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Biomedical subjects

S Goldfarb

Publications and source records attributed to S Goldfarb.

At least 145 records · Page 8Linked to original sources
PubMed1976

Studies of malformation syndromes of man XIB: the cerebro-hepato-renal syndrome of Zellweger: comparative pathology.

A study of 11 autopsied cases of the cerebro-hepato-renal syndrome of Zellweger (ZS) is reported. All cases had severe, persistent congenital hypotonia, hepatic lobular disarray, renal cortical cysts and pulmonary hypoplasia. Many had cardiovascular malformations, hepatomegaly, cerebral cortical gyral maldevelopment and pancreatic islet hyperplasia. Additional, less frequent findings are delineated. Results of iron content studies of hepatic and renal tissues are related to age of survival and possible development of fibrosis.

Abnormalities, Multiple↗
PubMed1976

Nephropathy and mixed cryoglobulinemia: evidence for an immune complex pathogenesis.

Mixed IgM-IgG cryoglobulins were present in the serum of a patient with the nephrotic syndrome, recurrent purpura, chronic active hepatitis and ascites. A renal biopsy demonstrated deposition of IgM, IgG, and complement components C3 and C4 in intracapillary 'coagula' and glomerular capillary walls. No glomerular deposition of alternate complement pathway components was noted. Serum levels of C3 and C1q were depressed, and the cryoprecipitate which contained monoclonal chi-type IgM and polyclonal IgG, behaved as an immune complex by in vitro C3 conversion tests. It is suggested that the renal disease resulted from entrapment of circulating cryoglobulin 'aggregates' having immunopathologic effects similar to those of immune complexes.

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↗
PubMed1976

Sex hormones and hepatic neoplasia.

The recent increase in hepatocellular neoplasms in women of child-bearing age taking oral contraceptives and in individuals of both sexes taking anabolic androgenic steroids is a phenomenon that requires urgent attention. Although most of the lesions are benign, reports of carcinomas in a few of these individuals and our own observation of an adenoma that shows borderline malignant transformation suggest that some of the adenomas are premalignant lesions. The pathology of our own cases and those reported in the literature are reviewed, and hypotheses are offered for a carcinogenic role of synthetic steroid sex hormones. These speculations are based on known toxic and metabolic actions of the drugs and are amenable to experimentation.

Adenoma↗
PubMed1976

Clinical usefulness of measuring prothrombin time as a routine admission test.

A questionnaire indicating the presence of a history or physical findings consistent with liver desease or bleeding disorders was completed by house officers on 301 admissions to a Veterans Administration medical service. Each patient had prothrombin time determined on admission. Only two of 107 patients for whom the prothrombin time was measured as a screening test had an abnormal results and one of these was normal when repeated. Of 73 patients with a history of alcoholism but no other pertient case history or physical examination results, only one had an abnormal prothrombin time. Of the remaining 121 patients, who had a pertinent history or physical examination, 41 had an abnormal admission prothrombin time. We conclude that measurement of prothrombin time adds little additional information to that obtained by history and physical examination in screening for liver disease and coagulation defects unless the patient has specific clinical evidence of liver disease, anticoagulation, or other conditions predisposing to bleeding disorders.

Alcoholism↗
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↗
PubMed1972

Stimulatory effect of dietary lipid and cholestyramine on hepatic HMG CoA reductase.

The diurnal cycle of hepatic HMG CoA reductase activity was studied under conditions of controlled feeding where the percentage of dietary lipid, alone or in combination with 2% cholestyramine, was varied. Cholestyramine caused an increase in HMG CoA reductase activity that began soon after feeding started and peaked 6 hr later. In contrast, a diet containing 20% corn oil was a much weaker inducer of the enzyme but caused a prolonged elevation that began late in the fasting part of the cycle. These patterns suggest two different mechanisms of action.

Alcohol Oxidoreductases↗
PubMed1971

Improved assay of 3-hydroxy-3-methylglutaryl coenzyme A reductase.

Two improvements are described for the assay of HMG CoA reductase. These are a simple synthesis of the substrate precursor HMG-3-(14)C anhydride and a double-label ((14)C and (3)H) method for determining the amount of mevalonate-3-(14)C that is formed from the substrate.

Alcohol Oxidoreductases↗