TY - JOUR T1 - Cell proliferation in the gastric corpus in Helicobacter pylori associated gastritis and after gastric resection. JF - Gut JO - Gut SP - 351 LP - 353 DO - 10.1136/gut.36.3.351 VL - 36 IS - 3 AU - D A Lynch AU - N P Mapstone AU - A M Clarke AU - P Jackson AU - M F Dixon AU - P Quirke AU - A T Axon Y1 - 1995/03/01 UR - http://gut.bmj.com/content/36/3/351.abstract N2 - Patients who have undergone gastric resection are at higher risk of developing gastric carcinoma than normal subjects, and bile reflux is believed to play a role in carcinogenesis. An increase in mucosal cell proliferation increases the likelihood of a neoplastic clone of epithelial cells emerging, particularly where there is chronic epithelial injury associated with bile reflux. Helicobacter pylori is considered a major risk factor for gastric cancer in the intact stomach. It has been shown previously that antral cell proliferation is increased in H pylori gastritis and falls to normal levels after eradication of the organism. Little is known of corpus cell proliferation in H pylori gastritis or after gastric resection. Using in vitro bromodeoxyuridine labelling of endoscopic biopsy specimens we have found that corpus cell proliferation is increased in H pylori gastritis. Cell proliferation was greater in corpus biopsy specimens of resected stomachs than in H pylori gastritis. Subgroup analysis of patients who had undergone gastric resection indicated that those positive for H pylori had higher levels of cell proliferation than those negative for the organism. These findings provide further evidence that H pylori and bile have a role in gastric carcinogenesis and suggest that their presence has a synergistic effect on gastric epithelial cell proliferation. ER -