A comparative study of cases of gastric intestinal metaplasia and atrophic gastritis concerning hyperhomocysteinemia and red cell distribution width (RDW)

Purpose: Hyperhomocysteinemia is a recognized independent risk factor for cardiovascular diseases, often linked to vitamin B12 and folate deficiencies. Atrophic gastritis (AG) and gastric intestinal metaplasia (GIM) represent distinct histological patterns of chronic gastric mucosal damage, both implicated in impaired vitamin B12 absorption. This study aimed to evaluate and compare serum homocysteine levels and their relationships with vitamin B12, folate and Red Cell Distribution Width (RDW) in patients diagnosed with GIM, AG, and non-atrophic, non-metaplastic chronic gastritis. Materials and methods: The study enrolled 110 individuals categorized into three groups: GIM (n=46), AG (n=31), and control subjects with chronic gastritis without atrophy or metaplasia (n=33). Biochemical measurements included vitamin B12, folate, RDW and homocysteine. Participants with known cardiovascular risks or vitamin supplementation were excluded to reduce confounding factors. Results: Both GIM (11.49±4.95 μmol/L) and AG (9.37±3.87 μmol/L) groups exhibited significantly elevated homocysteine levels compared to controls (7.03±6.64 μmol/L; p<0.01 and p=0.042, respectively). Vitamin B12 concentrations were considerably lower in GIM (253.88±95.78 pmol/L) and AG (251.83±63.70 pmol/L) patients versus controls (363.69±123.41 pmol/L; p<0.01 for both). Folate levels were significantly diminished in the GIM group compared to controls (p=0.02). RDW showed a slight, non-significant increase in the GIM and AG groups compared to controls (16.11±2.72, 16.23±2.32, 15.17±2.27, respectively; p=0.069). Logistic regression identified male gender and presence of GIM or AG as independent predictors of hyperhomocysteinemia. Conclusion: Similar to AG, GIM is linked to increased serum homocysteine levels likely due to compromised vitamin B12 absorption. These findings highlight GIM as a potential metabolic risk factor for vitamin B12-related abnormalities, especially in patients lacking traditional cardiovascular risk factors.