Much of what is currently accepted regarding Helicobacter pylori-associated
gastritis and its relationship with gastric adenocarcinoma rests on the as
sumption that atrophic gastritis can be correctly identified and reproducib
ly recognized, Several studies have indicated that pathologists have a low
level of agreement on this topic, and the terms 'gastric atrophy' and 'atro
phic gastritis' remain imprecisely defined and poorly understood, Furthermo
re, the genesis and progression of the atrophic changes that take place in
the gastric mucosa of some individuals infected with H. pylori are incomple
tely characterized. The lack of a strict definition of atrophic gastritis i
s at least partially responsible for recent concerns regarding the effects
of prolonged pharmacological gastric acid inhibition in patients with H. py
lori infection, One recent paper concluded that patients with reflux oesoph
agitis and H. pylori infection who are treated with longterm acid inhibitio
n have an increased risk of atrophic gastritis, As this term evokes associa
tions with an increased risk of gastric cancer, the possibility was subsequ
ently raised that anti-secretory maintenance therapy might increase the ris
k of cancer in H, pylori-positive patients. A second report, however, concl
uded that long-term acid-inhibitory therapy for an average of three years i
s no different from fundoplication in the development of gastric atrophy, A
lso, because no intestinal metaplasia developed in any of the patients, and
only atrophic gastritis associated with intestinal metaplasia is considere
d a precursor of gastric cancer, there is no evidence to support the hypoth
esis that long-term acid inhibition in individuals with H. pylori infection
increases the risk of gastric cancer. fur I Gastroenterol Hepatol 11 (supp
l 2):S29-S33 (C) 1999 Lippincott Williams & Wilkins.