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Biomedical subjects

I Singer

Publications and source records attributed to I Singer.

At least 109 records · Page 6Linked to original sources
PubMed1975

Paradoxical glucose-induced hyperkalemia. Combined aldosterone-insulin deficiency.

Severe hyperkalemia associated with spontaneous hyperglycemia as well as with the intravenous infusions of glucose occurred in an insulin-requiring diabetic patient in the absence of potassium administration, the use of diuretics which inhibit urinary potassium excretion or acidemia. Metabolic balance studies revealed, in addition to diabets, the presence of isolated aldosterone deficiency of the hyporeninemic type. Intravenous glucose infusions (0.5 g/kg body weight) produced significant hyperkalemia but desoxycortisone acetate (DOCA) therapy (10 mg/day) prevented the glucose-induced hyperkalemia. In this patient, the serum potassium concentration increases after the intravenous infusions of glucose because there is insufficient aldosterone and insulin to reverse the transfer of potassium to the extracellular fluid which normally occurs after hypertonic infusions of glucose. Although DOCA replacement modifies the distribution of potassium in the extracellular fluid and blunts the hyperkalemic effect of intravenous infusions of glucose, a rise in the insulin level is required for the usual hypokalemic response to intravenously administered glucose. These studies illustrate the risk of raising blood glucose levels in patients with combined aldosterone and insulin deficiency and the tendency towards hyperkalemia in diabetic patients under certain clinical conditions.

Aldosterone↗
PubMed1975

Endocrinology and metabolism in uremia and dialysis: a clinical review.

The salient information regarding the effects of uremia and dialysis on each of the metabolic fuels and hormones presented in the preceding sections is summarized in three tables. Tables 1 and 2 provide data on plasma levels, metabolism, dialysance, and literature references for each substance. Table 3 organizes the data according to the general mechanisms by which uremia and chronic dialysis may affect biological substances. Together these tables provide a reasonably complete summary of the information presently available. The pathophysiology of the uremic syndrome is still incompletely understood. The numerous metabolic and endocrine alterations associated with uremia and chronic dialytic therapy underscore the complexity of the problem and identify several specific areas for future research. One which deserves emphasis is the poolic and endocrine abnormalities found in uremia. A recent review by Chantler and Holliday (63) stressed in the importance of protein-calorie deficiency in the pathogensis of growth retardation and disturbed hormonal metabolism in children with chronic renal failure. The importance of this factor in adult patients with chronic uremia has been less well appreciated. However, striking similarities exist between the metabolic and endocrine abnormalities found in protein-calorie malnutrition and those found in uremia. These include, for example, altered albumin and amino acid metabolism, decreased levels of serum transferrin, peripheral insulin resistance and carbohydrate intolerance, elevated levels of glucagon, cortisol and growth hormone, and possibly diminished secretion of thyrotropin and thyroxine. Although not absolutely identical, the similarities between these two clinical syndromes suggest intriguing possible approaches to a better understanding of the pathophysiology of the uremic syndrome and its treatment.

Adult↗
PubMed1975

Demeclocycline treatment in the syndrome of inappropriate antidiuretic hormone secretion.

We have studied the effects of demeclocycline on the water metabolism of a patient with the syndrome of inappropriate antidiuretic hormone (ADH) secretion who presented with a serum sodium concentration of 110 meq/litre. Free water clearance was studied before, during, and after treatment with demeclocycline. This study shows that demeclocycline (900 mg/day) can at least partially inhibit the action of ADH in the setting of tumor-induced ADH secretion, with the production of a reversible, partial nephrogenic diabetes insipidus, and with few or no side effects. Demeclocycline may be useful in the treatment of chronic inappropriate ADH secretion.

Carcinoma, Small Cell↗
PubMed1974

Aldosterone-induced protein in toad urinary bladder.

Simultaneous electrophysiological and biochemical experiments demonstrated a specific aldosterone-induced protein in paired urinary hemibladders isolated from the toad Bufo marinus. Whenever aldosterone stinlmulated short-circuit current, aldosterone specifically increased [(35)S] methionine incorporation into a low-molecular-weight protein (about 12,000). Comparative studies with dexamethasone and insulin and inhibitory studies with spironolactone and actinomycin D suggest mineralocorticoid specificity.

Aldosterone↗
PubMed1972

Lithium-induced nephrogenic diabetes insipidus: in vivo and in vitro studies.

The physiological basis for the polyuria and polydipsia occurring in some manic-depressive patients treated with lithium salts was studied in vivo and in vitro. Three lithium-treated polyuric patients, in whom other causes of a concentrating defect were excluded, had abnormal urinary concentrating abilities after a standard water depreviation test. Two of these patients failed to respond to exogenous vasopressin (ADH) and one had a subnormal response. The abilities of these patients to excrete solute-free water (C(H2O)) was comparable to normal subjects during steady-state water diuresis, suggesting no gross abnormalities in sodium transport. However, each of these patients demonstrated abnormally low capacities to reabsorb solute-free water (T(C) (H2O)) under hydropenic conditions after administration of hypertonic saline and vasopressin. These in vivo findings demonstrate at least a nephrogenic basis for the diabetes insipidus syndrome manifested by these three patients. The defect in water transport was further characterized in toad urinary bladders in vitro. Short-circuit current (I) and water flow (W) were studied under basal, ADH-stimulated, and cyclic adenosine 3',5'-monophosphate (c-AMP)-stimulated conditions. Increasing mucosal [Li(+)] progressively inhibited basal I, and both I and W induced by ADH. Significant inhibition of basal and ADH-induced I was observed at mucosal [Li(+)] < 1.1 mEq/liter, and of ADH-induced W at mucosal [Li(+)] = 11 mEq/liter. On the other hand, at these lithium concentrations, neither c-AMP-stimulated W nor I was inhibited. Increasing serosal [Li(+)] produced significant inhibition of basal I only at [Li(+)] at least 50-fold greater than at the mucosal (urinary) surface. These in vitro studies confirm that mucosal lithium inhibits the action of ADH, but not c-AMP. Hence, lithium appears to be a significant inhibitor of ADH-stimulated water flow, probably acts from the urinary surface, and appears to exert its effect at a site biochemically proximal to c-AMP action.

Adult↗