February 7, 1925


JAMA. 1925;84(6):443. doi:10.1001/jama.1925.02660320035015

Observations on gallstone formation have, for many years, postulated in the case of the commonest concretions, the cholesterol calculi, that the chief source of their conspicuous component was in degenerating and desquamating cells of the gallbladder and biliary passages. A little reflection will indicate that something more than purely local conditions may become responsible for the genesis of cholesterol stones. They have been found in the absence of any detectable primary causes of inflammation. The physical chemists have attributed the deposition of gallstones to a reduction in the amount of "protective colloids" in the bile, brought about by abnormal conditions. In the normal bile, they argue, the bile salts and proteins act to keep the sparingly soluble substances in a colloidal state; when these protective colloids are destroyed, however, separation of the sparingly soluble compounds ensues.1

Students of the subject have been slow to reckon with the possibility that

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