Disparity of thyrotropin (TSH) and prolactin responses to TSH-releasing hormone in obesity.

The effect of TRH administration on TSH and PRL release was investigated in 11 obese women and 16 normal weight women. There were no differences in basal serum levels of estradiol, T3, T4, TSH, or PRL between the 2 groups. The increment of TSH levels in the obese group [mean maximum change (delta max), 19.

Aromatase inhibition by delta 1-testolactone does not relieve the gonadotropin-induced late steroidogenic block in normal men.

Aromatase inhibition by delta 1-testolactone [(17 oxa-D-homo 1,4 androstanediene-3,17 dione) 500 mg twice daily for 10 days] in nine normal men lowered circulating estradiol (E2) levels by about 25%, enhanced the secretion of FSH, 17-hydroxyprogesterone (17-OHP), and to a lesser degree testosterone (T), but did not affect serum LH levels. Despite E2 lowering there was greater accumulation of 17-OHP than of T after 7 days of treatment, suggesting 17,20-lyase inhibition. Unexpectedly, administration of delta 1-testolactone almost halved the T response to hCG (Pregnyl, 1500 IU), but did not affect the 17-OHP response.

ACTH and cortisol responses to ovine corticotrophin-releasing factor in patients with primary and secondary adrenal failure.

The ACTH and cortisol responses to an intravenous bolus injection of 100 micrograms ovine CRF were studied in 19 patients with adrenal failure. In all eight patients with primary adrenal failure, plasma ACTH levels increased from a mean basal level of 1494 +/- 431 (SEM) pg/ml to peak value of 2601 +/- 1220 pg/ml at 10 min. In comparison with healthy subjects absolute ACTH increments after ovine CRF were significantly augmented in the patients with Addison's disease (P* less than 0.

Disease-free interval and estrogen receptor activity in tumor tissue of patients with primary breast cancer: analysis after long-term follow-up.

Specific estrogen receptor activity (ER) was found in 115 of 175 (66%) tumors of patients treated for primary breast cancer in the period 1974-1981; 60 patients had ER-negative tumors. All patients were under observation for at least 48 months (median 76 months). The 24 patients who received adjuvant chemotherapy as part of their initial treatment, were excluded from the analysis of the disease-free interval (DFI).

Growth hormone responsiveness to human pancreatic growth hormone releasing factor in acromegaly: modulatory effects of basal hormone levels and of concomitant somatostatin administration.

Human pancreatic growth hormone releasing factor 1-44 (hpGRF), 100 micrograms was administered as an i.v. bolus injection to eleven patients with acromegaly.

Differential effects of ovine and human corticotrophin-releasing factor in human subjects.

Ten healthy subjects received 200 micrograms of human CRF (hCRF) and 200 micrograms of ovine CRF (oCRF) as an intravenous bolus injection on two different occasions. After hCRF plasma ACTH levels rose significantly (P less than 0.0005, by Friedman's nonparametric analysis of variance) from a basal value of 35 +/- 3 pg/ml (mean +/- SEM) to a peak value of 80 +/- 7 pg/ml 30 min after hCRF administration.

Concordance and discordance of estrogen and progesterone receptor content in sequential biopsies of patients with advanced breast cancer: relation to survival.

In 75 patients with advanced breast cancer, sequential biopsies were analyzed for estrogen receptor (ER). In 50 of these patients progesterone receptor (PgR) was also measured. All pairs of biopsies met the following criteria: (i) interval between the two biopsies: at least 6 weeks; (ii) biopsies performed at least 6 weeks after stopping endocrine therapy; and (iii) concordant histology.

Paradoxical responsiveness of growth hormone to corticotropin-releasing factor in acromegaly.

Corticotropin-releasing factor elicited an increase in serum GH in two of six patients with acromegaly. Both patients also responded paradoxically to LHRH administration and one of them also to TRH, further illustrating the dedifferentiation of the receptors of the somatotrophs in acromegaly.

Differential effect of single high dose and divided small dose administration of human chorionic gonadotropin on Leydig cell steroidogenic desensitization.

This study compared the effect of a single high dose of hCG (1500 IU) with that of the same dose administered in multiple small doses (300 IU, once daily for 5 days) on Leydig cell steroidogenesis. Administration of a single high dose of hCG to seven healthy men raised the mean plasma testosterone (T) level to peak levels 2.1 +/- 0.

Macronodular adrenocortical hyperplasia in long-standing Cushing's disease.

Clinical and biochemical findings in 13 patients (11 women and 2 men) with macronodular adrenocortical hyperplasia (MNH; nodule size, greater than 0.5 to 5.3 cm) were compared with those of 18 patients (15 women and 3 men) with Cushing's disease and diffuse (n = 9) or micronodular (n = 9) hyperplasia (DH).

Plasma adrenocorticotropin, cortisol, and aldosterone responses to corticotropin-releasing factor: modulatory effect of basal cortisol levels.

Two hundred micrograms of corticotropin-releasing factor (CRF) were administered as an iv bolus injection to 10 normal subjects (5 men and 5 women). Mean plasma ACTH levels rose significantly (P less than 0.0005, by Friedman's nonparametric analysis of variance) from a basal value of 27 +/- 5 pg/ml (mean +/- SEM) to a peak value of 63 +/- 8 pg/ml 30 min after CRF administration.

Responsiveness of the hypophyseal-adrenocortical axis to corticotropin-releasing factor in pituitary-dependent Cushing's disease.

Corticotropin-releasing factor [(CRF) 200 micrograms] was administered iv to five patients with classical pituitary-dependent Cushing's disease and to five normal subjects. In both groups no changes were observed in the plasma concentrations of hGH, PRL, TSH, LH, or FSH. In the normal subjects plasma ACTH levels rose from 41 +/- 9 (SEM) pg/ml to 87 +/- 28 pg/ml after 60 min (P less than 0.

Adrenocorticotropin and cortisol responsiveness to thyrotropin-releasing hormone and luteinizing hormone-releasing hormone discloses two subsets of patients with Cushing's disease.

In 23 consecutive patients with Cushing's disease and 52 control subjects, the responses of ACTH and cortisol to TRH and LRH were investigated. From the pattern of cortisol levels after the administration of the releasing hormone in the controls, a criterion for paradoxical responsiveness could be derived (maximum cortisol increase, greater than 6.0 micrograms/100 ml).

Enhancement of gonadotrophin induced 17,20-lyase suppression one week after human chorionic gonadotrophin priming.

A single injection of 1500 IU of human chorionic gonadotrophin (hCG) in normal men, induced a block in the conversion of 17-hydroxyprogesterone (17-OHP) to testosterone (T) which reached its maximum 24 h after hCG loading. One week after hCG administration both basal 17-OHP (3.8 +/- 0.

Tamoxifen versus ethinyl estradiol in the treatment of postmenopausal women with advanced breast cancer.

In a randomized study, 63 postmenopausal patients with advanced breast cancer were treated with ethinyl estradiol (EE2) or the antiestrogen tamoxifen to compare the efficacy and side effects of both drugs. EE2 was always given in combination with chlorothiazide to prevent fluid retention. Pretreatment characteristics of the patients of both groups did not differ significantly.

Tamoxifen suppresses gonadotropin-induced 17 alpha-hydroxyprogesterone accumulation in normal men.

Intramuscular administration of 1500 IU hCG daily for 3 days induced a transient accumulation of 17 alpha-hydroxyprogesterone (17 OHP) relative to testosterone (T) in normal men, reaching its maximum 24 h after the first injection (17 OHP to T ratio, 1.7 +/- 0.3 times baseline; P < 0.