Plasma Levels of Heparin Cofactor II (HCII) and Thrombin-HCII Complex in Patients with Disseminated Intravascular Coagulation

• Published in: Clinical and applied thrombosis/hemostasis Vol. 8; no. 3; pp. 265 - 271
• Main Authors: Noda, Ayako, Wada, Hideo, Kusiya, Fumihiko, Sakakura, Miho, Onishi, Katsuya, Nakatani, Kaname, Gabazza, Esteban C., Asahara, Naomi, Tsukada, Minoru, Nobori, Tsutomu, Shiku, Hiroshi
• Format: Journal Article
• Language: English
• Published: Thousand Oaks, CA SAGE Publications 01.07.2002; SAGE PUBLICATIONS, INC
• Subjects: Anticoagulants; Antithrombin III - analysis; Case-Control Studies; Disseminated Intravascular Coagulation - blood; Disseminated Intravascular Coagulation - etiology; Heparin Cofactor II - analysis; Heparin Cofactor II - metabolism; Humans; Infection - blood; Infection - complications; Inflammatory diseases; Neoplasms - blood; Neoplasms - complications; Peptide Hydrolases - blood; Plasma; Protein Binding; Thrombin - analysis; Thrombin - metabolism; Infection; Thrombin-heparin cofactor II complex; Heparin cofactor II; DIC
• ISSN: 1076-0296; 1938-2723
• DOI: 10.1177/107602960200800311

Plasma levels of heparin cofactor II (HCII), thrombin-HCII complex (THC), antithrombin (AT), and thrombin-AT complex (TAT) were evaluated in patients with disseminated intravascular coagulation (DIC) associated with several underlying diseases. Plasma levels of AT were significantly reduced in almost all underlying diseases associated with DIC, but the plasma levels of HCII and HCII/AT ratio were significantly reduced only in patients with infections. While the plasma level of TAT was significantly increased in patients with all underlying diseases associated with DIC, the increase of THC was not significant. Plasma levels of AT were significantly reduced in DIC and pre-DIC associated with almost all underlying diseases, but those of HCII were significantly reduced only in DIC and pre-DIC patients with inflammatory diseases. The plasma levels of TAT were significantly increased in DIC, pre-DIC, and non-DIC patients with all underlying diseases, and those of THC were significantly increased in DIC and pre-DIC patients with inflammatory diseases. The plasma levels of THC were not significantly increased in non-DIC patients of any disease group. The decrease of AT may be caused by thrombin generation or inflammatory reaction that occurs in DIC associated with underlying diseases, while the decrease of HCII might be caused by both thrombin generation and inflammatory reaction. Finally, AT inhibits thrombin more strongly than HCII in several underlying diseases associated with DIC except for inflammatory diseases. In inflammatory diseases, HCII might play an important role in preventing the onset of DIC.