HENRY GINSBERG, M. D.; HARRIET S. GILBERT, M.D.; JOYCE COREY GIBSON, D.SC.; NGOC-ANH LE, Ph.D.; W. VIRGIL BROWN, M.D.
Hypercholesterolemia reported in patients with myeloproliferative disorders prompted our investigation of lipoprotein metabolism in these patients. The production and fractional catabolic rates of very-low-density lipoprotein (VLDL) apoprotein-B were measured using 131I-VLDL; those of VLDL triglyceride, using 3H-glycerol; and those of low-density lipoprotein (LDL) apoprotein-B, using 125I-LDL. Plasma total and LDL cholesterol levels (mean ± SD) were significantly reduced in seven patients with myeloproliferative diseases, compared to five normal subjects (93.1 ± 20.3 mg/dL versus 166.8 ± 24.6 mg/dL and 50.3 ± 14.8 mg/dL versus 107 ± 20.8 mg/dL, respectively). The production rates of VLDL apoprotein-B and VLDL triglyceride were normal in the patients. The fractional catabolic rate of LDL apoprotein-B was increased in the patients with myeloproliferative diseases (0.89 ± 0.32/d versus 0.52 ± 0.10/d;p < 0.05); this increased rate was associated with reduced plasma LDL apoprotein-B levels (41.7 ± 7.1 mg/dL versus 57.0 ± 11.3 mg/dL; p < 0.05) despite normal or elevated LDL apoprotein-B production (16.7 ± 5.3 mg/kg body weight · d versus 12.9 ± 1.2 mg/kg body weight · d). The site (or sites) of increased LDL catabolism in these hypocholesterolemic patients with myeloproliferative disorders is under investigation.
GINSBERG H, GILBERT HS, GIBSON JC, et al. Increased Low-Density-Lipoprotein Catabolism in Myeloproliferative Disorders. Ann Intern Med. 1982;96:311–316. doi: 10.7326/0003-4819-96-3-311
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Published: Ann Intern Med. 1982;96(3):311-316.
Cardiology, Coronary Risk Factors, Dyslipidemia, Hematology/Oncology.
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