Poor outcome in disseminated intravascular coagulation or thrombotic thrombocytopenic purpura patients with severe vascular endothelial cell injuries.
Various hemostatic and vascular endothelial cell markers were measured in patients with disseminated intravascular coagulation (DIC), non-DIC, or thrombotic thrombocytopenic purpura (TTP) and in healthy volunteers to examine the relationships between the hemostatic abnormalities or vascular endothelial cell injuries and the patients' outcomes. Although the plasma levels of soluble fibrin monomer, thrombin-antithrombin complex, plasmin-plasmin inhibitor complex, and D-dimer were significantly increased in the DIC patients, there were no significant differences in these markers between the DIC patients who survived and those who died, suggesting that these markers might not be directly related to the patient outcome. The plasma thrombomodulin (TM) levels in the DIC and TTP patients were significantly higher than those in the healthy volunteers, and the plasma TM levels in the patients who died were significantly higher than those in the patients who survived. These findings showed that the TM level reflected the outcome, and that the outcome of the diseases underlying DIC and TTP might depend on vascular endothelial cell injuries. The plasma protein C and antithrombin activities were markedly reduced in the DIC, non-DIC, and TTP patients who died compared to those who survived. These findings suggest that reduced plasma antithrombin and protein C activities are useful markers of systemic vascular endothelial injuries. Although the plasma tissue factor (TF) levels were significantly increased in the DIC patients, there was no significant difference in the plasma TF levels between the DIC patients who died and those who survived. In conclusion, we found that the outcome of the diseases underlying DIC and TTP is related to vascular endothelial cells, and that plasma TM, antithrombin, and protein C are useful markers for systemic vascular endothelial cell injury.
Wada
H
H
Second Department of Internal Medicine, Mie University School of Medicine, Tsu-city, Japan.
Mori
Y
Y
Shimura
M
M
Hiyoyama
K
K
Ioka
M
M
Nakasaki
T
T
Nishikawa
M
M
Nakano
M
M
Kumeda
K
K
Kaneko
T
T
Nakamura
S
S
Shiku
H
H
D000933:Antifibrinolytic Agents / Q000032:analysis / Q000097:blood; D000990:Antithrombin III / Q000032:analysis; D000991:Antithrombins / Q000032:analysis; D004211:Disseminated Intravascular Coagulation / Q000401:mortality* / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000473:pathology*; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D005341:Fibrinolysin / Q000032:analysis; D005343:Fibrinolytic Agents / Q000032:analysis; D006463:Hemolytic-Uremic Syndrome / Q000097:blood; D006801:Humans; D010314:Partial Thromboplastin Time; D010447:Peptide Hydrolases / Q000032:analysis; D011486:Protein C / Q000032:analysis; D011517:Prothrombin Time; D011697:Purpura, Thrombotic Thrombocytopenic / Q000401:mortality* / Q000503:physiopathology*; D015996:Survival Rate; D018180:Thrombomodulin / Q000097:blood; D000979:alpha-2-Antiplasmin
D000933:Antifibrinolytic Agents; D000991:Antithrombins; D005338:Fibrin Fibrinogen Degradation Products; D005343:Fibrinolytic Agents; D011486:Protein C; D018180:Thrombomodulin; D000979:alpha-2-Antiplasmin; C046193:antithrombin III-protease complex; C036309:fibrin fragment D; C011468:fibrinmonomer; C037742:plasmin-plasmin inhibitor complex; D000990:Antithrombin III; D010447:Peptide Hydrolases; D005341:Fibrinolysin