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Biomedical subjects

B M Sherman

Publications and source records attributed to B M Sherman.

At least 37 records · Page 2Linked to original sources
PubMed1986

Prolactinoma and adrenal androgens.

Theories about the relationship between hyperprolactinemia and hyperandrogenism are conflicting. Several reports assert that prolactin affects the delta 5 and delta 4 pathways through its effect on the activity of 3beta-hydroxysteroid dehydrogenase (3beta-OHSD). We measured delta 5 and delta 4 steroids, prolactin and cortisol in 18 amenorrheic, hyperprolactinemic women before and after resection of prolactinomas. Similar determinations of delta 5: delta 4 steroids were made in a control group of five women. The ratios of individual delta 5: delta 4 steroids were also analyzed. Our results support a modification of delta 5, delta 4 pathways through an effect on the rate-limiting enzyme 3 beta-OHSD. In hyperprolactinemic women the differences between the preoperative and postoperative steroid levels were significant. Further, since the androgens decreased irrespective of the prolactin following surgery, there probably is a factor other than ACTH and prolactin modulating the adrenal androgens.

Adult↗
PubMed1985

Rhythm-related changes in pituitary-adrenal function in depression.

We measured plasma ACTH and cortisol at 20-min intervals for 24 h in depressed patients and healthy control subjects. The data were analyzed by the PULSAR program to quantitate the number of hormone pulses, their amplitude, length, maximum and interval. We found that in both healthy and depressed subjects the circadian pattern of pituitary-adrenal activity is the result of significant time-related changes in pulse amplitude with no change in pulse frequency. Depressed patients who had an abnormal response to dexamethasone also had changes in pituitary-adrenal rhythm in the unmedicated state. These included ACTH and cortisol pulses whose amplitude, maximum and duration were greater than in the controls as well as a phase advance in the cortisol circadian rhythm. Some of those features were shared by patients who responded normally to dexamethasone suggesting that rhythm-related indices of pituitary-adrenal function may be a more sensitive index of disturbed pituitary adrenal regulation than the Dexamethasone Suppression Test.

Adrenocorticotropic Hormone↗
PubMed1985

Clinical and biologic antecedents of the amenorrhea/hyperprolactinemia syndrome: a case-control study.

Clinical, reproductive, and biologic antecedents of women with the amenorrhea/hyperprolactinemia (A/H) syndrome, most with pituitary prolactinomas, and matched healthy subjects were examined in a case-control study. Women with A/H had more frequent irregularity in early menstrual cycle patterns and excess facial hair, had less frequent catamenial symptoms, and were heavier at the time of study when compared with control subjects. The patients reported a more frequent history of thyroid disease and chest trauma. There were no significant differences between the patients and control subjects with respect to prior use of oral contraceptives, estrogens, psychotropic drugs, alcohol, or other substances known to alter serum prolactin levels, nor were there significant differences in the family history of gynecologic conditions or malignancies or the syndromes of multiple endocrine neoplasia. The implications of these findings are discussed.

Adenoma↗
PubMed1985

Etomidate anesthesia inhibits the cortisol response to surgical stress.

Plasma cortisol was measured in 18 patients undergoing gynecological procedures under etomidate or methohexital and nitrous oxide anesthesia. Plasma ACTH was also measured in three patients in each group. The mean plasma cortisol concentration before anesthesia was comparable in both groups. Plasma cortisol increased in patients anesthetized with methohexital, while none of the patients anesthetized with etomidate had an increase in plasma cortisol. The increase in plasma ACTH was equivalent in the two groups. Therefore, etomidate is a potent inhibitor of the adrenal response to surgery. The absence of clinical consequences associated with the blunted response suggests that a major increase in adrenal hormone production may not be necessary during surgery.

Adrenal Cortex↗
PubMed1985

Oxytocin does not influence adrenocorticotropin secretion in man.

