As in previous years, developments in the field of ulcers and gastritis
have been dominated by new findings related to Helicobacter
pylori. With the decrease in the frequency of
H. pylori infection, the relative proportion of non-
H. pylori ulcers has increased. Attempts to reduce the endoscopy workload
by H. pylori or CagA screening have not been
successful, and are probably ill-advised. It has become increasingly clear
that curing H. pylori infection will not automatically
lead to complete relief of symptoms in patients with duodenal ulcer disease.
Post-therapy confirmation of cure will probably become the norm. Studies comparing
omeprazole to misoprostol or ranitidine for nonsteroidal anti-inflammatory
drug (NSAID) ulcer prevention in true NSAID ulcers have shown that omeprazole
is equal to full-dose misoprostol for ulcer healing and to the lowest useful
dose of misoprostol for ulcer prevention. H2-receptor antagonists
cannot be recommended for NSAID ulcer healing or prevention. Elimination of H. pylori increases the prevalence of gastroesophageal
reflux disease in a population in such a way that superficially, there appears
to be a choice between more gastroesophageal reflux disease or multifocal
atrophic gastritis. The risk of developing adenocarcinoma of the esophagogastric
junction is many times (10-fold to 60-fold) less than the risk of developing
gastric cancer from CagA-positive H. pylori infection
with multifocal atrophic gastritis - the “protective” lesion