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Smoking effect on colorectal neoplasia risk may vary by IBD type

Roshini Claire Anthony
05 Feb 2021

The impact of cigarette smoke exposure on the risk of colorectal neoplasia (CRN) in patients with inflammatory bowel disease (IBD) may differ according to IBD type, suggested results of a single-centre study presented at the recent Crohn’s and Colitis Congress 2021.

Participants in this retrospective study were 1,386 patients with IBD from the University Medical Center Groningen, the Netherlands, who had undergone 1 colorectal biopsy as per the Dutch nationwide pathology registry (PALGA). The patients underwent screening for CRN; of these, 11.5 percent (n=153) developed CRN.

Overall, exposure to cigarette smoke (ever smokers) was associated with a significantly increased risk of CRN in patients with Crohn’s disease (hazard ratio [HR], 2.04, 95 percent confidence interval [CI], 1.02–4.10; p=0.044) but not those with ulcerative colitis (HR, 1.38, 95 percent CI, 0.86–2.23; p=0.180). [Crohn’s and Colitis Congress 2021, session: The Latest in Transformative IBD Research and Featured Abstract Presentations; Clin Gastroenterol Hepatol 2021;doi:10.1016/j.cgh.2021.01.015]

Among patients with Crohn’s disease, active smokers had a significantly increased risk of CRN compared with never smokers (HR, 2.20, 95 percent CI, 1.02–4.75; p=0.044), while the risk was numerically but not significantly increased in former smokers (HR, 2.16, 95 percent CI, 1.00–4.70; p=0.051). The risk of CRN was increased in patients with passive smoke exposure, particularly those who experienced it during childhood (HR, 4.79, 95 percent CI, 1.72–13.34; p=0.003), and to a lesser extent in patients with current passive smoke exposure (HR, 1.87, 95 percent CI, 1.09–3.20; p=0.024).

Conflicting findings were observed in patients with ulcerative colitis, where CRN risk was raised in former compared with never smokers (HR, 1.73, 95 percent CI, 1.05–2.85; p=0.032), with no significant increase noted in active smokers (HR, 1.21; p=0.624) or those with passive smoke exposure be it current (HR, 1.05; p=0.846) or in childhood (HR, 1.14; p=0.623).

“Mucosal inflammation increases the risk of CRN in patients with IBD,” presented study author Dr Kimberley van der Sloot from the University of Groningen, Groningen, the Netherlands.

Smoking is a known risk factor for CRN in the general population. However, previous studies have shown that exposure to cigarette smoke has varying effects on inflammation in different IBD diseases, said the authors.

Research has suggested that while colorectal cancer risk may be declining in patients with IBD, certain subgroups are still at risk. Currently available screening strategies are underutilized yet remain a burden on healthcare resources and patients. As such, stratification of high-risk subgroups is warranted, they continued.

“[T]his study is the first to demonstrate a clear risk increasing association for active as well as passive cigarette smoke exposure and risk of CRN development in patients with Crohn’s disease, while former cigarette smoking was associated with CRN development in ulcerative colitis,” said the authors.

“Adding this risk factor improves the current risk stratification for CRN surveillance strategies,” van der Sloot pointed out.

Avenues for further research include establishing these findings in larger studies, examining the effect of concurrent lifestyle factors that may accompany smoking, and assessing the impact of the amount of cigarette smoke exposure (eg, pack years) on CRN risk, the authors said.

 

 

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