Recent studies suggest that oxytocin inhibits ACTH secretion in normal men, whereas previous animal studies indicate that oxytocin is a weak secretagogue of ACTH. We studied the effect of oxytocin on plasma ACTH and cortisol in normal men under three conditions. Using four different doses of oxytocin (30, 60, 90, and 120 mU/kg), given by iv bolus injection, we found no difference in the effect of oxytocin on morning ACTH and cortisol levels compared with the effect of a placebo. A prolonged infusion of oxytocin (90 mU/kg . h) given from 0300-0600 h did not suppress basal ACTH or cortisol levels or delay or blunt their normal circadian rise. In addition, pretreatment with oxytocin (50 mU/kg, iv bolus dose, followed by an infusion of 50 mU/kg . h) did not alter the ACTH and cortisol responses to vasopressin. We conclude that oxytocin is not a major regulator of pituitary-adrenal activity in normal men.

Adrenocorticotropic Hormone↗
PubMed1985

Serotonergic regulation of prolactin and growth hormone secretion in man.

Controversy still exists regarding the role of serotonin in the regulation of prolactin (Prl) and growth hormone (GH) secretion in man. We gave healthy male volunteers three oral doses (0.5, 1.0 and 1.5 mg/kg) of fenfluramine, a serotonin-releasing agent and uptake inhibitor, and a corresponding placebo. There was a significant dose-response effect of fenfluramine on Prl but not on GH levels. Following the highest dose of fenfluramine, mean Prl levels increased from 9.7 ng/ml to 42.3 ng/ml. In a separate study, subjects were pre-treated with cyproheptadine, a serotonin antagonist, before the administration of fenfluramine. Cyproheptadine did not significantly affect basal Prl or GH levels, but it did blunt the response of Prl to fenfluramine. Cyproheptadine pre-treatment did not alter plasma levels of fenfluramine. Our findings support a stimulatory role for serotonin in the regulation of Prl secretion in man. They also suggest that serotonin does not have a major influence on GH secretion in man.

Adult↗
PubMed1985

Hyperprolactinemia and contraception: a prospective study.

The authors measured serum concentrations by single and multiple sampling techniques in 347 women before, during, and after treatment with either hormonal or barrier methods of contraception. The prolactin responses to an intramuscular injection of estrogen also were evaluated in control and selected study patients. The incidence of hyperprolactinemia in oral contraceptive users was higher than control subjects (12 versus 5%). Hyperprolactinemia was best assessed by multiple blood sampling, it is often transient and resolves spontaneously in about 50% of women. The estrogen provocation study suggests that some women who develop hyperprolactinemia while taking oral contraceptives are more sensitive to the effects of exogenous estrogen and may be at greater risk of developing pill-related menstrual aberrations and hyperprolactinemia.

Adolescent↗
PubMed1984

Provocative endocrine testing in recovered depressives.

Twenty-eight patients underwent a series of provocative endocrine tests an average of one year after their last admission for depression. Hypersecretion of cortisol, early escape of cortisol from dexamethasone suppression, diminished growth hormone response to insulin-induced hypoglycemia and altered thyrotropin response to thyrotropin-releasing hormone reported in acute primary depression were not observed after recovery. There were no differences in these measures after recovery between previous suppressors and nonsuppressors to dexamethasone. The cortisol response to insulin-induced hypoglycemia was less than expected in 6 of 16 recovered patients tested. There were significant differences in post-dexamethasone urinary free cortisol and in basal and early post-insulin serum cortisol levels between patients who had been suppressors and those who had been nonsuppressors to dexamethasone during acute depression. Further studies need to be done to substantiate these findings. These data indicate that hormone responses in recovered depressives are largely normal, suggesting that abnormalities during depression are "state" related phenomena.

Adolescent↗
PubMed1984

Dissociation of plasma cortisol and ACTH responses to dexamethasone in healthy subjects.

We examined the plasma cortisol and ACTH concentrations after graded doses of dexamethasone in a group of young, healthy adults. The decrease in cortisol was uniform in all subjects, and in 8 subjects there was a high degree of correspondence with the plasma ACTH concentration. The remaining 5 subjects had no change in plasma ACTH concentration during dexamethasone administration. All subjects had an expected diurnal change in cortisol on 2 pretreatment days and there was a corresponding diurnal change in ACTH for those subjects who had associated ACTH and cortisol responses after dexamethasone, while those with dissociated ACTH and cortisol after dexamethasone had no diurnal ACTH pattern. These findings were consistent with the 24-hour pattern of ACTH and cortisol before and after 1.0 mg of dexamethasone in 2 of the same subjects. These results are further evidence for ACTH independent regulation of adrenal function and indicate that pituitary-adrenal regulation in man is more complex than the traditional model of ACTH-cortisol feedback would predict.

