Is It Rationale to Apply Strict Colonoscopic Surveillance in Patients with Helicobacter pylori Associated Chronic Atrophic Gastritis?

Colonic carcinogenesis is believed to be multifactorial process. In addition to hereditary and genetic factors, environmental factors such as Westernized dietary practice, smoking and alcohol consumption had also been contributed to increase the risk of colorectal cancer. 1 There has been growing interest in the relationship between infectious agents and colonic carcinogenesis. Especially, Heli-cobacter pylori, which is ubiquitous pathogen inducing chronic inflammation and eventually leading to development of chronic gastritis, peptic ulcer and even gastric cancer. There is also conflicting evidence on the relevance of chronic H. pylori infection as a risk factor for colorectal neoplasia. Several pathophysiologic mechanisms had been also suggested for this correlation between colorectal neoplasm and H. pylori infection. Increased serum gastrin caused by persistent H. pylori infection, which is estimated to have trophic effect on colonic mucosa, could contribute to colorectal carcinogenesis, 4 although this hypothesis was disputed by other reports showing discordant results. 5 The facts that measurement of nonamidated gastrin which seems to act as more important carcinogen of colorectal carcinoma is not available, and autocrine secretion of gastrin by colorectal cancer cells themselves may explain these inconsistent results. Intestinal dysbiosis induced by H. pylori-related chronic atro-phic gastritis resulting in hypochlorhydria was supposed to be another contributory to the colorectal carcinogenesis. 6,7 Although H. pylori is known as not to invade colonic mucosa, study reporting fecal shedding of viable H. pylori suggested the it may move through colonic lumen and locally activate co-lonic carcinogenesis. Study reporting higher detection rate of H. pylori in neoplastic lesion than normal mucosa also supported this hypothesis, 8 although exact pathophysiologic mechanism of H. pylori induced local activation of carcinogenesis should be evaluated. Enhanced systemic inflammatory response caused by H. py-lori, especially by Cag A-positive H. pylori infection, also had assumed to play a causative role in colorectal carcinogenesis. 4 Although the insufficient evidence for a definitive causal relationship , it appears that H. pylori related gastritis is associated with an increased, although modest, risk of colorectal adenoma and cancer. Lee et al. 9 tried retrospective cross-sectional study to evaluate the correlation between H. pylori, atrophic gastritis and colorec-tal neoplasm using a single center health check program. Authors analyzed 6,351 subjects who underwent screening colo-noscopy and H. pylori infection was confirmed with serology testing IgG antibody. This study showed H. pylori infection was a significantly associated with overall colorectal neoplasm. In addition, presence of atrophic gastritis, which was …