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| Chronic Gastritis |
| Etiology •Two major types of chronic gastritis are recognized •Type A associated with antibodies to gastric parietal cells and CD4 cell mediated immunity to parietal cells. •Type B associated primarily with infection by H.pylori •Miscellaneous causes include: bile reflux of any cause; graft vs. host disease; alcohol; smoking; Crohn's disease (usually considered as separate entity) |
| Pathogenesis •Type A (immunologic) gastritis is associated with a number of humoral autoantibodies against parietal cells, intrinsic factor and vit B12 •However, these antibodies are problably secondary to cell damage caused by a primary CD4-T cell mediated autoimmunity directed against parietal cells •Type B gastritis is most commonly due to infection by H.pylori (see H pylori for details), |
| Epidemiology •Type A chronic gastritis is much less common than Type B and is more prevalent in English speaking and Scandivaian countries. It occurs after the age of 50 and while familial clustering occurs, a specific genetic linkage has not been identified •Type A has a higher frequency of association with other autoimmune diseases such as autoimmune thyroiditis •Type B gastritis is worldwide and has a higher prevalence in third world countries due to its association with H.pylori •Epidemiologic studies have indicated a prevalence of >50% for Type B gastritis over the age of 50yrs. |
| General Gross Description •Type A gastritis affects the fundus and body sparing the antrum •Type B gastritis affects the antrum and involves the body and fundus to a much lesser degree •Both types of gastritis produce erythema due to vascular dilatation with some edema and loss of normal mucosal markings •As cell loss occurs, the mucosa becomes flattened, smooth and thin |
| General Microscopic Description •The hallmark of chronic gastritis is a chronic inflammatory infiltrate of lymphocytes and plasma cells in the lamina propria •Initially this is found superficially but with time involves the full thickness of the mucosa •Periods of active Type B disease are heralded by polys whose number correlate with the degree of activity •The lymphocytic infiltrate may form nodules and occasionally germinal centers are formed and called follicular gastritis •Active disease has congested vessels and microhemorrhages may be seen •Epithelial necrosis occurs in progressive disease with condensation of stroma, and loss of glands leading to thinning of the mucosa •As epithelial necrosis is occurring, regeneration may be seen •In Type A gastritis, the destruction of the parietal cells is a stimulus to G cell hyperplasia in the antrum •A later finding in both types of gastritis is repair by intestinal metaplasia •While goblet cells, Paneth cells and absorptive cells may be seen, the metaplastic epithelium shows biochemical and ultrastuctural differences from normal small intestine •In type B gastritis, H.pylori are never found above metaplastic epithelium •A late development is the development of dysplastic epithelium which shows cells with increased N/C ratio, increased nuclear chromatin, loss of cellular polarity, and abnormal nuclear shape |
| Clinical Correlation •Chronic gastritis is usually separated from acute gastritis •However, chronic gastritis should be viewed as a disease with episodes of acute activity superimposed on periods of clinical and histologic quiescence •Chronic active gastritis is commonly asymptomatic or may have low grade symptoms such as epigastric discomfort or nausea •The symptoms are more pronounced with development of associated illnesses such peptic ulcer disease, pernicious anemia, gastric outlet obstruction or carcinoma |
| References • Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 770-772 |
| Chronic Gastritis |
| Synopsis by: Martin Nadel. M.D. (T63000M73320)[565] |
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