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Chronic Atrophic Gastritis

Chronic atrophic gastritis, which is defined as the loss of specialized glandular tissue in its appropriate region of the stomach, is an established early morphologic change that occurs along the sequence toward the development of gastric cancer.13,185 The presence of atrophic gastritis has an annual incidence of progression to gastric cancer of approximately 0.5% to 1.0%.186-189 The extent of atrophic gastritis within the stomach correlates with risk of progression to cancer.190-192

There are 2 forms of atrophic gastritis (see Chapter 52). The more common is environmental multifocal atrophic gastritis (EMAG), which is associated with Hp infection and more likely to be associated with metaplasia. The presence of Hp infection is associated with an approximately 10-fold increased risk of atrophic gastritis.193 There is considerable regional variation in the prevalence of atrophic gastritis in Hp-infected individuals, with a roughly 3-fold increase in Asia compared to Western countries.193,194 The second form of atrophic gastritis, autoimmune metaplastic atrophic gastritis (AMAG), is associated with anti–parietal cell and intrinsic factor antibodies. This form of atrophy is confined to the body and fundus. AMAG is associated with pernicious anemia and an increased gastric cancer risk, albeit not as high as that seen with Hp-induced MAG, owing most likely to a lesser degree of inflammation.187,195

Mechanisms underlying the increased risk of gastric cancer in the setting of gastric atrophy may be related to low acid output (hypo- or achlorhydria), which predisposes to increased bacterial overgrowth with non-Helicobacter organisms, greater formation of N-nitroso compounds, and diminished ascorbate secretion into the gastric lumen. 196 Additionally, circulating gastrin levels increase in response to the reduced acid output. Gastrin is a known growth factor for gastric mucosal cells, and sustained elevations of gastrin may contribute to abnormal growth and increased risk of neoplastic progression.197,198