title: Antistreptokinase platelet-activating antibodies are common and heterogeneous.
abstract: BACKGROUND
  Platelet activation by antistreptokinase (SK) antibodies could impair the clinical effect of SK administration.
  
  
  OBJECTIVE
  To better describe anti-SK antibodies with particular emphasis on procoagulant activities as a result of platelet activation.
  
  
  METHODS
  Sera were collected from 146 patients with coronary artery disease: non-SK-treated, 95 from mainland France, 31 from French Polynesia; 20 patients from mainland in year 2 after SK treatment. Serum-induced SK-dependent platelet activation resulting in procoagulant activities was assessed with washed platelets from five donors representative of the known patterns of reactivities to IgG.
  
  
  RESULTS
  Concentrations (2-5252 microg mL(-1)) and fibrinolytic neutralization titres (< 10 to > 1280) were found in the expected wide range and correlated (rho = 0.66, P < 0.0001). Platelet activation was detected with 145 samples, but varied in intensity and pattern (depending on the donors), although there was no systematic hierarchy; it was presumably due to IgG (inhibited by an IgG Fc receptor-blocking antibody and recovered in the IgG fraction) and only partially affected by aspirin. Marked platelet activation could be detected in samples with concentration as low as 2 microg mL(-1), and/or no detectable neutralizing titers. The way of immunization to SK was not found to influence the functional profile of antibodies.
  
  
  CONCLUSIONS
  Anti-SK platelet-activating antibodies are widespread, heterogeneous, poorly predictable on the basis of their antifibrinolytic effect and strong enough to trigger procoagulant activities. Their clinical relevance should be formally assessed, using patients' own platelets for detection owing to the variation of platelet reactivity.
authors.affiliation: Inserm ERIT-M 0323 et EA 3452, UHP (Faculté de Médecine), Nancy, France.
authors.forename: V
authors.initials: V
authors.lastname: Regnault
authors.forename: G
authors.initials: G
authors.lastname: Helft
authors.forename: D
authors.initials: D
authors.lastname: Wahl
authors.forename: D
authors.initials: D
authors.lastname: Czitrom
authors.forename: A
authors.initials: A
authors.lastname: Vuillemenot
authors.forename: G
authors.initials: G
authors.lastname: Papouin
authors.forename: L
authors.initials: L
authors.lastname: Roda
authors.forename: N
authors.initials: N
authors.lastname: Danchin
authors.forename: T
authors.initials: T
authors.lastname: Lecompte
mesh_terms: D000328:Adult; D003324:Coronary Artery Disease / Q000188:drug therapy / Q000276:immunology; D005260:Female; D006801:Humans; D007106:Immune Sera / Q000494:pharmacology; D007074:Immunoglobulin G; D007518:Isoantibodies / Q000097:blood* / Q000502:physiology; D008297:Male; D015539:Platelet Activation / Q000276:immunology*; D010979:Platelet Function Tests; D013300:Streptokinase / Q000009:adverse effects / Q000276:immunology* / Q000627:therapeutic use; D013917:Thrombin / Q000096:biosynthesis
chemical_list: D007106:Immune Sera; D007074:Immunoglobulin G; D007518:Isoantibodies; D013300:Streptokinase; D013917:Thrombin