title: Impaired platelet function among platelet donors.
abstract: BACKGROUND
  Platelet transfusions are effective for the prevention and treatment of bleeding in patients with disorders of platelet number and/or function. In recent years plateletpheresis concentrates have outnumbered pooled platelet concentrates, albeit with significant differences between nations. Thus, the platelet quality of individual donors has become increasingly important. The aim of this study was to gain an estimate for the prevalence of impaired platelet function among platelet donors.
  
  
  METHODS
  We determined the inter-donor variability in platelet plug formation with a PFA-100 analyzer, the prevalence of impaired thromboxane formation, and effects of the density in alpha2 integrin polymorphism and density.
  
  
  RESULTS
  (i) Collagen-epinephrine induced closure time (CEPI-CT) showed a great inter-subject variability in platelet donors and was higher than in healthy controls (p = 0.008). One-fifth of donors had abnormal CEPI-CT values and 11% exceeded >300 s (max measurable value). (ii) Decreased serum thromboxane B2 levels were found in 9% of all donors, compatible with surreptitious intake of cyclooxygenase inhibitors or with an aspirin-like defect. CEPI-CT correlated inversely with TxB2-levels in donors and controls. (iii) The density of the alpha2-integrin correlated negatively with CEPI-CT and CADP-CT values in controls, but was not responsible for the observed impaired platelet function in donors. (iv) Finally, the ABO blood group system modulates closure times.
  
  
  CONCLUSIONS
  In sum, a large number of platelet donors present with prolonged closure times. Decreased thromboxane formation and frequent platelet donation partly account for this observation.
authors.affiliation: Department of Clinical Pharmacology-TARGET, Vienna University, Austria.
authors.forename: P
authors.initials: P
authors.lastname: Jilma-Stohlawetz
authors.forename: N
authors.initials: N
authors.lastname: Hergovich
authors.forename: M
authors.initials: M
authors.lastname: Homoncik
authors.forename: L
authors.initials: L
authors.lastname: Dzirlo
authors.forename: M
authors.initials: M
authors.lastname: Horvath
authors.forename: M
authors.initials: M
authors.lastname: Janisiw
authors.forename: S
authors.initials: S
authors.lastname: Panzer
authors.forename: B
authors.initials: B
authors.lastname: Jilma
mesh_terms: D000244:Adenosine Diphosphate / Q000494:pharmacology; D015703:Antigens, CD / Q000235:genetics; D001782:Blood Donors; D001791:Blood Platelet Disorders / Q000097:blood* / Q000453:epidemiology; D018955:CD36 Antigens / Q000032:analysis; D003094:Collagen / Q000494:pharmacology; D003430:Cross-Sectional Studies; D004837:Epinephrine / Q000494:pharmacology; D005434:Flow Cytometry; D006801:Humans; D039421:Integrin alpha2; D015539:Platelet Activation / Q000187:drug effects; D010979:Platelet Function Tests / Q000295:instrumentation; D019038:Platelet Glycoprotein GPIb-IX Complex / Q000032:analysis; D017713:Platelet Transfusion; D010983:Plateletpheresis; D011110:Polymorphism, Genetic; D015995:Prevalence; D011446:Prospective Studies; D013929:Thromboxane B2 / Q000097:blood; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D015703:Antigens, CD; D018955:CD36 Antigens; D039421:Integrin alpha2; D019038:Platelet Glycoprotein GPIb-IX Complex; D014841:von Willebrand Factor; D013929:Thromboxane B2; D000244:Adenosine Diphosphate; D003094:Collagen; D004837:Epinephrine