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PubMed1991

Dissolution of intraocular fibrinous exudate by streptokinase.

In a prospective, open, pilot study, the authors evaluated the effects of intraocular injection of streptokinase on intraocular fibrin. The study was composed of nine patients in whom fibrinous exudate developed after pars plana vitrectomy. There were seven male and two female patients with a mean age of 44 years (range, 27 to 65 years). Fibrinous exudates were seen 1 to 22 days after surgery with obstruction of the view of the posterior segment. Each patient received a single intraocular injection of 1000 IU of purified streptokinase. Four hours after the streptokinase injection, complete dissolution of the fibrin was noted in each patient. There were no clinically detectable adverse effects from the intraocular administration of streptokinase. Streptokinase may be considered in the dissolution of intractable intraocular fibrinous exudates after vitrectomy.

Adult↗

PubMed1986

Elevated serum D dimer: a degradation product of cross-linked fibrin (XDP) after intravenous streptokinase during acute myocardial infarction.

D dimer, a degradation product of cross-linked fibrin, is generated by lysis of fibrin but not by lysis of fibrinogen and can be reliably detected by specific monoclonal antibody techniques. The generation of D dimer after intravenous streptokinase in acute myocardial infarction was studied with the use of a semiquantitative latex agglutination immunoassay. This assay utilizes the monoclonal antibody DD-3B6/22, raised by conventional hybridoma technology, against a highly purified preparation of human D dimer and is adjusted to give a positive agglutination at a D dimer serum concentration of greater than 200 ng/ml (upper limit of normal). Twenty-one patients with acute transmural myocardial infarction of less than 3 hours' duration were studied. Fifteen patients received 0.75 to 1.5 million U intravenous streptokinase and 6 patients were treated conventionally without thrombolytic therapy. An elevated serum level of D dimer was detected before treatment in only 1 of 15 patients receiving intravenous streptokinase and within 2 hours of treatment in the remaining 14 patients who received streptokinase. In contrast, an elevated serum D dimer level was not detected during the first 24 hours in any of the six conventionally treated patients, including two patients who manifested the clinical syndrome of spontaneous reperfusion. The data suggest that in patients with acute myocardial infarction, an elevated serum level of D dimer, a cross-linked fibrin degradation product occurs early after administration of a large dose of streptokinase, but is infrequent during the first 24 hours in conventionally treated patients with acute infarction. Measurement of D dimer may be potentially useful for monitoring thrombolysis in patients with acute myocardial infarction.

Aged↗

PubMed1987

Paradoxic elevation of fibrinopeptide A after streptokinase: evidence for continued thrombosis despite intense fibrinolysis.

Elevated levels of fibrinopeptide A, a marker of thrombin activity associated with acute myocardial infarction, have been found to decrease after administration of streptokinase when reperfusion occurs. In contrast, in patients without reperfusion and those with reocclusion after streptokinase therapy, fibrinopeptide A remains elevated. In the present study early serial measurements of fibrinopeptide A were used to further characterize this paradoxic increase in thrombin activity after streptokinase and to characterize its response to heparin. In 19 patients with acute myocardial infarction fibrinopeptide A was elevated to 82.3 +/- 43.5 ng/ml (mean +/- SE) before therapy. Thirty minutes after the initiation of streptokinase, fibrinopeptide A increased to 300.1 +/- 117.4 ng/ml (p less than 0.01), consistent with extensive thrombin activity. Fibrinopeptide A remained elevated until 15 minutes after a heparin bolus injection when levels decreased to 15% of the poststreptokinase value (49.2 +/- 13.3 ng/ml) (p less than 0.001). These data document a prompt paradoxic increase in thrombin activity after administration of streptokinase that may be responsible for failure of therapy in some patients.

Cardiomyopathies↗

PubMed1987

Development and evaluation of anisoylated plasminogen streptokinase activator complex (APSAC) as a second generation thrombolytic agent.

