Gastritis

Inflammation of the gastric mucosa.

Gastritis can be classified based on the severity of mucosal injury, the site of involvement, or the inflammatory cell type. No classification scheme matches perfectly with the pathophysiology, and a large degree of overlap exists.

Erosive (hemorrhagic) gastritis: This type of gastritis may be caused by use of nonsteroidal anti-inflammatory drugs (NSAIDs), alcohol, ingestion of a corrosive, trauma, radiation therapy, ischemia, bile acids (due to reflux from the duodenum), congestive gastropathy, or sporadic idiopathic gastritis. The diagnosis is usually based on endoscopic appearance. Biopsy is not usually required, except to eliminate the possibility of infection in an immunocompromised patient or to rule out specific gastritis if it is suspected.

Nonerosive (chronic) gastritis: This type of gastritis has four major patterns. It is a histologic diagnosis that cannot be predicted by endoscopic appearance.

Antral gland gastritis (type B) is the most common pattern; it is associated with Helicobacter pylori and duodenal ulcers. In some persons, chronic superficial antral gland gastritis associated with H. pylori progresses to multifocal atrophic gastritis. However, the mechanism by which gastric atrophy occurs is unclear and is probably multifactorial. As the atrophy progresses, the presence of H. pylori decreases, possibly because hypochlorhydria creates an environment that is not conducive to the bacteria.

Fundic (oxyntic) gland gastritis (type A) can be associated with diffuse severe mucosal atrophy and pernicious anemia. Diffuse severe atrophic fundic gland gastritis primarily affects elderly patients, who develop achlorhydria, but with a residual ability to absorb vitamin B₁₂. Patients with pernicious anemia generally have antibodies against parietal cells (90%) and intrinsic factor (60%). Antiparietal cell antibodies also occur in 50% of patients with gastric atrophy without pernicious anemia (but without anti-intrinsic factor antibodies) and in 10 to 15% of normal persons.

In pangastritis (coexisting antral gland gastritis and fundic gland gastritis), the fundic gland gastritis is characterized by less severe inflammation than the antral gland gastritis. Pangastritis can result in extensive mucous gland (pseudopyloric) metaplasia and varying amounts of intestinal metaplasia. Nests of parietal cells commonly occur, even in the presence of achlorhydria.

Multifocal atrophic gastritis, which appears to begin near the incisura and extends proximally and distally, is commonly associated with intestinal metaplasia.

Specific (distinctive) gastritis: Specific gastritis may be caused by infections, Crohn's disease, eosinophilia, systemic disorders (eg, sarcoidosis), or physical agents (immunosuppressants, some chemotherapeutic agents [eg, 5-fluorouracil], radiotherapy). Distinctive histologic and sometimes endoscopic features allow a diagnosis or markedly narrow the differential diagnosis.

Treatment

Treatment should be directed at the underlying cause. Factors identified as contributing to the inflammatory process should be eliminated, if possible. Acid neutralization and suppression (with antacids, sucralfate, H₂ blockers, proton pump inhibitors) may be helpful.