Current development in the pathogenesis of gallstones.

Demonstration in 1968, of the association of cholesterol supersaturation of bile with cholesterol gallstones paved the way to a physical-chemical basis for gallstone formation. It however, soon became clear that other factors including nucleation of cholesterol crystal, binding together of these crystals with mucin, and hypomotility of the gallbladder played an equally important role in gallstone formation. Although the molecular events that underlie these processes are far from clear, many loose ends are beginning to tie. One knot recently tied is that an increase in biliary arachidonyl lecithin may lead to increased prostanoid synthesis which may be responsible for increased mucin secretion as well as gallbladder hypomotility. Research on similar lines is being done to unravel the pathogenesis of pigment gallstones, but much less has been gained in that field. An interesting outcome of some recent work is that biliary micelles and vesicles are important not only for the solubilisation of cholesterol but also for that of bilirubin and calcium which are the major constituents of pigment gallstones. This observation opens a common ground for the formation of both types of gallstones.