title: Platelet production and destruction in liver cirrhosis.
abstract: OBJECTIVE
  Thrombocytopenia is common in liver cirrhosis (LC) but the mechanisms are not fully understood. The purpose of our work was to evaluate platelet kinetics in LC with different etiologies by examining platelet production and destruction.
  
  
  METHODS
  Ninety-one consecutive LC patients (36 HCV, 49 alcoholics, 15 HBV) were enrolled. As controls, 25 subjects with idiopathic thrombocytopenic purpura, 10 subjects with aplastic anemia, and 40 healthy blood donors were studied. Plasma thrombopoietin (TPO) was measured by ELISA. Reticulated platelets (RP) were determined using the Thiazole Orange method. Plasma glycocalicin (GC) was measured using monoclonal antibodies. Platelet associated and serum antiplatelet antibodies were detected by flow cytometry. B-cell monoclonality in PBMC was assessed by immunoglobulin fingerprinting.
  
  
  RESULTS
  Serum TPO was significantly lower in LC (29.9±18.1 pg/ml) compared to controls (82.3±47.6 pg/ml). The GC levels were higher in LC (any etiology) than in healthy cases. Conversely, the absolute levels of RP were lower in LC (any etiology) than in healthy controls. The platelet-associated and serum anti-platelet antibodies were higher in HCV+ LC compared to healthy subjects (p<0.0064), alcoholic LC (p<0.018), and HBV+ LC (p<0.0001). B-cell monoclonality was found in 27% of the HCV+LC, while it was not found in HBV+ or alcoholic LC.
  
  
  CONCLUSIONS
  Patients with LC present decreased plasma TPO, accelerated platelet turnover, and reduced platelet production. This indicates that LC thrombocytopenia is a multifactorial condition involving both increased platelet clearance and impaired thrombopoiesis.
authors.affiliation: Blood Bank Service, Azienda Ospedaliero-Universitaria Ospedali Riuniti di Trieste, Trieste, Italy.
authors.forename: Paola
authors.initials: P
authors.lastname: Pradella
authors.forename: Stefania
authors.initials: S
authors.lastname: Bonetto
authors.forename: Stefano
authors.initials: S
authors.lastname: Turchetto
authors.forename: Laura
authors.initials: L
authors.lastname: Uxa
authors.forename: Consuelo
authors.initials: C
authors.lastname: Comar
authors.forename: Francesca
authors.initials: F
authors.lastname: Zorat
authors.forename: Vincenzo
authors.initials: V
authors.lastname: De Angelis
authors.forename: Gabriele
authors.initials: G
authors.lastname: Pozzato
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000741:Anemia, Aplastic / Q000097:blood / Q000276:immunology / Q000473:pathology; D001323:Autoantibodies / Q000097:blood; D001402:B-Lymphocytes / Q000276:immunology; D001792:Blood Platelets / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D002648:Child; D005260:Female; D006801:Humans; D008103:Liver Cirrhosis / Q000097:blood* / Q000276:immunology / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D019038:Platelet Glycoprotein GPIb-IX Complex / Q000378:metabolism; D016553:Purpura, Thrombocytopenic, Idiopathic / Q000097:blood / Q000276:immunology / Q000473:pathology; D013154:Spleen / Q000473:pathology; D034061:Thrombopoiesis / Q000502:physiology*; D013926:Thrombopoietin / Q000097:blood
chemical_list: D001323:Autoantibodies; D019038:Platelet Glycoprotein GPIb-IX Complex; C023592:glycocalicin; D013926:Thrombopoietin