Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.7 (plasmin)
 9,023 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to delineate the efficacy of plasmin-treated intravenous gamma-globulin (IVGG) in the treatment of Kawasaki syndrome, we compared the frequency of coronary artery abnormalities in children treated or not with IVGG for Kawasaki syndrome. Among 291 cases of Kawasaki syndrome diagnosed during the period of 1987 to 1991 without coronary abnormalities within 10 days of the onset of illness, 128 were treated with IVGG and aspirin and were compared with 163 treated with aspirin alone. IVGG was given in a dosage of 400 mg/kg/day for 4 consecutive days. The detection of coronary abnormalities was monitored by two dimensional echocardiography. Two weeks after enrollment coronary artery abnormalities were present in 37 (22.7%) of 163 children in the aspirin group and in 9 (9%) of 128 in the gamma-globulin group (P < 0.05). Seven weeks after enrollment, abnormalities were present in 20 (12.3%) of 163 children in the aspirin group and in 6 (4.6%) of 128 in the IVGG group (P < 0.05). We conclude that plasmin-treated IVGG is effective in reducing the prevalence of coronary artery abnormalities in Kawasaki syndrome and suggest a predominant role of the Fc gamma fragment of IgG in the therapeutic effect.
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PMID:Efficacy of plasmin-treated intravenous gamma-globulin for therapy of Kawasaki syndrome. 834 83

Streptokinase (SK) is one of the plasminogen activators currently used in therapeutics. SK antibodies may appear in the blood after thrombolytic therapy with SK or after-hemolytic streptococci infection. Such antibodies may both activate platelets and neutralize the ability of SK to convert plasminogen into plasmin. We previously demonstrated that platelet activation induced by the combination of IgG anti-SK and anisoylated plasminogen-SK activator complex (APSAC) is mediated by Fc gamma RIIa1 receptor. However, the mechanism by which IgG anti-SK and APSAC (or SK) transduce an activating signal across the platelet plasma membrane remains unknown. We have demonstrated in the present study that the platelet aggregation induced by the combination of IgG anti-SK and APSAC is accompanied by an increase in inositol phosphate, Ca2+ mobilization and thromboxane (Tx) A2 generation. Neomycin, erbstatin and GF 109203X, which inhibit phospholipase C (PLC), protein tyrosine kinase (PTK) and protein kinase C (PKC) activities, respectively, abolished platelet aggregation induced by IgG anti-SK plus APSAC, indicating the pivotal roles of the PLC, PTK and PKC pathways in this immunological activation. In addition, TxA2 generation is also important since aspirin, a cyclooxygenase inhibitor and SQ 29548, a TxA2 receptor antagonist, showed significant inhibition of the platelet response. The contribution of released ADP was confirmed using apyrase, which significantly inhibited IgG anti-SK plus APSAC-induced platelet aggregation. Finally, WEB 2086, a platelet-activating factor (PAF) receptor antagonist, was not effective, indicating that PAF is not involved in this process. APSAC- or SKinduced platelet activation may limit the therapeutic effectiveness of the drug and may contribute to the pathogenesis of early reocclusion. The study of the mechanism leading to APSAC-induced platelet activation could be relevant for a better understanding of the physiopathology of immune complex disorder diseases and thrombolytic treatment failure.
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PMID:Signal transduction in the platelet activation induced by IgG anti-streptokinase and anisoylated plasminogen-streptokinase activator complex. 1679 41