Table 7 Studies that measure activated protein C-related coagulation and fibrinolysis markers

[8] (2007)

PF1 + 2 increased as the ISS increased. In the presence of increased BD, protein C fell with increasing levels of PF1 + 2 and sTM. Low protein C was associated with low PAI-1 and increased t-PA and D-dimer levels. These changes were associated with prolonged PT and APTT.

[9] (2007)

Increasing ISS and BD were associated with high PF1 + 2, sTM levels and low levels of protein C levels. Brain injury and increased BD resulted in high t-PA and D-dimer levels. None of the results included the PAI-1 levels. These changes were associated with prolonged PT and APTT.

[10] (2008)

PF1 + 2 increased with increased ISS. Protein C fell with increasing levels of sTM. t-PA was increased in patients with BD > − 7.7; this was unrelated to PF1 + 2. The t-PA and D-dimer levels decreased in parallel with increases in PAI-1.

[43] (2009)

ACT patients had lag times that was 68% shorter and peak thrombin generation was three-fold higher in comparison to normal patients, indicating the presence of circulating procoagulants that were capable of initiating systemic coagulation. Increased systemic thrombin generation was associated with slower inhibition of thrombin generation and decreased antithrombin levels.

[44] (2010)

Patients with coagulopathy had higher procoagulant activity, tissue factor-like activity and D-dimer in comparison to normal controls and patients without coagulopathy. In patients with coagulopathy, 79% of the procoagulant activity was due to tissue factor-like activity, which was higher than that in patients without coagulopathy.

[45] (2011)

Patients with higher ISS (30–50 and > 50) showed extremely elevated PF1 + 2, TAT, and lower AT levels, which were associated with increased BD. Patients with higher ISS also showed lower platelet counts and fibrinogen levels, and prolonged PT and APTT.

[46] (2013)

In patients with severe fibrinolytic activity, the PAP, t-PA and D-dimer levels were higher than in patients with normal and moderate fibrinolysis. However, the PAI-1 levels did not change in association with changes in t-PA, D-dimer, and PAP levels. Patients with severe fibrinolytic activity also showed high PF1 + 2 and low AT levels. The PAP and D-dimer levels were increased in line with increases in the BD.

[47] (2014)

Severe fibrinolysis was associated with high active and total t-PA and a reduction of active and total PAI-1. Increased active t-PA and reduced active PAI-1 were both associated with fibrinolysis, as measured by PAP.

[48] (2016)

The total PAI-1 levels in hyperfibrinolytic trauma and healthy controls were equal; however, the levels of active PAI-1 were higher than in controls. The ratio of active to complexed PAI-1/t-PA was lower in hyperfibrinolytic trauma than in controls. Conversely, both total t-PA and active t-PA were higher than in healthy controls. Massive t-PA release overwhelms free PAI-1. There is no PAI-1 degradation.