Affiliation:
1. Division of Hematology, Department of Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand
2. Gastroenterology, Department of Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand
Abstract
Abstract
Background: Bleeding is an important complication of cirrhosis. Currently, there is no coagulation test that can reliably predict clinical hemorrhage. However, previous studies demonstrated significant correlations between hyperfibrinolysis and following bleeding in advanced cirrhotic patients. Objectives: Estimate the prevalence of hyperfibrinolysis in cirrhotic patients at stable conditions and to assess its role in predicting subsequent hemorrhage. Methods: The prospective cohort study included 58 consecutive cirrhotic patients at the Liver Clinic, Chulalongkorn Hospital. Assays for liver functions, PT, APTT, fibrinogen, fibrin degradation products (FDPs) and euglobulin lysis time (ELT) were performed at baseline. The subjects were followed-up for 10 months to observe clinical hemorrhage and survival. Results: The mean age was 56.4 years and 47% were male. The etiologies of liver diseases were virus (62.1%), alcohol (24.1%) or unknown (8.6%). Hyperfibrinolysis as reflected by ELT<120 minutes or FDPs>10 μg/mL was present in 32.8% and 74.1%, respectively. Fibrinolytic activity was significantly correlated with platelet counts and coagulation times, but not as much with liver function tests. By 10 months, 13 cases (22.4%) showed hemorrhagic episodes and 7 (12.1%) were expired, including 2 from bleeding. The significant predictors for death were Child class B or C, presence of ascites, hyperbilirubinemia, hypoalbuminemia, and prolonged APTT. However, none of the clinical, biochemical, or hemostatic factors was associated with clinical bleeding. Conclusion: Hyperfibrinolysis is common in cirrhotic outpatients. However, it cannot predict subsequent hemorrhage or survival. Novel hemostatic tests are required to assess the probability of bleeding in this disorder.
Reference23 articles.
1. 1. Comp PC, Jacocks RM, Rubenstein C, Radcliffe R. A lysine-absorbable plasminogen activator is elevated in conditions associated with increased fibrinolytic activity. J Lab Clin Med. 1981; 97: 637-45.
2. 2. Booth NA, Anderson JA, Bennett B. Plasminogen activators in alcoholic cirrhosis: demonstration of increased tissue type and urokinase type activator. J Clin Pathol. 1984; 37: 772-7.
3. 3. Hersch SL, Kunelis T, Francis RB Jr. The pathogenesis of accelerated fibrinolysis in liver cirrhosis: a critical role for tissue plasminogen activator inhibitor. Blood. 1987; 69: 1315-9.
4. 4. Leebeek FW, Kluft C, Knot EA, de Maat MP, Wilson JH. A shift in balance between profibrinolytic and antifibrinolytic factors causes enhanced fibrinolysis in cirrhosis. Gastroenterology. 1991; 101: 1382-90.
5. 5. Gresele P, Binetti BM, Branca G, Clerici C, Asciutti S, Morelli A, et al. TAFI deficiency in liver cirrhosis: relation with plasma fibrinolysis and survival. Thromb Res. 2008; 121: 763-8.
Cited by
5 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献