RESUMO

The relation of concentrations of endogenous estrogens and androgens to lipid and lipoprotein levels was examined in 176 white, postmenopausal women (mean age, 58 years) with an average of 9 years since the onset of menopause. All of the women were participants in a clinical trial of the effect of walking on postmenopausal bone loss. In that trial, women were randomized into either a walking group or a control group and were followed for 3 years. There were no differences in the serum hormones or lipids by randomized group, and hence, results from this study are presented for both groups combined. None of the women were on estrogen replacement therapy. Data were available from year 1 (1982-1983) of the trial for the estrogens, lipids, and lipoproteins. Information on androgens was available for 143 of these women. Hormone levels were determined by highly specific methods involving extraction, column chromatography, and radioimmunoassay. About 50% of the women had estradiol levels at or below the sensitivity level (2.5 pg/ml) of the assay; therefore, estradiol levels were viewed as dichotomous (measurable/not measurable), and the estradiol results should be interpreted with caution. There was little relation of the androgens to the lipid values. Univariate analyses suggested a direct relation between total cholesterol, low density lipoprotein cholesterol, and triglyceride levels with estradiol. An inverse relation was suggested between serum estrone and estradiol and total high density lipoprotein (HDL) cholesterol and HDL2 cholesterol, although none of these associations were statistically significant. Multiple regression analyses revealed that the primary determinant of the HDL cholesterol and triglyceride levels was the degree of obesity as estimated by the body mass index (weight (kg)/height (m)2). Addition of estrone or estradiol to the models did not contribute to the prediction of lipid levels. These results do not support the hypothesis of there being a relation between endogenous sex hormone levels and lipid levels in postmenopausal women. The results suggest that sex hormones cannot explain the sex difference in lipid levels and may not contribute to the rise in coronary heart disease that occurs in women around menopause.

Assuntos

RESUMO

The relation between cigarette smoking and serum sex hormone concentrations was examined in two samples of the Multiple Risk Factor Intervention Trial (MRFIT) population. One sample consisted of 121 men at the Pittsburgh, Pennsylvania MRFIT center who were followed longitudinally for four years. The other sample was drawn from the entire MRFIT cohort and consisted of 163 MRFIT participants who subsequently developed coronary heart disease and 163 matched controls. The results indicated a positive correlation between cigarette smoking and serum total androstenedione concentration. The association was independent of age, relative weight, alcohol drinking, blood pressure, and high density lipoprotein (HDL) cholesterol. Serum total and free testosterone concentrations were positively correlated with cigarette smoking among the longitudinal sample and the controls, but not for the baseline sera from the coronary heart disease cases. This positive correlation was also independent of age, relative weight, alcohol drinking, blood pressure, and HDL cholesterol. There was no association between either serum estradiol or estrone concentrations and cigarette smoking in this population. These observations may have important implications for epidemiologic studies of diseases with significant smoking relations.

Assuntos

Assuntos

RESUMO

The cortisol response to insulin hypoglycemia was determined in ten hypopituitary children treated for four months with both growth hormone and cyproheptadine, and in six other children with hypopituitarism treated for four months with hGH alone. All patients had previously normal responses to orally administered metyrapone. There was no demonstrable difference in the F responses to insulin hypoglycemia before and four months following its discontinuation in the patients receiving hGH alone. In the ten patients on combined therapy the F response to insulin hypoglycemia was normal in five and subnormal in five patients. These ten patients were retested at least two months after cessation of CPH therapy. The F response reverted to normal in four of the five patients in whom it had been subnormal. There was no significant change in the five patients with initial normal response. No patients had signs or symptoms of glucocorticoid insufficiency. In some cases, long-term administration of CPH to children with hypopituitarism is associated with decreased F response to insulin hypoglycemia; this may represent decreased adrenocortical reserve in these patients. The previously reported enhancement of growth of hypopituitary children treated with hGH and CPH may in part be a result of decreased F production.

Assuntos

RESUMO

The response of plasma progesterone, 17 alpha-hydroxyprogesterone (17-OHP), and cortisol to intravenous ACTH was determined in 16 control subjects and seven sets of parents of children with congenital virilizing adrenal hyperplasia. The baseline and poststimulation concentrations of hormones (of each group) were similar except for those of 17-OHP in the parents which were significantly greater following administration of ACTH. When rates of increase were determined, those of progesterone and 17-OHP but not cortisol were significantly greater in the parents. The combined rate of increase of progesterone and 17-OHP was calculated; 10 of the 14 parents had a combined rate of increase greater than the mean plus two standard deviations of the control group. This test provides a simple method for the detection of some heterozygous carriers for CVAH.

Assuntos

RESUMO

The endocrine findings in two adolescents with hyperthecosis are compared to those in a patient with an androgenic ovarian tumor. In patients with hyperthecosis, luteinizing hormone values were elevated or in the upper normal range, and plasma testosterone and androstenedione values were increased. Following dexamethasone suppression, testosterone and androstenedione values remained elevated, but after administration of human chorionic gonadotropin, they increased further in only one patient. Baseline 17-ketosteroid values were normal, suppressed with dexamethasone, and stimulated to baseline levels following HCG. The patient with a lipoid cell ovarian tumor had low baseline LH levels, and elevated testosterone, androstenedione, and 17-ketosteroid values. Dexamethasone produced little change in urinary or plasma values, but the 17-ketosteroids increased markedly after administration of HCG. The finding of low serum LH values in patients with hirsutism and elevated androgen secretion should alert the clinician to the possibility of a tumor.

Assuntos