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.
D000328:Adult; D001053:Apolipoproteins / Q000097:blood; D002675:Child, Preschool; D002784:Cholesterol / Q000097:blood; D006801:Humans; D006949:Hyperlipidemias / Q000209:etiology* / Q000378:metabolism; D007136:Immunoglobulins / Q000378:metabolism; D007945:Leukemia, Lymphoid / Q000150:complications* / Q000378:metabolism; D008071:Lipoprotein Lipase / Q000378:metabolism; D008079:Lipoproteins, VLDL / Q000378:metabolism*; D008297:Male; D013229:Stearic Acids / Q000097:blood; D014280:Triglycerides / Q000097:blood
D001053:Apolipoproteins; D007136:Immunoglobulins; D008079:Lipoproteins, VLDL; D013229:Stearic Acids; D014280:Triglycerides; D002784:Cholesterol; D008071:Lipoprotein Lipase