Prognostic value of activated protein C in patients with septic shock
CCCF ePoster library. Bosch K. Oct 31, 2016; 150896; 19
Katharina Bosch
Katharina Bosch
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Topic: Clinical Trial

Prognostic value of activated protein C in patients with septic shock


Tobias Becher, MD1; Jens Müller, PhD2 ; Ibrahim Akin, MD1; Stefan Baumann, MD1 ;Katharina Bosch, BSc1; Ibrahim El-Battrawy, MD1; Christian Fastner, MD1; Ksenija Stach, MD1; Martin Borggrefe, MD1; Bernd Pötzsch, MD2; Dirk Loßnitzer, MD1
1 First Department of Medicine, University Medical Centre Mannheim (UMM), Faculty of Medicine Mannheim, University of Heidelberg, Mannheim, Germany.
2 Institute for Experimental Haematology and Transfusion Medicine, University of Bonn Medical Centre (UKB), Bonn, Germany.
 


Grant acknowledgements:
Acknowledgment: This study was kindly supported by the Klaus Tschira foundation, Germany.

Abstract:

Introduction: Although the treatment of infectious sepsis has improved over the last decades with the implementation of early administration of antibiotics and the concept of early goal directed therapy, the mortality of patients with severe sepsis and septic shock remains high 1-3. The coagulation system is a major component that contributes to the dismal effects of systemic cytokine release in patients with sepsis. While systemic inflammation leads to activation of the coagulation system resulting in the formation of micro-thrombi and depletion of coagulation factors, the activation of the protein C system results in anti-inflammatory, anti-apoptotic and endothelial barrier-stabilizing effects. Protein C is activated through thrombomodulin via the endothelial protein C receptor (EPCR) 4. The mentioned protective effects are mediated through the EPCR and the protease-activated receptor 1 (PAR-1) 5. Although APC has been used extensively in patients with septic shock, little is known about levels of APC and their evolution during the course of sepsis.
Objectives: The rational of the study was therefore to characterize coagulation activation in patients with septic shock and to analyze the prognostic value of APC levels.
Methods: 36 consecutive patients presenting with septic shock to our intensive care unit (ICU) were included in our study. Blood samples were drawn on admission, day 2, day 4 and day 7. APC was measured by a clinical applicable oligonucleotide-enzyme-capture assay (OECA). D-Dimers, protein C activity, thrombin-antithrombin complexes (TAT) and F1 + F2 fragments were also measured to characterize coagulation activation.
Results: Of the 36 patients included in the study, 12 (33.3 %) died of septic shock. Although APC levels were elevated in all patients with septic shock, non-survivors had significantly higher APC values on admittance (0.88 vs. 0.39 ng/ml, p=0.004) and significantly higher peak APC levels (1.37 vs. 0.58 ng/ml, p=0.008) (Figure 1 and 2). Furthermore, TAT complexes were also higher in non-survivors on admission (19.34 vs. 9.95, p=0.010). Peak APC levels above a cutoff of 0.776 ng/ml were associated with increased mortality after 30 days (OR 5.24; 95 % CI 1.41 – 19.49, p=0.006) (Figure 3).
Conclusion: Levels of APC and TAT complex are both increased in patients with septic shock. Peak APC levels above a cutoff of 0.776 ng/ml are associated with an increased 30-day mortality.

 


References:

References:
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2.            Gu WJ, Wang F, Bakker J, Tang L, Liu JC. The effect of goal-directed therapy on mortality in patients with sepsis - earlier is better: a meta-analysis of randomized controlled trials. Crit Care. 2014; 18(5):570.
3.            Stevenson EK, Rubenstein AR, Radin GT, Wiener RS, Walkey AJ. Two decades of mortality trends among patients with severe sepsis: a comparative meta-analysis. Crit Care Med. 2014 ;42(3):625-631.
4.            Hayashi T, Suzuki K. Changes of expression of the protein C pathway components in LPS-induced endotoxemia--implication for sepsis. Cardiovasc Hematol Disord Drug Targets. 2015; 15(1):2-9.
5.            Bouwens EA, Stavenuiter F, Mosnier LO. Mechanisms of anticoagulant and cytoprotective actions of the protein C pathway. J Thromb Haemost. 2013; 11 Suppl 1:242-253.
 



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