4.7 Article

Cigarette Smoke Increases Risk for Colorectal Neoplasia in Inflammatory Bowel Disease

Journal

CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
Volume 20, Issue 4, Pages 798-+

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.cgh.2021.01.015

Keywords

Colorectal Neoplasia; Inflammatory Bowel Disease; Cigarette Smoke Exposure; Risk Stratification; Surveillance Guideline

Funding

  1. JSM MD-PhD trajectory grant from the Junior Scientific Masterclass of the University of Groningen, the Netherlands [16-22]

Ask authors/readers for more resources

This study highlights the significant role of cigarette smoke in the development of colorectal neoplasia in patients with inflammatory bowel disease (IBD). Adding smoking as a risk factor improves the accuracy of current surveillance strategies for colorectal neoplasia.
BACKGROUND & AIMS: Patients with inflammatory bowel disease are at increased risk of colorectal neoplasia (CRN) due to mucosal inflammation. As current surveillance guidelines form a burden on patients and healthcare costs, stratification of high-risk patients is crucial. Cigarette smoke reduces inflammation in ulcerative colitis (UC) but not Crohn's disease (CD) and forms a known risk factor for CRN in the general population. Due to this divergent association, the effect of smoking on CRN in IBD is unclear and subject of this study. METHODS: In this retrospective cohort study, 1,386 IBD patients with previous biopsies analyzed and reported in the PALGA register were screened for development of CRN. Clinical factors and cigarette smoke were evaluated. Patients were stratified for guideline-based risk of CRN. Coxregression modeling was used to estimate the effect of cigarette smoke and its additive effect within the current risk stratification for prediction of CRN. RESULTS: 153 (11.5%) patients developed CRN. Previously described risk factors, i.e. first-degree family member with CRN in CD (p-value = .001), presence of post-inflammatory polyps in UC (p-value = .005), were replicated. Former smoking increased risk of CRN in UC (HR 1.73; 1.05-2.85), whereas passive smoke exposure yielded no effect. For CD, active smoking (2.20; 1.02-4.76) and passive smoke exposure (1.87; 1.09-3.20) significantly increased CRN risk. Addition of smoke exposure to the current risk-stratification model significantly improved model fit for CD. CONCLUSIONS: This study is the first to describe the important role of cigarette smoke in CRN development in IBD patients. Adding this risk factor improves the current risk stratification for CRN surveillance strategies.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.7
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available