A RECENT editorial in the Journal 1 pointed out that despite the frequency of gallstones in the United States, research concerning their cause has lagged far behind that in many less prevalent disorders. The purpose of this report is to reclassify and summarize mechanisms of both clinical and experimental gallstone formation and perhaps to suggest direction for further research. The references have been chosen because of the completeness of their discussion or bibliography.For nearly a century and a half stasis, obstruction and inflammation have been mentioned in the literature as etiologic mechanisms in cholelithiasis.2 Although these concepts are important and . . .
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Donald Small (1968) studied this question.
Synapse has enriched 2 closely related papers on similar clinical questions. Consider them for comparative context: