Abstract
Increased risk of both cardiovascular disease (CVD) and bleeding has been found in patients with chronic hepatitis C (CHC) infection, and a re-balanced hemostasis has been proposed. The aim of this study was to investigate functional whole blood coagulation and platelet function in CHC infection. The prospective study included 82 patients with CHC infection (39 with advanced liver fibrosis and 43 with no or mild liver fibrosis) and 39 healthy controls. A total of 33 patients were treated for CHC infection and achieved sustained virological response (SVR). Baseline and post-treatment blood samples were collected. Hemostasis was assessed by both standard coagulation tests and functional whole blood hemostatic assays (thromboelastograhy (TEG), and platelet aggregation (Multiplate). Patients with CHC and advanced fibrosis had impaired platelet aggregation both compared to patients with no or mild fibrosis and to healthy controls. Patients with CHC and advanced fibrosis also had lower antithrombin, platelet count, and coagulation factors II-VII-X compared to healthy controls. In contrast, TEG did not differ between groups. In treated patients achieving SVR, post-treatment platelet count was higher than pre-treatment counts (p = 0.033) and ADPtest, ASPItest, and RISTOhightest all increased post treatment (all p < 0.05). All Multiplate tests values, however, remained below those in the healthy controls. CHC-infected patients displayed evidence of rebalanced hemostasis with only partly hemostatic normalization in patients achieving SVR. The implications of rebalanced hemostasis and especially the impact on risk of CVD and bleeding warrants further studies.
Highlights
Hepatitis C virus (HCV) is the cause of viral hepatitis, with an estimated 130–150 million persons with chronic hepatitis C infection (CHC) worldwide [1]
CHC infection is associated with thrombocytopenia and lower levels of coagulation factors, contributing to an increased risk of bleeding [7,8,9]
Due to study design, the CHC-infected group with advanced fibrosis had a higher level of fibrosis compared to patients with no or mild fibrosis (Table 1)
Summary
Hepatitis C virus (HCV) is the cause of viral hepatitis, with an estimated 130–150 million persons with chronic hepatitis C infection (CHC) worldwide [1]. 80% of those infected will develop CHC, and 10–15% of patients with CHC infection will develop advanced liver disease with cirrhosis and increased risk of hepatocellular carcinoma (HCC) [2]. Besides these well-known manifestations of CHC, increased risk of cardiovascular disease (CVD) and thromboembolic events has been documented [3,4,5,6]. Vascular inflammation and altered coagulation caused by CHC infection has been hypothesized to contribute to increased CVD risk. CHC infection is associated with thrombocytopenia and lower levels of coagulation factors, contributing to an increased risk of bleeding [7,8,9]. Evidence points towards manifestations of both hypo- and hypercoagulability
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