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Antistreptokinase platelet-activating antibodies are common and heterogeneous
1Inserm ERIT-M 0323 et EA 3452, UHP (Faculté de Médecine), Nancy, France.
Insights
Antibodies against streptokinase (SK) can activate platelets, potentially reducing SK treatment effectiveness. These anti-SK antibodies are common, varied, and can cause procoagulant activity, necessitating clinical relevance assessment using patient platelets.
Area of Science:
- Immunology
- Cardiovascular Medicine
- Thrombosis
Background:
- Platelet activation by antistreptokinase (SK) antibodies can negatively impact SK therapy efficacy.
- Understanding anti-SK antibodies is crucial for managing SK treatment outcomes.
Purpose of the Study:
- To characterize anti-SK antibodies, focusing on their role in platelet activation and resultant procoagulant activities.
- To investigate the relationship between antibody concentration, neutralizing capacity, and platelet activation.
Main Methods:
- Sera from 146 coronary artery disease patients (SK-treated and non-treated) were analyzed.
- SK-dependent platelet activation and procoagulant activity were assessed using washed platelets from representative donors.
Main Results:
- Anti-SK antibodies were widespread, with concentrations ranging from 2-5252 microg/mL and variable neutralizing titers.
- Platelet activation was detected in 145 samples, influenced by IgG and donor platelet reactivity, even at low antibody concentrations or without neutralizing activity.
- Antibody immunization route did not affect the functional profile.
Conclusions:
- Anti-SK platelet-activating antibodies are prevalent, diverse, and can induce procoagulant effects.
- Their clinical significance warrants formal evaluation, emphasizing the use of patient-specific platelets for accurate detection due to variable reactivity.
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.
Patients And 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.
Conclusion:
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.