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I thank Dr. Capurso and colleagues for their observations concerning the etiologic hypotheses I presented in my review of gastric pathophysiology, Helicobacter pylori, nitrite exposures, and pancreatic cancer. Studies in the literature provide a lot of suggestive evidence but are certainly not definitive for the hypotheses, and interpretations other than the ones I proposed are possible.

Capurso et al. mention two areas of potential controversy. The first concerns the relation between chronically increased gastric acid secretion and risk of pancreatic cancer. In support of this association, I cited studies of individuals with a history of duodenal ulcers, as well as studies of persons who had undergone gastrectomy for duodenal ulcer treatment. Capurso et al. are correct that gastrectomy usually decreases gastric acid output. Furthermore, duodenal ulcer patients treated with vagotomy and gastrojejunostomy or pyloroplasty can have elevated gastric nitrites and N-nitroso compounds that could be the reason for their increased risk of pancreatic cancer. However, as I noted in the review, a number of case–control studies examining only a history of duodenal ulcers, without considering gastrectomy, have shown an increased risk of pancreatic cancer.

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