this patient. According to the stimulation tests, the source of the elevated E2 levels was testicular.
The clinical features and hormonal abnormalities were surveyed in 117 men with cirrhosis of the liver. Compared with healthy men of similar ages, the patients had significantly lower metabolic clearance rates, plasma production rates and total and free levels of testosterone, reduced testosterone responses to human chorionic gonadotrophin stimulation, higher oestradiol, luteinizing hormone and follicle stimulating hormone levels and higher binding capacities of sex steroid binding globulin. The peripheral conversion of testosterone to oestradiol was also found to be significantly increased. However, the metabolic clearance and plasma production rates of oestradiol were not significantly different from those of healthy men. Patients who were severely ill with liver failure and one with haemochromatosis had low levels of luteinizing hormone and follicle stimulating hormone and sub-normal responses to clomiphene and luteinizing hormone-releasing hormone. Higher plasma oestradiol levels were found in patients with gynaecomastia and spider naevi than in those without these signs. However, the clinical features of androgen deficiency--that is, testicular atrophy, impotence and loss of secondary sex hair--were only poorly related to the low testosterone levels, and production rates and longtitudinal studies indicated that the hormonal levels, endocrine features and severity of the liver disease could change independently. It is concluded that the clearance of oestradiol from plasma is not limited by liver disease in all patients, and that reduced degradation of oestrogens is not the initial event in the sequence leading to the hormonal abnormalities of cirrhosis. While gonadotrophin deficiency occurs with liver failure and in some patients with haemochromatosis, the more usual findings are of elevated gonadotrophin levels and a poor Leydig cell response to chorionic gonadotrophin. These suggest that the hypogonadism is primary in most patients with cirrhosis. The causes of the high oestradiol levels were not discovered. Increased peripheral conversion of precursors to oestradiol or increased testicular secretion of oestradiol are possibilities. The high binding capacities of sex steroid binding globulin were not significantly correlated with either the low testosterone or high oestradiol level and the cause of this abnormality remains uncertain. The low metabolic clearance rates of testosterone appeared to result from the increased plasma protein binding of testosterone. The discrepancies in the expected relationships between the hormone and clinical changes suggest that factors other than those studied are also involved in the genesis of the endocrine features of hepatic cirrhosis.
In man both basal gonadotrophin levels and the pituitary responses to LHRH remained relatively constant throughout life. In women the pituitary sensitivity varied in the menstrual cycle due to the typical cyclic variation of oestradiol and progesterone. The max delta LH increase to 100 mug LHRH was observed in the periovulatory period (183 +/- 41 mU/ml); it was also significantly higher in the luteal (49 +/- 7 mu/ml) than in the early follicular phase (18 +/- 3 mU/ml). The effect of exogenous sex steroid hormones taken as contraceptive drugs was then studied in 15 women. Significantly lower LH and FSH basal values as well as responses to LHRH were observed in 8 normal women under oral combined contraceptives. Conversely, in 7 women under oral sequential contraceptives, basal LH and FSH remained in the normal range. The LH-FSH responses were increased and delayed when these tests were performed during the period of estrogen treatment. Thus, with combined oral contraceptives, constant and high levels of estrogens and progesterone not only inhibit the LH peak, but also decrease the basal LH-FSH levels and responses to releasing hormone. Conversely, with sequential oral contraceptives, the low level of estradiol does not inhibit these responses and even enhances them. In menopausal women both basal and gonadotrophin responses to LHRH were increased indicating an important pituitary reserve. In menstruating women a significant estradiol increase is observed 2 and 4 hours after a 100 mug LHRH injection, both during the follicular and the luteal phases whereas progesterone increases only in the luteal phase. In men, testosterone was found to increase 4 hours after a 100 mug LHRH injection. These studies show that in normal subjects, sex steroid hormones are important regulators of the sensitivity of the pituitary responsiveness to releasing hormone.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The serum gonadotropin response to LH-RH (100 mug e.v.) in a group of women with various types of amenorrhea was critically evaluated. Most patients responded to rapid LH-RH injection with a significant rise in plasma LH and FSH. In the authors' opinion this response is observed in healthy women as well as in those with lesions, even severe ones, of the pituitary, so that quantification of the response does not supply reliable information on diagnosis and prognosis. On the other hand, a negative response to the injection of 100 mug LH-RH does not necessarily imply a pituitary lesion but is often a sign of altered hypothalamic function which can be diagnosed and in some instances restored by clomiphene administration.
