Causal relationship analysis of MRI measurements of major human internal organs and liver disease

磁共振成像测量对人体主要内脏器官和肝脏疾病的因果关系分析

阅读:1

Abstract

BACKGROUND: This study aimed to explore the causal association between imaging measurement indicators of major internal organs and liver lesions using a two-sample Mendelian randomization (MR) method. METHODS: Data from the UK Biobank and GWAS Catalog platform were used to select single nucleotide polymorphisms (SNPs) associated with MRI or derived measurement results of various organ indicators as genetic instrumental variables. Data from the FinnGen project's R9 version were used to select liver lesion outcomes, such as nonalcoholic fatty liver disease (NAFLD), nonalcoholic cirrhosis, and primary hepatocellular carcinoma (HCC). UVMR analysis were utilized variable-by-variable, and MVMR was used to adjust for confounding on significant variables. Steiger directional test, heterogeneity, pleiotropy, and sensitivity tests were conducted to enhance reliability. RESULTS: Univariate Mendelian randomization analysis (UVMR) indicated that liver volume (LV), liver fat (LF), and subcutaneous adipose tissue measurement (SATM) are risk factors for NAFLD. The multivariable MR (MVMR) results for NAFLD showed that LV and LF remained significant, while SATM did not. For cirrhosis (NAC), UVMR suggested that LV, LF, and SATM are risk factors, but MVMR results showed that only LV and LF remained significant. Additionally, pancreatic volume (PV) was found to be a protective factor, while splenic volume (SV) was a pathogenic factor for NAC. For HCC, both UVMR and MVMR analyses suggested that LF and liver iron (LI) are risk factors, while SATM did not remain significant in the MVMR analysis. CONCLUSIONS: LV, LF, and SATM are associated with NAFLD. In the NAC stage, additional pathogenic effects of PV and SV were observed. The related results for LF and LI support the pathogenic effect of liver iron factors in the HCC stage.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。