Gastritis, although a common diagnosis used by clinicians and pathologists in most parts of the world, is not well understood, especially its pathophysiology. Two major forms are recognized.1 Type A gastritis, which involves the fundus, is associated with pernicious anemia, antibodies to parietal cells, and autoimmune conditions of other organs. Type B gastritis, which is much more common, appears to mainly affect the antrum, autoimmune phenomena are absent, and it has been considered idiopathic. Patients with peptic ulcer disease almost invariably also have type B gastritis, but the relationship of these two entities has not been satisfactorily resolved.2,3
See also p 1149.
Population-based studies of gastric histologic characteristics in adults in northern Europe performed a number of years ago indicated that gastritis was surprisingly common.4 The incidence of gastritis, nearly all type B, increased with age, reaching 78% in those over 50 years old. The gastritis observed