Differential target of oxidative damage in Helicobacter pylori-related and autoimmune atrophic gastritis: a single-center study

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Introduction Oxidative stress, which characterizes inflammatory and autoimmune diseases, is involved in atrophic gastritis progression. We aimed to compare the presence and patterns of oxidative stress in autoimmune atrophic gastritis (AAG) and multifocal atrophic gastritis (MAG), investigating its role in disease progression and the development of genomic damage. Materials and methods In this study, 120 consecutive patients with atrophic gastritis (70 AAG and 50 MAG) were collected. Serum/plasma dynamic reactive oxygen metabolites (dROM test-spectrophotometry), nitric oxide (NO-ELISA), advanced oxidation protein products (AOPPs—spectrophotometry), tissue levels of cytokines (IL-10 and TNFα–ELISA), and 8-hydroxydeoxyguanosine (8-OHdG) (HPLC-ED) were evaluated. Results No significant differences in dROMs, NO, and AOPP levels were demonstrated between AAG and MAG. In AAG patients, those with early atrophy exhibited higher levels of dROMs compared to those with advanced stages (p = 0.03), and those with early ECL-hyperplasia (ECL-H) exhibited higher dROMs and AOPP levels compared to those with advanced hyperplasia (p = 0.02). 8-OHdG levels were significantly higher in MAG patients than in AAG patients (p = 0.001). A ROC curve showed that patients with low 8-OHdG levels had a very low OR of belonging to the MAG group. A positive linear correlation was observed among serological biomarkers of atrophy and dROMs (p = 0.004). IL-10 was higher in patients with MAG vs. those with AAG (p = 0.008), and it was also higher when patients were sub-grouped according to the OLGA stages (p = 0.01). Conclusion Inflammatory responses and oxidative stress characterize atrophic gastritis, irrespective of etiology. However, a boost in inflammation-induced genomic damage is observed only in MAG, since AAG showed significantly lower 8-OHdG levels. Therefore, oxidative stress seem to play a minor role in the development of carcinoid and gastric cancer in AAG, and this finding may explain the lower risk of tumors in these patients.

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