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Treatment of familial hypercholesterolaemia: a controlled trial of the effects of pravastatin or cholestyramine therapy on lipoprotein and apolipoprotein levels
Author(s) -
WIKLUND O.,
ANGELIN B.,
FAGER G.,
ERIKSSON M.,
OLOFSSON S.O.,
BERGLUND L.,
LINDEN T.,
SJÖBERG A.,
BONDJERS G.
Publication year - 1990
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1111/j.1365-2796.1990.tb00225.x
Subject(s) - cholestyramine , pravastatin , placebo , medicine , cholesterol , apolipoprotein b , endocrinology , hydroxymethylglutaryl coa reductase , gastroenterology , concomitant , hmg coa reductase , chemistry , biochemistry , reductase , pathology , alternative medicine , enzyme
. The efficacy and safety of a new, selective inhibitor of cholesterol synthesis, pravastatin, and the bile acid‐binding resin, cholestyramine, were compared in a randomized, double‐blind study of 120 patients with familial hypercholesterolaemia. After a run‐in period of 8‐10 weeks with assessment of dietary habits, the patients were treated with pravastatin + placebo, placebo + cholestyramine, or placebo alone. Active pravastatin therapy was initiated with 10 mg b.i.d. for 6 weeks, and was increased to 20 mg b.i.d. for the following 6 weeks. Cholestyramine was given at 24 gd −1 , or the highest tolerable dose. After 6 weeks of therapy, serum total and LDL cholesterol levels were reduced by 17% and 21%, respectively, on pravastatin treatment, whereas the corresponding reductions with cholestyramine treatment were 24% and 30%, respectively. With an increased dose of pravastatin, serum and LDL cholesterol concentrations were reduced by 23% and 28%, respectively, after 12 weeks; the effect of cholestyramine was unchanged. HDL cholesterol levels increased in response to pravastatin, by 7% and 9% after 6 and 12 weeks, respectively. Concomitant changes in the concentrations of apolipoproteins B and AI were observed. Three patients discontinued the study because of side‐effects: two subjects were treated with pravastatin and one was given placebo. The prevalence of side‐effects (including laboratory abnormalities) was 35% for pravastatin, 30% for placebo, and 53% (significantly higher) for cholestyramine. We conclude that pravastatin, in a 40 mg daily dose, is as effective as cholestyramine in lowering LDL cholesterol in familial hypercholesterolaemia. Since the frequency of side‐effects is higher with cholestyramine, pravastatin offers a promising alternative for the therapy of this genetic disease.