Platelet function rather than plasmatic coagulation explains hypercoagulable state in cholestatic liver disease

Background/Aims: As compared to other chronic liver diseases, cholestatic disorders are associated with a better outcome of variceal bleeding and less blood loss at transplantation, suggesting the presence of a hypercoagulable state. We have assessed plasmatic coagulation and platelet function in patients with cholestatic and non-cholestatic liver disease. Methods: Thirty-seven patients with chronic cholestatic liver disease (primary biliary cirrhosis (PBC)/primary sclerosing cholangitis (PSC)), 53 patients with chronic hepatitis C (HCV) or alcoholic cirrhosis (C2), and 62 healthy controls were studied. Results: Thrombelastography revealed a hypercoagulable state in non-cirrhotic patients with PBC/PSC, but not in those with HCV (ma-value: 6.54[6.25–6.92, 95%CI] vs. 5.39[5.11–5.58], P<0.05) possibly due to higher fibrinogen levels in PBC/PSC patients (369[329–418] mg/dl vs. 263[250–275] mg/dl, P<0.05). PFA-100 closure time was prolonged in HCV/C2 patients with advanced cirrhosis, but not in cirrhotic patients with PBC/PSC (Child B; epinephrine stimulation: 192[161–229] s vs. 132[105–158] s, P<0.05). Flow cytometric studies of platelet receptors and granules revealed a higher surface expression of CD42b (112[105–119]% vs. 100[95–104]%, P<0.05) and LIBS-1 (261[184–348]% vs. 121[92–145]%, P<0.05) in patients with PBC/PSC than in those with HCV/C2. Conclusions: These results indicate that platelet function differs between patients with cholestatic and non-cholestatic liver disease and is stable or even hyperactive in patients with PBC and PSC