Adrenocorticotropic Hormone↗
PubMed1984

Serotonergic stimulation of adrenocorticotropin secretion in man.

Controversy still exists regarding the role of serotonin in the regulation of ACTH secretion. We gave normal men three oral doses (0.5, 1.0, and 1.5 mg/kg) of fenfluramine, a serotonin-releasing agent and uptake inhibitor, and a corresponding placebo. There was a significant dose-dependent stimulatory effect of fenfluramine on both ACTH and cortisol levels. After the highest dose of fenfluramine, mean ACTH and cortisol levels increased from 20.8 pg/ml and 7.3 micrograms/dl to 35.5 pg/ml and 15.1 micrograms/dl, respectively. In a separate study, normal men were pretreated with cyproheptadine, a serotonin antagonist, before the administration of fenfluramine. Cyproheptadine did not significantly alter basal ACTH or cortisol levels, but it did blunt the responses of both hormones to fenfluramine. Cyproheptadine pretreatment did not alter plasma levels of fenfluramine. These findings support a stimulatory role for serotonin in the regulation of ACTH secretion in man.

Adrenocorticotropic Hormone↗
PubMed1984

Analysis of the specificity of physostigmine stimulation of adrenocorticotropin in man.

Five normal men were given infusions of saline and three doses (6, 12, and 18 micrograms/kg) of physostigmine, a centrally acting anticholinesterase, after pretreatment with glycopyrrolate, a peripheral cholinergic antagonist. There was no increase in basal ACTH or cortisol concentrations in any of the subjects after saline or the two smaller doses of physostigmine. However, each subject had a marked increase in ACTH and cortisol levels after the largest dose of physostigmine. These changes were preceded in each subject by the occurrence of noxious side effects and were accompanied by a rise in PRL levels in four of the subjects. Four subjects who received physostigmine (12 micrograms/kg) without glycopyrrolate pretreatment also experienced noxious side effects; these symptoms were followed by elevations in ACTH, cortisol, and PRL levels. These findings suggest that physostigmine stimulates ACTH and cortisol secretion through a stress-mediated effect rather than through a specific cholinergic mechanism. Consequently, physostigmine is not a reliable tool for investigating the cholinergic regulation of ACTH and cortisol.

Adrenocorticotropic Hormone↗
PubMed1984

Hyperprolactinemia in polycystic ovary syndrome.

With the use of multiple blood sampling, the prevalence of hyperprolactinemia in 150 consecutive patients with polycystic ovary syndrome (PCO) was found to be 17%. To further compare these two groups of PCO patients, the pituitary responses to gonadotropin-releasing hormone and thyrotropin-releasing hormone and the adrenal responses to dexamethasone suppression and adrenocorticotropic hormone stimulation were evaluated in 40 normoprolactinemic and 10 hyperprolactinemic PCO patients. Adrenal and pituitary perturbation tests were normal in both groups of PCO patients. Besides the higher levels of prolactin, the hyperprolactinemic patients also had higher blood levels of thyrotropin and testosterone, a higher luteinizing hormone/follicle-stimulating hormone ratio, lower levels of follicle-stimulating hormone, and lower follicle-stimulating hormone responses to gonadotropin-releasing hormone. Our data are consistent with the hypothesis that in some cases, the pathogenesis of PCO may be due to a central deficiency in dopaminergic activity at the basal hypothalamus. The hyperprolactinemia observed in a significant number of PCO patients may reflect a greater deficiency of hypothalamic dopamine, as manifested by the basal elevations of both prolactin and thyrotropin levels.

Adrenal Cortex Hormones↗
PubMed1983

Differentiation of depressive subtypes by insulin insensitivity in the recovered phase.

