The causal relationship between atopic dermatitis and brain cancer: A bidirectional Mendelian randomization study

Skin Res Technol. 2024 Apr;30(4):e13715. doi: 10.1111/srt.13715.

Abstract

Background: Atopic dermatitis ranks among the prevalent skin disorders. Research has indicated a potential association with brain cancer. Yet, establishing a direct causal relationship between atopic dermatitis and brain cancer continues to be challenging.

Materials and methods: We extracted single nucleotide polymorphisms (SNPs) significantly associated with atopic dermatitis (sample size = 382 254) at a genome-wide level from a large Finnish Genome-Wide Association Study (GWAS) dataset (n cases = 15 208, n controls = 367 046). Summary data for 372 622 cases of brain cancer (n cases = 606, n controls = 372 016) were obtained via the IEU Open GWAS database. We employed the Inverse Variance Weighted (IVW) method as our primary analytical approach for Mendelian Randomization (MR) analysis. Additionally, heterogeneity was measured using Cochran's Q value, and horizontal pleiotropy was evaluated using MR-Egger 、Mendelian Randomization Pleiotropy RESidual Sum and Outlier and leave-one-out analyses.

Results: The risk of brain cancer increases with the presence of atopic dermatitis, as evidenced by the odds ratios (ORs) and 95% confidence intervals (CIs),(OR = 1.0005; 95% CI = 1.0001, 1.0009; p = 0.0096). However, when conducting the analysis in reverse, no significant link was observed.

Conclusion: The findings from our study indicate a causative link between atopic dermatitis and brain cancer, highlighting the importance of conducting broader clinical investigations into their potential association going forward.

Keywords: atopic dermatitis; brain cancer; mendelian randomization; original article.

MeSH terms

  • Brain Neoplasms* / genetics
  • Dermatitis, Atopic* / genetics
  • Finland / epidemiology
  • Genetic Predisposition to Disease / genetics
  • Genome-Wide Association Study*
  • Humans
  • Mendelian Randomization Analysis*
  • Polymorphism, Single Nucleotide*
  • Risk Factors