Sarah Bos

32 CHAPTER 2 There is an ongoing debate on the fibrinolytic status of patients with cirrhosis, with most studies describing either hyper- or normofibrinolysis. In the present study, using a plasma-based assays that has been extensively validated,(35) we found a hypofibrinolytic state, particularly in cholestatic disease and also in NASH cirrhosis. These results suggest, that at least in the population of CTP A/B cirrhosis, decreased fibrinolysis could contribute to thrombotic events, which is somewhat counterintuitive given the concept of hyperfibrinolysis in cirrhosis that has already been proposed in 1914.(36) It may be that hyperfibrinolysis only occurs in patients withmore advanced disease, but it will be of considerable interest to assess whether there are differences between etiologies of disease in a population with advanced disease. Our current findings, however, are in line with studies finding no evidence of hyperfibrinolysis by thromboelastography in a large cohort of patients with well compensated cirrhosis.(14) Despite the comprehensive analysis, this study has some limitations. Individual patient groups were still of moderate size and mainly consisted of patients with mild cirrhosis, which limits the possibility to draw firm conclusions. Nevertheless, many of the hemostatic changes seen in the present cohort, were also present in a cohort of critically ill patients we have recently analyzed.(37) Our in-depth hemostatic profiling of primary, secondary, and tertiary hemostasis in patients with CTP A/B cirrhosis showed a hypercoagulable profile without large differences between etiologies. This reinforces the need for studies on anticoagulant therapy for prevention and treatment of thrombotic events. Our data do not provide an explanation for the difference in incidence of thrombotic events between etiologies, and future studies are required to address this issue.