Cigarette smoking may be associated with a higher probability of developing colorectal neoplasia (CRN) among patients with inflammatory bowel disease (IBD), a finding that if confirmed could help to refine colorectal cancer surveillance guidelines. IBD patients undergo surveillance at specific time points of their disease with the aim to detect and potentially treat early CRN.
But these procedures are costly and burdensome to patients, and some previous studies have revealed a relatively low utility for patients, according to Kimberley van der Sloot, MD, a PhD candidate at the University Medical Center Groningen (the Netherlands). She presented the research at the annual congress of the Crohn’s & Colitis Foundation and the American Gastroenterological Association. The study was also published in Clinical Gastroenterology and Hepatology.
“We aimed to explore the role of cigarette exposure in colorectal neoplasia risk in patients with IBD, and we aimed to improve the CRN risk stratification model that we are currently using for these surveillance guidelines,” Dr. van der Sloot said during her talk.
Commenters during the Q&A period noted that the population database used in the study did not include measures of inflammation, which is a known risk for CRN. One review found that smoking worsens inflammation in Crohn’s disease but improves it in ulcerative colitis.
“It certainly raises the issue that we’ve always said, which is that people should quit smoking for other health reasons, but it doesn’t necessarily answer the question definitively,” said David Rubin, MD, who moderated the session and is professor of medicine at the University of Chicago and chair of the congress’s organizing committee. He added that the association between smoking and CRN risk may nevertheless inform future management surveillance guidelines if it is confirmed.
The researchers analyzed data from the 1000IBD cohort, which is prospectively following IBD patients in the Netherlands. The study included 1,386 patients who had at least one colorectal biopsy. Compared to a general population CRN incidence of 2.4%, Crohn’s disease patients who were never smokers had an incidence of 4.7% versus 10.3% among former or current smokers. In ulcerative colitis, the incidence was 12.5% among never smokers and 17.9% among former or current smokers.
In Crohn’s disease, previous or current smokers had about a twofold increased risk (hazard ratio, 2.04; P = .044). Compared to never smokers, former smokers trended toward an increased risk (HR, 2.16; P = .051), and active smokers had a significantly increased risk (HR, 2.20; P = .044). Passive smoke exposure was also associated with greater risk, both in childhood (HR, 4.79; P = .003) and current (HR, 1.87; P = .024).
In ulcerative colitis, the only statistically significant association between smoke exposure and CRN risk was among former smokers (HR, 1.73; P = .032).
The researchers also looked at patients with a disease duration longer than 8 years and stratified patients according to low risk (left-side ulcerative colitis, <50% of colon affected in Crohn’s disease; n = 425), medium risk (postinflammatory polyposis present or extensive colitis; n = 467), and high risk (concordant primary sclerosing cholangitis or having a first-degree relative with colorectal cancer; n = 143). In Crohn’s disease, current smoking was associated with greater CRN incidence (P = .046), and former smoking trended in that direction but was nonsignificant (P = .068). Former smoking also trended toward a risk in ulcerative colitis (P = .068), but there was no sign of an association for current smoking (P = .883).
In Crohn’s disease, after adjustment for risk stratification, greater CRN risk was associated with passive smoke exposure both during childhood (P = .001) and at present (P = .003).
“We believe this is the first study to describe the important role of cigarette smoking in development of colorectal neoplasia in IBD patients in a large, prospective, cohort, and I think [it] has shown the importance of lifestyle and smoking particularly in IBD. This is one more example. Alongside that, we’ve shown that adding this risk factor can improve the current risk stratification that is used for surveillance guidelines, and might be of benefit in the development of future guidelines,” said Dr. van der Sloot.
Dr. van der Sloot and Dr. Rubin had no relevant financial disclosures.
This article was updated Mar. 11, 2021.