Chronic Autoimmune Gastritis: Modern Diagnostic Principles

Abstract

This article summarizes and systematizes the available data from the literature on chronic autoimmune gastritis (CAG) in order to increase the awareness of specialists about the modern possibilities for diagnosing the disease, including its early stages. The clinical manifestation of the disease includes possible variants such as gastrointestinal, hematological (first of all, the formation of iron deficiency and B12-deficiency anemia), and neurological variants. Patients with chronic autoimmune gastritis are characterized by comorbidity with other autoimmune diseases. In this paper, data on the most informative serological markers for the diagnosis of CAG, as well as laboratory tests to detect micronutrient deficiencies, information on the characteristic changes in the gastric mucosa, and the prognosis of the disease, are presented. The diagnosis of CAG should be based on a multidisciplinary approach that combines a thorough analysis of a patient's complaints with a mandatory assessment of nutritional status, as well as the results of serological, endoscopic, and histological research methods.

Keywords: atrophic gastritis; chronic autoimmune gastritis; gastric adenocarcinoma; megaloblastic anemia; neuroendocrine tumors; nutritional status; vitamin B12 deficiency.

Figure 1

Autoimmune gastritis: initial stage. Biopsy from the gastric body. Lymphoplasmacytic inflammatory infiltration of the lamina propria with damage to the fundic glands. Hematoxylin and eosin stain. ×200 (from the personal archive of Professor S.I. Mozgovoi).

Figure 2

Autoimmune gastritis. Biopsy from the gastric body. Severe pseudopyloric metaplasia with the appearance of mucus-producing cells in place of the fundic glands (cytoplasm magenta staining). Periodic acid-Schiff stain. ×200 (from the personal archive of Professor S.I. Mozgovoi).

Figure 3

Autoimmune gastritis. Biopsy from the gastric body. Severe intestinal metaplasia (type I, complete), with intestinalization of gastric mucosa and villous transformation with absorptive and goblet cells; Paneth cells with acidophilic granular cytoplasm are presented at the base of the glands. Hematoxylin and eosin stain. ×200 (from the personal archive of Professor S.I. Mozgovoi).

Figure 4

Autoimmune gastritis. Biopsy from the gastric body. Marked pseudopyloric metaplasia. Signs of linear and micronodular hyperplasia of neuroendocrine cells. Immunohistochemical reaction with antibodies to chromogranin A. ×200 (from the personal archive of Professor S.I. Mozgovoi).

Figure 5

Autoimmune gastritis. Biopsy from the gastric body. Severe atrophy of the glands with pseudopyloric metaplasia. Adenomatous hyperplasia of neuroendocrine cells with the presence of cluster aggregates. Immunohistochemical reaction with antibodies to chromogranin A. ×100 (from the personal archive of Professor S.I. Mozgovoi).