The impact of hepatic steatosis on portal hypertension
Autoři:
Georg Semmler aff001; Bernhard Scheiner aff001; Philipp Schwabl aff001; Theresa Bucsics aff001; Rafael Paternostro aff001; David Chromy aff001; Albert Friedrich Stättermayer aff001; Michael Trauner aff001; Mattias Mandorfer aff001; Arnulf Ferlitsch aff003; Thomas Reiberger aff001
Působiště autorů:
Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria
aff001; Vienna Hepatic Hemodynamic Laboratory, Medical University of Vienna, Vienna, Austria
aff002; Department of Internal Medicine I, Hospital of St. John of God, Vienna, Austria
aff003
Vyšlo v časopise:
PLoS ONE 14(11)
Kategorie:
Research Article
doi:
https://doi.org/10.1371/journal.pone.0224506
Souhrn
Background and aims
Studies in animal models have suggested that hepatic steatosis impacts on portal pressure, potentially by inducing liver sinusoidal endothelial dysfunction and thereby increasing intrahepatic resistance. Thus, we aimed to evaluate the impact of hepatic steatosis on hepatic venous pressure gradient (HVPG) in patients with chronic liver disease.
Method
261 patients undergoing simultaneous HVPG measurements and controlled attenuation parameter (CAP)-based steatosis assessment were included in this retrospective study.
Results
The majority of patients had cirrhosis (n = 205; 78.5%) and n = 191 (73.2%) had clinically significant portal hypertension (CSPH; HVPG≥10mmHg). Hepatic steatosis (S1/2/3; CAP ≥248dB/m) was present in n = 102 (39.1%). Overall, HVPG was comparable between patients with vs. without hepatic steatosis (15.5±7.5 vs. 14.8±7.7mmHg; p = 0.465). Neither in patients with HVPG (<6mmHg; p = 0.371) nor in patients with mild portal hypertension (HVPG 6–9mmHg; p = 0.716) or CSPH (HVPG≥10mmHg; p = 0.311) any correlation between CAP and HVPG was found. Interestingly, in patients with liver fibrosis F2/3, there was a negative correlation between CAP and HVPG (Pearson’s ρ:-0.522; p≤0.001). In multivariate analysis, higher CAP was an independent ‘protective’ factor for the presence of CSPH (odds ratio [OR] per 10dB/m: 0.92, 95% confidence interval [CI]:0.85–1.00; p = 0.045), while liver stiffness was associated with the presence of CSPH (OR per kPa: 1.26, 95%CI: 1.17–1.36; p≤0.001). In 78 patients, in whom liver biopsy was performed, HVPG was neither correlated with percentage of histological steatosis (p = 0.714) nor with histological steatosis grade (p = 0.957).
Conclusion
Hepatic steatosis, as assessed by CAP and liver histology, did not impact on HVPG in our cohort comprising a high proportion of patients with advanced chronic liver disease. However, high CAP values (i.e. pronounced hepatic steatosis) might lead to overestimation of liver fibrosis by ‘artificially’ increasing transient elastography-based liver stiffness measurements.
Klíčová slova:
Etiology – Fatty liver – Fibrosis – Histology – Liver diseases – Liver fibrosis – Portal hypertension – Steatosis
Zdroje
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