Gastritis

– An acute or chronic inflammation of the gastric mucosa.

Causes and Incidence

Many factors can cause acute gastritis, including alcohol ingestion; drugs (e.g., aspirin, non-steroidal antiinflammatory agents [NSAIDs], cortico-steroids, cytotoxins, antimetabolites); ingested poisons (e.g., DDT, ammonia, mercury, carbon tetrachloride); ingestion of corrosive agents; trauma; burns; and endotoxins. Chronic gastritis is associated with peptic ulcer disease, renal disease, alcoholic cirrhosis, ulcerative colitis, and diabetes mellitus. Chronic use of NSAIDs, radiation treatments, genetics, diet, prolonged emotional stress, and gastrectomy may also be predisposing factors in chronic gastritis. Type B chronic gastritis is caused by a specific infection with Helicobacter pylori. Gastritis occurs five times more often in those who abuse alcohol than in the general population.

Disease Process

In acute gastritis the stomach mucosa erodes because of hydrochloric acid and one or more predisposing factors, which serve as irritants. The erosions, which are caused by back diffusion of the hydrogen ion and mucosal ischemia, involve the granular layer and lead to submucosal hemorrhage and inflammation. Spontaneous remission occurs if the irritant is removed.

Chronic gastritis begins as an inflammatory infiltration of the lamina propria by plasma cells and leukocytes. The surface epithelial cells become flattened and necrotic in what is labeled the superficial gastritis phase. In the atrophic gastritis phase, the plasma cells and leukocytes also invade the fundic glands and intraglandular spaces, and the glands atrophy as mucous thickness decreases and the muscularis mucosae hypertrophies. Finally, in the gastric atrophy phase, the fundic glands lose the parietal and chief cells as metaplasia occurs, with thinned mucosa and minimum inflammation with marked gland loss. If chronic gastritis involves the fundus, it is labeled type A. If it involves primarily the antrum with some fundic involvement, it is labeled type B.

Symptoms

Acute
Rapid onset of epigastric pain, indigestion, feeling of early fullness, anorexia, weight loss, cramping, nausea, vomiting, hematemesis, melena, general malaise

Chronic
Often asymptomatic; dyspepsia, flatulence, diarrhea, intolerance of spicy and fatty foods, no relief from antacids

Potential Complications

Individuals who have gastric atrophy often develop pernicious anemia. Untreated gastric disease can lead to obstruction, perforation, and peritonitis. Individuals with metaplasia have a higher risk of gastric cancer.

Diagnostic Tests

Clinical evaluation
History of exposure to one or more predisposing factors or agents

Endoscopy with biopsy/cytology
To visualize lesions, erosions, and bleeding sites and to rule out carcinoma

Stool guaiac
Positive

Nasogastric aspiration
Frank blood

Serum gastrin
Elevated in type A chronic gastritis

Intrinsic factor antibodies
Present in type A

Antibodies to gastrin-producing cells
Present in type B

Treatments

Surgery
Partial or total gastrectomy, pyloroplasty, vagotomy for major uncontrollable bleeding associated with acute gastritis.

Drugs
Antacids; histamine receptor antagonists and vasoconstrictors for acute gastritis; vitamins C and B12 in chronic gastritis with accompanying pernicious anemia; antibacterial agents in type B gastritis.

General
Removal of causative agents; ice water lavage to control bleeding; laser therapy by endoscopy; blood transfusions; with acute gastritis: NPO, then bland diet.