Volume 23 Issue 2
Feb.  2025
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YAN Jiawen, JI Junzhu, HAN Ruiting, YU Haibin. Association of uric acid with COPD and pulmonary ventilation based on Mendelian randomization method[J]. Chinese Journal of General Practice, 2025, 23(2): 186-189. doi: 10.16766/j.cnki.issn.1674-4152.003863
Citation: YAN Jiawen, JI Junzhu, HAN Ruiting, YU Haibin. Association of uric acid with COPD and pulmonary ventilation based on Mendelian randomization method[J]. Chinese Journal of General Practice, 2025, 23(2): 186-189. doi: 10.16766/j.cnki.issn.1674-4152.003863
shu

Association of uric acid with COPD and pulmonary ventilation based on Mendelian randomization method

doi: 10.16766/j.cnki.issn.1674-4152.003863
  • 1.

    Department of Respiratory Medicine, the First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, Henan 450003, China

Funds:

 2021JDZX005

 2022ZYZD04

 2023XTCX043

  • Received Date: 2024-01-24
    Available Online: 2025-03-27
    Abstract
  •   Objective   Relevant studies have indicated a correlation between blood uric acid (UA) levels and the occurrence and progression of chronic obstructive pulmonary disease (COPD) and pulmonary obstruction; In this study, Mendelian randomization analysis is used to further explore the causal relationship between them.  Methods   The gene loci related to COPD, blood uric acid, and pulmonary ventilation were screened from the aggregated data of genome-wide association studies and used as instrumental variables to conduct Mendelian randomization analysis using various analysis methods such as IVW. MR-PRESSO, MR-Egger intercept and, leave-one-out methods were used to analyze the sensitivity of relevant gene loci.  Results   IVW results showed no causal relationship between UA and the occurrence of COPD (OR = 1. 053, 95% CI: 0. 932-1. 189, P = 0. 406), and neither MR-PRESSO nor MR-Egger observed horizontal polymorphism and heterogeneity. No significant association between UA and first second forced expiratory volume ratio of the measured value to the predicted value (FEV1%) changes (β = -0. 006, P = 0. 686), No significant association between UA and FEV1 / forced vital capacity (FVC) changes (β = -0. 004, P = 0. 323), and horizontal polymorphism and heterogeneity were observed for MRPRESSO and MR-Egger, however, after excluding SNPs with horizontal pleiotropy, the results still showed no significant association (UA-FEV1% P = 0. 412, UA-FEV1 / FVC P = 0. 303). No significant changes in the above causal relationships were observed after the relevant gene loci were removed one by one by the leave-one-out method.  Conclusion   The results of this study show that UA is positively correlated with the development of COPD and negatively correlated with changes in FEV 1% and FEV1 / FVC, but none of these is a correlate causal relationship.

     

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