A comparison between streptokinase/streptodornase and streptokinase on delayed hypersensitivity skin testing

The use of streptokinase (SK) to replace streptokinase/streptodornase (SK/SD) in delayed hypersensitivity skin testing was evaluated in 325 patients. Sixty patients responded to SK/SD (100 U of SK per 25 U of SD) and 36 to SK (375 U). Thirty-two responded to SK/SD but not to SK, and eight responded to SK but not to SK/SD. SK, at the dosage used, is not a suitable substitute for SK/SD in delayed hypersensitivity testing. SD may be the more potent recall antigen. Perhaps more importantly is that of 250 positive responders to a recall-antigen battery consisting of SK/SD, SK, Candida, Trichophyton, tetanus toxoid, purified protein derivative, and coccidioidin, 99.2% (248) would have been detected had the testing for SK and SK/SD not been done.     

Henoch-Schoenlein purpura due to streptokinase

The syndrome of Henoch-Schoenlein purpura developed in a 74-year-old woman after receiving streptokinase as thrombolytic therapy for an acute myocardial infarction. Renal biopsy revealed mesangial hypercellularity with deposits of IgA. Skin biopsy also revealed IgA deposition. Immunological studies showed evidence of sensitization to streptokinase. Elevated IgG, IgA, IgM, and IgE antistreptokinase antibodies were detected in the acute serum. Positive immediate skin reactivity to streptokinase was also present. Serum precipitins to streptokinase disappeared when IgA was removed from the serum. Positive staining with biotinylated streptokinase was seen in the skin in the same pattern of distribution as IgA. These findings strongly support the role of streptokinase and IgA in the pathogenesis of Henoch-Schoenlein purpura in this patient. A control group of streptococcalinfected patients showed no immune response to streptokinase. Another control group of streptokinase-treated patients, who had no untoward reaction, had elevated immunoglobulin classes and precipitins to streptokinase. However, the precipitating antibody was IgG and streptokinase skin tests were negative.     

Guillain-Barré syndrome following streptokinase therapy

Summary Clinical and laboratory data from a patient with Guillain-Barré syndrome indicated a probable etiological correlation of polyradiculitis to the intravenous administration of streptokinase. Oligoclonal IgG bands in the cerebrospinal fluid and serum were shown to be specific for streptokinase. Serum titers of streptokinase were elevated 64-fold for IgG, 16-fold for IgM, and 4-fold for IgA compared to controls. Clinical symptoms of Guillain-Barré syndrome are thought to result from streptokinase antibody complex mediated damage to the local blood-nerve barrier. The pathogenic relevance of autoantibodies to albumin and proteins of the central and peripheral nervous systems, occurring early after onset of symptoms, remains to be determined.Abbreviations CNS central nervous system - CSF cerebrospinal fluid - GBS Guillain-Barré syndrome - IEF isoelectric focusing - NF-L neurofilament light - PNS peripheral nervous system - SDS sodium dodecyl sulfate     

Catheter-induced superior vena cava thrombosis-lysis with streptokinase and apsac (Anisoylated plasminogen streptokinase activator complex BRL 26921)

Ten patients were given thrombolytic therapy for obstructive thrombi in the superior vena cava (SVC) following catheterisation for total parenteral nutrition (TPN—8 cases) or chemotherapy (2 cases). Seven of the TPN patients were given intravenous APSAC (Beecham, BRL 26921); the other 3 were given streptokinase (SK). Five of the caval occlusions treated with APSAC cleared after between 1 and 5 doses; one of those given SK cleared after 3 days continuous infusions during which active thrombolytic potential was maintained.Intravenous APSAC should be considered for the relief of major SVC occlusive thrombosis secondary to central venous catheters.     

Immunologic responses to intravenous streptokinase in dogs

Streptokinase is used worldwide as a thrombolytic agent. Allergic reactions to streptokinase have been reported, but the immunologic mechanisms have not been well characterized. To develop a canine model of streptokinase immune responses analogous to human responses, four dogs received intravenous streptokinase infusions. Significant rises in IgG, IgA and IgM antibody levels occurred after streptokinase administration in three of four dogs; a fourth dog developed significant increases in IgG and IgA antibody levels. Two dogs developed immediate-type cutaneous hypersensitivity to streptokinase. One dog developed subacute dermatitis with eosinophilic infiltrates which was possibly a manifestation of an allergic reaction to streptokinase.     

