Tazuma S, Takizawa I, Kunita T, Mizuno T, Watanabe T, Teramen K, Horikawa K, Ochi H, Yamashita Y, Aihara N
Department of Internal Medicine, Hiroshima University School of Medicine, Japan.
Metabolism. 1995 Nov;44(11):1410-2. doi: 10.1016/0026-0495(95)90138-8.
We tested the possibility that pravastatin, a competitive inhibitor of hepatic hydroxymethyl glutaryl coenzyme A (HMG CoA) reductase, would alter cholesterol saturation of gallbladder bile by decreasing its cholesterol saturation index and/or degree of fatty acyl chain unsaturation in lecithin. Eighteen patients with type IIa hyperlipoproteinemia were treated with pravastatin 10 mg/d for 12 months. Gallbladder bile samples were aspirated with a duodenal tube by stimulating gallbladder contraction with intramuscular administration of cerulein before and after treatment. Serum cholesterol level was significantly reduced by 20% after 3 months, and this level was maintained after 12 months. In contrast, the cholesterol saturation index of gallbladder bile was not altered after 3 months (1.52 +/- 0.20 v 1.70 +/- 0.24), but it decreased significantly after 12 months (0.95 +/- 0.11, P < .01). The degree of fatty acyl chain unsaturation tended to decrease, although this was not statistically significant except for the decrease in molar percent of linoleate after 3 months. These findings suggest that long-term treatment with an inhibitor of HMG CoA reductase improves bile lithogenicity even at a comparatively low dose, and can decrease the incidence and complications of cholesterol gallstones.