Clinical suspicion arises with symptoms of epigastric pain and tenderness.
Diagnosis and classification into types is made by endoscopy coupled with biopsy.
Acute erosive gastritis
Infiltration of the lamina propria with inflammatory cells accompanied by superficial erosions that may be diffuse or localized.
Unlike ulcers erosions are superficial breaks that do not extend deeper than the mucosa itself.
Conservative measures + antacids and H2 receptor antagonists
- If the disease is localized, it may be amenable to endoscopic therapy.
- If diffuse vasopressin may be given iv or intra-arterially.
Chronic nonerosive gastritis
There are three pathological stages of mucosal damage
- Chronic superficial gastritis with lymphocyte and plasma cell infiltration of the superficial mucosa
- Atrophic gastritis with the development of deeper inflammation, loss of parietal and chief cells and occasionally intestinal metaplasia.
- Gastric atrophy with little evidence of inflammation but with thinning of the mucosa, loss of gastric glands and intestinal metaplasia which may be premalignant.
Type A (fundal gastritis)
Type A is usually due to autoimmune and affects the fundus and body. It is associated with circulating antibodies to parietal cells and intrinsic factor. It is seen in pernicious anemia, thyroid disease and diabetes. Maybe associated atrophy.
Associated with decreased basal acid secretion and hypergastrinemia + decreased intrinsic factor secretion.
No specific therapy exists, symptomatic.
Type B (antral)
Not associated with atrophic gastritis; however, it is associated with both peptic ulcer and Helicobacter pylori.
Treatment depends on the eradication of Helicobacter pylori infection and symptomatic therapy.