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Biomedical subjects

E L Cohen

Publications and source records attributed to E L Cohen.

At least 37 records · Page 2Linked to original sources
PubMed1981

Hormonal adaptation to the stresses imposed upon sodium balance by pregnancy and lactation in the Yanomama Indians, a culture without salt.

The Yanomama Indians of northern Brazil and southern Venezuela have been identified as a "no-salt" culture. In this study, data were obtained to determine in this population the adjustments of sodium-related hormones to the stresses imposed upon sodium balance by pregnancy and prolonged lactation. Controls against the possibility that findings in the Yanomama were ethnic rather than dietary were provided by similar observations in the Guaymi Indians of Panama, who have free access to salt. Urinary concentrations of sodium were approximately 1 mEq/l in male and female Yanomama, with 24-hour excretion rates in the males averaging 1 mEq, similar to our prior observation. The pregnant Yanomama had exceeding high urinary concentrations of aldosterone. These were associated with higher plasma renin activities and serum aldosterone concentrations than in all other subjects. Although pregnant Guaymi had elevations of serum and urinary aldosterone, these were significantly lower (p < 0.001) than those of the Yanomama. Prolonged lactation in the Yanomama was associated with elevation of plasma renin activity and serum and urinary aldosterone concentration compared with the Guaymi, but were not higher than those in nonlactating Yanomama females. The findings suggest that pregnancy in a salt-poor environment is associated with an exaggerated augmentation of hormonal responses that enhance positive sodium balance.

Adult↗
PubMed1979

Adenocarcinoma of gallbladder producing unilateral ureteral obstruction.

Ureteral obstruction is a common problem facing the urologist. Tumors, either primary in the urinary tract or metastases from other organs, may be the causal agent. Herein we present the first case reported of ureteral obstruction caused by metastases from adenocarcinoma of the gallbladder.

Adenocarcinoma↗
PubMed1979

17 alpha-Hydroxylase deficiency. A combination of hydroxylation defect and reversible blockade in aldosterone biosynthesis.

We have studied the hormonal secretion and excretion patterns in a patient with the XX type of 17 alpha-hydroxylase deficiency. In the untreated state, the patient's urine contained only those steroids which do not require 17-hydroxylation in their biosynthesis. Aldosterone was not produced in the patient and the metabolic product of its immediate precursor, 18-hydroxy-11-dehydro-tetrahydrocorticosterone, was excreted in markedly elevated amounts. This apparent complete block in 18 oxidation was reversible upon long-term ACTH suppression within 27 days. Direct in vitro incubation of the patient's adrenal gland removed at operation demonstrated, 1) the complete lack of 17 alpha-hydroxylase activity, 2) the functional block in the ability to oxidize the hydroxyl group at the 18 methyl side chain. The addition of physiological concentrations of angiotensin to the incubation medium further showed, 3) angiotensin mildly stimulated the entire aldosterone biosynthetic pathway, 4) angiotensin directly stimulated the conversion of 18-hydroxycorticosterone to aldosterone. We propose that in this patient, 17-hydroxylase deficiency produced a decreased plasma concentration of cortisol, followed by stimulation of deoxycorticosterone production by ACTH. The resultant increase in extracellular fluid volume suppressed plasma renin activity. This resulted in a low plasma concentration of angiotensin II which directly suppressed oxidation of 18-hydroxycorticosterone to aldosterone. This defect has been called corticosterone methyl oxidase defect type 2.

18-Hydroxycorticosterone↗
PubMed1978

Basal cell adenoma of prostate.

A case of basal cell adenoma originating in the prostate is presented. This lesion might develop from proliferation of basal epithelial cells of the prostate gland under unknown mechanism.

Aged↗
PubMed1978

Crossed fused renal ectopia presenting with blunt trauma.

A case is presented of crossed fused renal ectopia in a fifteen-year-old black male which was diagnosed because of blunt trauma. Workup and management are discussed and pertinent x-ray films shown. The literature is reviewed with respect to renal trauma associated with congenital anomalies of the kidney.

Adolescent↗
PubMed1977

Huntington's disease: clinical and chemical effects of choline administration.

Choline (Ch) administration sequentially increases blood Ch, brain Ch, and brain acetylcholine (ACh) levels in the rat and might be useful in Huntington's disease, a brain disorder thought to be associated with deficient cholinergic tone. Ten patients with Huntington's disease took Ch orally (8 to 20 gm per day) after the extent of their disabilities had been documented by clinical examination, movies, and combined electromyogram-accelerometer recordings. Choline levels in blood and cerebrospinal fluid increased markedly during treatment with Ch, affirming that oral Ch administration increases the amount of ACh precursor delivered to the brain. Although some of the patients exhibited transient improvement in speech, balance, and gait, treatment with Ch failed to bring about consistent or lasting improvement in any of the subjects.

