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World J Gastroenterol. Feb 28, 2006; 12(8): 1273-1277
Published online Feb 28, 2006. doi: 10.3748/wjg.v12.i8.1273
Does endothelium agree with the concept of idiopathic hepatic vessel thrombosis
Ozgur Harmanci, Yahya Buyukasik, Serafettin Kirazli, Ferhun Balkanci, Yusuf Bayraktar
Ozgur Harmanci, Yusuf Bayraktar, Hacettepe University Faculty of Medicine, Department of Gastroenterology, 06100 Sihhiye, Ankara, Turkey
Yahya Buyukasik, Serafettin Kirazli, Hacettepe University Faculty of Medicine, Department of Hematology, 06100 Sihhiye, Ankara, Turkey
Ferhun Balkanci, Hacettepe University Faculty of Medicine, Department of Radiology, 06100 Sihhiye, Ankara, Turkey
Co-first-authors: Yusuf Bayraktar
Supported by Hacettepe University Office of Scientific Research Center
Correspondence to: Dr. Ozgur Harmanci, Department of Gastroenterology, Hacettepe University Faculty of Medicine, 06100 Sihhiye, Ankara, Turkey. ozgurmd@hacettepe.edu.tr
Telephone: +90-312-3051713
Received: May 6, 2005
Revised: July 25, 2005
Accepted: August 3, 2005
Published online: February 28, 2006

AIM: To investigate the major steps of thrombogenesis and to identify the differences in these steps between idiopathic patient group and control group.

METHODS: Fibrinogenesis was studied by measuring the activated factor VII, total and free levels of tissue factor pathway inhibitor (TFPI). The fibrinolysis step was investigated by determining the global fibrinolytic capacity. The endothelial function was assessed by measuring the levels of soluble adhesion molecules, namely soluble intercellular adhesion molecule 1 (sICAM-1), soluble vascular cell adhesion molecule 1 (sVCAM-1) and soluble E-selectin molecule. The exclusion criteria from “idiopathic” patient group were abdominal surgery, pregnancy, use of oral contraceptives, anti-phospholipid syndrome, Behçet’s disease, cancer, myeloproliferative diseases. The congenital factors like mutations of factor-V Leiden and prothrombin, deficiencies of proteins C and S, antithrombin, hyperhomocysteinemia and hyperfibrinogenemia were ruled out. The total number of patients was reduced from 96 to 9 (7 with portal vein thrombosis, 2 Budd Chiari syndrome) by exclusion criteria.

RESULTS: The levels of adhesion molecules sICAM-1, sVCAM-1, free TFPI levels and global fibrinolytic capacity were significantly different (P < 0.05) in the patient group indicating an endothelial dysfunction and a lower fibrinolytic activity.

CONCLUSION: These results show that this patient group should be tested by means of endothelial dysfunction and managed differently.

Keywords: Portal vein thrombosis, Budd-Chiari syndrome, Endothelial dysfunction, Soluble adhesion molecules, Fibrinolysis