Autoimmune gastritis: when the body attacks itself
This form is less common than Helicobacter pylori-induced lesions and often goes hand in hand with other autoimmune diseases (Hashimoto's thyroiditis, hypoparathyroidism, Addison's disease). The pathogenesis is based on the production of two types of autoantibodies.
The first attack parietal cells (binding to the membrane of the intracellular canaliculus), blocking the proton pump — leading to achlorhydria. The second neutralize intrinsic factor, disrupting vitamin B12 absorption and triggering pernicious anemia.
Morphologically, the main blow is taken by the gastric body. Here, the mucosa is densely infiltrated by lymphocytes (including intraepithelial ones), and atrophy develops tens of times faster than in the general population. Meanwhile, the antrum structurally remains unchanged, but in response to the lack of hydrochloric acid, reactive G-cell hyperplasia is triggered within it.
Reactive gastritis: chemical burn of the mucosa
This variant of inflammation is associated with aggressive external factors or impacts from adjacent GI tract segments.
In reflux gastritis, duodenal contents are regurgitated back into the stomach. Bile acids literally dissolve the lipid membranes of the surface epithelium. An important nuance: true reflux gastritis develops only in a gastric stump if the patient has undergone partial resection.
Taking NSAIDs affects the mucosa differently. These drugs inhibit the COX-1 enzyme, which normally ensures regeneration. As a result, the most vulnerable layer — the surface foveolar epithelium — suffers.
Microscopic picture of reactive changes
The main feature of chemical damage is scant inflammatory infiltration and, as a rule, 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 characteristic subnuclear optically clear vacuoles appear in the surface-foveolar epithelium.
- Smooth muscle cells migrate into the lamina propria and interfoveolar zone.
In NSAID-induced gastritis, cell nuclei may enlarge, become hyperchromatic, the nuclear membrane thins, 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 closer to the surface the epithelium appears fully mature. Disruption of cell renewal can eventually lead to foci of intestinal metaplasia, dysplasia, and neoplasia.
Morphological assessment and atrophy criteria
To standardize the diagnosis, a semiquantitative visual analog scale is used (ranging from normal to pronounced changes). Bacterial colonization, activity (neutrophils), chronicity (mononuclear cells), atrophy, and metaplasia are evaluated.
- Chronic inflammation: reliably confirmed if more than 2 plasma cells per high-power field (×400) are visible among mononuclear cells.
- Atrophy: for its assessment, the muscularis mucosae must be included in the biopsy (representative volume). The diagnosis is made if fewer than 3–4 cross-sectioned glands remain in the high-power field (×400), replaced by connective tissue. For a long time, atrophy was considered irreversible, but since the late 1990s, it has been proven that its regression is possible after eradication of the infection.
- Intestinal metaplasia: a reliable marker of atrophy. It can be complete (type I, Paneth cells, goblet cells, and absorptive cells present) and incomplete (type II, one cell type predominates).
Briefly: answers to topical questions
Which classification system is used to grade and stage chronic gastritis based on histological data?
The stage and grade of chronic gastritis are classified using the OLGA prognostic system.
- Stage — an integrative assessment of mucosal atrophy across all regions of the stomach.
- Grade — an assessment of the severity of inflammatory infiltration.
A similar OLGIM system is also used, which is based on the same principles but analyzes intestinal metaplasia instead of atrophy.
What types of mucins and cells are characteristic of incomplete intestinal metaplasia types II and III?
Incomplete intestinal metaplasia type II is characterized by the appearance of goblet cells and the secretion of mixed mucins.
- Cells — goblet mucocytes containing mucus vacuoles of various sizes.
- Mucins — a mixture of sialomucins and sulfomucins (sulfo-mucin secretion is a prognostically unfavorable factor).
Information regarding the characteristics of incomplete intestinal metaplasia type III is not provided in the materials.
By what specific histological features is the activity grade of chronic gastritis assessed?
The activity grade of chronic gastritis is assessed by the presence and severity of neutrophil infiltration.
- Infiltrate localization — neutrophils infiltrate the lamina propria of the mucosa, as well as the surface and pit epithelium.
- Pit abscesses — accumulations of neutrophils directly within the gastric pits.
The number of neutrophils in the mucosa correlates in the vast majority of cases with the degree of Helicobacter pylori colonization.
From which sites of the stomach must biopsies be taken according to the updated Sydney system for adequate diagnosis?
For an adequate diagnosis, at least five biopsies must be taken from three different zones of the stomach.
- Antrum — two biopsies (from the greater and lesser curvature 3 cm from the pylorus).
- Gastric body — two biopsies (midpoint of the greater curvature and 4 cm proximal to the angulus on the lesser curvature).
- Gastric angulus (incisura angularis) — one biopsy (necessary to assess the severity of atrophy).
Additionally, sampling from every visible pathological lesion is mandatory.
To memorize the pathogenesis of autoimmune gastritis: Autoimmune = Antibodies to parietal cells → Achlorhydria → Anemia (pernicious) → Atrophy of the gastric body.
Class and exam questions
Why is the gastric body specifically affected in the autoimmune form?
Because it is precisely within the glands of the gastric body that the bulk of parietal cells, against which autoantibodies are produced, is concentrated.
How to distinguish reparative changes in NSAID-induced gastritis from dysplasia?
The key sign is the presence of a maturation gradient. During regeneration, maximal cellular atypia is observed in the deep parts of the glands, while the surface epithelium remains mature.
What is a reliable histological sign of chronic gastritis?
Detection of more than two plasma cells in a single microscopic field of view at ×400 magnification.
What else to study on this topic
- Visual analog scale for assessing gastritis (semiquantitative gradations)
- Mechanisms of development of intestinal metaplasia and its types
- Helicobacter-associated gastritis: pathogenesis and morphology
- Epithelial dysplasia and neoplasia in chronic inflammation
- Classification of gastritis by presence and topography of atrophy
Master the entire topic in the "Pathological Anatomy" course
This is a summary. The course covers everything tested in classes and exams.
- Complete study guide on "Autoimmune and Reactive Gastritis" and 4,414 more pages of the subject
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 153 video lessons on the subject
Other topics in the «Digestive System Diseases» section
Free video lessons: pathological anatomyShort lessons with study notes — no registration required.
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.