Cell proliferation in type C gastritis affecting the intact stomach

Aims-Type C gastritis caused by bile reflux has a characteristic appearance , similar to that seen in other forms of chemical gastritis, such as those associated with NSAIDs or alcohol. An increase in mucosal cell proliferatio n increases the likelihood of a neoplastic clone of epithelial cells emergi ng, particularly where there is chronic epithelial injury associated with b ile reflux. It has been shown previously that type C gastritis is associate d with increased cell proliferation in the postsurgical stomach. The aim of this study was to determine cell proliferation in type C gastritis caused by bile reflux affecting the intact stomach. Methods-Specimens from 15 patients with a histological diagnosis of type C gastritis on antral biopsy were obtained from the pathology archives betwee n 1994 and 1997. A control group of nine normal antral biopsies was also se lected and all underwent MIB-1 immunostaining. The gastric glands were divi ded into three zones (zone 1, gastric pit; zone 2, isthmus; and zone 3, gla nd base) and the numbers of positively staining nuclei for 500 epithelial c ell nuclei were counted in each zone to determine the percentage labelling index (LI%). Results-Cell proliferation was significantly higher in all three zones of t he gastric glands with type C gastritis compared with controls as follows: zone 1, median LI% in type C gastritis 64.7 (range, 7.8-99,2), controls 4.7 (range, 2.0-11.3); zone 2? median LI% in type C gastritis 94.7 (range, 28. 8-98.7), controls 40.2 (range, 23.1-70.3); and zone 3, median LI% in type C gastritis 20.0 (range, 1.3-96.0); controls 2.6 (range, 0.9-5.7). Conclusions-Bile reflux is thought to act as a promoter of gastric carcinog enesis in the postsurgical stomach. The same may be true in the intact stom ach.