Abstract

Of 77 duodenal ulcer patients consecutively subjected to Billroth-II-type gastric resection 56 patients were available for a follow-up study on an average 5.6 years postoperatively. In 43 out of 52 patients single biopsies from the fundal part of the stomach disclosed gastritis, which was associated with atrophic changes in 25 of them. Out of 53 patients 14 had achlorhydria. In 6 of them the production of intrinsic factor was markedly reduced. Manifest iron deficiency occurred in 17 patients. Circulating parietal cell antibodies were found in one patient only. Intrinsic factor antibodies were absent from the sera of all patients. In 49 out of 56 patients reflux to the stomach was demonstrated radiologically. The results suggest that reflux of duodenal contents to the stomach may advance the development of gastritis after gastric surgery. The possible relationship between iron deficiency and gastric mucosal atrophy is discussed. Autoimmunity seems to be without importance as to the postoperative gastritis.

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