Helicobacter pylori infection is not associated with increased risk of colorectal polyps in Taiwanese

A recent report by Mizuno et al.1 showed that Helicobacter pylori (H. pylori) infection was associated with increased risk of colorectal adenomatous polyps in Japanese. The prevalence of tubular adenoma were 42.4% and 18.9% in H. pylori infected and noninfected patients, respectively.1 We read that article with great interest and examined the relationships between H. pylori infection and colorectal polyps in Taiwanese. Asymptomatic individuals who underwent colonoscopy, esophagogastroduodenoscopy and 13C-urea breath test (13C-UBT) as part of health check-up were enrolled for analysis. 13C-UBT was performed with infrared spectrometer, which has the sensitivity of 97.8%, specificity of 96.8% and accuracy of 97.5%.2 Polyethylene glycol lavage solution (Klean-Prep; Norgine Limited, Harefield, Middlesex, UK), followed by glycerin enema were used for bowel preparation. Colonoscopy was performed by one of 7 board-certified gastroenterologists who had performed at least 500 colonoscopies using a standard colonoscope (CF-240AI; Olympus Optical Co, Tokyo, Japan). Chromoendoscopy with 0.2% indigo carmine was applied to all detected polypoid lesions for a more detailed assessment and description of colonoscopic morphology. Larger (>0.5 cm) polyps were removed with standard polypectomy snares whereas smaller (<0.5 cm) polyps were removed with a biopsy forceps. The criteria recommended by World Health Organization were used to classify the polyps.3 Advanced colonic neoplasm was defined as meeting any one of the following features: (1) an adenoma greater than 10 mm in diameter; (2) an adenoma containing villous architecture greater than 20%; (3) an adenoma with severe dysplasia or (4) invasive cancer. For analyses, findings such as juvenile or inflammatory polyps, lipomas, lymphoid aggregates and chronic nonspecific inflammation were regarded as normal mucosa. Our results were shown in Table I. The age and gender were not significantly different between the H. pylori infected and noninfected groups. In contrast to Mizuno et al.1 who showed a higher prevalence of tubular adenoma in H. pylori infected patients (42.4% vs. 18.9%, p < 0.0005), our data showed that the endoscopic findings were not significantly different between H. pylori infected and noninfected subjects (p = 0.513). The prevalence of nonadvanced adenoma was similar between the 2 groups (14.2% vs. 11.8%) and normal colonoscopy (without polyps) was also similar between the 2 groups (74.2% vs. 76.4%). Possible explanations for the contradictory results were as follows. First, we used the 13C-UBT to detect the presence of H. pylori infection in the stomach. Several species of Helicobacter other than Helicobacter pylori have been reported to colonize the lower intestinal tract of humans,4 which could be detected by a serologic test, but not by the 13C-UBT. Therefore, the increased risk of colorectal polyps in Helicobacter seropositive patients might be attributed to the colonization of species other than Helicobacter pylori in the colon, rather than to the H. pylori in the stomach. Besides, 13C-UBT detects the presence of current infection, whereas the serology test detects both the past and current infection. As hypergastrinemia has been reported to be associated with increased risk of colorectal carcinoma,5 the associations between the H. pylori infection and colorectal polyps might be mediated by hypergastrinemia, rather than by H. pylori itself. Second, the study populations were different. We enrolled asymptomatic individuals who underwent screening colonoscopy as a part of health check-up, whereas Mizuno et al. enrolled symptomatic patients who underwent colonoscopy for diagnostic purposes. Besides, the patients in our study were younger than those in their study (50 years vs. 60 years). Therefore, the overall prevalence of colorectal adenomatous polyps was lower in our study. Third, ethnic difference might also be an explanation for the contradictory results. Of course, a type II error in our study cannot be excluded. Finally, we were not able to answer whether different virulent strains of H. pylori have different impact on the carcinogenesis of colonic neoplasms, although 98% of Taiwanese have been reported to be infected with CagA positive strains.6 In summary, our data showed that current H. pylori infection in stomach was not associated with increased risk of colorectal adenomatous polyp in Taiwan. The roles of non-Helicobacter pylori helicobacters, which colonize the colon, different virulent strains of H. pylori and gastrin levels in the carcinogenesis of colon should be clarified by further well-designed large-scale population-based studies.