Atrophic Gastritis and Autoimmunity: Results from a Prospective, Multicenter Study
Malgorzata Osmola,
Caroline Hemont,
Nicolas Chapelle,
Marie-Anne Vibet,
David Tougeron,
Driffa Moussata,
Dominique Lamarque,
Edith Bigot-Corbel,
Damien Masson,
Justine Blin,
Maxime Leroy,
Regis Josien,
Jean-François Mosnier,
Jérôme Martin,
Tamara Matysiak-Budnik
Affiliations
Malgorzata Osmola
Department of Hematology, Transplantation and Internal Medicine, Medical University of Warsaw, 02-097 Warsaw, Poland
Caroline Hemont
Department of Immunology, University Hospital of Nantes, 44093 Nantes, France
Nicolas Chapelle
Institut des Maladies de l’Appareil Digestif (IMAD), Hepato-Gastroenterology & Digestive Oncology, University Hospital of Nantes, Hôtel Dieu, Place Alexis Ricordeau, CEDEX 1, 44093 Nantes, France
Marie-Anne Vibet
Department of Biostatistics, Centre Hospitalier Universitaire de Nantes, 44093 Nantes, France
David Tougeron
Department of Hepato-Gastroenterology, Poitiers University Hospital, University of Poitiers, 86000 Poitiers, France
Driffa Moussata
Department of Hepato-Gastroenterology, University Hospital of Tours, 37044 Tours, France
Dominique Lamarque
Department of Hepato-Gastroenterology, Ambroise-Paré Hospital, AP-HP, Paris Saclay University, University of Versailles Saint-Quentin-en-Yvelines, Institut National de la Santé et de la Recherche Médicale (INSERM), Infection and Inflammation, 91190 Paris, France
Edith Bigot-Corbel
Faculty of Medicine, University of Nantes, 44300 Nantes, France
Damien Masson
Faculty of Medicine, University of Nantes, 44300 Nantes, France
Justine Blin
Faculty of Medicine, University of Nantes, 44300 Nantes, France
Maxime Leroy
Department of Biostatistics, Centre Hospitalier Universitaire de Nantes, 44093 Nantes, France
Regis Josien
Department of Immunology, University Hospital of Nantes, 44093 Nantes, France
Jean-François Mosnier
Faculty of Medicine, University of Nantes, 44300 Nantes, France
Jérôme Martin
Department of Immunology, University Hospital of Nantes, 44093 Nantes, France
Tamara Matysiak-Budnik
Institut des Maladies de l’Appareil Digestif (IMAD), Hepato-Gastroenterology & Digestive Oncology, University Hospital of Nantes, Hôtel Dieu, Place Alexis Ricordeau, CEDEX 1, 44093 Nantes, France
Despite a global decrease, gastric cancer (GC) incidence appears to be increasing recently in young, particularly female, patients. The causal mechanism for this “new” type of GC is unknown, but a role for autoimmunity is suggested. A cascade of gastric precancerous lesions, beginning with chronic atrophic gastritis (CAG), precedes GC. To test the possible existence of autoimmunity in patients with CAG, we aimed to analyze the prevalence of several autoantibodies in patients with CAG as compared to control patients. Sera of 355 patients included in our previous prospective, multicenter study were tested for 19 autoantibodies (anti-nuclear antibodies, ANA, anti-parietal cell antibody, APCA, anti-intrinsic factor antibody, AIFA, and 16 myositis-associated antibodies). The results were compared between CAG patients (n = 154), including autoimmune gastritis patients (AIG, n = 45), non-autoimmune gastritis patients (NAIG, n = 109), and control patients (n = 201). ANA positivity was significantly higher in AIG than in NAIG or control patients (46.7%, 29%, and 27%, respectively, p = 0.04). Female gender was positively associated with ANA positivity (OR 0.51 (0.31–0.81), p = 0.005), while age and H. pylori infection status were not. Myositis-associated antibodies were found in 8.9% of AIG, 5.5% of NAIG, and 4.4% of control patients, without significant differences among the groups (p = 0.8). Higher APCA and AIFA positivity was confirmed in AIG, and was not associated with H. pylori infection, age, or gender in the multivariate analysis. ANA antibodies are significantly more prevalent in AIG than in control patients, but the clinical significance of this finding remains to be established. H. pylori infection does not affect autoantibody seropositivity (ANA, APCA, AIFA). The positivity of myositis-associated antibodies is not increased in patients with CAG as compared to control patients. Overall, our results do not support an overrepresentation of common autoantibodies in patients with CAG.
