R K Siddheshwar1, K B Muhammad, J C Gray, S B Kelly. 1. Department of Surgery, Regional School of Medicine, North Tyneside General Hospital, Tyne & Wear, North Shields, England.
Abstract
OBJECTIVES: The role of Helicobacter pylori in the pathogenesis of colorectal polyps and colorectal carcinoma is unknown. H. pylori infection causes fasting and meal stimulated hypergastrinemia. Gastrin increases colorectal mucosal proliferation and promotes tumor growth. We performed a prospective study to determine the seroprevalence of H. pylori in patients with colorectal polyps and colorectal carcinoma and in controls. METHODS: Blood samples were collected from 189 patients with colorectal carcinoma, 57 patients with colorectal polyps, and 179 controls. H. pylori serology was determined by an ELISA assay. RESULTS: Logistic regression showed no difference in seroprevalence of H. pylori between patients with colorectal cancer and controls (odds ratio, 1.1; 95% confidence interval, 0.7 to 1.8) or between patients with colorectal polyps and controls (odds ratio 1.3; 95% confidence interval, 0.7 to 2.5). Age and sex were not found to be associated with H. pylori infection. Patients in social classes IV and V were 2.3 times more likely to have H. pylori infection than those in social classes I, II, and III (95% confidence interval, 1.3 to 4.2). CONCLUSIONS: This study shows that there is no increase in the seroprevalence of H. pylori in patients with colorectal polyps or colorectal carcinoma compared with controls. These results do not support the hypothesis that there is a relationship between H. pylori infection and the development of colorectal neoplasia.
OBJECTIVES: The role of Helicobacter pylori in the pathogenesis of colorectal polyps and colorectal carcinoma is unknown. H. pyloriinfection causes fasting and meal stimulated hypergastrinemia. Gastrin increases colorectal mucosal proliferation and promotes tumor growth. We performed a prospective study to determine the seroprevalence of H. pylori in patients with colorectal polyps and colorectal carcinoma and in controls. METHODS: Blood samples were collected from 189 patients with colorectal carcinoma, 57 patients with colorectal polyps, and 179 controls. H. pylori serology was determined by an ELISA assay. RESULTS: Logistic regression showed no difference in seroprevalence of H. pylori between patients with colorectal cancer and controls (odds ratio, 1.1; 95% confidence interval, 0.7 to 1.8) or between patients with colorectal polyps and controls (odds ratio 1.3; 95% confidence interval, 0.7 to 2.5). Age and sex were not found to be associated with H. pyloriinfection. Patients in social classes IV and V were 2.3 times more likely to have H. pyloriinfection than those in social classes I, II, and III (95% confidence interval, 1.3 to 4.2). CONCLUSIONS: This study shows that there is no increase in the seroprevalence of H. pylori in patients with colorectal polyps or colorectal carcinoma compared with controls. These results do not support the hypothesis that there is a relationship between H. pyloriinfection and the development of colorectal neoplasia.
Authors: Rack Cheon Bae; Seong Woo Jeon; Han Jin Cho; Min Kyu Jung; Young Oh Kweon; Sung Kook Kim Journal: World J Gastroenterol Date: 2009-12-07 Impact factor: 5.742