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Observational Study
. 2017 Dec 21;21(1):321.
doi: 10.1186/s13054-017-1894-8.

Copeptin in acute decompensation of liver cirrhosis: relationship with acute-on-chronic liver failure and short-term survival

Annarein J C Kerbert  1 , Hein W Verspaget  2 , Àlex Amorós Navarro  3 , Rajiv Jalan  4 , Elsa Solà  5 , Daniel Benten  6 , François Durand  7 , Pere Ginès  5 , Johan J van der Reijden  2 , Bart van Hoek  2 , Minneke J Coenraad  2 ; CANONIC Study Investigators of the EASL-CLIF Consortium
Affiliations
Observational Study

Copeptin in acute decompensation of liver cirrhosis: relationship with acute-on-chronic liver failure and short-term survival

Annarein J C Kerbert et al. Crit Care. .

Abstract

Background: Acute-on-chronic liver failure (ACLF) is characterized by the presence of acute decompensation (AD) of cirrhosis, organ failure, and high short-term mortality rates. Hemodynamic dysfunction and activation of endogenous vasoconstrictor systems are thought to contribute to the pathogenesis of ACLF. We explored whether copeptin, a surrogate marker of arginine vasopressin, is a potential marker of outcome in patients admitted for AD or ACLF and whether it might be of additional value to conventional prognostic scoring systems in these patients.

Methods: All 779 patients hospitalized for AD of cirrhosis from the CANONIC database with at least one serum sample available for copeptin measurement were included. Presence of ACLF was defined according to the CLIF-consortium organ failure (CLIF-C OF) score. Serum copeptin was measured in samples collected at days 0-2, 3-7, 8-14, 15-21, and 22-28 when available. Competing-risk regression analysis was applied to evaluate the impact of serum copeptin and laboratory and clinical data on short-term survival.

Results: Serum copeptin concentration was found to be significantly higher in patients with ACLF compared with those without ACLF at days 0-2 (33 (14-64) vs. 11 (4-26) pmol/L; p < 0.001). Serum copeptin at admission was shown to be a predictor of mortality independently of MELD and CLIF-C OF scores. Moreover, baseline serum copeptin was found to be predictive of ACLF development within 28 days of follow-up.

Conclusions: ACLF is associated with significantly higher serum copeptin concentrations at hospital admission compared with those with traditional AD. Copeptin is independently associated with short-term survival and ACLF development in patients admitted for AD or ACLF.

Keywords: Acute-on-chronic liver failure; Biomarker; Cirrhosis; Copeptin; Organ failure.

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Conflict of interest statement

Ethics approval and consent to participate

The present study is an ancillary study of the prospective observational CANONIC study [2], which was performed in 29 university hospitals from eight European countries. Written informed consent was obtained from each patient included in that study and the study protocol conformed to the ethical guidelines of the 1975 Declaration of Helsinki as reflected a priori by the individual institution’s Medical Ethics Committees as described elsewhere [2]. Ethical bodies that approved the study can be found at www.clifconsortium.com/centres.

Consent for publication

Not applicable.

Competing interests

RJ has served on a Scientific Advisory Board for Conatus Pharma, has received lecture fees from Gambro, has an on-going research collaboration with Gambro and Grifols, and is the Principal Investigator of an industry-sponsored study (Sequana Medical). He is also inventor of the drug, l-ornithine phenyl acetate (OCR-002), which UCL has licensed to Ocera Therapeutics. He is also the founder of UCL spin-out companies Yaqrit Ltd. and Cyberliver Ltd. The remaining authors declare that they have no competing interests.

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Figures

Fig. 1
Fig. 1
Association of ACLF grades with serum copeptin concentration and the presence of renal failure. Distribution of serum copeptin concentration within subgroups of patients with acute-on-chronic liver failure (ACLF) and patients with and without ascites and no ACLF at time of admission for acute decompensation of cirrhosis. Dots represent serum copeptin concentrations of individual patients. Horizontal lines denote median values
Fig. 2
Fig. 2
Association of the estimated probability of death using the chronic liver failure-consortium organ failure (CLIF-C OF) score at 28 days (a) and 90 days (b) of follow-up, stratified according to serum copeptin concentration. The optimal cut-off point of serum copeptin in predicting 28- and 90-day mortality was defined using the Youden Index
See this image and copyright information in PMC

References

    1. Jalan R, Williams R. Acute-on-chronic liver failure: pathophysiological basis of therapeutic options. Blood Purif. 2002;20:252–61. doi: 10.1159/000047017. - DOI - PubMed
    1. Moreau R, Jalan R, Gines P, et al. Acute-on-chronic liver failure is a distinct syndrome that develops in patients with acute decompensation of cirrhosis. Gastroenterology. 2013;144:1426–37. doi: 10.1053/j.gastro.2013.02.042. - DOI - PubMed
    1. Olson JC, Wendon JA, Kramer DJ, et al. Intensive care of the patient with cirrhosis. Hepatology. 2011;54:1864–72. doi: 10.1002/hep.24622. - DOI - PubMed
    1. APASL Acute-on-chronic liver failure: consensus recommendations of the Asian Pacific Association for the study of the liver (APASL) Hepatol Int. 2009;3:269–82. doi: 10.1007/s12072-008-9106-x. - DOI - PMC - PubMed
    1. Bernardi M, Moreau R, Angeli P, et al. Mechanisms of decompensation and organ failure in cirrhosis: from peripheral arterial vasodilation to systemic inflammation hypothesis. J Hepatol. 2015;63:1272–84. doi: 10.1016/j.jhep.2015.07.004. - DOI - PubMed

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