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. 2010 Jan;25(1):116-21.
doi: 10.1111/j.1440-1746.2009.05921.x. Epub 2009 Aug 3.

Protein C and D-dimer are related to portal vein thrombosis in patients with liver cirrhosis

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Protein C and D-dimer are related to portal vein thrombosis in patients with liver cirrhosis

Donglei Zhang et al. J Gastroenterol Hepatol. 2010 Jan.

Abstract

Background and aim: To profile changes of coagulation, anticoagulation and fibrolytic factors associated with liver function failure and portal vein thrombosis (PVT) formation in chronic liver cirrhosis patients.

Methods: A total of 116 cirrhotic patients admitted to our hospital from June 2006 to October 2008 were included in our study. All patients were classified into two groups: PVT group (31 patients), composed of patients with PVT and a control group (85 patients), including patients without PVT. Platelet, prothrombin time (PT), activated partial prothrombin time (APTT) and fibrinogen were measured. Also, plasma samples from the patients were analyzed for the levels of antithrombin III (AT-III), protein C (PC), protein S (PS), D-dimer, tissue-type plasminogen activator as well as plasminogen activator inhibitor-1. Statistical analyses were carried out to evaluate the correlation of specific variations with the disease status.

Results: In general, the higher Child-Pugh scores, indicating the aggravation of hepatic impairment of the patients, correlated well with the prolonged PT/APTT and increased D-dimer, as well as decreased platelet, fibrinogen, PC and AT-III levels in the serum. Furthermore, we found that the PC, PS and D-dimer levels in PVT patients were 2.32 +/- 0.72 mg/L, 17.14 +/- 3.62 mg/L and 0.99 +/- 0.36 mg/L, respectively, both representing a significant difference compared with those in the control group without PVT. Logistic regression model shows that the odds ratio value of one unit of increase of PC and D-dimer were 0.48 and 15.57.

Conclusions: Cirrhotic patients displayed dysfunctions in the coagulation, anti-coagulation and fibrolytic systems. The development of PVT in these patients may be independently associated with the decrease of PC, PS and D-dimer. Furthermore, decreasing PC and increasing D-dimer may be risk factors inducing PVT in cirrhotic patients.

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