Presence of NOD2 mutations is not associated with hepatic or systemic hemodynamic abnormalities of cirrhosis

Dig Liver Dis. 2023 Oct;55(10):1362-1367. doi: 10.1016/j.dld.2023.05.016. Epub 2023 Jun 13.

Abstract

Background: Patients with cirrhosis who carry NOD2 mutations are susceptible to bacterial infections. The aim was to evaluate the association of NOD2 mutations with hepatic and systemic hemodynamics in cirrhosis.

Patients and methods: This is a secondary analysis of a prospectively collected database in the context of the screening for the INCA trial (EudraCT 2013-001626-26). This cross-sectional study compared hemodynamic findings according to NOD2 status in 215 patients. Patients were genotyped for NOD2 variants (p.N289S, p.R702W, p.G908R, c.3020insC, rs72796367). Hepatic hemodynamic study and right heart catheterization were performed.

Results: Patients had a median age of 59 (IQR 53-66) years, and 144 (67%) were men. Most patients (64%) were Child-Pugh stage B. Sixty-six patients (31%) carried a NOD2 mutation, which was slightly more common among Child-Pugh stage C (p = 0.05), without differences in MELD [wild-type: 13 (10-16); NOD2 variants 13 (10-18)]. No differences in hepatic and systemic hemodynamics were observed according to NOD2 status. If excluding patients on prophylactic or therapeutic antibiotics, again no association between hepatic or systemic hemodynamics and NOD2 status could be observed.

Conclusion: NOD2 mutations are not associated with hepatic or systemic hemodynamic abnormalities in patients with decompensated cirrhosis, suggesting that other mechanisms leading to bacterial translocation predominate.

Keywords: Bacterial translocation; Hepatic venous pressure gradient; Liver cirrhosis; Portal hypertension.

MeSH terms

  • Aged
  • Cross-Sectional Studies
  • Female
  • Hemodynamics*
  • Humans
  • Liver Cirrhosis* / complications
  • Liver Cirrhosis* / genetics
  • Male
  • Middle Aged
  • Mutation
  • Nod2 Signaling Adaptor Protein / genetics

Substances

  • NOD2 protein, human
  • Nod2 Signaling Adaptor Protein