Peptic ulcer disease (PUD) is thought to result from an imbalance betw
een aggressive (excessive) [especially gastric acid and pepsin] and pr
otective (diminished) factors (gastric mucus and bicarbonate, prostagl
andins and others) in the stomach. Recent attention has focused on the
role of Helicobacter pylori as a cause of chronic active gastritis an
d a pathogenic factor in PUD. Antiulcer medications with proven effica
cy in the treatment of acute PUD include histamine2 (H-2)-receptor ant
agonists, H+/K+-ATPase (proton pump) inhibitors, antacids, sucralfate
and prostaglandin analogues. The advent of proton pump inhibitors in p
articular has resulted in effective therapy for ulcers that previously
would have been considered refractory. H-2-receptor antagonists and s
ucralfate are also useful for maintenance therapy of PUD. Recent inter
est has focused on strategies aimed at eradicating H. pylori and the e
nsuing change in the natural history of PUD, specifically a marked dec
rease in ulcer recurrence. In contrast, with standard treatment regime
ns there is a high rate of ulcer relapse (50 to 90%) after acute ulcer
healing. Eradication of H. pylori has until now required a triple dru
g regimen of bismuth and 2 antibiotics, and is too cumbersome for rout
ine use. It is likely, however, that treatment aimed at eradicating H.
pylori will be routine in the near future and will represent a cost-e
ffective alternative to standard long term maintenance therapy.