胃食管反流病、肥胖症的遗传易感性以及特发性肺纤维化的风险。
Genetic liability to gastro-esophageal reflux disease, obesity, and risk of idiopathic pulmonary fibrosis.
作者信息
Cotton Caroline, Alton Philip, Hughes David M, Zhao Sizheng Steven
机构信息
Department of Rheumatology, Liverpool University Hospitals NHS Foundation Trust, Liverpool, UK.
Accident and Emergency Department, Liverpool University Hospitals NHS Foundation Trust, Liverpool, UK.
出版信息
Respir Investig. 2023 May;61(3):335-338. doi: 10.1016/j.resinv.2023.02.005. Epub 2023 Mar 16.
BACKGROUND
Gastro-esophageal reflux disease (GORD) has been associated with a greater risk of idiopathic pulmonary fibrosis (IPF) in observational studies, but results are limited by confounding. We used multivariable Mendelian randomization to examine their causal relationship, adjusting for BMI.
METHODS
We selected genetic instruments for GORD from genome-wide association studies of 80,265 cases and 305,011 controls. Genetic association data for IPF were obtained from 2668 cases and 8591 controls, and BMI from 694,649 individuals. We used the inverse-variance weighted method and a series of sensitivity analyses including weak instrument robust methods.
RESULTS
Although genetic liability to GORD increased IPF risk (OR 1.58; 95% CI 1.10-2.25), this result was attenuated to include the null after adjusting for BMI (OR 1.14; 95% CI 0.85-1.52).
CONCLUSION
Intervention for GORD alone is unlikely to reduce the risk of IPF, whereas reducing obesity may be a better approach.
背景
在观察性研究中，胃食管反流病（GORD）与特发性肺纤维化（IPF）的风险增加有关，但结果受混杂因素影响而受限。我们使用多变量孟德尔随机化来研究它们的因果关系，并对体重指数（BMI）进行了调整。
方法
我们从80265例病例和305011例对照的全基因组关联研究中选择了GORD的遗传工具变量。IPF的遗传关联数据来自2668例病例和8591例对照，BMI数据来自694649人。我们使用了逆方差加权法和一系列敏感性分析，包括弱工具变量稳健方法。
结果
尽管GORD的遗传易感性增加了IPF风险（比值比1.58；95%置信区间1.10 - 2.25），但在调整BMI后，该结果减弱至包括无效值（比值比1.14；95%置信区间0.85 - 1.52）。
结论
单独针对GORD进行干预不太可能降低IPF风险，而减轻肥胖可能是更好的方法。
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