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Family Studies of Hypergastrinemic, Hyperpepsinogenemic I Duodenal Ulcer

I. L. TAYLOR, M.D., Ph.D.; J. CALAM, M.D.; J. I. ROTTER, M.D.; C. VAILLANT, Ph.D.; I. M. SAMLOFF, M.D.; A. COOK, M.D.; E. SIMKIN, M.D.; and G. J. DOCKRAY, Ph.D.
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Grant support: by grants from the Medical Research Council and grant AM 17328 (Peptic Ulcer Center), clinical investigator award AM 00523 (to Dr. Rotter), and research grant AM 13233 from the National Institute of Arthritis, Metabolism, and Digestive Diseases.

▸Requests for reprints should be addressed to I.L. Taylor, M.D.; Division of Gastroenterology, Sepulveda Veterans Administration Hospital; Sepulveda, CA 91343.

Liverpool, England; and Torrance, Sepulveda, and Los Angeles, California

© 1981 American College of PhysiciansAmerican College of Physicians

Ann Intern Med. 1981;95(4):421-425. doi:10.7326/0003-4819-95-4-421
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Antral G-cell hyperfunction is a rare cause of hypergastrinemia, hyperchlorhydria, and duodenal ulcer disease. We found evidence for a familial basis for this disorder. The probands were two young men with aggressive duodenal ulcer who had basal and postprandial hypergastrinemia, hyperpepsinogenemia I, and basal and pentagastrin-stimulated hyperchlorhydria. All characteristics returned to normal after antrectomy and vagotomy. Antral gastrin concentrations and quantitative G-cell counts were normal, indicating hyperfunction of G-cells rather than hyperplasia. Four of 10 first-degree relatives of the two patients shared with them the combination of postprandial hypergastrinemia and hyperpepsinogenemia I. The aggregation of these abnormalities in two families, each identified by a proband with hypergastrinemic, hyperpepsinogenemic I duodenal ulcer, suggests that antral G-cell hyperfunction may have a genetic basis.





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