TY - JOUR
T1 - Effects of pravastatin, a new HMG-CoA reductase inhibitor, on vitamin D synthesis in man
AU - Dobs, Adrian S.
AU - Levine, Michael A.
AU - Margolis, Simeon
N1 - Funding Information:
From The Johns Hopkins University School of Medicine, Baltimore, MD. Suppotted in part by National institutes of Health Grant No. 5MOIRROO722 to the Outpatient General Clinical Research Center, The Johns Hopkins Hospital. Baltimore, MD and Bristol-Myers Squibb Corporation. Portions of this study have been presented in abstract form at the 1988 National American Heart Association Meeting. Address reprint requests to Adrian S. Dobs, MD, The Johns Hopkins University School of Medicine, 600 N Wolfe St, 906B Blalock Building, Baltimore, MD 21205. Copyright 0 1991 by W.B. Saunders Company 0026-049519114005-0014$03.00/0
PY - 1991/5
Y1 - 1991/5
N2 - The HMG-CoA reductase inhibitors, a new class of lipid-lowering agents being used with increasing frequency, inhibit synthesis of cholesterol in vivo. Thus, one potential side effect of these drugs is alteration of other metabolic pathways requiring intermediates in the cholesterol biosynthetic pathway. We hypothesized that pravastatin, a new HMG-CoA reductase inhibitor, may impair vitamin D3 synthesis in the skin and alter mineral homeostasis by diminishing the availability of vitamin D precursors. Basal serum levels of calcium, phosphorus, parathyroid hormone (PTH), vitamin D3, and 1,25-dihydroxyvitamin D were measured, and dietary intakes of calcium and vitamin D were calculated in a control hypercholesterolemic group and an experimental group treated with pravastatin 10, 20, and/or 40 mg orally twice daily for at least 3 months. Basal parameters of mineral metabolism were similar in the two groups. To assess the capacity of the skin to synthesize vitamin D3 and as an indirect measure of its precursors, all subjects received whole body ultraviolet irradiation (UVI) in a phototherapy chamber for varying time intervals. Subjects in both groups showed significant (P < .001) dose-dependent increases in vitamin D3 production after equivalent UVI exposures. However, for equivalent UVI exposure, the serum vitamin D3 response was identical in controls versus pravastatin-treated subjects. We conclude that hypercholesterolemic patients have normal mineral metabolism and the use of pravastatin at these doses for up to 3 months does not alter vitamin D3 synthesis in the skin.
AB - The HMG-CoA reductase inhibitors, a new class of lipid-lowering agents being used with increasing frequency, inhibit synthesis of cholesterol in vivo. Thus, one potential side effect of these drugs is alteration of other metabolic pathways requiring intermediates in the cholesterol biosynthetic pathway. We hypothesized that pravastatin, a new HMG-CoA reductase inhibitor, may impair vitamin D3 synthesis in the skin and alter mineral homeostasis by diminishing the availability of vitamin D precursors. Basal serum levels of calcium, phosphorus, parathyroid hormone (PTH), vitamin D3, and 1,25-dihydroxyvitamin D were measured, and dietary intakes of calcium and vitamin D were calculated in a control hypercholesterolemic group and an experimental group treated with pravastatin 10, 20, and/or 40 mg orally twice daily for at least 3 months. Basal parameters of mineral metabolism were similar in the two groups. To assess the capacity of the skin to synthesize vitamin D3 and as an indirect measure of its precursors, all subjects received whole body ultraviolet irradiation (UVI) in a phototherapy chamber for varying time intervals. Subjects in both groups showed significant (P < .001) dose-dependent increases in vitamin D3 production after equivalent UVI exposures. However, for equivalent UVI exposure, the serum vitamin D3 response was identical in controls versus pravastatin-treated subjects. We conclude that hypercholesterolemic patients have normal mineral metabolism and the use of pravastatin at these doses for up to 3 months does not alter vitamin D3 synthesis in the skin.
UR - http://www.scopus.com/inward/record.url?scp=0025755375&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0025755375&partnerID=8YFLogxK
U2 - 10.1016/0026-0495(91)90235-O
DO - 10.1016/0026-0495(91)90235-O
M3 - Article
C2 - 1902546
AN - SCOPUS:0025755375
SN - 0026-0495
VL - 40
SP - 524
EP - 528
JO - Metabolism
JF - Metabolism
IS - 5
ER -