Gastric Intestinal Metaplasia (GIM)
Interpretation, risk stratification, management & point-of-care decision algorithm — AGA, ESGE, BSG Guidelines
Sections
Pathogenesis & Correa Cascade
Gastric intestinal metaplasia (GIM) is the replacement of normal gastric mucosa by intestinal-type epithelium in response to chronic gastric inflammation. It is a premalignant condition that sits within the Correa cascade — the stepwise progression toward gastric adenocarcinoma.
The Correa Cascade
• Prevalence: 5–15% of patients undergoing EGD in Western populations
• Up to 40%+ in high-risk ethnic groups (East Asian, Hispanic, African American)
• Baseline annual cancer risk: 0.16%/year (~1.6% at 10 years)
• H. pylori accounts for >90% of cases
H. pylori-associated (EMAG): Begins at incisura, spreads proximally. All gastric epithelium at risk. Antibodies to H. pylori. Variable gastrin. Associated with MALToma/adenocarcinoma.
Autoimmune (AMAG): Corpus-predominant, antrum sparing. Anti-parietal cell & anti-intrinsic factor antibodies. Elevated gastrin. B12 deficiency. Associated with type 1 gastric NETs.
Clinical Pearl
GIM on histology almost invariably implies underlying atrophic gastritis — even when not explicitly noted on the pathology report. A diagnosis of GIM should always prompt a coordinated assessment of extent and severity.