Noémi Zádori1, Dávid Németh2, Lajos Szakó3, Szilárd Váncsa4, Nóra Vörhendi5, Zsolt Szakács6, Levente Frim7, Péter Hegyi8, Jozsef Czimmer9. 1. Institute for Translational Medicine, Medical School, University of Pécs, Pécs; János Szentágothai Research Centre, University of Pécs, Pécs, Hungary. . znoeemi@gmail.com. 2. Institute for Translational Medicine, Medical School, University of Pécs, Pécs, Hungary. davidsum96@gmail.com. 3. Institute for Translational Medicine, Medical School, University of Pécs, Pécs; János Szentágothai Research Centre, University of Pécs, Pécs, Hungary. szaklaj@gmail.com. 4. Institute for Translational Medicine, Medical School, University of Pécs, Pécs; János Szentágothai Research Centre, University of Pécs, Pécs, Hungary. vancsaszilard@gmail.com. 5. Institute for Translational Medicine, Medical School, University of Pécs, Pécs; János Szentágothai Research Centre, University of Pécs, Pécs, Hungary. vorinocci@gmail.com. 6. Institute for Translational Medicine, Medical School, University of Pécs, Pécs; First Department of Internal Medicine, University of Pécs, Medical School, Pécs, Hungary. szaki92@gmail.com. 7. Institute for Translational Medicine, Medical School, University of Pécs, Pécs, Hungary. levi.frim@gmail.com. 8. Institute for Translational Medicine, Medical School, University of Pécs, Pécs; János Szentágothai Research Centre, University of Pécs, Pécs; Centre for Translational Medicine, Semmelweis University, Budapest; Division of Pancreatic Diseases, Heart and Vascular Center, Semmelweis University, Budapest, Hungary. p.hegyi@tm-centre.org. 9. nstitute for Translational Medicine, Medical School, University of Pécs, Pécs; Division of Gastroenterology, First Department of Internal Medicine, Medical School, University of Pécs, Pécs, Hungary. czimmer.jozsef@pte.hu.
Abstract
BACKGROUND AND AIMS: The underlying aetiology of chronic gastritis (CG) often remains unknown due to its underrated significance in clinical practice. However, the role of chronic inflammation of the stomach in the development of atrophy, intestinal metaplasia (IM) and eventually of gastric cancer is well documented. We aimed to explore the possible aetiological factors of CG, determine the prevalence of systemic autoimmune disorders in patients with CG of unknown aetiology, and clarify the role of autoantibodies in the development of precancerous lesions in the stomach. METHODS: This is a retrospective, cross-sectional study, conducted from January 2016 to January 2020, including data from 175 patients with CG. Exclusion criteria were: (1) acute gastritis; (2) reactive gastropathy; (3) gastric cancer; (4) subjects without any serology testing results; and (5) Helicobacter pylori positivity. The primary endpoint was a composite endpoint involving gastric atrophy and IM. RESULTS: Fifty-five per cent of patients with CG had autoantibodies. Systemic lupus erythematosus (SLE)-related antibodies were positive in most of the cases, including antinuclear antibody (ANA) positivity, which was found in 19.13% of the patients. Autoimmune positivity was shown to be associated with precancerous lesions in the stomach (p<0.001): IM, atrophy and IM with atrophy. Anti-parietal cell antibody positivity seems to be a significant risk factor for IM and IM with atrophy. Autoimmune thyroiditis-related antibodies and ANA positivity by itself were only associated with atrophy; SLE-related antibodies and inflammatory bowel diseases related antibodies (ASCA and ANCA) correlated either with IM or with atrophy. No significant relation was found between any other investigated autoimmune disease-related antibodies and precancerous lesions. CONCLUSIONS: Autoimmune positivity often underlies gastritis of unknown aetiology and predisposes to precancerous lesions in the stomach. These antibodies can serve as non-invasive markers for the of optimal timing of an endoscopic follow-up strategy. Furthermore, CG can be an early symptom of a systemic autoimmune disorder.
BACKGROUND AND AIMS: The underlying aetiology of chronic gastritis (CG) often remains unknown due to its underrated significance in clinical practice. However, the role of chronic inflammation of the stomach in the development of atrophy, intestinal metaplasia (IM) and eventually of gastric cancer is well documented. We aimed to explore the possible aetiological factors of CG, determine the prevalence of systemic autoimmune disorders in patients with CG of unknown aetiology, and clarify the role of autoantibodies in the development of precancerous lesions in the stomach. METHODS: This is a retrospective, cross-sectional study, conducted from January 2016 to January 2020, including data from 175 patients with CG. Exclusion criteria were: (1) acute gastritis; (2) reactive gastropathy; (3) gastric cancer; (4) subjects without any serology testing results; and (5) Helicobacter pylori positivity. The primary endpoint was a composite endpoint involving gastric atrophy and IM. RESULTS: Fifty-five per cent of patients with CG had autoantibodies. Systemic lupus erythematosus (SLE)-related antibodies were positive in most of the cases, including antinuclear antibody (ANA) positivity, which was found in 19.13% of the patients. Autoimmune positivity was shown to be associated with precancerous lesions in the stomach (p<0.001): IM, atrophy and IM with atrophy. Anti-parietal cell antibody positivity seems to be a significant risk factor for IM and IM with atrophy. Autoimmune thyroiditis-related antibodies and ANA positivity by itself were only associated with atrophy; SLE-related antibodies and inflammatory bowel diseases related antibodies (ASCA and ANCA) correlated either with IM or with atrophy. No significant relation was found between any other investigated autoimmune disease-related antibodies and precancerous lesions. CONCLUSIONS: Autoimmune positivity often underlies gastritis of unknown aetiology and predisposes to precancerous lesions in the stomach. These antibodies can serve as non-invasive markers for the of optimal timing of an endoscopic follow-up strategy. Furthermore, CG can be an early symptom of a systemic autoimmune disorder.
Authors: Noémi Zádori; Dávid Németh; Levente Frim; Nóra Vörhendi; Lajos Szakó; Szilárd Váncsa; Péter Hegyi; József Czimmer Journal: Int J Gen Med Date: 2022-10-12