Antistreptokinase antibodies influence Adenosine diphosphate-inducible platelet aggregation
More details
Hide details
Educational and Scientific Centre “Institute of Biology”, National Taras Shevchenko University, Kiev, Ukraine
Nataliia Burlova-Vasilieva   

National Taras Shevchenko University, Kiev, Educational and Scientific Centre “Institute of Biology”, Volodimirska Street 64, 01601, Kiev, Ukraine.
J Pre Clin Clin Res. 2010;4(2):92–95
The objective of the study was to investigate the effect of streptokinase/antistreptokinase antibodies on Adenosine 5-diphosphate (ADP)-inducible platelet aggregation under steptokinase treatment. ADP-inducible platelet aggregation was determined using light transmission aggregometry (LTA). Baseline rabbits (7) and subjects after intravenous infusion of streptokinase (7) were observed. The presence of antistreptokinase antibodies and plasminogen activators inhibitor type 1 (PAI-1) were determined using ELISA. 7 days after intravenous infusion of streptokinase (Sk) ADP-inducible platelet aggregation in platelet rich plasma (PRP) did not increase baseline level, and was inhibited by Sk in a dose-dependent manner. Sk in a concentration of 16 mkg/ml was associated with significantly reduced ADP-inducible platelet aggregation. Concentration of PAI-1 was significantly elevated in platelet fraction. ADP-inducible platelet aggregation peaked at 7 weeks after intravenous infusion of Sk; Sk-inducible inhibition was not observed. 7 days after administration of Sk ADP-inducible platelet aggregation was normal, although PAI-1 level was elevated in platelet fraction. Platelet aggregation in response to ADP was significantly increased at 7 weeks after Sk administration when compared to baseline level. Inhibition effect of streptokinase on ADP-inducible platelet aggregation was not observed.
Courval M, Palisaitis DA, Diodati JG, Lesperance B, Pharand C: Inhibition of streptokinase-induced, antibody-mediated platelet aggregation with tirofiban after exposure to streptokinase or streptococcal infection. Pharmacotherapy 2004, 24, 558-563.
Vaughan DE, Kirshenbaum JM, Loscalzo JI: Streptokinase-induced, antibody-mediated platelet aggregation: a potential cause of clot propagation in vivo. J Am Coll Cardiol 1988, 11, 1343-1348.
Perler B: Thrombolytic therapies: The current state of affairs. J Endovasc Ther 2005, 12, 224-232.
McRedmond JP, Harriott P, Walker B, Fitzgerald DJ: Streptokinaseinduced platelet activation involves antistreptokinase antibody and cleavage of protease-activated receptor-1. Blood 2000, 95, 1301- 1388.
Lee HS, Cross S, Davidson R, Reid T, Jennings K: Raised levels of antistreptokinase antibody and neutralization titers from 4 days to months after administration of streptokinase or anistreplase. Eur Heart J 1993, 14, 640-643.
Breet NJ, van Werkum JW, Bouman HJ, Kelder JC, Ruven HJ, Bal ET, Deneer VH, Harmsze AM, van der Heyden JA, Rensing BJ, Suttorp MJ, Hackeng CM, van Berg JM: Comparison of platelet function tests in predicting clinical outcome in patients undergoing coronary stent implantation. JAMA 2010, 303, 754-762.
Jeong YH, Hwang JY, Kim IS, Park Y, Hwang SJ, Lee SW, Kwak CH, Park SW: Adding cilostazol to dual antiplatelet therapy achieves greater platelet inhibition than high maintenance dose clopidogrel in patients with acute myocardial infarction: Results of the adjunctive cilostazol versus high maintenance dose clopidogrel in patients with AMI (ACCEL-AMI) study. Circ Cardiovasc Interv 2010, 3, 17-26.
Schuhmann CG, Sohn HY, Nagel J, Spannagl M, Klauss V, Krotz F: Clinical management of clopidogrel inefficiency by point of care platelet function testing and individual adjustment of anti-platelet therapyinitial experiences. Platelets 2009, 20, 498-504.
Gemmill JD, Hogg KJ, Dunn FG, Rae AP, and Hillis WS: Pre-dosing antibody levels and efficacy of thrombolytic drugs containing streptokinase. Br Heart J 1994, 72, 222–225.
