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Activated protein C plays no major roles in the inhibition of coagulation or increased fibrinolysis in acute coagulopathy of trauma-shock: a systematic review

Authors
  • Gando, Satoshi1
  • Mayumi, Toshihiko2
  • Ukai, Tomohiko3
  • 1 Hokkaido University Graduate School of Medicine, Division of Acute and Critical Medicine, Department of Anesthesiology and Critical Care Medicine, N15W7, Kita-ku, Sapporo, 060-8638, Japan , Sapporo (Japan)
  • 2 School of Medicine, University of Occupational and Environmental Health, Department of Emergency Medicine, Kitakyushu, Japan , Kitakyushu (Japan)
  • 3 Graduate School of Medicine, Osaka University, Department of Social Medicine, Osaka, Japan , Osaka (Japan)
Type
Published Article
Journal
Thrombosis Journal
Publisher
BioMed Central
Publication Date
Jun 19, 2018
Volume
16
Issue
1
Identifiers
DOI: 10.1186/s12959-018-0167-3
Source
Springer Nature
Keywords
License
Green

Abstract

BackgroundThe pathophysiological mechanisms of acute coagulopathy of trauma-shock (ACOTS) are reported to include activated protein C-mediated suppression of thrombin generation via the proteolytic inactivation of activated Factor V (FVa) and FVIIIa; an increased fibrinolysis via neutralization of plasminogen activator inhibitor-1 (PAI-1) by activated protein C. The aims of this study are to review the evidences for the role of activated protein C in thrombin generation and fibrinolysis and to validate the diagnosis of ACOTS based on the activated protein C dynamics.MethodsWe conducted systematic literature search (2007–2017) using PubMed, the Cochrane Database of Systematic Reviews (CDSR), and the Cochrane Central Register of Controlled Trials (CENTRAL). Clinical studies on trauma that measured activated protein C or the circulating levels of activated protein C-related coagulation and fibrinolysis markers were included in our study.ResultsOut of 7613 studies, 17 clinical studies met the inclusion criteria. The levels of activated protein C in ACOTS were inconsistently decreased, showed no change, or were increased in comparison to the control groups. Irrespective of the activated protein C levels, thrombin generation was always preserved or highly elevated. There was no report on the activated protein C-mediated neutralization of PAI-1 with increased fibrinolysis. No included studies used unified diagnostic criteria to diagnose ACOTS and those studies also used different terms to refer to the condition known as ACOTS.ConclusionsNone of the studies showed direct cause and effect relationships between activated protein C and the suppression of coagulation and increased fibrinolysis. No definitive diagnostic criteria or unified terminology have been established for ACOTS based on the activated protein C dynamics.

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