The glucose response to a standard insulin tolerance test (ITT) has been reported to be blunted in the acute phase of heterogeneous depressive disorders and to be normal in the recovered phase. We studied the glucose response to ITT in the recovered phase depression in patients who had previously been subclassified according to familial and clinical characteristics. All patients with depressive spectrum disease had an adequate glucose response to the ITT, whereas only 40% of patients with familial pure depressive disease and 56% of patients with bipolar illness had an adequate hypoglycemic response. There was also a trend toward a decrease in insulin sensitivity in patients who had been nonsuppressors to dexamethasone when depressed. These findings suggest that the glucose response to ITT may be a useful tool in differentiating among the heterogeneous depressive disorders.

Adult↗
PubMed1983

Dexamethasone suppression, protirelin stimulation, and insulin infusion in subtypes of recovered depressive patients.

Twenty-eight patients (10 bipolar, 13 depressive spectrum disease, and 5 familial pure depressive), recovered from depression for an average of 1 year, underwent a series of basal and provocative endocrine tests. No significant differences were found among depressive subtypes in thyrotropin, cortisol, or growth hormone measurements either before or after provocative testing with the exception of growth hormone response to insulin-induced hypoglycemia. Patients with depressive spectrum disease showed a significantly different growth hormone response to insulin-induced hypoglycemia than patients with bipolar disorder, a finding which suggests differences in alpha-adrenergic receptor sensitivity between these groups.

Adult↗
PubMed1982

Effect of danazol on plasma lipid and lipoprotein levels in normal women.

Prior studies of lipid and lipoprotein levels alterations associated with the administration of danazol, a testosterone derivative, in patients treated for endometriosis have been conflicting. We administered danazol to 7 normal menstruating women and measured plasma lipid and lipoprotein cholesterol levels prior to and 2 months after treatment. Small, non-significant decreases in total plasma cholesterol and triglyceride levels were seen, largely due to a dramatic decline in one woman with type IV hyperlipoproteinemia. No significant change in low density or very low density lipoprotein cholesterol levels was seen. However, a marked (40%) reduction of high density lipoprotein cholesterol level in the mean was found. These findings have implications for the atherogenic potential of danazol, the treatment of hyperlipidemia, and the relationship between gonadal hormones and lipoprotein levels.

Adult↗
PubMed1982

Regulation of the glucocorticoid receptor in human lymphocytes.

The presence of a glucocorticoid receptor in human lymphocytes is well established, but factors affecting its regulation have not been described. Using a competitive binding whole cell assay, we have examined the binding of [3H]-dexamethasone at 24 and 37 degrees C in untreated normal subjects and in healthy subjects taking various glucocorticoid preparations. At 24 degrees C normal human lymphocytes had 6000 binding sites/cell and a dissociation constant of 4 x 10(-9) M. The administration of 1 mg of dexamethasone, 5 mg of prednisone, and 37.5 mg of cortisone acetate resulted in a 30% decrease in binding sites after 1 week with no change in binding affinity. No changes in the number of binding sites was noted before 1 week and the diminished number persisted for 1 week after discontinuation of glucocorticoid treatment. Lymphocytes from hospitalized patients taking 40-60 mg of dexamethasone daily demonstrated the same change in number of binding sites that was seen in normal subjects taking 1 mg of dexamethasone. When binding assays were carried out at physiologic temperature there was the same decrease in number of binding sites after dexamethasone administration, and in addition, there was a two-fold increase in binding affinity. Glucocorticoid administration results in a time-dependent decrease in the number of lymphocyte glucocorticoid binding sites that is independent of the type of glucocorticoid administered. This is the first in vivo demonstration that glucocorticoids modulate their own receptors in man.

Binding, Competitive↗
PubMed1982

A case-control study of breast cancer and psychotropic drug use.

The relative risk of breast cancer incidence and tumor promotion associated with psychotropic drug consumption was evaluated in 151 patients with newly diagnosed neoplasms and 151 hospital controls. No significantly altered risk of breast cancer was found in association with the use of diazepam, chlordiazepoxide, antidepressants, major tranquillizers, sedatives or hypnotics, even after adjustment for known menstrual and reproductive risk factors. No substantial evidence of tumor promotion effects was found, as measured by altered age-at-onset of disease or altered clinical stage at presentation. Psychotropic drug use was inversely related to subject ponderosity (measured by the Quetelet Index) and while this did not confound risk estimates, it may be important in exploring biologic hypotheses of psychotropic drug use and breast cancer.

Aged↗