ArticleClinical rheumatology2024
Systemic lupus erythematosus and Atopic dermatitis: A two sample Mendelian randomization study.
Article in Clinical rheumatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- Mendelian randomization studies in atopic dermatitis: causal insights across omics layers.Frontiers in immunology · 2026Review
- No causal association between pneumoconiosis and three inflammatory immune diseases: a Mendelian randomization study.Frontiers in public health · 2024Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSystemic lupus erythematosus (SLE) and atopic dermatitis (AD) are common diseases in human populations. Previous studies have suggested a potential association between SLE and AD. However, the causal relationship and direction between the two conditions remain unclear.
objectiveThe aim of this study is to evaluate the causal relationship between SLE and AD.
methodsIn this study, we employed Mendelian randomization (MR) analysis to investigate the causal relationship between SLE and AD. MR analysis has the advantage of reducing confounding factors, determining the direction of causality, and providing quantitative effect estimates. We obtained summary data from genome-wide association studies (GWAS) on SLE and AD from publicly available databases. Five MR methods, namely MR Egger, weighted median, inverse variance weighted, simple mode, and weighted mode, were used to assess the causal relationship between SLE and AD. Several techniques, including MR-Egger intercept, MR-PRESSO, and Cochran's Q test, were utilized to evaluate heterogeneity and pleiotropy.
resultsOur study demonstrated a causal relationship between the prevalence of SLE and an increased risk of AD (MR Egger OR: 1.567, 95% CI: [1.041, 1.285], P = 0.009; IVW OR: 1.085, 95% CI: [1.005, 1.143], P = 0.035). Furthermore, sensitivity analyses did not detect heterogeneity or pleiotropy.
conclusionOur research finds that SLE is a contributing factor to the development of AD, providing valuable insights into the pathogenesis and prevention of both diseases. Key Points • Currently, there is no research that clearly indicates a causal relationship between SLE and AD. This study, for the first time, identified a positive causal relationship between SLE and AD. • The results of this study contribute to our understanding of the pathogenesis and treatment strategies for SLE and AD, providing some guidance for future clinical practice.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.