To the Editor: Reihnér et al. (July 26 issue)1 should be commended for their interesting study and their methodologic groundwork.2 , 3 It would be premature, however, to draw conclusions about the relative quantitative roles of inhibition of cholesterol synthesis and stimulation of uptake mediated by low-density lipoprotein receptors in the hypocholesterolemic effects of pravastatin. Reihnér et al. did not measure the rate of cholesterol synthesis directly but estimated it indirectly from the ratio of serum free lathosterol to free cholesterol. This technique is based on rather simplistic assumptions: that cellular steroid concentrations must all exhibit a simple metabolite crossover4 at 3-hydroxy-3-methylglutaryl-coenzyme. . .
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