Z Gastroenterol 2022; 60(08): e484
DOI: 10.1055/s-0042-1754737
Abstracts | DGVS/DGAV
Leber und Galle
Leberzirrhose: Grundlagen II
Donnerstag, 15. September 2022, 10:10 – 11:14, Saal 5

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

R Greinert
1   Universitätsklinikum Halle, Klinik für Innere Medizin I, Halle, Deutschland
,
A Zipprich
2   Universitätsklinikum Jena, Klinik für Innere Medizin IV, Jena, Deutschland
,
A Hauptmann
3   Universitätsklinikum des Saarlands, Innere Medizin II, Homburg, Deutschland
,
M Casper
3   Universitätsklinikum des Saarlands, Innere Medizin II, Homburg, Deutschland
,
M Reichert
3   Universitätsklinikum des Saarlands, Innere Medizin II, Homburg, Deutschland
,
F Lammert
3   Universitätsklinikum des Saarlands, Innere Medizin II, Homburg, Deutschland
,
C Ripoll
2   Universitätsklinikum Jena, Klinik für Innere Medizin IV, Jena, Deutschland
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    Introduction Presence of NOD2 Mutation has been associated to infections in cirrhosis. This association is more evident in compensated patients (pts) (PMID: 30702490). According to the systemic inflammation hypothesis, bacterial translocation is one of the main drivers of complications of end-stage liver disease

    Aims Aim was to evaluate the association of NOD2 mutations with hepatic and systemic hemodynamics

    Methods The presence of NOD2 risk variants (p.N289S, p.R702W, p.G908R, c.3020insC, rs72796367) were evaluated in 825 pts (screening in context of INCA trial: EudraCT 2013-001626-26). From these, 215 pts received a hepatic hemodynamic study and right heart catheterization. This cross-sectional study compared hepatic hemodynamic and systemic hemodynamics according to NOD2 status. Variables are described with median (IQR) or proportions. Mann Whitney U or Chi-square test were applied

    NOD2 wild-type

    NOD2 Variants

    p value

    MAP (mmHg)

    83 (76-89)

    83 (75-91)

    0.961

    CI (l/min/m2)

    2.93 (2.47-3.52)

    3.31 (2.59-3.95)

    0.075

    SVRI (dyn·sec/cm 5 /m 2 )

    2016 (1641-2490)

    1814 (1473-2399)

    0.315

    PAP (mmHg)

    16 (13-20)

    17 (14-20)

    0.285

    PCWP (mmHg)

    11 (7-15)

    12 (8-15)

    0.237

    PVR (dyn·sec·cm -5 )

    75 (43-112)

    65 (32-112)

    0.542

    VCI (mmHg)

    8 (6-12)

    8 (5-11)

    0.395

    WHVP (mmHg)

    29 (23-32)

    28(23-35)

    0.483

    FHVP (mmHg)

    12 (8-15)

    12 (7-15)

    0.982

    HVPG (mmHg)

    19 (15-22)

    19 (15-23)

    0.994

    Results Two-hundred-fifteen pts were included [median age 59 (IQR 53-66); male 67%; 76% alcohol associated cirrhosis]. Most pts were Child Pugh stage B (A 25%, B 64%, C 11%).Sixty-six pts (31%) carried a NOD2 risk variant, of which 64 were heterozygous pts. Although there was an increase in the proportion of NOD2 risk variants among Child Pugh stage C (p=0.05), no differences were observed in MELD score [wild-type: 13 (10-16); NOD2 variants 13 (10-18)]. No significant differences in hepatic and systemic hemodynamics were observed when comparing patients with and without NOD2risk variants (table 1). Analyses were repeated excluding patients who were on prophylactic or therapeutic antibiotics and again no association between hepatic or systemic hemodynamic parameters and NOD2risk variants could be observed

    Conclusions The presence of NOD2 mutations is not associated with hepatic or systemic hemodynamic abnormalities in patients with cirrhosis, suggesting that other mechanisms leading to bacterial translocation predominate


     

    Publication History

    Article published online:
    19 August 2022

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