Acetylcholine↗
PubMed1977

Systemic capillary leak syndrome and monoclonal IgG gammopathy; studies in a sixth patient and a review of the literature.

The clincical and laboratory features of a sixth patient with periodic systemic capillary leak syndrome are reported. During an attack metabolic studies demonstrated a marked shift of plasma (10 to 70%) from the intravascular to the extravascular space resulting in hemoconcentration (highest hematocrit of 82). At the termination of the attack there was a return of the electrolytes, water and proteins to the intravascular compartment. The cardiovascular, renal and endocrine compensation was appropriate to this insult and no underlying abnormalities were demonstrated in these systems. The effector pathways of coagulation, complement, bradykinin generation, prostaglandins and histamine metabolism did not appear to be responsible for the altered capillary permeability. The patient was not missing inhibitors of these same pathways. The only persistently abnormal finding was a monoclonal IgG gammopathy. However, further studies of this paraprotein did not uncover a link between it and the abnormal capillary permeability. Five similar cases are reviewed; at least four and possibly all of these patients also had an IgG paraprotein. Treatment of these attacks was unsuccessful. Attemps to prevent the episodes with a wide variety of therapeutic agents failed. Treatment of the acute attacks with administration of intravenous fluids, did not maintain an adequate intravascular volume and may lead to fluid overload upon return of normal capillary integrity. Pressor agents were of no apparent value and may cause increased cardiac irritability. Although the clinical features and pathophysiology of the capillary leak syndrome have been defined, the etiology remains unknown.

Adult↗
PubMed1977

A new and superior adrenal imaging agent, 131I-6beta-iodomethyl-19-nor-cholesterol (NP-59): evaluation in humans.

We have reported tissue distribution studies in rats and dogs with a new adrenal imaging agent. 131I-6beta-iodomethyl-19-nor-cholesterol (NP-59). This agent concentrated five times higher in the adrenal cortex than 131I-19-iodocholesterol without increased concentration in non-adrenal tissues. We now report in 34 patients, the findings on scintigraphy with NP-59 compared with angiograms and/or adrenal vein hormone levels and histopathology, including 13 patients with hypercortisolism, 12 with primary aldosteronism, 2 with low renin hypertension, 5 with catecholamine excess, 1 with a liver metastasis from an aldosterone producing adrenal cortical carcinoma, and 1 with anaplastic adrenal cortical carcinoma. NP-59 adrenal cortical uptake was more rapid and intense and background activity was less prominent, allowing earlier and more definite interpretation of images than was possible with 131I-19-iodocholesterol.

Adrenal Cortex Neoplasms↗
PubMed1977

Renin reactivity, renin activity and renin concentration in patients with normal and low renin essential hypertension.

Renin activity, concentration, substrate and reactivity were determined in normal subjects as well as in hypertensive subjects with suppressed and normal plasma renin activity. Renin substrate measurements were similar in all groups. Renin reactivity, a measure of circulating modifiers of the renin reaction, was significantly increased in both hypertensive groups. Reactivity was significantly greater in the normal renin hypertensive group than the low renin hypertensive group. Renin concentration was significantly suppressed in both hypertensive groups, but to a greater degree in the low renin hypertensives. These findings suggest that plasma renin concentration may be suppressed in most hypertensive subjects. Furthermore, plasma renin activity may be "normalized" in most hypertensive subjects by the effect of circulating modifiers of the renin reaction. While renin reactivity in the plasma of low-renin hypertensive subjects is accelerated to a lesser degree than that of the normal-renin hypertensives, this finding alone does not explain the low plasma renin activity.

Angiotensinogen↗
PubMed1977

Renin-renin substrate kinetic constants in the plasma of normal and estrogen-treated humans.

The renin-renin substrate Michaelis constant (Km) and maximal velocity (Vmax) were determined in the plasmas of normal subjects. The mean Km was 0.7 microgram/ml. Under these conditions, the in vitro reaction of renin with physiologic concentrations of renin substrate will proceed at only 70% of its maximal velocity. Following estrogen administration, Km doubled to a value of 1.3 microgram/ml. Vmas increased by 81%. Analysis of the changes induced in the in vitro reaction velocity demonstrated that estrogen-induced acceleration of the renin reaction is dependent upon both an increase in renin substrate concentration as well as an increase in Vmas. The latter appears to be quantitatively more important. These findings suggest the emergence of modifying factors in the renin-renin substrate interaction following estrogen administration.

Angiotensinogen↗