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

ORCID
0000-0002-7561-6294
Zugehörigkeit
Department of Internal Medicine I, Martin-Luther University Halle Wittenberg, Halle
Greinert, Robin;
GND
1211611256
Zugehörigkeit
Internal Medicine IV, Jena University Hospital, Jena
Zipprich, Alexander;
Zugehörigkeit
Department of Medicine II, Saarland University Medical Center, Homburg
Casper, Markus;
Zugehörigkeit
Department of Medicine II, Saarland University Medical Center, Homburg
Reichert, Matthias Christian;
Zugehörigkeit
Department of Medicine II, Saarland University Medical Center, Homburg
Lammert, Frank;
GND
1210053217
ORCID
0000-0002-9704-4741
Zugehörigkeit
Internal Medicine IV, Jena University Hospital, Jena
Ripoll, Cristina

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.

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