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January 10, 1972

Cholera, Prostaglandins, and CAMP

JAMA. 1972;219(2):213. doi:10.1001/jama.1972.03190280051012

Though cholera's visitations continue despite advances in prophylaxis and therapy, much of their mystery has been dispelled by a better understanding of etiology and basic mechanisms of the disease. Isolation of the causative organism and its enterotoxic exotoxin, and subsequent identification of the electrolyte and water disturbances caused by the latter have made cholera more understandable and easier to control. Currently, studies at the molecular level are providing deeper insights into the fundamental processes which underlie the pathophysiology of the disease.

How does cholera enterotoxin provoke the observed characteristic changes in the movement of water and solutes across the epithelium of the small bowel? Field and co-workers1 noted that cholera toxin placed on the luminal side of isolated rabbit ileal mucosa stimulated active secretion of chloride and inhibited absorption of sodium. The changes were the same as those previously observed2 with cyclic adenosine monophosphate (CAMP) or theophylline—the latter