Biomedical subjects
Publications and source records attributed to E L Cohen.
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.
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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.
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.
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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.
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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.
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.
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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.
A growing number of brain diseases are characterized by decreased levels of one or more of the neurotransmitters. Recent experimental evidence indicates that nutritional factors strongly influence the regulation of two of these neurotransmitters, serotonin and acetylcholine. As a result, attempts are now being made to treat diseases associated with low levels of serotonin or acetylcholine by administering their dietary precursors, tryptophan and choline, respectively. This treatment may increase the amount of the deficient neurotransmitter at synapses and produce clinical benefit. Such efforts to elevate brain neurotransmitter levels with a naturally occurring precursor represent a new approach in medical therapeutics and will probably continue. We review the scientific basis for such treatment and show that brain levels of serotonin and acetylcholine depend upon the amounts of tryptophan and choline available to the brain; these, in turn, fluctuate according to dietary factors.
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In the course of studies designed to develop a radioimmunoassay system for the detection of renin, we have identified in human plasma a potent inhibitor that interferes with the renin-antirenin reaction. Utilizing gel filtration, this renin-antirenin inhibitory activity was found to have the same molecular size as renin substrate. However, it could be separated from renin substrate by ion-exchange chromatography. When fractions containing this activity were tested in an in vitro system containing renin and renin substrate, they were found to inhibit the generation of angiotensin I.