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Biomedical subjects

E Koren

Publications and source records attributed to E Koren.

94 records · Page 6Linked to original sources

Hyperlipidemia in acute lymphoblastic leukemia.

Studies were conducted on lipemic serum obtained from a 26 month old male to determine possible mechanisms for the association of a Type V hyperlipidemic phenotype with advanced lymphoblastic leukemia (ALL). Antibodies to apolipoproteins and endogenous heparin were not detected as previously reported. Fatty acid analysis of the triglyceride esters revealed a high proportion of stearic-acid (18:0) which was associated with a slower in vitro degradation of very low density lipoproteins (VLDL) by human milk lipoprotein lipase (LPL). This suggests that a cause of the hyperlipidemia could be abnormal composition of triglycerides which render the VLDL a poor substrate for lipoprotein lipase. Hyperlipidemia in leukemia may be more prevalent than previously realized since nine other cases of newly diagnosed ALL have been studied who had moderate hypertriglyceridemia associated with elevated ApoB and low ApoA-I levels, but normal triglyceride composition. These findings suggest that the abnormal triglyceride composition is a late feature of the hyperlipidemia in leukemia, as observed in the case studied.

Adult↗

Serotonin in the portal vein after acidification.

To test whether serotonin release from the argentaffin cells of the intestinal tract can elicit peptic ulcer, rats were given intraduodenal infusions of N/10 and N/20 hydrochloric acid. Serotonin measured in the portal venous blood of rats which had had an intraduodenal infusion of N/20 HCl for five minutes was significantly higher than in the portal (P less than 0.05) or systemic (P less than 0.01) blood of control animals. After longer intervals serotonin release tapered off and measurements obtained 30 minutes after an infusion of N/10 HCl did not differ significantly from those in the controls.

Animals↗

Rhabdomyolysis associated with clozapine treatment in a patient with decreased calcium-dependent potassium permeability of cell membranes.

A 21-year-old patient developed rhabdomyolysis during his nineteenth week of treatment with clozapine for drug-resistant schizophrenia. No risk factors for rhabdomyolysis were found, but the calcium-dependent potassium efflux, normally responsible for membrane hyperpolarization and muscle refractoriness, was severely decreased in the patient's red blood cells. Clozapine is speculated to cause rhabdomyolysis in patients with defective calcium-activated K+ channels.

Adult↗