Gastric epithelial cell proliferation in patients with liver cirrhosis

Citation
A. Zullo et al., Gastric epithelial cell proliferation in patients with liver cirrhosis, DIG DIS SCI, 46(3), 2001, pp. 550-554
Citations number
38
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
DIGESTIVE DISEASES AND SCIENCES
ISSN journal
01632116 → ACNP
Volume
46
Issue
3
Year of publication
2001
Pages
550 - 554
Database
ISI
SICI code
0163-2116(200103)46:3<550:GECPIP>2.0.ZU;2-Y
Abstract
An increased risk for gastric cancer in patients with liver cirrhosis has r ecently been reported. This study was performed in order to determine gastr ic epithelial cell proliferation in cirrhotic patients and to evaluate the role of congestive gastropathy (CG) and Helicobacter pylori infection in th is process. Thirty-six cirrhotic patients and 18 controls were enrolled in the study. All patients underwent endoscopy and three biopsies were perform ed in the antrum and three in the gastric body. The presence of H. pylori i nfection was assessed by a rapid urease test and histology. The antral biop sies were used for gastric cell proliferation assessment by an immunohistoc hemical analysis (Ki-67). There was no significant difference in epithelial cell proliferation between cirrhotics and controls. Gastric proliferation values were higher in patients with H. pylori infection compared with uninf ected patients, both in cirrhotic (P = 0.003) and in control groups (P = 0. 06). Among the cirrhotic group, we found a progressive increase in gastric cell proliferation values related to the degree of CG, the highest values b eing observed in cirrhotic patients with severe CG. Moreover, cirrhotics wi th both severe CG and H. pylori infection had the highest proliferation val ues when compared with all other subgroups. In conclusion, this study found that: (1) CG significantly affects epithelial cell proliferation in gastri c mucosa in cirrhotic patients, (2) H. pylori infection plays a similar rol e in gastric cell proliferation in both cirrhotic and non-cirrhotic patient s, and (3) CG and H. pylori could act synergistically in this process.