Neuroendocrine differentiation in gastric adenocarcinomas associated with severe hypergastrinemia and/or pernicious anemia

Authors

  • Gunnar Qvigstad,

    1. Norwegian University of Science and Technology, Faculty of Medicine, Departments of Intra-abdominal Diseases and Physiology & Biomedical Engineering, Trondheim and Central Hospital of Møre and
    Search for more papers by this author
  • Tor Qvigstad,

    1. Romsdal, Departments of Medicine and Pathology, Ålesund, orway
    Search for more papers by this author
  • Bjørn Westre,

    1. Romsdal, Departments of Medicine and Pathology, Ålesund, orway
    Search for more papers by this author
  • Arne K. Sandvik,

    1. Norwegian University of Science and Technology, Faculty of Medicine, Departments of Intra-abdominal Diseases and Physiology & Biomedical Engineering, Trondheim and Central Hospital of Møre and
    Search for more papers by this author
  • Ejliv Brenna,

    1. Norwegian University of Science and Technology, Faculty of Medicine, Departments of Intra-abdominal Diseases and Physiology & Biomedical Engineering, Trondheim and Central Hospital of Møre and
    Search for more papers by this author
  • Helge L. Waldum

    Corresponding author
    1. Norwegian University of Science and Technology, Faculty of Medicine, Departments of Intra-abdominal Diseases and Physiology & Biomedical Engineering, Trondheim and Central Hospital of Møre and
      Helge Waldum, Department of Medicine, University Hospital, N-7006 Trondheim, Norway.
      e-mail: helge.waldum@medisin.ntnu.no
    Search for more papers by this author

  • Received August 31, 2001.

    Accepted October 10, 2001.

Helge Waldum, Department of Medicine, University Hospital, N-7006 Trondheim, Norway.
e-mail: helge.waldum@medisin.ntnu.no

Abstract

Patients with hypergastrinemia secondary to achlorhydria have an increased risk of developing ECL cell carcinoids and gastric adenocarcinomas. Hypergastrinemia is central in the pathogenesis of ECL cell carcinoids, but the link between gastrin and gastric carcinomas is controversial. During neoplastic transformation ECL cells may, however, lose many of their neuroendocrine characteristics, making them difficult to recognise as neuroendocrine with conventional immunohistochemical techniques. Neuroendocrine differentiation was therefore examined in eight gastric adenocarcinomas found in seven patients with severe hypergastrinemia and/or pernicious anemia using a monoclonal antibody towards chromogranin A and immunohistochemistry without and with a sensitive signal amplification technique. The Sevier-Munger method was used as a more specific marker of ECL cells. Seven of the carcinomas contained scattered neuroendocrine tumour cells. When using signal amplification, an increase in the number of immunoreactive neoplastic cells was seen. In many tumours, clusters or confluent sheets of such cells were disclosed, suggesting a neuroendocrine and ECL cell origin. These tumours may therefore be ECL cell carcinomas and hypergastrinemia may thus be involved in the tumourigenesis.

Ancillary