Plasma levels of activated protein C-protein C inhibitor complex in patients with hypercoagulable states.
Plasma levels of activated protein C (APC)-protein C inhibitor (PCI) were significantly increased in patients with disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic purpura (TTP), acute myocardial infarction (AMI), pulmonary embolism (PE), or deep vein thrombosis (DVT) and in patients undergoing hemodialysis (HD). Plasma levels of APC-alpha(1)-antitrypsin (AT) complex were significantly increased in patients with DIC and in those with TTP. Plasma levels of PCI were significantly decreased in patients with DIC, non-DIC, or TTP and in those undergoing HD. In the pre-DIC stage, the plasma levels of APC-PCI complex were significantly increased but not those of APC-alpha(1)-AT complex. These data suggest that measurements of APC-PCI complex and APC-alpha(1)-AT complex may be useful for the diagnosis of DIC. After treatment of DIC, the plasma levels of APC-PCI complex and APC-alpha(1)-AT complex were significantly decreased, but not those of PCI. Plasma levels of thrombin-antithrombin complex (TAT), plasmin-alpha(2)-plasmin complex (PPIC), D-dimer, and soluble fibrin monomer (SFM) were markedly increased in patients with DIC or pre-DIC and were moderately increased in patients with non-DIC, TTP, AMI, PE, or DVT and in those undergoing HD. The receiving operating characteristic (ROC) analysis showed that SFM and the APC-PCT complex are useful markers for diagnosis of DIC. The specificity of plasma TAT and PPIC levels was low. The positive rate of APC-PCI complex was higher than 90% with DIC, TTP, AMI, PE, and it was higher than 60% with DVT and HD. Since the APC-PCI complex was elevated not only in patients with venous thrombosis but also in those with arterial thrombosis, components of the protein C pathway might be useful markers for the diagnosis of arterial thrombosis.
Second Department of Internal Medicine, Mie University School of Medicine, Tsu-city, Mie-ken, Japan.
R
R
Watanabe
H
H
Wada
M
M
Sakakura
Y
Y
Mori
T
T
Nakasaki
Y
Y
Okugawa
E C
EC
Gabazza
T
T
Hayashi
J
J
Nishioka
K
K
Suzuki
H
H
Shiku
T
T
Nobori
D000990:Antithrombin III / Q000032:analysis; D004211:Disseminated Intravascular Coagulation / Q000097:blood; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D006801:Humans; D009203:Myocardial Infarction / Q000097:blood; D010447:Peptide Hydrolases / Q000032:analysis; D011486:Protein C / Q000032:analysis*; D018046:Protein C Inhibitor / Q000097:blood*; D011655:Pulmonary Embolism / Q000097:blood; D011697:Purpura, Thrombotic Thrombocytopenic / Q000097:blood; D006435:Renal Dialysis; D019851:Thrombophilia / Q000097:blood*; D020246:Venous Thrombosis / Q000097:blood; D000979:alpha-2-Antiplasmin / Q000032:analysis
D005338:Fibrin Fibrinogen Degradation Products; D011486:Protein C; D018046:Protein C Inhibitor; D000979:alpha-2-Antiplasmin; C046193:antithrombin III-protease complex; C036309:fibrin fragment D; C011468:fibrinmonomer; D000990:Antithrombin III; D010447:Peptide Hydrolases