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Dive into the research topics where Carl H. Bivens is active.

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Featured researches published by Carl H. Bivens.


The New England Journal of Medicine | 1973

Inhibition of hypoglycemia-induced growth hormone secretion by the serotonin antagonists cyproheptadine and methysergide.

Carl H. Bivens; Harold E. Lebovitz; Jerome M. Feldman

Abstract Growth hormone secretion is provoked by hypoglycemia. Since hypothalamic serotonin content increases during insulin-induced hypoglycemia, the role of hypothalamic serotonin in growth hormo...


The American Journal of the Medical Sciences | 1975

Growth hormone and prolactin secretion in the carcinoid syndrome.

Jerome M. Feldman; James W. Plonk; Carl H. Bivens; Harold E. Lebovitz; Stuart Handwerger

We evaluated plasma growth hormone (GH) and plasma prolactin (PRL) levels in ten patients with metastatic carcinoid tumors and the carcinoid syndrome (“active tumors”) and seven patients with metastatic carcinoid tumors without the carcinoid syndrome (“inactive tumors”). The patients with active tumors had elevated serum serotonin levels and increased urinary 5-hydroxyindoleacetic acid (5-HIAA) while these values were normal in patients with inactive tumors. Forty-five per cent of patients with active tumors had elevated fasting plasma GH levels that were either not suppressed or showed a paradoxical increase in response to I.V. glucose. There was a positive correlation between the plasma GH levels and serotonin production by the tumor. Twenty-eight per cent of patients with inactive tumors had elevated fasting plasma GH levels. GH levels were decreased by the administration of serotonin antagonists in some but not all of the patients. Parachlorophenylalanine (PCPA) an inhibitor of serotonin synthesis caused a paradoxical rise in GH levels. GH release in response to insulin hypoglycemia was normal. Plasma prolactin levels were normal in most of the patients with metastatic carcinoid tumors. PCPA administration did not systematically alter plasma prolactin levels. We conclude that elevated plasma GH levels are frequently present in patients with the carcinoid syndrome. Both serotonin produced by the tumors and the tumor itself may be responsible for the elevated GH levels.


Clinical Endocrinology | 1976

Inhibitory effect of serotonin antagonists on growth hormone release in acromegalic patients.

Jerome M. Feldman; James W. Plonk; Carl H. Bivens

We evaluated the effect of the serotonin antagonists cyproheptadine (Cypro) and methysergide (Methy) on growth hormone secretion in six patients with acromegaly. Two days administration of Cypro deceased the plasma GH concentration during oral glucose tolerance tests in four of the six patients evaluated; 2 days administration of Methy reduced the plasma GH levels of only one of the four patients evaluated. The one patient whose palsma GH concentration was lowered by Methy, did not have a decerase in plasma GH concentration after Cypro administration. Acromegalic patients have normal serum serotonin concentration and normal 5‐hydroxyindoleacetic acid excretion. If Cypro lowers plasma GH by antagonizing serotonin, our data would suggest that serotoninergic neruonal pathways are important in the regulation of pituitary GH secretion in some patients with acromegaly.


The New England Journal of Medicine | 1973

Peyronie's Disease — A Presenting Complaint of the Carcinoid Syndrome

Carl H. Bivens; Raymond L. Marecek; Jerome M. Feldman

ALTHOUGH the earliest clinical manifestations of the carcinoid syndrome are usually facial flushing and diarrhea, other symptoms may herald this syndrome. In the cases reported below the carcinoid ...


The American Journal of the Medical Sciences | 1973

Carcinoid tumors: effect on thyroid function.

Carl H. Bivens; Raymond L. Marecek; Jerome M. Feldman

The purpose of the present study was to determine if serotonin alters human thyroid function. Fifteen patients with carcinoid tumors underwent clinical and laboratory evaluation of thyroid function. Ten of the subjects had excessive serotonin levels with the carcinoid syndrome; five of the subjects had normal serotonin levels. Five subjects also underwent monthly reevaluation for from five to 17 months after the initial evaluation. On initial evaluation 47 per cent of the patients had an abnormality of at least one of four tests of thyroid function (serum thyroxine, serum triiodothyronine, triiodothyronine resin uptake, or free thyroxine index). These abnormalities were found in patients with and without the carcinoid syndrome. Despite these abnormal laboratory tests, all of the patients were clinically euthyroid, and none had goiters. Although there is a high incidence of abnormal thyroid function tests in patients with carcinoid tumors, these alterations can not be attributed to serotonin.


The Journal of Clinical Endocrinology and Metabolism | 1974

Inhibition of Hypoglycemia-Induced Cortisol Secretion by the Serotonin Antagonist Cyproheptadine

James W. Plonk; Carl H. Bivens; Jerome M. Feldman


Hormone and Metabolic Research | 1975

Failure of 5-Hydroxytryptophan to Stimulate Prolactin and Growth Hormone Secretion in Man

S. Handwerger; Plonk Jw; Harold E. Lebovitz; Carl H. Bivens; Jerome M. Feldman


Diabetes | 1975

Glucose Intolerance in the Carcinoid Syndrome

Jerome M. Feldman; James W. Plonk; Carl H. Bivens; Harold E. Lebovitz


Hormone and Metabolic Research | 1975

The role of cortisol and growth hormone in the counter-regulation of insulin-induced hypoglycemia.

Jerome M. Feldman; Plonk Jw; Carl H. Bivens


Hormone and Metabolic Research | 1975

Effect of cyproheptadine administration on insulin secretion in acromegalic, diabetic and normal subjects

Jerome M. Feldman; Carl H. Bivens; Skyler Js; Harold E. Lebovitz

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