The development and growth pattern of solitary and multiple cholesterol gallbladder stones was defined using cholecystography in a prospective study of 48 patients whose initial cholecystograms indicated a stone-free gallbladder and who developed gallstones within the subsequent 5 years. Radiological observations performed over 365 patient-years were complemented by macroscopic examination, radiograms, scanning electron microscopy, and chemical analysis of gallstones from these and other patients obtained at cholecystectomy. Solitary gallstones were found to develop after a precursor phase of over 2 years during which free-floating crystal laminae of cholesterol formed. These laminae subsequently aggregated loosely and underwent external compaction and internal remodeling by movement of cholesterol molecules to form compact spheroids. A single lamina was observed to function as a nucleus for the development of a solitary stone shaped as an ellipsoid. About 10% of solitary stones were found to have a solitary pigment stone in their center. In contrast, multiple cholesterol gallstones formed without a precursor phase. Innumerable, very thin cholesterol crystals appeared which very abruptly aggregated to form spheres of up to 1 mm in diameter. Within 3 months a second aggregation took place in which these spheres colaesced to form mulberry stones. Mulberry stones in turn were transformed either to faceted stones (if many were present in the gallbladder) or to barrel stones (if few were present) over a period of 3 years. It is proposed that temporary occlusion of the cystic duct leads to supersaturation of bile with calcium bilirubinate and/or calcium carbonate which in turn promotes deposition of either or both of these calcium salts on the surface of single or multiple gallstones. For multiple gallstones, this process or the deposition of additional cholesterol crystals seals the gallstone surface and is followed by metamorphosis of the stone center.

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Over a period of 32 years 689 patients with upper abdominal symptoms were examined radiologically at least twice for gall-bladder polyps and stones. All were without evidence of stones initially, but 181 had gall-bladder polyps on first examination. During a mean observation period of 9 1/2 years gall-bladder stones occurred in 18% (pigment stones in about 24%, solitary cholesterol stones in 30% and multiple ones in 46%), regardless of the presence or absence of gall-bladder polyps. There was no evidence for a change from polyps to stones. Cholesterolosis runs through four stages in the course of decades; accumulation of cholesterol esters in subepithelial foam-cell nests is characteristic. 95% of gall-bladder polyps are cholesterol polyps which gradually empty. Prophylactic cholecystectomy for gall-bladder polyps is justified only if they are more than 10 mm in diameter.