Z Gastroenterol 2018; 56(05): e48
DOI: 10.1055/s-0038-1654662
POSTER
Hepatologie
Georg Thieme Verlag KG Stuttgart · New York

Controlled attenuation parameter (CAP®) does not predict hepatic decompensation in patients with compensated advanced chronic liver disease

L Steininger
1   Medical University of Vienna, Department of Internal Medicine III, Division of Gastroenterology & Hepatology, Vienna, Austria
,
B Scheiner
1   Medical University of Vienna, Department of Internal Medicine III, Division of Gastroenterology & Hepatology, Vienna, Austria
,
G Semmler
1   Medical University of Vienna, Department of Internal Medicine III, Division of Gastroenterology & Hepatology, Vienna, Austria
,
P Schwabl
1   Medical University of Vienna, Department of Internal Medicine III, Division of Gastroenterology & Hepatology, Vienna, Austria
,
T Bucsics
1   Medical University of Vienna, Department of Internal Medicine III, Division of Gastroenterology & Hepatology, Vienna, Austria
,
R Paternostro
1   Medical University of Vienna, Department of Internal Medicine III, Division of Gastroenterology & Hepatology, Vienna, Austria
,
A Ferlitsch
1   Medical University of Vienna, Department of Internal Medicine III, Division of Gastroenterology & Hepatology, Vienna, Austria
,
M Trauner
1   Medical University of Vienna, Department of Internal Medicine III, Division of Gastroenterology & Hepatology, Vienna, Austria
,
T Reiberger
1   Medical University of Vienna, Department of Internal Medicine III, Division of Gastroenterology & Hepatology, Vienna, Austria
,
M Mandorfer
1   Medical University of Vienna, Department of Internal Medicine III, Division of Gastroenterology & Hepatology, Vienna, Austria
› Author Affiliations
Further Information

Publication History

Publication Date:
09 May 2018 (online)

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Background and Aims:

Transient elastography (TE)-based controlled attenuation parameter (CAP®) is a non-invasive marker of hepatic steatosis. Recently, CAP® has been proposed as a predictor of decompensation in patients with compensated advanced chronic liver disease (cACLD). Our aim was to evaluate the prognostic value of CAP® in patients with cACLD and decompensated cirrhosis (DC).

Method:

189 patients who underwent simultaneous TE (stiffness ≥10kPa) and hepatic-venous pressure gradient (HVPG) measurements between 01/2014 and 12/2016 were included in this retrospective analysis. In cACLD-patients, hepatic decompensation was defined by new onset of ascites, hepatic encephalopathy, or variceal bleeding. In patients with DC, requirement of paracentesis, admission for grade III/IV hepatic encephalopathy, or liver-related death were considered as (further) hepatic decompensation.

Results:

The study population was stratified into patients with cACLD (without prior hepatic decompensation, n = 86) and patients with DC (n = 103). Hepatic decompensation occurred in 13 (15.1%) cACLD patients and in 33 (32.0%) patients with DC during a mean follow-up of 23.2 and 16.1 months, respectively. CAP® was not predictive of (further) hepatic decompensation in cACLD patients (per 10 dB/m; OR: 0.999, 95%CI: 0.990 – 1.008, p = 0.884) or in patients with DC (OR: 0.998, 95%CI: 0.992 – 1.004, p = 0.499). Adjusting for baseline characteristics including the presence of clinically significant portal hypertension/HVPG did affect these results. Using the well-established CAP®-cutoff of ≥248 dB/m for any steatosis, the incidence of (further) hepatic decompensation was comparable between CAP® groups (cACLD: p = 0.657; DC: p = 0.743). Serum albumin levels (per mg/dL; OR: 0.773, 95%CI: 0.684 – 0.874, p < 0.001) and HVPG (per mmHg; OR: 1.087, 95%CI: 1.005 – 1.175, p = 0.036) were the only parameters independently associated with (further) hepatic decompensation in patients with cACLD and DC, respectively.

Conclusion:

CAP® does not predict the development of (further) hepatic decompensation in patients with cACLD or DC, while serum albumin levels and HVPG are of prognostic value.