Peptic ulcer disease was once thought of simply as a prob-lem of hypersecretion of acid and pepsin. However, it is now clear that an ulcer is the end result of an imbalance between aggressive and defensive factors in the gastroduodenal mucosa. H. pylori, NSAIDs, and acid secretory abnormalities are the major factors that disrupt this equilibrium. Whereas acid pep-tic injury is necessary for ulcers to form, acid secretion is nor-mal in almost all patients with gastric ulcers and increased in approximately one third of patients with duodenal ulcers. Zollinger Ellison syndrome accounts for 0.1% of patients who present with peptic ulcer disease. A defect in bicarbonate pro. duction, and hence acid neutralization in the duodenal bulb, is also seen in patients with duodenal ulcer disease. This abnor-mality resolves with eradication of H. pylori if it is present.

Duodenal and gastric ulcers develop in a minority of pa-tients infected with H. pylori. Acute infection results in short. lived acid hyposecretion that then resolves despite persistence of the organism. Chronic infection increases the basal gastrin, the gastrin response to a meal, basal acid output, and gastrin stimulated acid output. Regulation of antral G cells may be al-tered by abnormalities in the ability of adjacent somatostatin-producing D cells to shut down gastrin release. All of these ab-normalities resolve after eradication of the organism. Gastric ulcers may develop in the setting of intense gastritis associated with certain strains of H. pylori. The development of duodenal ulcers is more complex and probably involves enhanced gastric acid secretion caused by dysregulation of somatostatin and gas-trin: gastrin release is increased, whereas the inhibitory influ-ence of somatostatin is diminished. This results in duodenal gastric metaplasia and subsequent H. pylori colonization and in-flammation in the duodenum. Duodenal bicarbonate production is also inhibited by H. pylori infection.

NSAII)s clearly predispose patients to ulcers, both duode-nal and gastric, as well as to complications of ulcer disease, in-cluding hemorrhage, perforation, and obstruction. The risk for gastric ulcers is somewhat greater than that for duodenal ulcers. It is estimated that symptomatic ulceration occurs in 2% to 4 % of patients treated with NSAIDs for 1 year. Many more individuals will develop asymptomatic ulcers of uncertain significance. NSAID-induced ulceration occurs with all NSAIDs, except for the newer cyclooxygenase-2 selective a-gents such as celecoxib (Celebrex), regardless of enteric coat-ing or delivery as a prodrug formulation. The risk of NSAID-induced ulceration and complications is dose related and in-creases with age older than 60, concurrent corticosteroid use, increasing duration and dose of therapy, anticoagulant thera-py, and a history of prior ulcer disease.

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