Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Exploring the Relationship Between NOD2 Risk Variants and First Decompensation Events in Cirrhotic Patients With Varices.

Liver international : official journal of the International Association for the Study of the Liver - 1 Apr 2025

Karbannek Henrik, Reichert Matthias C, Greinert Robin, Zipprich Alexander, Lammert Frank, Ripoll Cristina

Abstract excerpt

BACKGROUND AND AIMS: NOD2 mutations are associated with impaired gut mucosal barrier function. According to the systemic inflammation hypothesis, bacterial translocation is central in the development of decompensation. The aim was to evaluate whether the presence of NOD2 variants is associated with the development of first decompensation. METHOD: Secondary analysis of prospectively collected consecutive patients...

Topics

Join the communities discussing this publication.

Aged
NOD2 gene
Genetic Predisposition to Disease
Liver Cirrhosis
Mutation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Nod2 Signaling Adaptor Protein

Source

Open in PubMed Open full text

Identifiers

PMID: 39469976
DOI: 10.1111/liv.16143
PMCID: PMC11891376

Genes

NOD2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026.

Community interpretation

Discuss the evidence

Ask a question, add context or challenge an interpretation. Community activity is separate from scientific evidence strength.

0

discussions

0

replies

Citations encouraged

Claims remain attributable.

No discussion yet

Be the first to add a careful, cited interpretation.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Exploring the Relationship Between NOD2 Risk Variants and First Decompensation Events in Cirrhotic Patients With Varices.PMID 39469976Read ↗

NOD2 gene variants confer risk for secondary sclerosing cholangitis in critically ill patients.Semantic proximity Read ↗

Presence of NOD2 mutations is not associated with hepatic or systemic hemodynamic abnormalities of cirrhosis.Semantic proximity Read ↗

NOD2 gene variants are a risk factor for culture-positive spontaneous bacterial peritonitis and monomicrobial bacterascites in cirrhosis.Semantic proximity Read ↗

Nucleotide‐binding oligomerization domain containing 2 (NOD2) variants are genetic risk factors for death and spontaneous bacterial peritonitis in liver cirrhosis†Semantic proximity Read ↗

The prognostic power of the NOD2 genotype for complicated Crohn's disease: a meta-analysis.Semantic proximity Read ↗

Functional polymorphisms of innate immunity receptors are not risk factors for the non-SBP type bacterial infections in cirrhosis.Semantic proximity Read ↗

The INCA trial (Impact of NOD2 genotype-guided antibiotic prevention on survival in patients with liver Cirrhosis and Ascites): study protocol for a randomized controlled trial.Semantic proximity Read ↗

Predictors of Non-Variceal Hemorrhage in a National Cohort of Patients with Chronic Liver DiseaseSemantic proximity Read ↗

NOD1 and NOD2 genetic variants: Impact on hepatocellular carcinoma susceptibility and progression in Moroccan population.Semantic proximity Read ↗

A variant in the nuclear dot protein 52kDa gene increases the risk for spontaneous bacterial peritonitis in patients with alcoholic liver cirrhosis.Semantic proximity Read ↗

Nucleotide-Binding Oligomerization Domain-Containing Protein 2 Variants in Patients with Spontaneous Bacterial Peritonitis.Semantic proximity Read ↗

Toll-like receptor (TLR) 2 promoter and intron 2 polymorphisms are associated with increased risk for spontaneous bacterial peritonitis in liver cirrhosis.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.