IBD Clinical and Research Centre, University of Manitoba, Winnipeg, Manitoba, Canada.
Am J Gastroenterol. 2010 Sep;105(9):1994-2002. doi: 10.1038/ajg.2010.140. Epub 2010 Apr 6.
We aimed to determine whether any of the nonsteroidal anti-inflammatory drugs (NSAIDs), antibiotics, infections, and stress trigger symptomatic flares of inflammatory bowel diseases (IBDs).
Participants drawn from a population-based IBD research registry were surveyed every 3 months for 1 year. They simultaneously tracked the use of NSAIDs, antibiotics, infections, major life events, mood, and perceived stress. Social networks, childhood socioeconomic status, and smoking were assessed at baseline. Disease flare was identified using the Manitoba Inflammatory Bowel Disease Index, a validated disease activity index. Across any two consecutive survey periods, participants were categorized as having a flare (inactive/active), having no flare (inactive/inactive), or remaining active (active/active). Potential triggers were evaluated for the first 3-month period to determine predictive rather than concurrent relationships. Data from only one pair of 3-month periods from an individual were analyzed.
A total of 704 participants completed the baseline survey; 552 (78.3%) returned all 5 surveys. In all, 174 participants who had a flare were compared with 209 who had no flare. Perceived stress, negative affect (mood), and major life events were the only trigger variables significantly associated with flares. There were no differences between those who flared and those who did not, in the use of NSAIDs, antibiotics, or in the presence of infections. Multivariate logistic regression analyses indicated that only high-perceived stress (adjusted odds ratio=2.40 (1.35, 4.26)) was associated with an increased risk of flare.
This study adds to the growing evidence that psychological factors contribute to IBD symptom flares. There was no support for differential rates of use of NSAIDS, antibiotics, or for the occurrence of (non-enteric) infections related to IBD flares.
我们旨在确定非甾体抗炎药(NSAIDs)、抗生素、感染和应激是否会引发炎症性肠病(IBD)的症状发作。
从基于人群的 IBD 研究登记处抽取的参与者每 3 个月接受一次调查,为期 1 年。他们同时跟踪 NSAIDs、抗生素、感染、重大生活事件、情绪和感知压力的使用情况。在基线时评估社会网络、儿童社会经济地位和吸烟情况。使用曼尼托巴炎症性肠病指数(一种经过验证的疾病活动指数)来确定疾病发作。在任何两个连续的调查期间,将参与者分为发作(缓解/活动)、无发作(缓解/缓解)或持续活动(活动/活动)。在最初的 3 个月期间评估潜在触发因素,以确定预测而不是并发关系。仅分析单个参与者的一对 3 个月期的数据。
共有 704 名参与者完成了基线调查;552 名(78.3%)人完成了所有 5 次调查。共有 174 名发作参与者与 209 名无发作参与者进行了比较。感知压力、负性情绪(情绪)和重大生活事件是唯一与发作显著相关的触发变量。在使用 NSAIDs、抗生素或感染方面,发作组和未发作组之间没有差异。多变量逻辑回归分析表明,只有高感知压力(调整后的优势比=2.40(1.35,4.26))与发作风险增加相关。
本研究增加了越来越多的证据表明,心理因素会导致 IBD 症状发作。没有证据表明 NSAIDs、抗生素的使用率或与 IBD 发作相关的(非肠道)感染发生率存在差异。