The gastroduodenal mucosa is a dynamic barrier restricting entry of gastric acid and other potentially hostile luminal contents. Mucosal HCO3(-) is a key element in preventing epithelial damage, and knowledge about HCO3(-) transport processes, including the role of the cystic fibrosis transmembrane conductance regulator channel, and their neurohumoral control are in rapid progress.

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The defensive factors that prevent the human duodenal mucosa from acidic and peptic damage have not been fully evaluated. To determine whether duodenal mucosal bicarbonate production was altered in patients with inactive duodenal ulcer, we measured basal and acid-stimulated bicarbonate output from the duodenal bulb and the distal duodenum in healthy subjects and patients with inactive duodenal ulcer. As compared with 16 normal subjects, the 12 patients had significantly less mean (+/- SE) basal proximal duodenal mucosal bicarbonate secretion (185 +/- 13 vs. 107 +/- 18 mumol per centimeter per hour; P less than 0.001). Moreover, in response to a physiologic amount of hydrochloric acid (2 mmol per five minutes) instilled directly into the duodenal bulb, peak proximal duodenal bicarbonate output in the patients was 41 percent of the normal response (263 +/- 65 vs. 642 +/- 77 mumol per centimeter per hour; P less than 0.01). There was little overlap between groups. In contrast, bicarbonate outputs in the distal duodenum were similar in the two groups. We conclude that most patients with duodenal ulcer disease have decreased proximal duodenal mucosal bicarbonate production at rest, in response to hydrochloric acid, and in relation to peak gastric acid secretion. Impaired proximal duodenal mucosal bicarbonate secretion may be an important factor in the development and natural history of duodenal ulcer.

EPCS permanently stopped variceal bleeding, rarely became occluded, was accomplished with a low incidence of portal-systemic encephalopathy, and compared with EST, produced greater longterm survival. The widespread practice of using surgical procedures mainly as salvage for failure of endoscopic therapy is not supported by the results of this trial (clinicaltrials.gov #NCT00690027).