Rectal cell proliferation and colon cancer risk in patients with hypergastrinaemia

Background—The influence of gastrin on the colonicmucosa is still uncertain. Some authors have suggested a stimulatingeffect on the growth of normal and malignant colonic epithelium, while others have shown no association between gastrin and neoplastic development.
Aims—To evaluate the effect of gastrin oncolorectal cell proliferation, patients with chronic endogenoushypergastrinaemia underwent proctoscopy. Biopsy specimens were taken inorder to study rectal cell kinetics.
Patients and controls—Ten patients with chronicautoimmune gastritis (CAG), six patients with Zollinger-Ellisonsyndrome (ZES), and 16 hospital controls took part in this study.Patients with CAG and ZES had basal serum gastrin concentrationssignificantly higher than controls (p<0.001).
Methods—Immunohistochemistry was performed on 3 µm sections of rectal biopsy specimens incubated with5'-bromodeoxyuridine.
Results—The percentage of proliferating cells inthe entire crypts (overall labelling index) was similar in all thegroups. However, the labelling frequency in the upper two fifths of the glands (ϕh value) was significantly higher in patients with CAG orZES compared with controls (p<0.01 in both patient groups versus controls).
Conclusions—Endogenous hypergastrinaemia isassociated with rectal cell proliferation defects, similar to thoseobserved in conditions at high risk for colon cancer. The effect of theincreased serum concentrations of gastrin on the colorectal mucosaafter treatment with drugs inhibiting gastric acid secretion should be investigated.