RECTAL CELL-PROLIFERATION AND COLON-CANCER RISK IN PATIENTS WITH HYPERGASTRINEMIA

Citation
M. Renga et al., RECTAL CELL-PROLIFERATION AND COLON-CANCER RISK IN PATIENTS WITH HYPERGASTRINEMIA, Gut, 41(3), 1997, pp. 330-332
Citations number
25
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
GutACNP
ISSN journal
00175749
Volume
41
Issue
3
Year of publication
1997
Pages
330 - 332
Database
ISI
SICI code
0017-5749(1997)41:3<330:RCACRI>2.0.ZU;2-K
Abstract
Background-The influence of gastrin on the colonic mucosa is still unc ertain. Some authors have suggested a stimulating effect on the growth of normal and malignant colonic epithelium, while others have shown n o association between gastrin and neoplastic development. Aims-To eval uate the effect of gastrin on colorectal cell proliferation, patients with chronic endogenous hypergastrinaemia underwent proctoscopy. Biops y specimens were taken in order to study rectal cell kinetics. Patient s and controls-Ten patients with chronic autoimmune gastritis (CAG), s ix patients with Zollinger-Ellison syndrome (ZES), and 16 hospital con trols took part in this study. Patients with CAG and ZES had basal ser um gastrin concentrations significantly higher than controls (p<0.001) . Methods-Immunohistochemistry was performed on 3 mu m sections of rec tal biopsy specimens incubated with 5'-bromodeoxyuridine. Results-The percentage of proliferating cells in the entire crypts (overall labell ing index) was similar in all the groups. However, the labelling frequ ency in the upper two fifths of the glands (phi h value) was significa ntly higher in patients with CAG or ZES compared with controls (p<0.01 in both patient groups versus controls). Conclusions-Endogenous hyper gastrinaemia is associated with rectal cell proliferation defects, sim ilar to those observed in conditions at high risk for colon cancer. Th e effect of the increased serum concentrations of gastrin on the color ectal mucosa after treatment with drugs inhibiting gastric acid secret ion should be investigated.