Our study indicates that gastric H. pylori infection, confirmed by immunohistochemistry staining of gastric biopsies, associates with an increased risk of colorectal lesions in African Americans. The same association was true in 3 meta-analyses which included studies from different ethnic groups. In particular, Zumkeller et al.  included 11 studies regardless of the diagnostic tests used for H. pylori, and Zhao et al.  included 10 out of 13 case–control studies that used only IgG antibody for H. pylori to demonstrate previous H. pylori infection in patients with colonic lesions. Jones et al.  used immunohistochemistry methods to demonstrate that H. pylori do reside in the subjects’ colon biopsies and associates with colorectal neoplasm.
Our previous report showed colorectal polyps’ incidence begins to increase significantly at age forty in African Americans  with or without family history of CRC, thus it has been chosen as a cutoff age in this study. Aging male patients are at a higher risk of adenomatous and hyperplastic polyps , and are more likely to associate with H. pylori positivity which is consistent with findings in other ethnic groups . In this study, we were not able to establish a correlation between histopathological subtypes, size, and location of colorectal polyps with H. pylori infection.
Other confounders such as BMI, smoking, alcohol consumption, diabetes, socioeconomic status, diet and lack of physical activity are known risk factors for colorectal polyp/cancer. Our retrospective epidemiological study did not adjust for these factors because of lack of corresponding information. Previous studies reported an association between H. pylori and colorectal adenoma which was not altered even after adjustment for confounding factors [14, 50].
To our knowledge, no previous study has linked H. pylori infection with colorectal polyps or cancer in African Americans. The higher prevalence of colorectal polyps in H. pylori infected patients and the higher seropositivity could be explained by their environmental and genetic differences as well. Potentially, such differences may alter host gastric and/or colorectal mucosa in response to H. pylori carcinogenic effect among some ethnic groups. For instance, Indians have a low rate of gastric cancer and high rate of H. pylori infection which was not significantly associated with intestinal metaplasia, gastric tumor site, and patient’s age . Moreover, despite the high prevalence of gastric cancer in Finland, there was no association between atrophic gastritis or H. pylori infection with colorectal cancer among Finnish male smokers [19, 52].
High risk features when combined at presentation were more predictive for colorectal polyps, As such, they can be useful clinical criteria to prioritize access to colonoscopy. The risk prediction of colorectal polyps based on gastric lesions recovered from gastroscopy depend on the nature of such lesions. The highest prevalence of colorectal polyps among H. pylori positive subjects was found among those who had chronic active gastritis. Such polyps were more likely to be neoplastic (adenomatous). Due to the retrospective nature of the study, the time lapse between the H. pylori infection and the colonic lesions occurrence is unknown. Meira et al.  reported after infecting mice with H. pylori, the chronic inflammation induced DNA damage in alkyladenine DNA glycosylase deficit mice and enhances inflammation-associated colon tumorigenesis. It also predisposed to the development of gastric cancer precursor lesions.
As gastric lesions progressed, H. pylori positivity decreased and the risk of colorectal polyps increased, being highest in patients with chronic atrophic gastritis with intestinal metaplasia, but the number of associated colorectal polyps was too small to make meaningful conclusions. The annual progression from chronic non-atrophic gastritis to atrophic gastritis is 1 to 3% [53, 54]. H. pylori in advanced gastric lesions has probably decreased because of migration through the gastrointestinal tract . This suggests that with advanced gastric lesions, gastric lesions but not H. pylori status would be appropriate in the prediction of colorectal polyps [23, 56, 57]. Bulajic et al.  found only 1.2% of malignant colorectal tissues were positive for H. pylori in contrast to 6% positive normal tissues from cancer patients. This could be explained by migration phenomena too  and would suggest that H. pylori gastric effect could be similar to its colonic effect. Once H. pylori’s infection is established, it likely elicits robust and lasting inflammatory and immune responses that may potentially influence the development of diseases that occur later in life such as cancer.
The strengths of our study; are in its comprehensive nature since it linked the real time presence of gastric H. pylori, the symptoms it may produce, and the associated gastric lesions with its extra-gastric colonic effects . Gold standard tools were utilized to diagnose colorectal polyps (complete colonoscopy) and H. pylori infection (gastric biopsy). We used immunohistochemistry to diagnose H. pylori in gastric biopsies as it is highly sensitive and specific particularly in patients who have been partially treated. Besides, we had a fairly large sample size (n = 1256). Moreover, the findings with this large sample were further confirmed serologically.
Because our study was retrospective and hospital-based rather than population-based, it has its own limitations. The underestimation of H. pylori’s prevalence and its associated gastric lesions in the prediction of colorectal polyps could be explained by gastric sampling errors and unknown received treatments. Also, our serology testing sampling was smaller (n = 163) than the sampling for the epidemiological study (n = 1256). Despite that, we were able to prove positive association between H. pylori and colorectal polyps consistent with the colon cancer mouse models studies . Also, we were able to show that there is a trend of increased chance of having polyps in the presence of Cag-A positive H. pylori infections.