SynthesisScientific reports2025
Spleen volume in relation to ulcerative colitis and Crohn's disease: a Mendelian randomization study.
Synthesis in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- The impact for causal associations between common diseases and inflammatory bowel disease: a disease-wide bidirectional Mendelian randomization study.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Genetic evidence against a causal relationship between myocardial infarction and urological malignancies.The Canadian journal of urology · 2026Article
- Causal effects of antibody-mediated immunity to pathogens on five ophthalmic diseases: a Mendelian randomization study.Experimental biology and medicine (Maywood, N.J.) · 2026Article
- Modifiable Dietary Habits, Inflammatory Mediation, and Senile Cataract: Unraveling Causality via Mendelian Randomization.Food science & nutrition · 2025Article
- Evaluating spleen volume in inflammatory bowel disease.Annals of gastroenterologyReview
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Prior research has established the significance of spleen volume (SV) in the pathogenesis and advancement of ulcerative colitis (UC) and Crohn's disease (CD). Nevertheless, these investigations are predominantly observational, thereby leaving their causal associations ambiguous. Moreover, the breadth of existing research is constrained by various uncontrollable variables in clinical settings. This study aims to deduce the causal link between SV and the susceptibility to UC and CD through a genetic perspective. The objective of this study was to investigate the genetic association between SV and inflammatory bowel disease (IBD) risk using Mendelian randomization (MR) analysis. Single nucleotide polymorphisms (SNPs) associated with SV were used as instrumental variables. Genetic associations for UC and CD were extracted from the International Inflammatory Bowel Disease Genetics Consortium (IIBDGC), the FinnGen study, and other publicly available genome-wide association studies (GWAS). Methods such as inverse variance weighted, Bayesian weighted Mendelian randomization (BWMR), contamination mixture (ConMix), along with sensitivity analyses and the Steiger test were used in the study. A meta-analysis was conducted to synthesize the results. The study found that genetically predicted SV was associated with an increased risk of UC in the IIBDGC dataset (OR = 1. 223, 95% CI: 1. 055-1. 417, P = 0. 008), FinnGen (OR = 1. 169, 95% CI: 1. 003-1. 363, P = 0. 045), the GWAS study by Sakaue S (OR = 1. 188, 95% CI: 1. 008-1. 399, P = 0. 040), and in the meta-analysis (OR = 1. 115, 95% CI: 1. 014-1. 227, P = 0. 025). Similarly, genetically predicted SV was associated with an increased risk of CD in the IIBDGC dataset (OR = 1. 235, 95% CI: 1. 026-1. 488, P = 0. 026), FinnGen (OR = 1. 308, 95% CI: 1. 026-1. 667, P = 0. 030), the GWAS study by Zorina-Lichtenwalter K (OR = 1. 316, 95% CI: 1. 037-1. 670, P = 0. 024), and in the meta-analysis (OR = 1. 272, 95% CI: 1. 133-1. 428, P < 0. 001). According to the meta-analysis results, for each standard unit increase in SV, the risk of developing UC increases by 11. 5%, and the risk of developing CD increases by 27. 2%. This study presents findings that suggest a positive causal association between SV and the onset of IBD.
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