Fig 1.
The study design overview and flowchart of MR analysis in this study.
GWAS, genome-wide association studies; SNP, single nucleotide polymorphisms; IVs, instrument variables; MR, Mendelian randomization; PRESSO, pleiotropy residual sum and outlier; IVW, inverse variance weighted; CD, Crohn’s diseaseor; UC, ulcerative colitis; IBD, inflammatory bowel disease.
Fig 2.
Summary of univariate Mendelian randomization (MR) analyses of the causal effects between Crohn’s disease (CD) and the risk of autoimmune hepatitis (AIH).
OR, odds ratio; CI, confidence interval; FDR, false discovery rate.
Fig 3.
Summary of multivariable Mendelian randomization (MR) analyses of the causal effects between Crohn’s disease (CD) or ulcerative colitis (UC) and the risk of autoimmune hepatitis (AIH) using inverse variance weighted (IVW) method.
OR, odds ratio; CI, confidence interval.
Table 1.
Sensitivity analysis of the MR analysis result of exposure and outcome.
Fig 4.
Summary of univariate Mendelian randomization (MR) analyses of the causal effects between ulcerative colitis (UC) and the risk of autoimmune hepatitis (AIH).
OR, odds ratio; CI, confidence interval; FDR, false discovery rate.
Fig 5.
Summary of univariate Mendelian randomization (MR) analyses of the causal effects between inflammatory bowel disease (IBD) and the risk of autoimmune hepatitis (AIH).
OR, odds ratio; CI, confidence interval.
Fig 6.
The effect of risk factors (Crohn’s disease (CD), ulcerative colitis (UC), and inflammatory bowel disease (IBD)) on the risk of autoimmune hepatitis (AIH) in replication analysis and meta-analysis.
OR, odds ratio; CI, confidence interval.