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Current concepts in cholesterol gallstone pathogenesis

Pathogenesis of cholesterol gallstones is related to the failure of bile to maintain cholesterol in micellar solution. The predominant defect is supersaturation of bile with cholesterol caused mainly by hepatic secretion of free cholesterol. A measure for this defect is the conventional cholesterol supersaturation index (CSI). This parameter seems to over‐estimate the ‘effective supersaturation’ in terms of thermodynamic activity of cholesterol monohydrate in bile. The basic information about cholesterol solubilization has been derived from systematic studies of model bile systems at equilibrium. The various cholesterol carriers in bile are summarized in Fig. 8. Mixed micelles and unilamellar vesicles appear to be the major cholesterol carriers. The absolute amount, however, carried by each lipid aggregate cannot be precisely determined by the current methodology. Fusion of cholesterol‐rich vesicles and aggregation into large lamellar liquid crystals is correlated with appearance of solid cholesterol crystals. Therefore, it has been postulated that cholesterol crystals nucleate from these liquid crystalline aggregates. Further growth occurs by apposition of cholesterol molecules, presumably derived from unilamellar vesicles. Recently, however, evidence has been provided that the lecithin and cholesterol of liquid crystalline aggregates may derive directly from both micelles and vesicles [87].