Abstract
Background
Previous observational studies have found that lichen planus (LP) is associated with autoimmune diseases. To determine the association between LP and 15 autoimmune diseases, we applied the Mendelian randomization (MR) approach, which uses genetic variants as a tool to improve causal inference.
Methods
We performed a two-sample MR with the genetic instruments identified for 15 autoimmune diseases. Genome-wide association study (GWAS) data for LP was sourced from the FinnGen (1,865 cases and 212,242 non-cases). The instrumental variables (IVs) for LP were genetic variations highly associated (P < 5 × 10− 6) with LP in the European population. UK Biobank, FinnGen data and IEU Open GWAS database were utilized for autoimmune diseases GWAS data. To calculate causal effects, odds ratios (ORs) with 95% confidence intervals (CIs) are employed.
Results
We found genetic liability to LP was associated with a decreased risk of atopic dermatitis and ankylosing spondylitis, OR [95%CI] = 0.96[0.94, 0.99], PIVW = 0.013 and OR [95%CI] = 0.88[0.77, 0.99], PIVW = 0.047, respectively. Furthermore, it presents increased risk of higher odds ratios in: Type 1 diabetes (OR [95%CI] = 1.07[1.01, 1.14], PIVW = 0.027).
Conclusion
The MR study suggests that there may not be a significant association for LP contributing to the development of vitiligo, thyroid disease, SLE and Sjogren’s syndrome. On the contrast, we found that patients with LP are at decreased risk of AD and ankylosing spondylitis. no strong causal evidence of LP on the risk of vitiligo, thyroid disease, SLE and Sjogren’s syndrome.