Cholesterol gallstone disease is one of the most prevalent and the most costly digestive diseases in Western
countries. Its pathogenesis is a complex paradigm resulting from the interaction of genetic factors, hepatic hypersecretion
of cholesterol, increased intestinal absorption of cholesterol, a constantly “supersaturated” bile, crystallization of biliary
cholesterol, and gallbladder stasis. De novo cholesterol biosynthesis, biliary cholesterol output, and intestinal cholesterol
absorption are therefore key steps involved in cholesterol homeostasis. Establishing the right pharmacological therapy for
cholesterol gallstones is of major importance in Western healthcare systems. Certain drugs might independently influence
cholesterol gallstone formation by blocking the 3-hydroxy-3-methylglutaryl-coenzyme A reductase and inhibiting cholesterol
biosynthesis in the liver (statins) or blocking cholesterol absorption in the small intestine apical membrane by specifically
inhibiting the Niemann-Pick C1-like 1 protein (ezetimibe). This review will focus on the possibility that statins
and ezetimibe, by acting at different levels of cholesterol homeostasis, might represent novel therapeutic approaches to
prevent cholesterol gallstones in selected subjects at risk.
Keywords: Cholelithiasis, cholesterol synthesis, cholesterol absorption, enterohepatic circulation, metabolic syndrome, Niemann-
Pick C1-like 1, obesity.
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Published on: 19 March, 2014
Page: [1435 - 1447]