Abstract

Introduction: Chronic hepatitis B (CHB) infection has been associated with malignancy, most notably hepatocellular carcinoma. Previous research has shown that hepatitis C is associated with increased colorectal adenomas and neoplasia. Currently, there are no studies on the association of CHB and colorectal adenomas. We aimed to identify a possible link between CHB and colorectal adenoma. Methods: A retrospective chart review was performed on 555 consecutive patients undergoing screening or diagnostic colonoscopy that were previously screened or diagnosed with hepatitis B. Comparisons between categorical variables were analyzed with the Chi-squared test and t-test for continuous variables. Unconditional logistic regression was used to generate age-, gender-, and race-adjusted odds ratios (ORs) and their 95% confidence intervals (CIs). Statistical analyses were performed with SAS 9.3 software. Results: Four hundred eighty-four patients were analyzed in the control group (non-hepatitis B) versus 71 in the CHB group. The adenoma detection rate was 23.9% in CHB versus 15.9% in the non-hepatitis B group for all-cause colonoscopy; however, this did not reach statistical significance. There was a significantly higher number of adenomas present in the distal colon compared to control (OR 2.16; 95%CI 1.06-4.43; p=0.04; Table 1). There were no significant associations found between CHB infection with size, multiplicity, or presence of proximal adenomas. There was a significant difference in regards to BMI, smoking history, and diabetes between the 2 groups (Table 2).Table 1: Presence of Adenomas in CHB vs. Control GroupTable 2: BMI, Smoking History, and Diabetes Between CHB vs. Control GroupConclusion: Although the adenoma detection rate was higher in the CHB population, this did not reach statistical significance. However, we did find an association between CHB infection and the presence of distal colorectal adenomas. Larger prospective studies are needed to strengthen our findings along with future studies examining HBV and mechanisms inducing colorectal carcinogenesis.

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