Edris M Alkozai1, Robert J Porte2, Jelle Adelmeijer3, Alberto Zanetto4, Paolo Simioni5, Marco Senzolo4, Ton Lisman6. 1. Surgical Research Laboratory, University of Groningen, University Medical Center Groningen, Groningen, Netherlands; Section of Hepatobiliairy Surgery and Liver Transplantation, Department of Surgery, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands. 2. Section of Hepatobiliairy Surgery and Liver Transplantation, Department of Surgery, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands. 3. Surgical Research Laboratory, University of Groningen, University Medical Center Groningen, Groningen, Netherlands. 4. Department of Surgical and Gastroenterological Sciences, University Hospital of Padua, Padua, Italy. 5. Department of Cardiologic, Thoracic and Vascular Sciences, University Hospital of Padua, Padua, Italy. 6. Surgical Research Laboratory, University of Groningen, University Medical Center Groningen, Groningen, Netherlands; Section of Hepatobiliairy Surgery and Liver Transplantation, Department of Surgery, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands. Electronic address: j.a.lisman@umcg.nl.
Abstract
INTRODUCTION: Cancer is a major risk factor for developing venous thromboembolism (VTE). Plasma hypercoagulability is an established risk factor for cancer-related VTE. In addition, thrombocytosis and hyperreactive platelets have been implicated in VTE and cancer progression. Cirrhosis is associated with changes in platelet number and function. The platelet activation status of patients with cirrhosis and hepatocellular carcinoma has not yet been established. Here we assessed the platelet activation status in patients with hepatitis-related cirrhosis in presence or absence of HCC. MATERIALS AND METHODS: We performed a cross-sectional study including thirty-eight consecutive patients with hepatitis B- or C- related liver cirrhosis in presence or absence of HCC. We studied basal and agonist-induced platelet activation using flow cytometry. In addition, we studied the plasma levels of von Willebrand factor (VWF) and the VWF-cleaving protease ADAMTS13. Twenty healthy volunteers served as controls. RESULTS: We found no evidence of basal platelet activation in patients with cirrhosis compared to controls. However, we found reduced agonist-induced platelet activation in patients. No differences in the basal and agonist-induced platelets activation status between patients with or without HCC were detected. Plasma levels of VWF were increased and the levels of ADAMTS13 activity were decreased in patients compared to controls. No differences between the levels of VWF and ADAMTS13 in patients with or without HCC were detected. CONCLUSIONS: HCC development or recurrence in patients with hepatitis B- or C-related cirrhosis does not appear to be associated with platelet activation and changes in pivotal proteins in primary hemostasis.
INTRODUCTION:Cancer is a major risk factor for developing venous thromboembolism (VTE). Plasma hypercoagulability is an established risk factor for cancer-related VTE. In addition, thrombocytosis and hyperreactive platelets have been implicated in VTE and cancer progression. Cirrhosis is associated with changes in platelet number and function. The platelet activation status of patients with cirrhosis and hepatocellular carcinoma has not yet been established. Here we assessed the platelet activation status in patients with hepatitis-related cirrhosis in presence or absence of HCC. MATERIALS AND METHODS: We performed a cross-sectional study including thirty-eight consecutive patients with hepatitis B- or C- related liver cirrhosis in presence or absence of HCC. We studied basal and agonist-induced platelet activation using flow cytometry. In addition, we studied the plasma levels of von Willebrand factor (VWF) and the VWF-cleaving proteaseADAMTS13. Twenty healthy volunteers served as controls. RESULTS: We found no evidence of basal platelet activation in patients with cirrhosis compared to controls. However, we found reduced agonist-induced platelet activation in patients. No differences in the basal and agonist-induced platelets activation status between patients with or without HCC were detected. Plasma levels of VWF were increased and the levels of ADAMTS13 activity were decreased in patients compared to controls. No differences between the levels of VWF and ADAMTS13 in patients with or without HCC were detected. CONCLUSIONS: HCC development or recurrence in patients with hepatitis B- or C-related cirrhosis does not appear to be associated with platelet activation and changes in pivotal proteins in primary hemostasis.
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