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Biomedical subjects

I Singer

Publications and source records attributed to I Singer.

At least 91 records · Page 5Linked to original sources
PubMed1977

Guidelines for drug therapy in renal failure.

Five tables are presented that provide guidelines for drug usage in patients with renal insufficiency. The data are derived from the current medical literature. If specific information about a drug is unavailable, emphasis is given to normal pharmacokinetic variables in arriving at recommendations for therapy. Nephrotoxicity of adverse effects in patients with renal disease are noted and adjustments for dialysis suggested.

Acute Kidney Injury↗
PubMed1976

Hysterical polydipsia (compulsive water drinking) in children.

Two patients had entirely different clinical presentations of hysterical polydipsia: convulsions and coma in a 5-year-old boy with intrinsic renal disease and a single kidney, and abnormal behavior in a 3-year-old girl with normal kidneys. In neither case was the correct diagnosis made on initial evaluation. Physiological studies demonstrated primary polydipsia to be responsible for both clinical presentations. The differential diagnosis of polydipsia and polyuria is reviewed, and the nonuniform presentation of hysterical polydipsia is emphasized. In children with intrinsic renal disease, hysterical polydipsia may be life-threatening.

Child, Preschool↗
PubMed1976

Renal failure, hemodialysis, and nafcillin kinetics.

Nafcillin (N) pharmacokinetics was studied in 27 subjectswith and without renal failure (RF) (determined by endogenous creatinine clearance, Ccr). Elimination rate constants (K) were calculated from serial serum levels of N measured from 2 to 12 hr after a single 500-mg intramuscular injection. Only 4 of 9 hemodialysis patients had measurable levels of N at 24 hr. The K values for the groups with normal renal function,moderate RF, severe RF, and on hemodialysis were 0.477 hr(-1), 0.432 hr (1), 0.369 hr(-1), and 0.306 hr (-1), respectively...

Adult↗
PubMed1976

Acute hyperkalemia induced by hyperglycemia: hormonal mechanisms.

Two insulin-requiring diabetics with isolated hyporeninemic hypoaldosteronism cpontaneously developed hyperkalemia that was aggravated whenever blood glucose concentration rose. Acute glucose infusions raised the serum potassium concentration in these patients with combined insulin and aldosterone deficiency but lowered, or did not change, the serum potassium concentration in normal subjects and in patients with either aldosterone or insulin deficiency alone. The paradoxical hyperkalemic response to glucose in patients with combined hormonal deficiency was blunted by prior administration of desoxycorticosterone acetate and abolished by prior administration of insulin. Our studies emphasize the crucial roles played by insulin and aldosterone in regulating the serum potassium concentration in man, and the need to avoid hyperglycemia in patients with combined insulin and aldosterone deficiency.

Acute Disease↗
PubMed1975

Actions of insulin, epinephrine, and dibutyryl cyclic adenosine 5'-monophosphate on fat cell protein phosphorylations. Cyclic adenosine 5'-monophosphate dependent and independent mechanisms.

Endogenous and hormone-induced protein (polypeptide) phosphorylations were studied in isolated rat fat cells, in fat pads, and in subcellular fractions obtained from fat tissue under different physiological conditions. Insulin (25-100 muU/ml) increased the incorporation of 32P into two proteins: insulin-phosphorylated proteins (IPP 140 and IPP 50; similar to 140,000 and 50,000 daltons, respectively). Epinephrine (10(-7)-10(-6) M) increased the incorporation of 32P into another protein: epinephrine-phosphorylated protein (EPP 60-65; similar to 60,000-65,000 daltons). Endogenous IPP 140 phosphorylation in fat cells obtained from fasted and refed rats was similar to that of insulin in normal cells. Studies of insulin and epinephrine interactions showed that insulin increased IPP 140 phosphorylation even in the presence of epinephrine or lithium (25 mM times 10(-3) M). dibutyryl cyclic AMP (5 times 10(-4) M) markedly stimulated EPP 60-65 phosphorylation, but neither epinephrine (10(-7)-10(-6) M) nor dibutyryl cyclic AMP reproduced insulin's phosphorylation of APP 140. Lithium inhibited both endogenous and epinephrine-stimulate EPP 60-65 phosphorylation, but did not inhibit that induced by dibutyryl cyclic AMP. These findings suggest that insulin stimulated a specific, cyclic AMP independent protein kinase for IPP 140 phosphorylation. Cell-free extracts from insulin-treated fat tissue catalyzed the specific transfer of 32P from ATP to IPP 140 more rapidly than control extracts. No differences in the total receptor protein or total protein kinase activity using [gamma(-32P]ATP were noted between insulin-treated and control preparations. IPP 140 may be either (a) an insulin-sensitive protein kinase (phosphotransferase) or (b) a protein whose function is regulated by an insulin-sensitive protein kinase or phosphatase.

Adipose Tissue↗
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↗