In primary hypogonadism (n=73) FSH basal levels and responses are elevated. LH basal levels and/or responses are elevated in 68 cases. In idiophatic oligospermia FSH and/or response are elevated in 28% cases, normal in 68% cases, decreased in 4% cases. LH and/or LH response are elevated in 44% cases normal in 53% cases and decreased in 4% cases. High significant correlation is found between FSH basal levels and FSH response, and between FSH and LH response.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Tumours and proliferates of the testes from spermatogenic epithelium were treated with estrogens, and those from the interstitial cells-with androgens and 17-hydrosyprogesterone caproate. Depression of the folliculo-stimulating function of the pituitary body with a simultaneous stimulation of the luteinizing hormones (LH) production under the effect of estrogen led to cessation of teratoma and seminoma growth, and to the resolution of the proliferates. When androgens or 17-hydroxyprogesterone caproate were used, depression of the LH led to cessation of the tumour growth, and to the resolution of proliferion of proliferates from the interstitial cells.
The effect of intramuscular triamcinolone acetonide (TCA-A) on pituitary gonadotropins and ovarian hormones was studied in a normally menstruating woman. Serum levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), as well estradiol 17-beta (E2) and progesterone (P), were determined daily in a normal "ovulatory" pretreatment cycle. A total of 160 mg of TCA-A was then administered in four injections over two and a half months. Daily serum levels of LH, FHS, E2, and P were again measured during a period beginning thirty days after the last injection of TCA-A. Cyclicity of all these hormones was absent after treatment. Both LH and FSH were suppressed in the first half of the post-treatment period when compared with the pretreatment ovulatory cycle. A potent corticosteroid such as TCA-A is apparently capable of producing anovulatory cycles in humans by disruption of cyclic pituitary gonadotropin secretion.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The contraceptive effect of continuous treatment with low dose progestogens (minipill) has been attributed mainly to alterations of the cervical mucus and the endometrium. This study was undertaken to investigate the effect of low dose progestogens on hypothalamic-pituitary-ovarian function. Plasma concentrations of follicle stimulating hormone (FSH), luteininzing hormone (LH), estradiol-17 beta (E-2) and Progesterone were measured daily during apparently ovulatory menstrual cycles and during treatment cycles with different low dose progestogens. From the results obtained it was concluded that the minipill has a clear-cut effect on the LH/FSH peak at midcycle and on corpus luteum function. A cyclic secretion of E-2 is maintained in the majority of cases. In a few treatment cycles however, follicular maturation was suppressed as indicated by low E-2 concentrations. It was concluded that the minipill exerts a profound effect at the central and ovarian level which contributes to its satisfactory contraceptive efficacy.
Serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin, estradiol, and progesterone concentrations were measured in 58 ovulating women in different age groups (20 to 29, 34 to 39, 40 to 44, and 45 to 50 years) at five- to seven-day intervals through a single menstrual cycle and in 18 postmenopausal women sampled weekly five to six times. The over-all hormone patterns were similar in four premenopausal groups. However, mean serum FSH levels increased with age and significantly higher concentrations were found in the 40 to 50 years group than in the 20 to 29 year group. Serum LH levels did not show a similar rise with age, although follicular LH levels in the oldest group were higher than in the 20 to 29 year group. Prolactin and estradiol concentrations did not change with age prior to the menopause, but luteal progesterone levels were lower in the three older premenopausal groups than in the 20 to 29 year group. Postmenopausal women showed elevated FSH and LH, decreased prolactin, and negligible estradiol and progesterone levels. There was an over-all significant linear correlation between prolactin and estradiol concentrations. It appears that the menopause is preceded by several years of rising gonadotropin, predominantly FSH, levels. During this period, ovarian estrogen production appears to be maintained and ovulation continues, but luteal progesterone levels decline. It is likely that these premenopausal alterations in pituitary-ovarian relationships reflect depletion of ovarian follicles.