Atrophic Body Gastritis: A Challenge for the Presumptive Endoscopic and Histologic Diagnosis of Autoimmune Gastritis

Abstract

The diagnosis of glandular atrophy of the gastric mucosa (gastric atrophy) remains a challenge in the areas of gastrointestinal endoscopy and pathology. The importance of an endoscopic suspicion of this regressive tissue change is the possibility of alerting the pathologist to its presence. Patients with gastric atrophy, especially in more advanced stages, are more prone to develop intestinal metaplasia, dysplasia and gastric carcinoma, known as the Correa cascade (Correa, 1984, 1992). The most common type of gastric atrophy is that associated with Helicobacter pylori (H. pylori) infection. In such cases, the glandular atrophy usually occurs in parallel to the course of the inflammatory process that takes place in the gastric antrum (antral gastritis, multifocal gastritis) or in both gastric antrum and body (pangastritis, multifocal gastritis). In contrast, in most cases the chronic atrophic gastritis selective of the gastric body and sparing the antral mucosa is a consequence of an autoimmune inflammatory process. For the purpose of this chapter, the chronic gastritis presenting this histopathological pattern will be called atrophic body gastritis (ABG). Exceptionally, some patients with H. pylori-associated gastritis develop gastric lesions with histological pattern very similar to that of ABG which can lead to uncertainty about the differential histologic diagnosis with chronic gastritis of autoimmune origin. Therefore, the two most important inflammatory diseases of the gastric mucosa, multifocal chronic gastritis and autoimmune gastritis, tend to progress to glandular atrophy of the gastric mucosa. In the first case, gastric atrophy may not occur or it develops more slowly, becoming conspicuous usually in later stages of life. In the second case, which is also more frequent with advancing age, gastric atrophy progresses more rapidly and may induce severe gastric changes also in the younger age groups. This differential course of the development of gastric atrophy in these two inflammatory diseases of the stomach involves different clinical and pathophysiological consequences. Those associated with H. pylori infection usually do not involve important pathophysiological changes, while the atrophy resulting from autoimmune disease often leads to well-known pathophysiological changes of the gastric mucosa, often culminating in pernicious anemia. Furthermore, the H. pyloridependent glandular atrophy is considered to be a condition predisposing to gastric adenocarcinoma, which has high rates of morbidity and mortality, while the autoimmune-