title: Platelet function rather than plasmatic coagulation explains hypercoagulable state in cholestatic liver disease.
abstract: OBJECTIVE
  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.
authors.affiliation: Medizinische Klinik III, Klinikum der Ludwig-Maximilians-Universität - Grosshadern, 81377 München, Germany. rudolf.pihusch@med3.med.uni-muenchen.de
authors.forename: Rudolf
authors.initials: R
authors.lastname: Pihusch
authors.forename: Andreas
authors.initials: A
authors.lastname: Rank
authors.forename: Peter
authors.initials: P
authors.lastname: Göhring
authors.forename: Markus
authors.initials: M
authors.lastname: Pihusch
authors.forename: Erhard
authors.initials: E
authors.lastname: Hiller
authors.forename: Ulrich
authors.initials: U
authors.lastname: Beuers
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001760:Bleeding Time; D001792:Blood Platelets / Q000378:metabolism*; D015550:Cell Degranulation; D015209:Cholangitis, Sclerosing / Q000097:blood* / Q000503:physiopathology; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D008104:Liver Cirrhosis, Alcoholic / Q000097:blood / Q000503:physiopathology; D008105:Liver Cirrhosis, Biliary / Q000097:blood* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D011956:Receptors, Cell Surface / Q000378:metabolism; D013916:Thrombelastography; D019851:Thrombophilia / Q000097:blood* / Q000503:physiopathology
chemical_list: D011956:Receptors, Cell Surface