Department of Gastroenterology and Hepatology, Groningen, the Netherlands; Department of Epidemiology, Groningen, the Netherlands.
Department of Pathology, Groningen, the Netherlands.
Clin Gastroenterol Hepatol. 2022 Apr;20(4):798-805.e1. doi: 10.1016/j.cgh.2021.01.015. Epub 2021 Jan 13.
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.
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. Cox-regression modeling was used to estimate the effect of cigarette smoke and its additive effect within the current risk stratification for prediction of CRN.
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.
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.
由于黏膜炎症,炎症性肠病(IBD)患者结直肠肿瘤(CRN)的风险增加。由于当前的监测指南给患者和医疗保健成本带来了负担,因此对高危患者进行分层至关重要。吸烟可减轻溃疡性结肠炎(UC)的炎症,但不会减轻克罗恩病(CD)的炎症,并且是普通人群中 CRN 的已知危险因素。由于这种关联不同,吸烟对 IBD 中 CRN 的影响尚不清楚,也是本研究的主题。
在这项回顾性队列研究中,对 PALGA 登记处分析并报告了先前活检的 1386 例 IBD 患者,以筛查 CRN 的发生。评估了临床因素和吸烟情况。根据基于指南的 CRN 风险对患者进行分层。使用 Cox 回归模型估计吸烟及其在当前风险分层内的附加效应对 CRN 预测的影响。
153 例(11.5%)患者发生了 CRN。以前描述的危险因素,即 CD 中一级亲属有 CRN(p 值=0.001)、UC 中有炎症后息肉(p 值=0.005),得到了复制。以前吸烟会增加 UC 中 CRN 的风险(HR 1.73;1.05-2.85),而被动吸烟则没有影响。对于 CD,主动吸烟(2.20;1.02-4.76)和被动吸烟(1.87;1.09-3.20)显著增加了 CRN 的风险。将吸烟暴露因素添加到当前的风险分层模型中,显著改善了 CD 的模型拟合度。
本研究首次描述了吸烟在 IBD 患者 CRN 发展中的重要作用。添加此危险因素可改善当前的 CRN 监测策略风险分层。