Immunology of streptokinase in human subjects.

Antigens of Plasmodium falciparum, in supernatants of in vitro cultures of the parasite were affinity purified on columns prepared with the IgG fraction of the serum of an immune individual. The purified antigens induced proliferation of lymphocytes from persons who had recently had malaria. The responses were strongest with lymphocytes from individuals infected with falciparum and ovale malaria; vivax malaria infections induced a lower level of response and lymphocytes of unsensitized individuals were little affected. Lymphocytes from unsensitized individuals did not respond to the affinity purified antigen preparations from malaria patients' sera indicating that significant amounts of non-specific mitogens were not present.     

The streptokinase domain responsible for plasminogen binding

The limited proteolysis of soluble recombinant streptokinase by Sepharose-immobilized human plasmin(ogen) complexed with recombinant streptokinase is described. A 17 kDa streptokinase fragment comprising residues Val143 (Glu148) to Arg289 (Lys293) has been shown to be the smallest stable plasminogen binding domain. Moreover, this region seems also to be important for plasminogen activation.     

尿激酶和链激酶对大鼠血小板功能的影响

目的：观察尿激酶（UK）和链激酶（SK）是否能直接激活血小板。方法：在体外制备大鼠血小板，以血小板聚集、血小板释放丙二醛（MDA）及5-羟色胺（5-HT）、血小板内游离钙（[Ca²⁺]_i）为指标，观察UK和SK对血小板的直接作用；在体内观察它们对电刺激诱导大鼠动脉形成血栓的影响。结果：在体外2×10⁶ U/L的UK与SK对凝血酶及ADP诱导的血小板聚集、对凝血酶诱导的血小板释放MDA含量、5-HT含量和血小板[Ca²⁺]_i无明显影响。在体内4×10⁴ U/kg的UK和SK对电刺激诱导的大鼠动脉血栓形成有一定的抑制作用。结论：UK和SK不能直接激活血小板。     

Sequence-directed DNA bending upstream of the streptokinase promoter

A 450-base pair (bp) HinfI restriction fragment from the chromosome of Streptococcus equisimilis H46A contains the early coding region of the streptokinase gene (skc), the skc promoter, and a stretch of DNA 5' to the--35 region of the skc promoter. Two-dimensional polyacrylamide (PA) gel electrophoresis at two different temperatures showed that this fragment migrates anomalously slowly on PA gels, suggesting the existence of a bent DNA conformation. Inspection of the nucleotide sequence confirmed this suggestion by revealing numerous oligomeric dA.dT tracts, some of which are in phase with the helix screw. Computer analysis of the sequence predicted the existence of two bending loci, one of which is located upstream of the skc promoter. In addition to showing DNA bending, the 450-bp HinfI fragment contains multiple 13-bp sequences homologous to the Escherichia coli integration host factor DNA-binding consensus sequence. Insertion of IS1 into a site immediately upstream of the--35 region decreased the expression level of skc in E. coli, suggesting that DNA conformation upstream of the promoter has a role in skc expression.     

Detection of nephritis strain-associated streptokinase by monoclonal antibodies

Monoclonal antibodies (MAbs) N-59 and RU-1 were produced by immunisation of mice with streptokinase secreted by Streptococcus group A, type 12, strain A374 isolated from a patient with post-streptococcal glomerulonephritis (PSGN) and were characterised by Western blot analysis. MAb N-59 recognised antigenic determinants shared by both nephritis strain-associated streptokinase (NSA-SKase) and streptokinase of Streptococcus group C (C-SKase); MAb RU-1 reacted only with NSA-SKase. All nephritis-associated group A streptococcal strains tested reacted with MAb N-59; 87.5% of these strains reacted with MAb RU-1. MAb N-59 reacted with SKase produced by group G streptococcal strains isolated from patients with PSGN, and MAb RU-1 recognised SKase in two out of three of these strains.