ROBERT M. VOGEL, M.D.; L. DONALD WEINSTEIN, M.D.; TEODORO HERSKOVIC, M.D.; HOWARD M. SPIRO, M.D., F.A.C.P.
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Diarrhea is a prominent clinical feature of the Zollinger-Ellison syndrome (1). In approximately one half of the well-studied cases of non-beta islet cell adenomas diarrhea is associated with marked gastric hypersecretion and intractable peptic ulcer disease; it is within this group that steatorrhea and malabsorption occur (1-13). Although the gastric hypersecretion may be responsible for the diarrhea, the precise etiologic mechanism has not been fully elucidated. Theoretically, hyperacidity must lead to steatorrhea by two possible mechanisms:  inactivation of pancreatic enzymes, particularly lipase, by acid duodenal contents or  production of jejunal abnormalities. If this hypothesis is correct, drastic reduction
VOGEL RM, WEINSTEIN LD, HERSKOVIC T, et al. Mechanisms of Steatorrhea in the Zollinger-Ellison Syndrome. Ann Intern Med. 1967;67:816–822. doi: 10.7326/0003-4819-67-4-816
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Published: Ann Intern Med. 1967;67(4):816-822.
Celiac Disease and Malabsorption, Endocrine and Metabolism, Endocrine Cancer, Gastroenterology/Hepatology, Hematology/Oncology.
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