Cargando…

Incidence and prevalence of gastric neuroendocrine tumors in patients with chronic atrophic autoimmune gastritis

BACKGROUND: The incidence of type I gastric neuroendocrine neoplasms (gNENs) has increased significantly over the past 50 years. Although autoimmune gastritis (AIG) increases the likelihood of developing gNENs, the exact incidence and prevalence of this association remain unclear. AIM: To evaluate t...

Descripción completa

Detalles Bibliográficos
Autores principales: Massironi, Sara, Gallo, Camilla, Elvevi, Alessandra, Stegagnini, Marta, Coltro, Lorenzo Andrea, Invernizzi, Pietro
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Baishideng Publishing Group Inc 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10473929/
https://www.ncbi.nlm.nih.gov/pubmed/37663936
http://dx.doi.org/10.4251/wjgo.v15.i8.1451
Descripción
Sumario:BACKGROUND: The incidence of type I gastric neuroendocrine neoplasms (gNENs) has increased significantly over the past 50 years. Although autoimmune gastritis (AIG) increases the likelihood of developing gNENs, the exact incidence and prevalence of this association remain unclear. AIM: To evaluate the incidence and prevalence of type I gNENs in a cohort of patients with a histological diagnosis of AIG. METHODS: Patients with a histological diagnosis of AIG were enrolled between October 2020 and May 2022. Circulating levels of CgA and gastrin were assessed at enrollment. Included patients underwent regular endoscopic follow-up to detect gastric neoplastic lesions, enterochromaffin-like (ECL) cell hyperplasia, and the development of gNEN. RESULTS: We included 176 patients [142 women (80.7%), median age 64 years, interquartile range (IQR) 53–71 years] diagnosed with AIG between January 1990 and June 2022. At enrollment. One hundred and sixteen patients (65.9%) had ECL hyperplasia, of whom, 29.5% had simple/linear, 30.7% had micronodular, and 5.7% had macronodular type. The median follow-up time was 5 (3–7.5) years. After 1032 person-years, 33 patients developed a total of 50 type I gNENs, with an incidence rate of 0.057 person-years, corresponding to an annual cumulative incidence of 5.7%. Circulating CgA levels did not significantly differ between AIG patients who developed gNENs and those who did not. Conversely, gastrin levels were significantly higher in AIG patients who developed gNENs [median 992 pg/mL IQR = 449–1500 vs 688 pg/mL IQR = 423–1200, P = 0.03]. Calculated gastrin sensitivity and specificity were 90.9% and 1.4%, respectively, with an overall diagnostic accuracy of 30% and a calculated area under the gastrin receiver operating characteristic curve (AUROC or AUC) of 0.53. CONCLUSION: Type I gNENs are a significant complication in AIG. Gastrin’s low diagnostic accuracy prevents it from serving as a marker for early diagnosis. Effective strategies for early detection and treatment are needed.