Postdissolution gallstone recurrence. A clinical perspective.

Abstract

The intuitive assumption that gallstones will rapidly recur in all patients is clearly incorrect. At least 50% of patients do not develop stones within three to five years of complete dissolution, and the risk may decrease after the first two or three years. This is not so surprising when one considers the complexity of the pathogenic process. Bile must be sufficiently supersaturated with cholesterol, an imbalance in nucleating and antinucleating factors must occur, at least transiently, and, for some patients, a defect in gallbladder emptying may be necessary. Occasionally, pathogenic mechanisms that had been present, eg, estrogens, obesity, or medications such as clofibrate, may no longer be active. The best method to reduce the risk of recurrence is to reverse one or more of the essential pathogenic mechanisms. Desaturating bile in cholesterol by oral therapy with a bile acid such as ursodiol should be effective. A search for other safe, effective, and cost-effective approaches persists, eg, for novel bile acids resistant to bacterial degradation and for various dietary regimens. Alteration of cholesterol nucleation with nonsteroidal antiinflammatory agents is also under investigation. In addition, enhancement of gallbladder emptying is an interesting approach that is worth studying. If stones do recur, the course of action is not always clear. Recurrent stones are usually "silent," and we do not usually treat asymptomatic stones. These small cholesterol stones are temptingly easy to dissolve, however. At least in those patients whose level of surgical risk would be high if symptoms developed, prophylactic dissolution therapy may be desirable.