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Progression From Antral G-Cell Hyperplasia to Gastric Neuroendocrine Tumor in a Patient With Autoimmune Gastritis

Autoimmune metaplastic atrophic gastritis is caused by immune-mediated destruction of gastric parietal cells. This leads to the absence of gastric acid production, which causes compensatory hyperplasia of gastric antral G-cells leading to hypergastrinemia. The excess gastrin binds to enterochromaffi...

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Detalles Bibliográficos
Autores principales: Brown, Patrick, Tetali, Bhavana, Suresh, Suraj, Varma, Adarsh
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wolters Kluwer 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8386912/
https://www.ncbi.nlm.nih.gov/pubmed/34476276
http://dx.doi.org/10.14309/crj.0000000000000649
Descripción
Sumario:Autoimmune metaplastic atrophic gastritis is caused by immune-mediated destruction of gastric parietal cells. This leads to the absence of gastric acid production, which causes compensatory hyperplasia of gastric antral G-cells leading to hypergastrinemia. The excess gastrin binds to enterochromaffin-like cells causing hyperplasia, which may progress to dysplasia and rarely to gastric neuroendocrine tumors. We present a rare case of autoimmune metaplastic atrophic gastritis associated with G-cell hyperplasia showing the full developmental spectrum of enterochromaffin-like cell proliferation from hyperplasia to dysplasia to neuroendocrine tumor.