Gastric atrophy, diagnosing and staging

Abstract

H. pylori is now accepted as the cause of gastritis and gastritis-associated diseases, such as duodenal ulcer, gastric ulcer, gastric carcinoma, and gastric MALT lymphoma. The natural history of H. pylori gastritis includes inflammation progressing from the antrum into the adjacent corpus resulting in an atrophic front of advancing injury leading to a reduction in acid secretion and eventual loss of parietal cells and development of atrophy. Sub-typing intestinal metaplasia has no clinical value to the patient, the pathologist, or the endoscopist. The pattern, extent, and severity of atrophy, with or without intestinal metaplasia, is a far more important predictor than is intestinal metaplasia subtype. The challenge remains to identify a reliable marker that relates to pre-malignant potential.

Figure 1

Duodenal ulcer and gastric ulcer represent two ends of one disease “H pylori infection”. Unlike gastric ulcer patients, duodenal ulcer patients have a long lag period before developing gastric atrophy. Disease progression is dependent on H pylori infection (cured/uncured) and other environmental factors such that in some countries DU would be considered protective against the development of gastric carcinoma.

Figure 2

The diagnosis of pseudopyloric metaplasia can be facilitated by using pepsinogen I immunostain. Pepsinogen I (PG I) is localized in chief cells, mucous-neck cells and transitional mucous-neck/chief cells of the human fundic mucosa[78] and is negative in antral gland cells.