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. 2019 Jan;39(1):127-135.
doi: 10.1111/liv.13943. Epub 2018 Sep 22.

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

Bernhard Scheiner  1   2 , Lisa Steininger  1   2 , Georg Semmler  1   2 , Lukas W Unger  2   3 , Philipp Schwabl  1   2 , Theresa Bucsics  1   2 , Rafael Paternostro  1   2 , Arnulf Ferlitsch  1   2 , Michael Trauner  1 , Thomas Reiberger  1   2 , Mattias Mandorfer  1   2
Affiliations

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

Bernhard Scheiner et al. Liver Int. 2019 Jan.

Abstract

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 < 0.001) and MELD-Na (per point; HR: 1.15, 95% CI: 1.04-1.28, P = 0.006) in cACLD and MELD-Na (per point; HR: 1.12, 95% CI: 1.05-1.19, P < 0.0001) in DC patients were the only parameters independently associated with first and further hepatic decompensation, respectively.

Conclusion: Controlled attenuation parameter does not predict the development of first (cACLD)/further (DC) hepatic decompensation, while serum albumin levels and MELD-Na are of prognostic value.

Keywords: compensated advanced chronic liver disease; controlled attenuation parameter; decompensated cirrhosis; hepatic decompensation.

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Conflict of interest statement

The authors have nothing to disclose regarding this study.

Figures

Figure 1
Figure 1
Patient flow chart showing the number of included and excluded patients as well as the number of patients assigned to the group of compensated advanced chronic liver disease and decompensated cirrhosis. CAP, controlled attenuation parameter; cACLD, compensated advanced chronic liver disease; DC, decompensated cirrhosis; HVPG, hepatic venous pressure gradient; HCC, hepatocellular carcinoma; HCV, hepatitis C virus; TE, transient elastography
Figure 2
Figure 2
Incidence of first/further hepatic decompensation according to baseline CAP </≥248 dB/m in (A) patients with compensated advanced chronic liver disease and (B) patients with decompensated cirrhosis. CAP, controlled attenuation parameter; M, months
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