Autoimmune metaplastic atrophic gastritis and association with neuroendocrine tumors of the stomach a study of patients at a large tertiary medical center

Autoimmune gastritis (AIG), a chronic inflammatory condition characterized by the immune-mediated destruction of gastric parietal cells, leads to atrophic gastritis predominantly in the gastric fundus and body. This condition is associated with an increased risk of gastric neuroendocrine neoplasms (g-NENs), a heterogeneous group of tumors arising from enterochromaffin-like cells. Understanding the link between AIG and g-NENs is crucial for early detection, management, and improving patient outcomes. AIG is often asymptomatic but can lead to vitamin B12 deficiency, iron deficiency anemia, and gastric neuroendocrine tumors (NETs). g-NENs, although rare, present a significant risk due to their potential for malignancy. The pathogenesis involves chronic hypergastrinemia, stimulating neuroendocrine cell proliferation. Early detection and differentiation from other gastric pathologies are essential for effective management. This study aimed to investigate the clinical, biochemical, and histological characteristics of patients with AIG and explore the association between AIG and the development of g-NENs, focusing on identifying potential predictive biomarkers and risk factors for g-NENs in this patient population. Methods: Conducting a retrospective analysis on a prospectively collected database from Molinette Hospital, Turin, between September 1996 and September 2022, the study encompassed patients with confirmed AIG diagnoses. It assessed clinical data, biometric data, laboratory findings, and histological examination results. The study analyzed serum gastrin levels, chromogranin A levels, the presence of autoantibodies, and histological features of atrophic gastritis and g-NENs. The study identified 62 patients with AIG, highlighting a female predominance and a high prevalence of concomitant autoimmune disorders. Elevated serum gastrin levels were significantly associated with the presence of g-NENs, suggesting its role as a potential biomarker for early detection. Additionally, the borderline significance of focal carcinoid cell hyperplasia suggests a potential trend toward an association between this histological feature and the development of g-NENs. Histological findings emphasized the importance of atrophic gastritis, intestinal metaplasia, and ECL cell hyperplasia in the context of AIG and g-NENs. To summarize, the study shed light on the significant association between AIG and the development of g-NENs, it advocates for a biomarker-driven approach in the surveillance of AIG patients to facilitate early detection and intervention for g-NENs, potentially improving patient outcomes. Further research is necessary to explore the molecular mechanisms underlying this association and to validate the use of gastrin and focal carcinoid hyperplasia as a predictive biomarker for g-NEN development in AIG patients.