IBD: Where there’s smoke, there’s colorectal neoplasia
For inflammatory bowel disease (IBD) patients, smoking cigarettes or just being exposed to secondhand smoke raises the risk of developing colorectal neoplasia (CRN), a study has found.
“This study is the first to describe the important role of cigarette smoke in CRN development in IBD patients,” according to a team of researchers from the University of Groningen and University Medical Center Groningen, the Netherlands, led by Dr Kimberley van der Sloot.
In Crohn’s disease (CD) specifically, active smoking more than doubled the risk of CRN (hazard ratio [HR], 2.20, 95 percent confidence interval [CI], 1.02–4.76; p=0.044), current passive smoke exposure carried an 87-percent risk increase (HR, 1.87, 95 percent CI, 1.09–3.20; p=0.024), and secondhand smoke exposure during childhood conferred a more than fourfold increase (HR, 4.79, 95 percent CI, 1.72–13.34; p=0.003) relative to no exposure at all. [Clin Gastroenterol Hepatol 2021;10.1016/j.cgh.2021.01.015]
On the other hand, only former smoking contributed to an increased risk of CRN in ulcerative colitis (UC; HR, 1.73, 95 percent CI, 1.05–2.85; p=0.032).
Pinpointing high-risk patients
While it is not news that the risk of CRN is elevated in IBD and that cigarette smoking contributes to CRN in the general population, the present data have important implications for stratification of IBD patients at high risk of CRN in surveillance strategies, according to van der Sloot.
When compared to the risk stratification as prescribed by current guidelines, adding 'history of secondhand smoke exposure in childhood' (p=0.001) and 'current passive smoke exposure' (p=0.029) largely improved the prediction accuracy of CRN development in CD.
“Since current surveillance strategies are costly [and have a low uptake], the improvement of risk prediction due to the addition of cigarette smoking might allow for better stratification and further refinement of guidelines in the near future,” she added.
Just as important is to beef up efforts to promote smoking cessation in the IBD population, given its proven effect of decreasing the risk of flares in CD, which can, in turn, favourably influence the future risk of CRN, the researcher said. [Gastroenterology 2001;120:1093-1099]
Lighting up and inflammation
The analysis included a cohort of 1,313 IBD patients with previous biopsies. CRN occurred in 62 out of 724 CD patients (mean age, 48.7 years; 71 percent female) and in 89 out of 589 UC patients (mean age, 51.7 years; 38.2 percent female). CRN patients in the CD group were more likely to have a first-degree relative with colorectal cancer (p=0.001) and nonextensive colon involvement (p=0.046), while those in the UC group commonly presented with postinflammatory polyps (p=0.005).
The proportions of patients with CRN were 4.7 percent among never smokers versus 10.3 percent among ever smokers in the CD group, and 12.5 percent versus 17.9 percent, respectively, in the UC group.
“Cigarette smoke has been associated with divergent alterations of inflammatory status in CD and UC. While the overall risk of CRN in CD remains lower than in UC, the increased risk of CRN after cigarette smoke exposure in CD could be due to the increase of inflammation,” van der Sloot noted. [Best Pract Res Clin Gastroenterol 2004;18:481-496]
“For UC, the opposite association is seen, with a decrease of inflammation in active smokers leading to a decreased relapse risk,” she explained, adding that quitting leads to a rise in complication rate. [Inflamm Bowel Dis 2009;15:1199-1207; Aliment Pharmacol Ther 2016;43:549-561]
Van der Sloot called for further research into the role of cigarette smoke exposure in more detail, that is to evaluate the possible dose-dependent effect of pack years as described in the general population, as well as while taking other lifestyle associated factors into account.
“This should … allow for more precise evaluation of location of inflammation as well as disease activity parameters, medication escalation, and hospitalizations,” she said.