Inflammatory bowel disease in Spain: problems grow

Román, Antonio; Bermejo, Fernando

doi:10.4321/s1130-01082004000500001

Cited by 4 publications

(1 citation statement)

References 7 publications

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“…The involvement of the appendix in the pathogenesis of UC has been postulated; however, the precise nature and underlying mechanisms of this association remain elusive 4,5 . Numerous observational studies have demonstrated a notable decrease in the incidence of UC among individuals diagnosed with appendicitis when compared to control subjects [6][7][8][9] . Furthermore, several investigations have highlighted the potential of appendectomy to reduce the risk of UC and enhance clinical outcomes [10][11][12][13][14][15] .…”

Section: Introductionmentioning

confidence: 99%

Evidence for genetic correlation between appendix and inflammatory bowel disease: a bidirectional Mendelian randomization study

Liu,

Dan,

Yan

et al. 2024

Preprint

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Observational studies highlighted an association between the appendix and inflammatory bowel disease (IBD). However, it's unclear whether the identified association is causal because of difficulties in establishing a clear temporal sequence. We investigated the association between acute appendicitis, appendectomy, and IBD by using two-sample bidirectional univariable Mendelian randomization (UVMR), multivariable MR (MVMR) and linkage disequilibrium score regression (LDSC) analyses. Eligible instrumental variables were screened from previous genome-wide association studies (GWAS) of European ancestry for analysis. The inverse variance-weighted (IVW) method was used for the primary analysis. Sensitivity analyses were used to detect and correct pleiotropy. LDSC analysis determined SNP-based heritability (h2) for acute appendicitis, IBD, Crohn's disease (CD), and ulcerative colitis (UC). Following that, cross-trait LDSC analysis assessed genetic correlations (rg) between these traits using GWAS summary data. Genetically predicted UC was associated with a significantly lower risk of acute appendicitis (OR = 0.933, P < 0.001) and appendectomy (OR = 0.954, P < 0.001), but conversely, acute appendicitis or appendectomy had no causal effect on IBD, UC or CD (all P > 0.05). CD had a suggestive association with appendectomy (OR = 0.981, P = 0.018) but was not significant after excluding the effect of UC by MVMR (OR = 0.999, P = 0.889). Furthermore, LDSC suggested a negative genetic correlation between UC and acute appendicitis (rg = -0.205, P = 0.005). In conclusion, our study confirms UC casually leads to a decreased risk of acute appendicitis and appendectomy, but neither acute appendicitis nor appendectomy reduces the risk of IBD, UC, and CD.

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