Controlled attenuation parameter does not predict hepatic decompensation in patients with advanced chronic liver disease

• Published in: Liver international 2019-01, Vol.39 (1), p.127-135
• Main Authors: Scheiner, Bernhard, Steininger, Lisa, Semmler, Georg, Unger, Lukas W., Schwabl, Philipp, Bucsics, Theresa, Paternostro, Rafael, Ferlitsch, Arnulf, Trauner, Michael, Reiberger, Thomas, Mandorfer, Mattias
• Format: Article
• Language: English
• Subjects: Adult; Aged; Albumin; Ascites; Attenuation; Bleeding; Cirrhosis; Cirrhosis and Liver Failure; compensated advanced chronic liver disease; Confidence intervals; controlled attenuation parameter; decompensated cirrhosis; Elasticity Imaging Techniques; Fatty liver; Female; hepatic decompensation; Hepatic encephalopathy; Humans; Liver; Liver - diagnostic imaging; Liver cirrhosis; Liver Cirrhosis - complications; Liver diseases; Liver Failure - diagnosis; Liver Failure - mortality; Male; Middle Aged; Multivariate Analysis; Parameters; Patients; Predictive Value of Tests; Prognosis; Proportional Hazards Models; Retrospective Studies; Serum albumin; Serum Albumin, Human - analysis; Steatosis; Stiffness
• ISSN: 1478-3223; 1478-3231
• DOI: 10.1111/liv.13943

Background & Aims Assessment of hepatic steatosis by transient elastography (TE)‐based controlled attenuation parameter (CAP) might predict hepatic decompensation. Therefore, we aimed to evaluate the prognostic value of CAP in patients with compensated advanced chronic liver disease (cACLD) and decompensated cirrhosis (DC). Methods A total of 430 patients who underwent TE (liver stiffness ≥10 kPa) and CAP measurements were included in this retrospective analysis. Half of patients (n = 189) underwent simultaneous HVPG measurement. In cACLD patients, first hepatic decompensation was defined by new onset of ascites, hepatic encephalopathy or variceal bleeding. In patients with DC, the following events were considered as further hepatic decompensation: requirement of paracentesis, admission for/development of grade 3/4 hepatic encephalopathy, variceal (re‐)bleeding or liver‐related death. Results First hepatic decompensation occurred in 25 of 292 (9%) cACLD patients, while 46 of 138 (33%) DC patients developed further hepatic decompensation during a median follow‐up of 22 and 12 months respectively. CAP was not predictive of first (cACLD; per 10 dB/m; hazard ratio [HR]: 0.97, 95% confidence interval [95% CI]: 0.91‐1.03, P = 0.321) or further hepatic decompensation (DC; HR: 0.99, 95% CI: 0.94‐1.03, P = 0.554) in adjusted analysis. Using the well‐established CAP cut‐off of ≥248 dB/m for hepatic steatosis, the incidence of first (cACLD; P = 0.065) and further hepatic decompensation (DC; P = 0.578) was similar in patients with hepatic steatosis or without. Serum albumin levels (per mg/dL; HR: 0.83, 95% CI: 0.77‐0.89, P