Tatu-Chiţoiu G, Teodorescu C, Dan M, Guran M, Căpraru P, Istrăţescu O, Tatu-Chiţoiu A, Bumbu A, Chioncel V, Arvanitopol S, Dorobanţu M: Streptokinase-induced hypotension has no detrimental effect on patients with thrombolytic treatment for acute myocardial infarction. A substudy of the Romanian Study for Accelerated Streptokinase in Acute Myocardial Infarction (ASK-ROMANIA). Rom J Intern Med 2004, 42, 557-573.
Varvara C Karagkiozaki, Stergios D Logothetidis, Spyridon N Kassavetis, Giannoglou GD: Nanomedicine for the reduction of the thrombogenicity of stent coatings. Int J Nanomedicine 2010, 5, 239– 248.
Altman R, Scazziota A, de Lourdes Herrera M, Gonzalez CD: The hemostatic profile of recombinant activated factor VII. Can low concentrations stop bleeding in off-label indications? Thromb J 2010, 8, 8.
Brogren H, Karlsson L, Andersson M, Wang L, Erlinge D, Jern S: Platelets synthesize large amounts of active plasminogen activator inhibitor 1. Blood 2004, 104, 3943-3948.
Juhan-Vague I, Alessi MC, Morange PE: Hypofibrinolysis and increased PAI-1 are linked to atherothrombosis via insulin resistance and obesity. Ann Med 2000, 32, 78-84.
Aso Y: Plasminogen activator inhibitor (PAI)-1 in vascular inflammation and thrombosis. Front Biosci 2007, 12, 2957-2966.
Soeki T, Tamura Y, Fukuda N, Ito S: Plasma and Platelet Plasminogen Activator Inhibitor-1 in Patients With Acute Myocardial Infarction. Jpn Circ J 2000, 64, 547-53.
Raised levels of antistreptokinase antibody and neutralization titres from 4 days to 54 months after administration of streptokinase or anistreplase. Eur Heart J 1993, 14, 84-89.
S Patel, S Jalihal, D P Dutka, G K Morris, 1993, 'Streptokinase neutralisation titers up to 866 days after intravenous streptokinase for acute myocardial infarction. Br Heart J 1993, 70, 119.
Regnault V, Helft G, Wahl D, Czitrom D, Vuillemenot A, Papouin G, Roda L, Danchin N, Lecompte T: Antistreptokinase platelet activating antibody are common and heterogeneous. J Thromb Haemost 2003, 1, 1055-1061.
Helft G, Lecompte T, Le Feuvre C, Metzger JP, Vacheron A, Samama MM: Anti-streptokinase antibody. Arch Mal Coeur Vaiss 1997, 90, 975-980.
Gemmill JD, Hogg KJ, Dunn FG, Rae AP, Hillis WS: Pre-dosing antibody levels and efficacy of thrombolytic drugs containing streptokinase. Br Heart J 1994, 72, 222-225.
Muhl D, Furedi R, Gecse K, Ghosh S, Falusi B, Bogar L, Roth E, Lantos : Time course of platelet aggregation during thrombolytic treatment of massive pulmonary embolism. Blood Coagul Fibrinolysis 2007, 18l, 661-667.
Moser M, Nordt T, Peter K, Ruef J, Kohler B, Schmittner M, Smalling R, Kubler W, Bode C: Platelet function during and after thrombolytic therapy for acute myocardial infarction with reteplase, alteplase, or streptokinase. Circulation 1999, 100, 1858-1864.
Huang TC, Graham DA, Nelson LD, Alevriadou BR: Fibrinolytic agents inhibit platelet adhesion onto collagen type I-coated surfaces at high blood flow conditions. Blood Coagul Fibrinolysis 1998, 9, 213-226.
Krasnobryzha EM, Burlova-Vasyl’eva NK, Savchuk O M, Volkov GL: Process of platelets activation by streptokinase. Ukr Biochem J 2007, 79(6), 60-64.
. Marcucci R, Gori AM, Paniccia R, Giusti B, Valente S, Giglioli C, Buonamici P, Antoniucci D, Abbate R, Gensini GF: Cardiovascular death and nonfatal myocardial infarction in acute coronary syndrome patients receiving coronary stenting are predicted by residual platelet reactivity to ADP detected by a point-of-care assay: a 12 month followup. Circulation 2009, 119, 237-242.
Gremmel T, Steiner S, Seidinger D, Koppensteiner R, Panzer S, Kopp CW: Adenosine diphosphate-inducible platelet reactivity shows pronounced age dependency in the initial phase of antiplatelet therapy with clopidogrel. J Thromb Haemost 2010, 8(1), 37-42.