FAILURE OF INHIBITION OF CHOLESTEROL BIOSYNTHESIS TO RETARD ATHEROMA

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Abstract
In two patients with gross hypercholesterolemia triparanol (MER-29) treatment failed to inhibit the rapid deposition of sterols in the aorta and the skin. Analysis of lesions laid down, partly or wholly during MER-29 treatment, suggested that desmosterol participated equally with cholesterol in the formation of atheromatous and xanthomatous lesions. No evidence has been obtained to suggest that triparanol in any way influences the course of rapidly developing atheroma or xanthomatosis.