Related Experiment Video
Updated: Aug 29, 2026
A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry
Published on: June 5, 2019
Platelet activity and antibody titers after exposure to streptokinase or streptococcal infection
Maryse Courval1, Donald A Palisaitis, Jean G Diodati
1Research Center, Hôpital du Sacré-Coeur de Montréal and Faculty of Pharmacy, Université de Montréal, Montreal, Quebec, Canada.
Insights
Antibodies to streptokinase can activate and aggregate platelets, potentially hindering treatment effectiveness in acute myocardial infarction. This platelet reactivity was observed in patients treated with streptokinase or those with prior streptococcal infections.
Area of Science:
- Cardiology
- Immunology
- Hematology
Background:
- Streptokinase (SK) therapy for acute myocardial infarction faces challenges with reperfusion failure (60%) and reocclusion (16%).
- These failures may stem from systemic SK inactivation, SK-induced platelet activation, and aggregation driven by antibodies formed after SK administration or streptococcal infections.
Purpose of the Study:
- To investigate the incidence of streptokinase-induced, antibody-mediated platelet activation and aggregation.
- To assess these phenomena following SK administration or in patients with a history of streptococcal infection.
Main Methods:
- Studied 45 healthy volunteers, 45 patients treated with streptokinase, and 13 patients with recent severe streptococcal infections.
- Measured streptokinase-induced, antibody-mediated platelet activation and aggregation.
- Assessed anti-streptokinase antibody titers and streptokinase resistance.
Main Results:
- Streptokinase-induced, antibody-mediated platelet activation occurred in 49% of SK patients versus 17% and 15% in streptococcal infection and control groups (p<0.05).
- Streptokinase-induced platelet aggregation was seen in 23% of SK and streptococcal infection patients, but none of the controls (p<0.05).
Conclusions:
- Streptokinase-induced, antibody-mediated platelet activation and aggregation are linked to high anti-streptokinase antibody titers.
- These immune responses may contribute to streptokinase therapy failure.
- Patients with streptococcal infections exhibit similar platelet reactivity to streptokinase in vitro as those treated with the drug.
Introduction:
Streptokinase use, in acute myocardial infarction, is hindered by failure to reperfuse (60%) and early reocclusion (16%). This phenomenon may, among other causes, be due to systemic inactivation of streptokinase, as well as streptokinase-induced platelet aggregation and clot propagation from antibodies to streptokinase produced after streptokinase administration or streptococcal infections. The purpose of this study was to determine the incidence of streptokinase-induced, antibody-mediated, platelet activation and aggregation after administration of SK or development of a streptococcal infection.
Materials And Methods:
We included 45 normal volunteers (Control group), as well as 45 patients who had received streptokinase (Streptokinase group) and 13 who had suffered a severe streptococcal infection (Streptococcal infection group) within the past 3 years. Extent of streptokinase-induced, antibody-mediated, platelet activation and aggregation, as well as anti-streptokinase antibody and streptokinase resistance titers (lowest streptokinase concentration to cause clot lysis within 10 min) were measured.
Results:
Whereas streptokinase-induced, antibody-mediated, platelet activation was observed in 49% of streptokinase patients and in only 17% and 15% of streptococcal infection patients and normal volunteers (p<0.05 Streptokinase vs. Control and Streptokinase vs. Streptococcal infection), streptokinase-induced platelet aggregation was observed in 23% of streptokinase patients and streptococcal infection patients, and in none of the control patients (p<0.05).
Conclusions:
Streptokinase-induced, antibody-mediated, platelet activation and aggregation occur in patients with high titers of anti-streptokinase antibody and may play a role in failure of streptokinase therapy. Streptococcal infection patients behave like streptokinase patients in terms of the reactivity of their platelets to subsequent streptokinase dose in vitro.
Related Concept Videos
01:22Formation of the Platelet Plug
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
01:16Clot Retraction and Fibrinolysis