ROBERT M. VOGEL, M.D.; L. DONALD WEINSTEIN, M.D.; TEODORO HERSKOVIC, M.D.; HOWARD M. SPIRO, M.D., F.A.C.P.
VOGEL RM, WEINSTEIN LD, HERSKOVIC T, SPIRO HM. 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.
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
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Celiac Disease and Malabsorption, Endocrine and Metabolism, Endocrine Cancer, Gastroenterology/Hepatology, Hematology/Oncology.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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