Startseite Copeptin – a biomarker of short-term mortality risk (7 days) in patients with end-stage liver disease
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Copeptin – a biomarker of short-term mortality risk (7 days) in patients with end-stage liver disease

  • Christoph Schneider , Johannes Remmler , Jeffrey Netto , Daniel Seehofer , Cornelius Engelmann , Thomas Berg , Joachim Thiery und Thorsten Kaiser EMAIL logo
Veröffentlicht/Copyright: 13. Juni 2019
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Abstract

Background

For many patients with end-stage liver disease, liver transplantation represents the only curative therapy. Transplant recipients are scored and ranked using the model for end-stage liver disease (MELD/MELD-Na). Circulatory impairment is known to deteriorate outcomes; however, it is not incorporated into the current allocation system’s score. The aim of our study is to analyze the predictive value of copeptin as a biomarker of circulatory impairment and increased short-term mortality risk in patients with end-stage liver disease.

Methods

We conducted a retrospective observational study of 615 patients with end-stage liver disease. Patients were recruited using assessments performed during the evaluation process for liver transplantation. Copeptin values were analyzed in comparison to MELD-Na, interleukin 6 (IL-6), and C-reactive protein (CRP).

Results

Elevated levels of copeptin, IL-6 and CRP, as well as high MELD-Na scores, were significantly correlated with mortality. In a comparison of copeptin-tertiles, patients in group T3 (16.3 pmol/L or more) showed a significantly higher mortality risk (hazard ratio 11.2, p < 0.001). After adjusting for MELD-Na, copeptin remains an independent predictor of mortality. It shows its greatest prognostic strength in short-term mortality, where it performs comparable to MELD-Na (AUROC for 7 day-mortality, 0.941/0.939; p = 0.981) and shows an additional predictive value to MELD-Na for short-term mortality (7 days, p: 0.046; 30 days, p: 0.006).

Conclusions

Copeptin presents a valuable individual biomarker in detecting patients at risk for short-term mortality. Further studies should be performed to confirm our findings.


Corresponding author: Dr. med. Thorsten Kaiser, Institute of Laboratory Medicine, Clinical Chemistry and Molecular Diagnostics, University Hospital Leipzig, Paul-List-Str. 13-15, 04103 Leipzig, Germany, Phone: +49 341 9722200, Fax: +49 341 22209
aChristoph Schneider and Johannes Remmler contributed equally to this work.
  1. Author contributions: Study concept and design: C.S., J.R., J.N., D.S., C.E., T.B., J.T., T.K.; acquisition of data: C.S., J.N.; analysis and/or interpretation of data: C.S., J.R., J.N., D.S., C.E., T.B., J.T., T.K.; statistical analysis: J.R., C.E., T.K.; drafting the manuscript: C.S., J.R., T.K.; critical revision of the manuscript for important intellectual content: C.S., J.R., J.N., D.S., C.E., T.B., J.T., T.K.; final approval of the version to be published: C.S., J.R., J.N., D.S., C.E., T.B., J.T., T.K.; study supervision: T.K. All the authors have accepted responsibility for the entire content of this submitted manuscript and approved submission.

  2. Research funding: None declared.

  3. Employment or leadership: None declared.

  4. Honorarium: None declared.

  5. Competing interests: The funding organization(s) played no role in the study design; in the collection, analysis, and interpretation of data; in the writing of the report; or in the decision to submit the report for publication.

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Supplementary Material

The online version of this article offers supplementary material (https://doi.org/10.1515/cclm-2019-0023).


Received: 2019-01-07
Accepted: 2019-05-09
Published Online: 2019-06-13
Published in Print: 2019-11-26

© 2019 Walter de Gruyter GmbH, Berlin/Boston

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