Skip to main content

Advertisement

Table 4 Studies that measure activated protein C

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

Reference (year) Main results
[35] (2011) ACOTS showed lower levels of protein C, and higher levels of sTM and D-dimer however, there were no differences in the levels of activated protein C, PF1 + 2, TAT, t-PA, or PAI-1 between ACOTS and non-ACOTS. In ACOTS, activated protein C showed no correlation with PF1 + 2. ACOTS showed consumption coagulopathy.
[36] (2012) Patients with ISS > 15 and BD > − 6 showed high activated protein C and lower protein C levels. Activated protein C > 6 ng/mL was associated with prolonged PT, APTT, low FV and FVIII activities, and high levels of t-PA and D-dimer. Markers of thrombin generation, sTM and PAI-1 were not measured. Neither activated protein C nor protein C levels were shown in patients with acute traumatic coagulopathy (defined as PTINR> 1.3).
[37] (2012) The high histone group showed higher ISS, and activated protein C, t-PA, and D-dimer levels. The markers of thrombin generation, sTM and PAI-1 were not measured. There were no differences between high and low histone groups with regard to the levels of protein C, AT, or BD, or the FVII, FV and FVIII activities.
[38] (2013) The sTBI/E group showed high ISS and a high incidence of ACOTS. The sTBI/E groups showed decreased protein C and AT levels, and increased D-dimer and sTM levels. There were no differences in the levels of BD, activated protein C, PF1 + 2, TAT, t-PA, or PAI-1 among the three groups.
[39] (2013) PTINR-based coagulopathy: The coagulopathy group showed higher activated protein C levels and lower protein C levels but there were no differences in the D-dimer levels. Both protein C and activated protein C were independent predictors of coagulopathy. APTT-based coagulopathy: Coagulopathy was associated with increased activated protein C and D-dimer levels and decreased protein C levels. There were inconsistencies between PTINR- and APTT-based coagulopathy. Factors V, VII, and VIII were decreased in both types of coagulopathy.
[40] (2016) Activated protein C levels were more decreased in ACOTS than controls and non-ACOTS. ACOTS showed the same results as DIC.
[41] (2017) ATC showed higher activated protein C, PF1 + 2, PAP and D-dimer levels and lower protein C, AT and fibrinogen levels in comparison to non-ATC. Activated protein C reduced the Factors V and VIII activities and the fibrinogen levels in a dose-dependent manner, while the thrombin generation capacity was preserved. The PAI-1 levels did not differ between patients with low and high activated protein C levels.
[42] (2013) ACOTS showed normal prothrombinase activity, increased soluble fibrin and sTM, and decreased AT in comparison to normal controls and non-ACOTS. The results related to ACOTS coincided with those of DIC.
  1. ACOTS acute coagulopathy trauma shock, AIS abbreviated injury scale, APTT activated partial thromboplastin time, AT antithrombin, ATC acute traumatic coagulopathy, BD base deficit, E extracranial injury, ED emergency department, DIC disseminated intravascular coagulation, ISS injury severity score, iTBI isolated traumatic brain injury, m multicenter, PAI-1 plasminogen activator inhibitor-1, PAP plasmin α2-antiplasmin complex, PF1 + 2 prothrombin fragment 1 + 2, PT prothrombin time, PTINR prothrombin time international normalized ratio, ROTEM rotational thromboelastometry, s single center, SD standard deviation, sTBI severe traumatic brain injury, sTM soluble thrombomodulin, TAT thrombin antithrombin complex, t-PA tissue-type plasminogen activator