Chronic Gastritis

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Chronic gastritis is chronic inflammation of the gastric mucosa eventually leading to atrophy (chronic atrophic gastritis).

a. Fundic type (type A) chronic gastritis is an autoimmune atrophic gastritis that involves the body and the fundus. It is due to auto antibodies directed against parietal cells and/or intrinsic factor. This leads to loss of parietal cells, decreased acid secretion, increased serum gastrin (G-cell hyperplasia), and pernicious anemia (megaloblastic anemia due to lack of intrinsic factor and B12 malabsorption).

  • Pathologically, there is grossly a loss of rugal folds in the body and fundus.
  • Microscopically, fundic type chronic gastritis is characterized by mucosa atrophy with loss of glands and parietal cells, chronic lympho plasmacytic inflammation, intestinal metaplasia, and increased risk of gastric carcinoma.

b. Antral type (type B) chronic gastritis (also called Helicobacter pylori gastritis) is the most common form of chronic gastritis in the United States.

  • Pathologically,  Helicobacter pylori organisms are involved which are curved, gram-negative rods that produce urease. The risk of infection increases with age, and infection is associated with chronic gastritis (type B), duodenal and gastric peptic ulcers, and gastric carcinoma.
  • Microscopically, H. pylori organisms are visible in the mucous layer of the surface epithelium. Other microscopic features include foci of acute inflammation, chronic inflammation with lymphoid follicles, and intestinal metaplasia.
  • Antral-type chronic gastritits predisposes for gastric carcinoma.
CLINICAL CO-RELATE The ability of H. pylori to produce urease is clinically used for detection by the [13C]-urea breath test and clofazimine (CLO) tests. Other methods of detection include biopsy (Histologic identification is the gold standard) and serology
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