Hypergastrinemia is associated with adenocarcinomas in the gastric corpus and shorter patient survival.
Hypergastrinemia causes carcinoids or carcinomas in the gastric corpus in animal models. Helicobacter pylori (HP) infection in patients causes atrophy, hypergastrinemia and promotes gastric carcinogenesis. Many patients with gastric cancer have hypergastrinemia and it has therefore been hypothesized that hypergastrinemia promotes carcinogenesis. We have examined the associations between serum gastrin, the anatomical localization of gastric cancer, histological classification and patient survival. Patients with non-cardia gastric adenocarcinomas were included prospectively (n = 80). Tumour localization, histological classification according to Laurén and disease stage were recorded. Preoperative fasting serum gastrin was analysed by radioimmunoassay and HP serology by ELISA. Patient survival was determined after a median postoperative follow-up of 16.5 years. Hypergastrinemic patients had carcinomas located in the gastric corpus more often compared to normogastrinemic patients (81.8 vs 36.2%, p = 0.002). Patients with disease stage 2-4 and hypergastrinemia had shorter survival than normogastrinemic patients [5.0 (1.1-8.9) vs 10.0 (6.4-13.6) months (p = 0.04)]. There was no significant difference in serum gastrin or survival between patients with intestinal and diffuse type carcinomas. Hypergastrinemia was associated with adenocarcinomas in the gastric corpus and shorter survival. The findings support the hypothesis that hypergastrinemia promotes carcinogenesis and affects biological behaviour.
Department of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.|Department of Gastroenterology and Hepatology, St. Olav's University Hospital, Trondheim, Norway.
Reidar
R
Fossmark
Department of Gastroenterology and Hepatology, St. Olav's University Hospital, Trondheim, Norway.
Liv
L
Sagatun
Department of Pathology and Medical Genetics, St. Olav's University Hospital, Trondheim, Norway.|Department of Laboratory Medicine, Children's and Women's Health, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.
Ivar S
IS
Nordrum
Department of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.|Department of Gastroenterology and Hepatology, St. Olav's University Hospital, Trondheim, Norway.
Arne K
AK
Sandvik
Department of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.|Department of Gastroenterology and Hepatology, St. Olav's University Hospital, Trondheim, Norway.
Helge L
HL
Waldum
D000230:Adenocarcinoma / Q000209:etiology / Q000401:mortality* / Q000473:pathology*; D000368:Aged; D053379:Chromogranin A / Q000097:blood; D005260:Female; D005500:Follow-Up Studies; D005753:Gastric Mucosa / Q000473:pathology; D005755:Gastrins / Q000097:blood; D016481:Helicobacter Infections / Q000150:complications / Q000382:microbiology / Q000401:mortality* / Q000473:pathology; D016480:Helicobacter pylori / Q000302:isolation & purification; D006801:Humans; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D013270:Stomach / Q000473:pathology*; D013274:Stomach Neoplasms / Q000209:etiology / Q000401:mortality* / Q000473:pathology*; D015996:Survival Rate
D053379:Chromogranin A; D005755:Gastrins
Gastric cancer; Helicobacter pylori; adenocarcinoma; chromogranin A; gastrin