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Plasma and lipoprotein lipid responses to four hypolipid drugs
Author(s) -
Hazzard William R.,
Wahl Patricia W.,
Gagne Claude,
ApplebaumBowden Deborah,
Warnick G. Russell,
Albers John J.
Publication year - 1984
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/bf02534494
Subject(s) - triglyceride , medicine , clofibrate , cholesterol , very low density lipoprotein , chemistry , endocrinology , lipoprotein
The responses of 14 hyperlipidemic subjects to 4 hypolipidemic agents were compared by measureing cholesterol and triglyceride in whole plasma, very low density lipoproteins (VLDL), low density lipoproteins (LDL), and high density lipoproteins (HDL) monthly for 2 months before and 3 months during treatment with each of 4 drugs: clofibrate, 2 g/d; colestipol, 20 g/d; para‐aminosalicylic acid‐ascorbate (PAS‐C), 6–8 g/d; and oxandrolone, 7.5 mg/d. Lipid responses proved to be stable by the first monthly evaluation both off and on each drug. Mean adherence was high and similar for all agents (81–92% of the prescribed dose). Clofibrate was associated with significant decreases in mean plasma cholesterol (−16%, p<.01), plasma triglyceride (−51%, p<.005), VLDL‐cholesterol (−61%, p<.005) and VLDL‐triglyceride (−61%, P<.005), while HDL cholesterol increased (+20%, p<.01), and the LDL‐cholesterol/HDL ratio declined (−24%, p<.05). Colestipol was associated with decreases in mean plasma cholesterol (−15%, p<.01) and LDL‐cholesterol (−22%, p<.05), while VLDL‐triglyceride increased (+41%, p<.05), and the LDL‐cholesterol/HDL‐cholesterol ratio declined (−25%, p<.05). PAS‐C was associated with decreases in VLDL‐cholesterol (−30%, p<.05), and VLDL‐triglyceride (−29%, p<.05), while the LDL‐cholesterol/HDL‐cholesterol ratio remained unchanged. Oxandrolone was associated with increases in mean plasma cholesterol (+7%, p<.05), LDL‐cholesterol (+45%, p<.005 [+25% excluding one subject who increased 298%]), and LDL‐triglyceride (+24%, p<.01), while decreases occurred in plasma triglyceride (−31%, p<.05), VLDL‐cholesterol (−26%, p<.05), VLDL‐triglyceride (−42%, p<.005), HDL‐cholesterol (−45%, p<.005), and HDL‐triglyceride (−43%, p<.01). The mean LDL‐cholesterol/HDL‐cholesterol ratio increased by 109% (p<.005), reflecting the reciprocal changes in LDL and HDL. Thus, while both clofibrate and colestipol were associated with significant, equivalent reductions in theoretical atherogenic risk, oxandrolone produced a net effect that was not only adverse but 4 times that magnitude, suggesting caution in its long‐term use, even for the management of hypertriglyceridemia.

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