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Diagnosis of Gastrinoma: Much Ado about Nothing?

M. Michael Wolfe, MD
[+] Article and Author Information

Grant Support: Supported in part by grant RO1 DK35636 from the National Institutes of Health and grant RRO1032 from the General Research Center Program of the Division of Research Resources.

Requests for Reprints: M. Michael Wolfe, MD, Brigham and Women's Hospital, Division of Gastroenterology, 75 Francis Street, Boston, MA 02115.


Brigham and Women's Hospital
Boston, Massachusetts


Ann Intern Med. 1989;111(9):697-699. doi:10.7326/0003-4819-111-9-697
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Few disorders have attracted as much clinical interest as duodenal ulcer disease, particularly regarding pathogenesis and treatment. Many gaps remain in our understanding of the pathophysiology of this disease; however, the role of gastric acid is well established. As Karl Schwarz so eloquently stated it in 1910 (1): "Ohne saueren Magensaft, kein peptisches Geschwür": that is, "no acid, no ulcer." Although basal acid production is increased in patients with duodenal ulcer as a group (2), rates vary enormously, and approximately 50% to 60% of patients secrete normal amounts of acid in the basal state (3). Even in these latter

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