2021 Volume 63 Issue 12 Pages 2460-2466
A 61-year-old male was referred to our hospital due to anorexia and further evaluation of his gastric lesions. Esophagogastroduodenoscopy (EGD) revealed an erythematous surface polypoid lesion measuring 13-mm in diameter, with a central depression on the anterior wall of the lower body, and multiple submucosal lesions with or without a central depression on the middle to the upper body. EGD also revealed a corpus-dominant advanced gastric atrophy. Endoscopic biopsy specimens of the gastric polypoid lesions revealed a grade 2 gastric neuroendocrine tumor (G-NET).
The serological examination was negative for anti-gastric parietal cell antibodies and intrinsic factor antibodies, and positive for immunoglobulin G antibodies against Helicobacter pylori (HP). The patient’s serum gastrin levels were elevated at 16,030 pg/mL. A computed tomography and positron emission tomography/computed tomography revealed no abnormal lesions.
The patient was diagnosed to have a type ⅠG-NET. He underwent total gastrectomy and lymphadenectomy. Pathological examination of the tumor specimens revealed NET G2 and lymph node metastasis. Moreover, enterochromaffin-like (ECL) cell hyperplasia and endocrine cell micronests were observed in the gastric mucosa around the tumor.
The patient’s HP infection-induced hypergastrinemia. The onset of which has been explained by the gastric mucosal atrophy resulting in low acid output and the production of antibodies. Additionally, cytokines and inflammatory mediators released during chronic inflammation induced by HP infection promoted ECL proliferation. Therefore, HP infection is a risk factor for G-NET, by inducing hypergastrinemia.
This case is of interest because it reports a patient with multiple G-NETs and extreme hypergastrinemia, following type B chronic gastritis due to HP infection. Further studies are necessary to elucidate how HP infection was implicated in the pathogenesis of G-NET.
