Autoimmune Gastritis: When the Body Attacks Itself
This form is less common than Helicobacter pylori-induced gastritis and frequently coexists with other autoimmune disorders (Hashimoto thyroiditis, hypoparathyroidism, Addison disease). The pathogenesis is driven by two main types of autoantibodies.
The first type attacks parietal cells (binding to the secretory canaliculus membrane), blocking the proton pump and resulting in achlorhydria. The second type neutralizes intrinsic factor, impairing vitamin B12 absorption and triggering pernicious anemia.
Morphologically, the primary target is the gastric body. The mucosa here is densely infiltrated by lymphocytes (including intraepithelial lymphocytes), and atrophy develops tens of times faster than in the general population. Meanwhile, the antrum remains structurally unchanged, though a reactive G-cell hyperplasia is triggered in response to the lack of hydrochloric acid.
Reactive Gastritis: Chemical Injury to the Mucosa
This inflammatory variant is linked to aggressive exogenous factors or agents from adjacent gastrointestinal segments.
In reflux gastritis, duodenal contents reflux into the stomach. Bile acids literally dissolve the lipid membranes of the superficial epithelial cells. An important caveat: true reflux gastritis develops exclusively in a gastric remnant following partial gastric resection.
NSAIDs damage the mucosa through a different mechanism. These drugs inhibit the COX-1 enzyme, which normally ensures epithelial regeneration. As a result, the most vulnerable layer—the surface foveolar epithelium—suffers.
Microscopic Findings in Reactive Changes
The hallmark of chemical injury is sparse inflammatory infiltration and typically the absence of H. pylori colonization. The tissue attempts to compensate for the damage:
- Foveolar hyperplasia develops (gastric pits become deformed, elongated, and tortuous).
- Mucocytes actively proliferate, and the surface-foveolar epithelium exhibits characteristic subnuclear optically clear vacuoles.
- Smooth muscle cells migrate into the lamina propria and the interfoveolar zone.
In NSAID-induced gastritis, cell nuclei may enlarge and become hyperchromatic, nuclear membranes thin out, and mitoses appear. To distinguish this reparative reaction from a neoplastic process, pathologists look for a maturation gradient: cellular atypia is maximal at the base of the glands, whereas the epithelium near the surface appears fully mature. Impaired cell renewal can eventually lead to foci of intestinal metaplasia, dysplasia, and neoplasia.
Morphological Evaluation and Atrophy Criteria
To standardize the diagnosis, a semiquantitative visual analog scale is used (ranging from normal to marked changes). Bacterial load, activity (neutrophils), chronicity (mononuclear cells), atrophy, and metaplasia are evaluated.
- Chronic inflammation: reliably confirmed when mononuclear infiltrates at ×400 magnification reveal more than 2 plasma cells per high-power field.
- Atrophy: for accurate assessment, the biopsy must include the muscularis mucosae (representative sample). The diagnosis is established if fewer than 3–4 cross-sectioned glands remain per high-power field (×400), replaced by connective tissue. Atrophy was long considered irreversible, but since the late 1990s, it has been proven that regression is possible following eradication of the infection.
- Intestinal metaplasia: a reliable marker of atrophy. It can be complete (Type I, featuring Paneth cells, goblet cells, and absorptive enterocytes) or incomplete (Type II, dominated by a single cell type).