Reviewers: Elliot Weisenberg, M.D. (see Reviewers page)
Revised: 4 August 2012, last major update August 2012
Copyright: (c) 2003-2012, PathologyOutlines.com, Inc.
● Chronic mucosal inflammatory changes leading to mucosal atrophy and epithelial metaplasia, usually without erosions
● Most cases are type B or non-autoimmune gastritis
● Associated with chronic Helicobacter pylori infection (Am J Surg Pathol 2006;30:242), toxins (alcohol, tobacco), reflux of bilious duodenal secretions (post-antrectomy or other), obstruction (bezoars, atony), radiation
● Incidence increases with age; in Europe/Japan, affects 50% at age 60+
● Histology does not correlate well with symptoms
Superficial chronic gastritis:
● Inflammation confined largely to mucosa occupied by gastric pits
● Plasma cells, lymphocytes, occasional lymphoid follicles
● May have eosinophils and neutrophils also
● May have reduced cytoplasmic mucin, reactive epithelial changes (nuclear and nucleolar enlargement)
● May have subnuclear vacuolation in antral glands or pits (PAS negative), probably represents degenerative response to cell injury
● Intestinal metaplasia: affects antral and body/fundic mucosa, with partial replacement by metaplastic goblet cells of intestinal morphology, absorptive cells and Paneth cells; extensive if involves 25% of biopsy tissue
● Immunophenotypically distinct from intestinal metaplasia of GE junction or Barrett’s esophagus (Am J Surg Pathol 2001;25:87)
● Complete intestinal metaplasia: mucosal pattern resembles small bowel epithelium with goblet and absorptive cells, villi and crypts; sialomucins predominate
● Incomplete intestinal metaplasia: no absorptive cells, columnar cells resemble gastric foveolar cells; neutral mucins and sulfomucins are present
Enterochromaffin cell hyperplasia
End of Stomach > Gastritis > Chronic gastritis
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