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.; G. J. DOCKRAY, Ph.D.
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.
I. L. TAYLOR, J. CALAM, J. I. ROTTER, C. VAILLANT, I. M. SAMLOFF, A. COOK, et al. Family Studies of Hypergastrinemic, Hyperpepsinogenemic I Duodenal Ulcer. Ann Intern Med. 1981;95:421–425. doi: 10.7326/0003-4819-95-4-421
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Published: Ann Intern Med. 1981;95(4):421-425.
Gastroenterology/Hepatology, Peptic Disease, Peptic Ulcer.
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