SynthesisWiener klinische Wochenschrift2022
Inflammatory bowel disease and risk of coronary heart disease : A Mendelian randomization study.
Synthesis in Wiener klinische Wochenschrift, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 4 citations in OpenAlex.
- Heart Under Pressure: Divergent Cardiac Molecules Responses to Azathioprine and Anti-TNF Therapy in Ulcerative Colitis.International journal of molecular sciences · 2025Observational
- Causal relationship between inflammatory bowel disease and cardiovascular disease: a two-sample Mendelian randomized study.Archives of medical science : AMS · 2025Article
- Causal association between gastrointestinal diseases and coronary artery disease: a bidirectional Mendelian randomization study.Frontiers in endocrinology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundInflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD), has been reported to be associated with an increased risk of coronary heart disease (CHD); however, the causal link between IBD and CHD is unclear. We performed Mendelian randomization (MR) analysis to investigate the association between genetically predicted IBD and CHD risk.
methodsExposure summary data were obtained from genome-wide association studies (GWAS) with cohorts of IBD (12,882 cases and 21,770 controls), UC (6968 cases and 20,464 controls), and CD (5956 cases and 14,927 controls) of European descent to identify single nucleotide polymorphisms (SNPs) as instrumental variables. Outcome summary data were obtained from a meta-analysis of 22 GWAS including 22,233 cases and 64,762 controls of European descent. To estimate MR, four methods were used, including inverse variance-weighted (IVW), MR-Egger, simple mode, and weighted median methods. Sensitivity analysis was also performed. The Bonferroni method was used to correct the bias of multiple testing.
resultsThree sets of SNPs (69 SNPs of IBD, 40 SNPs of UC, and 58 SNPs of CD) were used to estimate the causal effect between genetically predicted IBD and CHD. Using the IVW method, we found that no causal relationship between genetically predicted IBD and CHD after Bonferroni correction, and there was no causal relationship between UC/CD and the development of CHD. No evidence of significant heterogeneity and pleiotropy was found.
conclusionThe results of this study suggested that genetically predicted IBD may have no causal effect on CHD risk in a population with European ancestry.
Indexed as
Identifiers
What 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.