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Performance of Controlled Attenuation Parameter in Patients with Advanced Chronic Liver Disease and Portal Hypertension

BACKGROUND: Liver stiffness (LS) measured by vibration-controlled transient elastography (VCTE) is influenced by liver fibrosis and hepatic perfusion pressure. VCTE-based controlled attenuation parameter (CAP) is a noninvasive marker for hepatic steatosis (HS). AIMS: To investigate the diagnostic pe...

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Detalles Bibliográficos
Autores principales: Semmler, Georg, Stift, Judith, Scheiner, Bernhard, Wöran, Katharina, Schwabl, Philipp, Paternostro, Rafael, Bucsics, Theresa, Stättermayer, Albert Friedrich, Pinter, Matthias, Ferlitsch, Arnulf, Trauner, Michael, Reiberger, Thomas, Mandorfer, Mattias
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6858384/
https://www.ncbi.nlm.nih.gov/pubmed/31209721
http://dx.doi.org/10.1007/s10620-019-05702-7
Descripción
Sumario:BACKGROUND: Liver stiffness (LS) measured by vibration-controlled transient elastography (VCTE) is influenced by liver fibrosis and hepatic perfusion pressure. VCTE-based controlled attenuation parameter (CAP) is a noninvasive marker for hepatic steatosis (HS). AIMS: To investigate the diagnostic performance of CAP in patients with advanced chronic liver disease (ACLD)/portal hypertension (PHT: hepatic venous pressure gradient (HVPG) ≥ 6 mmHg). METHODS: Eighty-eight patients with LS ≥ 10 kPa and/or HVPG ≥ 6 mmHg who underwent simultaneous liver biopsy, CAP, and HVPG measurement were included. HS was histologically graded according to the modified Brunt classification. RESULTS: Patient characteristics: Mean MELD:11 (standard derivation [SD] ± 4), median HVPG:16 (interquartile range [IQR]10–19) mmHg, median LS:27.4 (IQR 16.2–48.9) kPa, and mean CAP:221 (SD ± 75) dB/m. According to histology, 47 (53.4%) patients had no HS (S0), 28 (31.8%) had S1, 11 (12.5%) had S2, and 2 (2.3%) had S3. The area under the receiver operating characteristic curve (AUROC) of CAP for diagnosing any HS (S0 vs. ≥ S1) was 0.692 (95% confidence interval [95% CI] 0.582–0.802) in the overall cohort, 0.830 (95% CI 0.637–1.0) in patients with HVPG < 10 mmHg, and 0.629 (95% CI 0.497–0.761) in patients with clinically significant portal hypertension (CSPH; HVPG ≥ 10 mmHg; n = 69). Using the established cutoff for any HS (248 dB/m), the sensitivity/specificity of CAP was only 48.8%/76.6%, respectively. In contrast, the AUROC and sensitivity/specificity (cutoff 268 dB/m) for diagnosing HS ≥ S2 were 0.842 (95% CI 0.747–0.936) and 84.6%/81.3%, respectively. CAP correlated with the percentage of steatotic hepatocytes (Spearman’s ρ = 0.402; p ≤ 0.001) and showed a weak correlation with liver stiffness (ρ = 0.225; p = 0.035). CONCLUSIONS: The diagnostic performance of CAP for any HS seems to be limited in patients with ACLD, if CSPH is present. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1007/s10620-019-05702-7) contains supplementary material, which is available to authorized users.