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Robert A. Kozol, MD

Arch Surg. 1995;130(10):1040.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

OPERATIONS currently performed for peptic ulcer disease were designed prior to the identification of Helicobacter pylori as a major cofactor in ulcerogenesis. These operations decrease gastric acid secretion by eliminating vagal stimulation and gastrin production and/or by diminishing the parietal cell mass. The complications and ulcer recurrence rates for each antiulcer operation can be recited by most surgical residents. Most of these data were collected prior to the widespread use of fiberoptic endoscopy and therefore probably represent modest estimates.¹ Prospective trials with almost complete endoscopic follow-up have identified ulcer recurrences in 30% to 95% of patients medically treated for peptic ulcer.^2,3 Few, if any, patient populations have been systematically screened by endoscopy for recurrent ulcer after surgical therapy for peptic ulcer. In fact, most surgical series have used endoscopic follow-up only in patients with hematemesis, perforation, or persistent, severe dyspepsia.^4,5

Helicobacter pylori infection of the gastric mucosa . . . [Full Text PDF of this Article]

Author Affiliations
Detroit, Mich

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