The Relationship between Helicobacter pylori Infection and Gastric Carcinoid Tumor Yuichi Sato 1 , Ken Nishikura 2 , Hidenobu Watanabe 2 , Mituya Iwafuchi 3 , Jun-ichi Ueki 4 1he Third Department of Internal Medicine, Niigata University School of Medicine 2The First Department of Pathology, Niigata University School of Medicine 3The Department of Pathology, Niigata University School of Health Science 4Department of Gastroenterology, Niigata Prefectural Central Hospital Keyword: 胃カルチノイド , Helicobacter pylori , 自己免疫性胃炎 , 抗壁細胞抗体 pp.1417-1421
Published Date 2000/10/25
DOI https://doi.org/10.11477/mf.1403104897
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 We divided 11 patients with gastric carcinoid tumor (GCT) into two groups ; parietal cell antibody (PCA) -positive group and PCA-negative group, and compared the serum gastrin level, pepsinogen Ⅰ, Ⅱ, and the histological characteristics in the corpus mucosa in both groups. All the PCA-negative GCT patients were antiHelicobacter pylori (H. pylori ) antibody positive and except for one patient with Type Ⅲ GCT, showed that hypergastrinemia, low pepsinogen I levels and low pepsinogen Ⅰ/Ⅱ ratio were not equal to those in the PCA-positive GCT patients or the patients group with autoimmune gastritis showing Type-A chronic atrophic gastritis. Moreover, the patterns of corpus atrophic gastritis in the PCA-negative GCT patients group mimic those in the PCA-positive GCT patients group. These results suggested that H. pylori infection would induce hypergastrinimia via corpus mucosal atrophy in spite of the lack of classical PCA in serum and would be a factor in the birth and growth of GCT.

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