S1617 Incomplete Intestinal Metaplasia Is Rare in Autoimmune Gastritis

Abstract

Introduction: Incomplete intestinal metaplasia (IM) is reportedly associated with greater risk for gastric cancer (GC). AGA Guidelines recommend including IM type in pathology reports. In a long-term follow-up of a large cohort of patients with Helicobacter-naïve autoimmune atrophic gastritis (AIG), we did not detect any excess risk for CG (Rugge et al. Gut, In press). We hypothesized that if incomplete IM is a reliable harbinger of GC, it should be uncommon in patients with AIG. Methods: We assessed the IM type in biopsies from 377 subjects with IM and one of the following gastric phenotypes: 1) minimal-change gastritis (MCG – 58 subjects); 2) reactive gastropathy (RG – 135 subjects); 3) H. pylori chronic active gastritis (Hp-CAG, 136 subjects); 4) AIG (48 subjects). To minimize inclusion of patients with previous H. pylori infection we used strict criteria for the diagnosis of AIG, (uninflamed antrum without IM; corpus-restricted atrophy; and ECL-cell hyperplasia). All biopsies were reviewed to confirm diagnosis and location and to categorize the type of IM (complete or incomplete). The prevalence of incomplete IM was compared across gastritis groups. Differences were evaluated using odds ratios (OR) and their 95% confidence intervals (95% CI). Results: Table 1 summarizes the prevalence of incomplete IM in the 4 different groups. Compared to subjects with H. pylori-CAG, those with AIG were >4 times less likely to have the incomplete type of IM (OR 0.23; 0.08 – 0.70; P < .01) Conclusion: Compared to subjects with H. pylori gastritis – a condition known to carry a high risk of GC – patients with AIG had a low prevalence of incomplete IM, providing further support to the concept that AIG, in the absence of previous or concurrent Helicobacter infection, is not associated with a high GC risk. Most studies suggesting a GC risk associated with AIG likely included patients from the pre-Helicobacter era, and the cancer risk may have been induced by unrecognized H. pylori infection. Table 1. - Prevalence of incomplete IM in 4 gastric phenotypes Phenotype of the gastric mucosa Total cases Median Age (range) Female (%) Incomplete IM (%) Atrophic autoimmune gastritis 48 68 (40 – 82) 33 (68.8) 4 (8.3) H. pylori gastritis 136 66 (30 – 90) 78 (57.4) 53 (38.2) Reactive gastropathy 135 61 (14 – 96) 86 (63.7) 7 (5.2) Normal 58 59 (7 – 91) 37 (63.8) 0