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Dictionary The Gastrointestinal System

Gastritis

Synonyms :  

Clinical features, Diagnosis, Management, Prognosis,

Clinical features:  < BACK TO TOP >

Chronic Gastritis

Chronic gastritis is characterised by the presence of chronic mucosal inflammatory changes leading eventually to mucosal atrophy (thinning) and epithelial intestinal metaplasia (conversion of gastric epithelium into the intestinal one which is presumably more resistant to stress). The two forms of chronic gastritis are described: autoimmune chronic atrophic gastritis (type A) and environmental H. pylori gastritis (type B).

1. Type A gastritis is the less common form of chronic gastritis that characteristically involves the fundus and body of the stomach, with relative sparing of the antrum. Antibodies to parietal cells and intrinsic factor can usually be identified, suggesting the autoimmune pathogenesis. The resultant destruction and mucosal atrophy may lead to decreased gastric acid and intrinsic factor production. Insufficient amounts of intrinsic factor are responsible for malabsorption of vitamin B12, with resulting haematologic and/or neurologic consequences characteristic of pernicious anaemia.

2. Type B gastritis is more common and it principally involves the antrum, especially in younger patients. In older patients after 15-20 years of long-standing chronic gastritis, the entire stomach is usually affected. The prevalence of this type of chronic gastritis increases with age, reaching 80% in individuals over age 50 and virtually 100% after age 70! It has been confirmed that H. pylori is the agent responsible for type B gastritis and that eradication of H. pylori leads to resolution of the histologic findings. In general, the degree of histologic abnormality correlates with the number of organisms. Epithelial metaplasia found in the later stages of chronic gastritis seems to be linked to gastric carcinoma. In other words, H. pylori infection appears to be an important risk factor for gastric carcinoma (however, not all patients with gastric carcinoma are infected with H. pylori). And finally, H. pylori-induced proliferation of lymphoid tissue within the gastric mucosa has been implicated as a precursor of gastric lymphoma.

  • Chronic gastritis usually causes few or no symptoms; upper abdominal discomfort, heaviness, bloating, anorexia, nausea and occasionally vomiting can occur.
  • When severe parietal cell loss occurs, especially in the setting of autoimmune gastritis, hypochlorhydria or achlorhydria (referring to levels of gastric hydrochloric acid) are characteristically present, leading to incomplete digestion and malabsorption.
  • Also in autoimmune gastritis other features of pernicious anaemia can occur (megaloblastic anaemia, peripheral neuropathy with sensory symptoms, muscle weakness, even dementia).
  • Most important is the relationship of chronic H. pylori gastritis to the development of peptic ulcer (most patients with peptic ulcer, whether duodenal or gastric, have H. pylori infection).

Diagnosis:  < BACK TO TOP >

  • Gastroscopy followed by biopsy is the only reliable means for identification and classification of chronic gastritis.
  • H. pylori is detected using the tests described in section about peptic ulcer.
  • Blood analysis can be useful for cases of pernicious anaemia when low count of abnormally large erythrocytes, together with reduced haemoglobin concentration, is the most striking abnormality.

Management  < BACK TO TOP >

  • Treatment procedures are still a matter of intensive discussion.
  • It is clear that pernicious anaemia requires lifelong regular parenteral vitamin B12 administration.
  • Symptomatic patients could qualify for anti-Helicobacter treatment.
  • The role of this treatment is still controversial in asymptomatic patients, and at this stage it is not clear whether and to what extent early eradication of H. pylori actually decreases risk for gastric carcinoma and lymphoma (it decreases risk for peptic ulcer though). At the same time some observations indicate that eradication of H. pylori increases risk for gastro-oesophageal reflux disease and adenocarcinoma of the oesophagus.

Prognosis  < BACK TO TOP >

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