ArticleArchives of dermatological research2025
Exploring the shared genetic mechanisms of atopic dermatitis and alopecia areata via bioinformatics approaches.
Article in Archives of dermatological research, 2025. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Precision therapeutics in non-scarring alopecia: a systemic genomic and pathway-based framework for targeted interventions.ADMET & DMPK · 2026Review
- Bioinformatics analysis of immune infiltration and cell cycle hub genes in atopic dermatitis.Biochemistry and biophysics reports · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atopic dermatitis (AD) and alopecia areata (AA) are chronic inflammatory skin diseases. While studies suggest a possible immune defense mechanism link between the two, the causal relationship remains unclear, and current methodologies have limitations. This study aims to investigate the causal relationship between AD and AA using genome-wide association study statistics from the Integrative Epidemiology Unit Open Genome-Wide Association Study (IEU Open Gwas) project. We utilized the inverse variance weighting (IVW) method as our primary analysis approach for assessing the causal association between AD and AA. To enhance the robustness of our findings, we also employed supplementary validation methods, including the weighted median, MR-Egger method, and other analytical approaches. Our analysis revealed a significant increase in the risk of AA associated with single-nucleotide polymorphisms (SNPs) linked to AD (odds ratio (OR) = 1.84, 95% confidence interval (CI): 1.19-2.85, p-value (p) = 0.006). While MR-Egger analysis did not show a significant association (OR = 1.04, 95% CI: 0.29-3.68, p = 0.957), weighted median analysis demonstrated a significant association (OR = 2.08, 95% CI: 1.16-3.71, p = 0.013). Additionally, MR-Egger intercept and MR-PRESSO analysis showed no evidence of potential pleiotropy or horizontal pleiotropy between AD and AA. This study indicates that AD increases the risk of AA, providing valuable insights into the pathogenesis and prevention of these two diseases. Future research should explore the underlying mechanisms to better understand this relationship.
Indexed as
Identifiers
39976767What OpenQuestion holds
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.