Chronic gastritis

Chronic active gastritis consists of an infiltration of the lamina propria with lymphocytes and plasma cells. This can lead to the development of atrophic changes in the mucosa including loss of parietal and chief cells, and subsequent intestinal metaplasia. Helicobacter pylori is the chief cause of chronic active gastritis affecting the antrum and body of the stomach. Other causes include:
AUTOIMMUNE GASTRITIS; affecting the fundus and body of the stomach (pangastritis) resulting in pernicious anaemia. Autoantibodies to gastric parietal cells and intrinsic factors are found in the serum (perniciousanaemia ).
CHRONIC INGESTION OF SAIDs, aspirin  and possibly biliary reflux produces gastritis.


A consistent relationship between upper gut symptoms and histological chronic gastritis has not been established. There may be a subset of patients in whom the gastritis may account for the symptoms. Most chronic gastritis is asymptomatic and requires no treatment. Helicobacter pylori and the upper gastrointestinal tract. This spiral-shaped urease-producing bacterium  is found in the stomach and in areas of gastric metaplasia in the duodenum. H. pylori is found in greatest numbers under the mucus layers in gastric pits in close apposition to gastric epithelial cells. Intrafamilial clustering suggests person-to-person spread, but the exact mode of transmission is unclear. Childhood acquisition of H. pylori is very prevalent in developing countries. There is a clear relationship between the age of acquisition and lower socio-economic status worldwide. A relationship between H. pylori infection and crowded domestic living conditions in childhood has been established.


Initially, H. pylori infection produces acute gastritis which rapidly becomes chronic active gastritis and in some peptic ulcer disease may develop. Long-standing chronic active gastritis leads to atrophy, intestinal metaplasia and increases the risk of gastric carcinoma.
Thus the earlier the H. pylori is acquired, the greater the risk of atrophy and metaplasia.H. pylori is present in a greater proportion of patients with non-ulcer dyspepsia than in asymptomatic controls, but the relationship with symptoms is poor.


1 Invasive endoscopy
(a) Rapid urease test: biopsies are added to a urea solution containing phenol red. If H. pylori is present, the urease enzyme splits the urea to release ammonia which raises the pH of the solution and causes a rapid colour change.
(b) H. pylori can be Gram stained or cultured on special medium and sensitivities to antibodies can be ascertained.
(c) H. pylori can also be detected histologically with routine stained sections.

2 Non-invasive
(a) Urea breath test with 13Cor 14C , but using urea as the substrate). This is a quick and easy way of detecting the presence of H. pylori and is used as a screening test and also to demonstraten eradication of the organism following treatment.
(b) Serum antibodies. Reasonably sensitive and specific serological tests are available and are used mainly for epidemiological studies.


In patients with peptic ulcer disease, it is necessary to eradicate the organism as this leads to a ‘cure’ with very low recurrence of ulceration unless reinfection occurs; this is, however, uncommon. The best regimen for eradication is not yet clear, but all regimens must take into account the following factors:
• A good compliance with treatment regimens is required
• The high incidence of antibiotic resistance to metronidazole (25%+)
• That oral metronidazole, when given, increases the side-effects of treatment
• That bismuth chelate is unpleasant to take even as tablets.
Two regimens are currently used, but these will undoubtedly change over the years:
1 Triple therapy-bismuth chelate, 2 tablets four times daily for 4 weeks, 30 min before a meal, metronidazole 400 mg three times daily for the first week, tetracycline, 500 mg three times daily for the first week.

2 An alternative therapy is omeprazole 40 mg daily, together with amoxycillin, or possibly clarithromycin, 500 mg three times per day for 1-2 weeks. All these treatments give eradication figures of approximately 80%.
Patients with gastritis without peptic ulceration should not be treated, but this is an area which is increasingly changing as more is discovered about the organism and better eradication therapy is found.

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