Inflammatory Bowel Diseases Before and After 1990.
Inflammatory Bowel Diseases Before and After 1990.
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DOI：
10.1016/j.gastha.2022.08.001
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发表时间：
2023
期刊：
影响因子：
--
通讯作者：
Brant, Steven R
中科院分区：
文献类型：
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作者：
Truta, Brindusa;Begum, Ferdouse;Datta, Lisa Wu;Brant, Steven R
炎症性肠病(IBD)是由遗传和环境危险因素相互作用引起的。我们评估了1990年后北美发病率增加的潜在决定因素。使用拟合的广义线性模型，我们评估了1990年前和1990年后国立糖尿病、消化和肾脏疾病IBD遗传学联合会数据库中克罗恩病(CD)和溃疡性结肠炎(UC)的临床特征、吸烟和遗传风险评分(GRS)。在2744例(55.00%CD，42.2%UC)患者中，吸烟状况和GRS是影响诊断年龄的主要因素。1990年后，UC和CD的初诊吸烟率均显著下降(分别为34.1%比20.8%，P<；.001和14.7%比8.7%，P=0.06)。在UC组，戒烟率增加(9%比15%，P<；.001)，不吸烟率保持不变，而CD组，戒烟率保持不变。CD-GRS和IBD-GRS与年轻的诊断年龄、犹太民族、IBD家族史和手术显著相关。在多变量分析中，1990年后CD-GRS显示边缘显著下降(P=.058)，但仅当排除模型中的手术时；CD和UC的手术数在1990年后均显著减少。CD-GRS与确诊时吸烟呈负相关(P<；.001)，这表明，在吸烟的情况下，CD可能只需要较低的遗传风险就能发生。1990年后，戒烟显著增加与UC发病率相关。相反，尽管CD发病率上升，但吸烟风险在1990年后显著降低。同样，CD-GRS在1990年后也有下降的趋势，但不考虑CD手术的显著减少。因此，我们推断不明的危险因素(如饮食、肥胖、抗生素的使用、卫生条件的改善等)。或者，更多地发现或存在轻度CD可能是1990年后CD发病率增加的原因。
Inflammatory bowel disease (IBD) is caused by interaction of genetic and environmental risk factors. We evaluated potential determinants of the post-1990 increased incidence in North America. Using fitted generalized linear models, we assessed clinical features, smoking and genetic risk scores (GRS) for Crohn’s disease (CD) and ulcerative colitis (UC) in the National Institutes of Diabetes, Digestion and Kidney Diseases IBD Genetics Consortium database, before and post 1990. Among 2744 patients (55% CD, 42.2% UC), smoking status and GRS were the main determinants of diagnosis age. After 1990, smoking at diagnosis declined significantly in both UC and CD (34.1% vs 20.8%, P < .001, and 14.7% vs 8.7%, P = .06, respectively). In UC, ex-smoking increased (9% vs 15%, P < .001), and nonsmoking rates remained unchanged, whereas in CD, ex-smoking remained unchanged. CD-GRS and IBD-GRS were significantly associated with young diagnosis age, Jewish ethnicity, IBD family history, and surgery. CD-GRS showed a borderline significant decrease (P = .058) in multivariate analysis post 1990 but only when excluding surgery in the model; surgery significantly decreased post 1990 in both CD and UC. CD-GRS inversely correlated with smoking at diagnosis (P < .001) suggesting that, in the presence of smoking, CD may only require a low genetic risk to develop. Significantly increase in ex-smoking correlates with UC incidence post 1990. Conversely, smoking risk decreased significantly post 1990 despite rising CD incidence. CD-GRS likewise trended to decrease post 1990 only when not accounting for a significant decrease in CD surgery. We therefore deduce that unaccounted risk factors (eg, dietary, obesity, antibiotic use, improved hygiene, etc.) or greater detection or presence of mild CD may underlie post-1990 increased CD incidence.