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At least 109 records · Page 6Linked to original sources
PubMed1975

Clinics in endocrinology and metabolism. Investigative procedures.

In patients with hypogonadism, the exact cause of the deficient androgenisation is not always clinically apparent. The data presented demonstrate that by means of hormone measurements, basally or after stimulation tests, the exact level of the lesion can usually be determined. This allows a decision with regard to appropriate therapy to be made on the basis of an accurate diagnosis. In many instances basal measurements of pituitary and gonadal hormones are all that is required to decide the level of the lesion. Care in interpreting basal levels is required, however, in view of methodological limitations and of known physiological variations with age, time of day and hour-to-hour fluctuations. If the basal hormone levels are borderline, or if the 'reserve function' of part or all of the hypothalamic-pituitary-gonadal axis needs to be assessed, than the appropriate stimulation test should be performed. The indication for these stimulation procedures and results obtained in different conditions are described and problems of interpretation discussed.

Adult↗
PubMed1975

An apparently direct inhibitory effect of oestrogen on the human testis.

In men suffering from prostatic cancer, i.v. administration of 12 g diethylstilboestrol diphosphate within 20 days resulted in a decrease of the LH serum level to about 50% (P less than 0.05), whereas the total testosterone level decreased to less than 5% (P less than 0.001) and the apparently free testosterone level to less than 2% of the initial values (P less than 0.001). Hence, the "systemic antiandrogenic effect" of oestrogen can be explained (1) by indirect inhibition of testicular androgen secretion via diminution of hypophyseal gonadotrophin secretion, (2) by direct inhibition of testicular androgen secretion and (3) by elevation of the capacity of testosterone binding beta-globulin.

Aged↗
PubMed1978

Androgen and estrogen formation in women with ovarian hyperthecosis.

Women with ovarian hyperthecosis were studied and found to have a plasma testosterone production rate of 2.1 mg/day, a value eight times greater than that of nonhirsute, ovulatory women. The severity of hirsutism and virilization in these women was more closely correlated with the amount of testosterone produced than with plasma testosterone concentrations. The mean plasma production rates of androstenedione in these women, 8.6 mg/day, was more than three times that found in young women with no evidence of androgen excess. There was a marked gradient between ovarian and peripheral venous plasma concentrations for both C19 steroids. Following ovarian wedge resection or oophorectomy, there was a precipitous fall in the peripheral venous concentrations of these steroids. These observations support the view that the major source of excess androstenedione and testosterone secretion in these subjects was the ovaries. The rate of estrone formation in these women, 106-345 microgram/day, was the result of extraglandular aromatization of plasma androstenedione.

Adolescent↗
PubMed1978

Anovulation and increased androgenic activity as breast cancer risk in women with fibrocystic disease of the breast.

The urine of 26 otherwise healthy women with fibrocystic disease of the breast was assayed by gas chromatography for testosterone and androstanediol (5alpha-androstane-3alpha, 17beta-diol), the major metabolite of dihydrotestosterone. The mean values for both androgens were significantly higher than in 18 normal women in the same age range. Sixteen of the 26 fibrocystic disease patients also had endometrial hyperplasia. Since the endometrial specimen was obtained in the premenstrual period, the presence of hyperplasia proved that the menstrual cycle in over two-thirds of the fibrocystic disease patients was nonovulatory.

Adult↗
PubMed1977

A syndrome of functional hypogonadotropic hypogonadism and sterility in a male with elevated serum estradiol.

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.

Adolescent↗
PubMed1975

[Plasma concentrations of LH and of sex steroids during the normal menstrual cycle and during contraceptive treatment].

The authors have studied the long-term effects of combined oestrogen-progestogen on the secretion of gonadotrophins and on ovarian function. Estimation of the radio-immune levels of the plasma concentrations of the pituitary luteinizing hormone (LH), of oestradiol (E2), of progesterone (P) and of 20 alpha hydroxyprogesterone (20 alpha OHP) and of testosterone (T) served as a base for this study. A test cycle and 8 cycles in which a combination of 50 micrograms of ethinyl-oestradiol and 0.5 mg of norgestrel were administered were studied in 4 normal volunteer women. A pituitary stimulation test using 50 micrograms of gonadotrophin "releasing factor" (LH-RH) was given during the 7th cycle. Ovarian stimulation using human menopausal gonadotrophins (HMG) was given during the 8th cycle of treatment in 3 of the women and in 3 other subjects. Pituitary secretion of LH and ovarian secretion of E2 and P are partially inhibited. Pituitary response to the injection of LH-RH stays normal but 5 out 6 patients had no response to stimulation by gonadotrophins. These results allow us to conclude that the lowering of production of gonadotrophins during treatment with combination oestrogen and progestagens is responsible for inhibition of ovarian activity, and that there is a delay before the latter respond to stimulation by either endogenous or exogenous gonadotrophins.

Adult↗
PubMed1976

A study of the endocrine manifestations of hepatic cirrhosis.

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.

Adult↗
PubMed1975

[Effect of the steroid sex hormones on the LH and FSH responses to LHRH in the normal subject].

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.

Contraceptives, Oral, Combined↗
PubMed1978

Treatment of acne with cyproterone acetate and ethinyl estradiol.

Tablets containing 2 mg cyproterone acetate and 0.05 mg ethinyl estradiol in a calendar package of 21 days were used as an oral contraceptive to treat acne. The series comprised 20 patients. The women were 18--43 years of age, and all had acne which had previously been resistant to therapy. The treatment was continued for 6 months. Serum testosterone, 17-OHCS, 17-KS, serum ALAT and gamma-GT were recorded prior to the treatment at 3 and 6 months. Ten patients responded well to the treatment, 5 responded moderately well, 3 experienced no change, and 2 became worse. The serum testosterone level fell during the therapy and the ALAT level rose, though only one pathological ALAT value was recorded.

17-Hydroxycorticosteroids↗
PubMed1976

Quantitative study of spermatogenesis in vasectomized mice.

Adult mice were vasectomized under semi-sterile conditions and examined five weeks later. The weight of the epididymis was increased but none of the animals had developed spermatic granulomas. The concentration of testosterone in the plasma, the body weight and the weight of the testes were not affected by vasectomy. Cross sections of the testes were prepared for histological examination and the nuclei of the various types of germinal cells were enumerated at stage VII of spermatogenesis. Vasectomy caused a small, but statistically significant, decrease in the number of preleptotene spermatocytes, pachytene spermatocytes and step 7 spermatids.

Animals↗
PubMed1977

Inhibitory effects of sexual steroidal hormones on the responses of the isolated guinea-pig lleum to acetylcholine and histamine.

Six sexual steroidal hormones (progesterone, pregnenolone, testosterone, ethinyl-oestradiol, oestriol and oestrone) inhibit acetylcholine- and histamine-induced contractions of the isolated guinea-pig ileum. Different degrees of inhibitory capacity were found. High concentrations of PGE1 and F2alpha reverse some of these inhibitions. This reversal seems to be non-specific and probably related to sensitization of the ileal smooth muscle by prostaglandins. The inhibitory action of sexual steroids might be non-specific as well. But a "corticoid-like" effect cannot be excluded.

Acetylcholine↗
PubMed1977

Androstenedione metabolism in patients with endometrial cancer.

The plasma concentration of androstenedione and the instantaneous conversion of androstenedione to estrone was increased in patients with endometrial cancer as compared to postmenopausal control subjects. Moreover, the per cent of estrone derived from androstenedione was increased in the cancer group.

Androstenedione↗