■急性胰腺炎(AP)是炎症性肠病(IBD)的肠外表现。许多观察性研究报道了诊断为IBD的患者AP的风险增加。然而,由于观察性研究的局限性,IBD或其亚型与AP发展之间的因果关系和方向性尚不清楚.本研究采用孟德尔随机化(MR)方法探讨IBD或其亚型与AP风险的关系。
■进行了双样本双向MR研究,从国际炎症性肠病遗传学联盟(IIBDGC)和FinnGen数据库中选择与IBD和AP相关的遗传变异作为工具变量,分别。逆方差加权(IVW)方法用作因果推断的主要方法。采用CochranQ检验进行异质性评估。使用MREgger截距测试进行敏感性分析,MR-Presso,和留一法。
■结果显示,IBD(OR=1.049,95%CI=1.010-1.090,p=0.013)和溃疡性结肠炎(UC)(OR=1.057,95%CI=1.013-1.102,p=0.011)与AP风险增加显著相关。然而,克罗恩病(CD)(OR=1.023,95%CI=0.993-1.055,p=0.134)与AP的风险无因果关系。有趣的是,提示AP与CD风险降低相关(OR=0.797,95%CI=0.637-0.997,p=0.047)。此外,AP与IBD(OR=0.886,95%CI=0.753-1.042,p=0.144)或UC(OR=0.947,95%CI=0.773-1.159,p=0.595)的风险之间无因果关系.
■总而言之,这项研究提供了遗传证据支持IBD(特别是UC)对AP的因果影响,而CD似乎对AP没有因果关系。
UNASSIGNED: Acute pancreatitis (AP) is an extraintestinal manifestation of inflammatory bowel disease (IBD). Numerous observational studies have reported an increased risk of AP in patients diagnosed with IBD. However, the causal association and directionality between IBD or its subtypes and the development of AP remains unclear due to the limitations of observational research. This study aims to explore the relationship between IBD or its subtypes and AP risk using Mendelian Randomization (MR) method.
UNASSIGNED: A two-sample bidirectional MR study was conducted, selecting genetic variants associated with IBD and AP as instrumental variables from the International Inflammatory Bowel Disease Genetics Consortium (IIBDGC) and FinnGen databases, respectively. The inverse-variance weighted (IVW) method used as the primary approach for causal inference. The Cochran Q test was employed for heterogeneity assessment. Sensitivity analyses were performed using the MR Egger intercept test, MR-Presso, and Leave-one-out method.
UNASSIGNED: The results revealed that IBD (OR = 1.049, 95% CI = 1.010-1.090, p = 0.013) and ulcerative colitis (UC) (OR = 1.057, 95% CI = 1.013-1.102, p = 0.011) were significantly associated with an increased risk of AP. However, Crohn\'s disease (CD) (OR = 1.023, 95% CI = 0.993-1.055, p = 0.134) did not show a causal association with the risk of AP. Interestingly, AP was suggestively associated with a decreased risk of CD (OR = 0.797, 95% CI = 0.637-0.997, p = 0.047). Furthermore, there was no causal association between AP and the risk of IBD (OR = 0.886, 95% CI = 0.753-1.042, p = 0.144) or UC (OR = 0.947, 95% CI = 0.773-1.159, p = 0.595).
UNASSIGNED: In conclusion, this study provides genetic evidence supporting the causal influence of IBD (specifically UC) on AP, while CD does not appear to have a causal impact on AP.