C. J. GLUECK, M.D.; A. P. KAPLAN, M.D.; R. I. LEVY, M.D.; H. GRETEN, M.D.; H. GRALNICK, M.D.; D. S. FREDRICKSON, M.D.
Exogenous hypertriglyceridemia in two patients with systemic lupus erythematosus and one with lymphoma was associated with depression of plasma postheparin lipolytic activity and specifically the activity of triglyceride lipase and monoglyceride hydrolase. Larger doses of heparin elevated plasma lipolytic enzyme activities into the normal range and promoted clearing of chylomicrons. Resistance to the action of heparin was also seen in the coagulation system in vivo and in vitro by lack of prolongation of thrombin and coagulation times. IgG isolated from plasma of the patients with lupus and IgA: IgM from the lymphoma patient preferentially bound 3H-heparin, and removal of IgM from the latter fraction caused loss of binding activity. Preincubation of heparin with these fractions depressed the effect of heparin on release of rat adipose tissue lipoprotein lipase and prolongation of the thrombin time in vitro. The association of heparin-binding immunoglobulins with exogenous hyperlipoproteinemia adds support to a role of endogenous heparin in the maintenance of tissue lipolysis and the removal of triglycerides from plasma.
GLUECK CJ, KAPLAN AP, LEVY RI, GRETEN H, GRALNICK H, FREDRICKSON DS. A New Mechanism of Exogenous Hyperglyceridemia. Ann Intern Med. 1969;71:1051–1062. doi: 10.7326/0003-4819-71-6-1051
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Published: Ann Intern Med. 1969;71(6):1051-1062.
Cardiology, Coronary Risk Factors, Dyslipidemia.
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