title: Safety issues of plateletpheresis: comparison of the effects of two cell separators on the activation of coagulation, fibrinolysis, and neutrophils and on the formation of neutrophil-platelet aggregates.
abstract: BACKGROUND
  Although many donors undergo repeated plateletpheresis, data on the consequences of plateletpheresis for the donor's health remain scarce. Thus, the effect of plateletpheresis on the activation of coagulation, fibrinolysis, and neutrophils was investigated.
  
  
  METHODS
  Part 1: Sixteen healthy men were randomly assigned to undergo plateletpheresis on a cell separator (AMICUS, Fenwal Baxter; or MCS 3p, Haemonetics). The effects of plateletpheresis on plasma levels of prothrombin fragment (F(1+2)), D-dimer, plasmin-plasmin inhibitor (PPI) complexes, and plasminogen activator inhibitor (PAI-1); on the activation of neutrophils (% L-selectin+); and on the frequency of platelet-neutrophil aggregates (% CD41+ neutrophils) were compared. Part 2: Ten healthy men received infusions of ACD-A and placebo without apheresis in a randomized, double-blind crossover study to control for the pharmacologic effects of citrate.
  
  
  RESULTS
  Part 1: No change in F(1+2) occurred (p>0.05), which indicated that plateletpheresis did not enhance coagulation. Levels of D-dimer, PPI, and PAI-1 decreased over time on the AMICUS (p<0.001). Plateletpheresis did not activate neutrophils (p>0.05), but it decreased the percentage of CD41+ neutrophils (p<0.003). An approximately 80-percent drop in mononuclear cells was observed in the extracorporeal circulation of the AMICUS (p<0.001 vs. baseline and p = 0.005 vs. MCS 3p), and circulating lymphocyte and monocyte counts decreased concomitantly. Part 2: Infusion of ACD-A slightly decreased D-dimer levels (p<0.05), and both infusions decreased the circulating lymphocyte counts.
  
  
  CONCLUSIONS
  Plateletpheresis can be regarded as safe with respect to the activation of coagulation or neutrophils. The consequences for the donor's health of the decrease in D-dimer, PPI, and PAI-1 may deserve further investigation.
authors.affiliation: Department of Clinical Pharmacology, TARGET, Vienna University Hospital School of Medicine, Austria.
authors.forename: P
authors.initials: P
authors.lastname: Stohlawetz
authors.forename: S
authors.initials: S
authors.lastname: Kapiotis
authors.forename: D
authors.initials: D
authors.lastname: Seidl
authors.forename: N
authors.initials: N
authors.lastname: Hergovich
authors.forename: M
authors.initials: M
authors.lastname: Zellner
authors.forename: H G
authors.initials: HG
authors.lastname: Eichler
authors.forename: G
authors.initials: G
authors.lastname: Stiegler
authors.forename: G
authors.initials: G
authors.lastname: Leitner
authors.forename: P
authors.initials: P
authors.lastname: Höcker
authors.forename: B
authors.initials: B
authors.lastname: Jilma
mesh_terms: D000328:Adult; D001777:Blood Coagulation; D005342:Fibrinolysis; D006801:Humans; D008297:Male; D018375:Neutrophil Activation; D009504:Neutrophils / Q000502:physiology*; D010974:Platelet Aggregation; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000032:analysis; D010983:Plateletpheresis / Q000009:adverse effects*
chemical_list: D019039:Platelet Glycoprotein GPIIb-IIIa Complex