Complications of gastritis

Complications of acute gastritis

The most frequent and favorable outcome of acute gastritis (especially catarrhal) is complete restitution—the restoration of the normal mucosal structure. However, in deep lesions, such as necrotic (corrosive) or acute ulcerative gastritis, severe consequences develop:

• Bleeding. It arises from eroded (pathologically destroyed) vessels of the submucosal layer.
• Perforation. Perforation of the gastric wall with the release of contents into the abdominal cavity causes severe peritonitis.
• Cicatricial strictures. A characteristic long-term outcome of deep chemical burns in corrosive gastritis, leading to narrowing and deformation of the organ.
• Chrozinization (transition to chronic form). The transition to a chronic form occurs with the persistence of the damaging factor (e.g., infection or regular intake of nonsteroidal anti-inflammatory drugs).

Peptic ulcer disease and bleeding

The ulcer phenotype of Helicobacter pylori-associated gastritis triggers a pathological chain: antral gastritis → hypergastrinemia → hydrochloric acid hypersecretion. This results in a high risk of duodenal or gastric ulcers.

The complicated course of an ulcer manifests as erosive bleeding (due to necrosis of large vessel walls in scar tissue) and perforation (when fibrinoid necrosis penetrates all the way to the serosa).

Clinical presentation of acute blood loss:

1. Sudden relief of epigastric pain (due to the buffering effect of the shed blood).
2. Sharp weakness, pallor of the skin, and dizziness.
3. Vomiting of blood (hematemesis).
4. Melena — foul-smelling black stools.

Pre-hospital care: the patient must be placed in a horizontal position, and the airway must be controlled to prevent aspiration of vomit. Intake of any food and liquid is strictly prohibited.

Oncological complications

Chronic gastritis can develop via a cancer phenotype through the so-called Correa cascade: pangastritis transforms into multifocal atrophy, followed by hypochlorhydria, intestinal metaplasia, and finally invasive adenocarcinoma. Atrophic gastritis of the gastric body is a proven predictor of cancer. An important nuance: an ulcer detected against the background of atrophic pangastritis is highly likely an ulcerated cancer.

A specific complication is gastric MALT lymphoma. The pathogenesis is associated with T-lymphocytes (bearing CD40) sensitized to H. pylori. They stimulate the proliferation of B-lymphocytes, which accumulate genetic abnormalities, in particular the translocation t(11,18)(q21;q21).

Morphologically, the process manifests as diffuse infiltration of the lamina propria by centrocyte-like cells. A pathognomonic sign of the lymphoma is lymphoepithelial lesions (complexes), in which lymphocytes literally destroy the gland epithelium and basement membrane. Eradication of H. pylori can halt tumor progression.

Pernicious anemia and barrier dysfunction

Vitamin B12 deficiency (pernicious) anemia is a classic complication of chronic autoimmune gastritis (type A). The pathogenesis is based on the production of autoantibodies against gastric cells or intrinsic factor (gastromucoprotein), which leads to severe atrophy and the inability to absorb vitamin B12.

Three types of antibodies are distinguished:

• Canalicular antibodies against parietal cells (found in 90% of patients).
• Blocking antibodies (in 60%) — prevent the formation of the "B12 - intrinsic factor" complex.
• Binding antibodies (in 50%) — prevent the already formed complex from attaching to receptors in the ileum.

Such gastritis is often associated with other autoimmune pathologies: thyroiditis, Addison's disease, and type 1 diabetes mellitus. Additionally, chronic inflammation impairs the mucosal barrier function (permeability increases, which is proven by sucrose tests), contributing to further tissue destruction.

Class and exam questions

What else to study on this topic

• Mechanisms of the Correa cascade formation and the OLGA atrophy staging system
• Pathogenesis of lymphoepithelial complex formation in MALT lymphoma
• Differential diagnosis of peptic ulcer disease and ulcerated gastric cancer
• The role of T-lymphocytes and the CD40 molecule in the progression of HP-associated lymphoma
• Gastric mucosal permeability tests (sucrose test)

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.