Department of Health Sciences, University of Leicester, Leicester, LE1 7RH, UK.
Groningen Research Institute of Pharmacy, University of Groningen, Groningen, 9700 AB, Netherlands.
Nat Commun. 2019 Apr 5;10(1):1561. doi: 10.1038/s41467-019-09381-w.
Following numerous genome-wide association studies of disease susceptibility, there is increasing interest in genetic associations with prognosis, survival or other subsequent events. Such associations are vulnerable to index event bias, by which selection of subjects according to disease status creates biased associations if common causes of incidence and prognosis are not accounted for. We propose an adjustment for index event bias using the residuals from the regression of genetic effects on prognosis on genetic effects on incidence. Our approach eliminates this bias when direct genetic effects on incidence and prognosis are independent, and otherwise reduces bias in realistic situations. In a study of idiopathic pulmonary fibrosis, we reverse a paradoxical association of the strong susceptibility gene MUC5B with increased survival, suggesting instead a significant association with decreased survival. In re-analysis of a study of Crohn's disease prognosis, four regions remain associated at genome-wide significance but with increased standard errors.
在对疾病易感性进行了大量全基因组关联研究之后,人们越来越关注与预后、生存或其他后续事件相关的遗传关联。如果未考虑发病率和预后的共同原因,那么这种关联容易受到起始事件偏倚的影响,即根据疾病状况选择研究对象会导致关联存在偏差。我们提出了一种使用遗传效应与预后的回归残差对遗传效应与发病率的回归残差进行调整的方法,以消除起始事件偏倚。当直接遗传效应对发病率和预后的影响独立时,我们的方法可以消除这种偏差,否则在实际情况下可以减少偏差。在一项特发性肺纤维化的研究中,我们扭转了强烈易感性基因 MUC5B 与生存率增加之间的矛盾关联,提示其与生存率降低有显著关联。在对克罗恩病预后的一项研究的重新分析中,四个区域仍然与全基因组意义显著相关,但标准误差增加。