Hypercoagulability in End-Stage Liver Disease: Prevalence and Its Correlation With Severity of Liver Disease and Portal Vein Thrombosis

Abstract

Contrary to well-recognized bleeding diathesis in chronic liver disease, thrombotic events can occur in these patients due to reduction or loss of synthesis of anticoagulant proteins. Forty-seven consecutive patients with end-stage liver disease (ESLD) were investigated for activity of protein C, protein S, antithrombin, and factor V Leiden mutation. Forty-two (89.4%) patients had low levels of at least 1 while 33 (70.2%) patients were deficient for all anticoagulant proteins studied. Forty-six (97.9%) patients were negative for factor V Leiden mutation. The deficiencies were more marked in hepatitis C virus–positive patients and patients with model for end-stage liver disease (MELD) score >15. Six (12.8%) patients had portal vein thrombosis (PVT), and all had diminished protein S activity. In conclusions, deficiency of anticoagulant proteins occur in early phase of chronic liver disease. The severity of deficiency is proportional to the severity of liver disease. Despite the high prevalence of hypercoagulability, the incidence of PVT is low. Further studies with larger cohort of patients are needed to support these conclusions and to study other associated factors.

Decreased protein C function predicts mortality in patients with cirrhosis

“…The other natural anticoagulants analysed did not show this trend. This finding further validates the role of PrC in plasmatic hypercoagulability in CLD as theorized in previous studies Tripodi et al observed decreased plasma PrC levels in cirrhosis (median of nearly 40%) in patients with CLD and they showed that a PrC‐deficient status contributed to the high index of procoagulant imbalance in these patients. Our results of significant decrease in PrC levels with increasing severity of liver dysfunction support this concept that there occurs a state of procoagulant imbalance in CLD due to reduced PrC.…”

Intraoperative hypercoagulability during liver transplantation as demonstrated by thromboelastography

“…In liver disease, the endogenous anticoagulants as well as procoagulant factors are all reduced, and the balance of procoagulants to anticoagulants may be altered in favor of a prothrombotic state, but the INR reflects primarily procoagulant activity . It is increasingly recognized that patients with cirrhosis are at risk of thrombotic complications as a result of low endogenous anticoagulant levels . Viscoelastic monitoring adds valuable qualitative information to the management of these cases …”

“…40 It is increasingly recognized that patients with cirrhosis are at risk of thrombotic complications as a result of low endogenous anticoagulant levels. 41 Viscoelastic monitoring adds valuable qualitative information to the management of these cases. 42 What remains unclear is what action should be taken when hypercoagulability is demonstrated on TEG.…”

Value of D-dimer and protein S for diagnosis of portal vein thrombosis in patients with liver cirrhosis

“…33 While coagulation function is altered by liver dysfunction, anticoagulant factors such as protein S decrease in a higher proportion in patients with cirrhosis. 6 Thus, a relatively hypercoagulable state can develop with a large amount of protein S consumed after the formation of PVT. Both liver function deterioration and PVT formation can contribute to decreased protein S concentrations, which have been associated with venous thromboembolism and ischaemic stroke.…”