Anisoylated plasminogen streptokinase activator complex (APSAC) was developed as a second generation thrombolytic agent in an attempt to overcome some of the limitations to the intravenous application of streptokinase for coronary artery thrombolysis. Temporary protection of the active site on the plasminogen molecule by acylation allows APSAC to be given by rapid injection, confers semiselectivity for clot (at lower doses) and prolonged fibrinolytic action. These properties may simplify intravenous administration, improve coronary reperfusion response and reduce reocclusion potential. Clinical trials with APSAC, still ongoing, allow the following tentative conclusions: the efficacy of intravenous APSAC appears to be equivalent to that of intracoronary streptokinase, when given within 4 hours of the onset of symptoms of myocardial infarction, and superior to that of intravenous streptokinase, but it is easier to administer. Early APSAC therapy leads to reperfusion rates of 60 to 65% and patency rates of 70 to 80%. Early reocclusion rates (within 24 hours) appear to be as low as or lower than those obtained with other agents. Bleeding complications and allergic manifestations after APSAC are acceptably low and comparable with those of equivalent doses of streptokinase. The potential for mortality benefit after APSAC appears to be high and is undergoing additional study. Thus, APSAC therapy, which can be given by simple injection over 2 to 5 minutes, appears promising as a future first line approach to reperfusion therapy in acute myocardial infarction.

Animals↗

PubMed1993

Polymorphism of the streptokinase gene: implications for the pathogenesis of post-streptococcal glomerulonephritis.

Recent studies of streptokinase genes from epidemiologically and clinically defined streptococci of groups A, C and G have provided evidence of the polymorphism of the streptokinase locus in the chromosome of pathogenic streptococci. This review considers genetic and pathogenetic data suggesting that there exists a causal relationship between nephritis strain-associated streptokinase production and the initial stages of post-streptococcal glomerulonephritis (PSGN). Currently available sequence information allows to recognize, in the middle of the streptokinase molecule, a major variable region, V1, of about 70 amino acid residues in which sequence identity drops to below 50% when the proteins from nephritogenic and non-nephritogenic strains are compared. The V1 regions, although showing microheterogeneity within either protein category, appear to be more hydrophobic and possess a higher content of ordered secondary structures in the "nephritogenic" molecules. As a working hypothesis, they may be considered the nephrotropic domain(s) with which streptokinases from nephritogenic strains bind to glomerular structures and activate plasminogen in situ, thus triggering the cascade of proteolytic processes leading to PSGN.

Amino Acid Sequence↗

PubMed1994

Substitution of arginine 719 for glutamic acid in human plasminogen substantially reduces its affinity for streptokinase.

In isolation human plasminogen possesses no enzymatic activity, yet upon formation of an equimolar complex with the bacterial protein streptokinase, it acquires a plasminogen activator function. The region(s) of plasminogen and of streptokinase which mediate complex formation has (have) not been previously published. Here it is reported that a single-residue substitution (Arg719-->Glu) in the serine protease domain of full-length Glu-plasminogen substantially reduces its affinity for streptokinase. The plasminogen variant displays no other significant differences from the wild-type molecule with respect to activation by two-chain urokinase-type plasminogen activator, recognition by monoclonal antibodies, or ability to undergo conformational change. It is concluded that Arg719 in human plasminogen is an important determinant of the streptokinase binding site, although further sites are likely to contribute both to the affinity of plasminogen for streptokinase and to mechanisms by which the active site is formed within the complex.

Animals↗

PubMed1987

Pharmacokinetics of streptokinase in patients based on amidolytic activator complex activity.

The purpose of this study was to determine the pharmacokinetics of intravenous streptokinase in humans. Five patients with myocardial infarction, six patients with venous thromboembolism, and two normal volunteers were studied. The patients with myocardial infarction received 500,000 U over 30 minutes, the patients with venous thromboembolism received 250,000 U over 30 minutes followed by 100,000 U/hr over 16 to 78 hours, and the normal volunteers received 100,000 U over 15 minutes. Plasma streptokinase levels were measured based on the amidolytic activity of the streptokinase-plasminogen complex on the chromogenic substrate S-2251. Pharmacokinetic parameters were: biologic half-life 82 +/- 25 minutes, total clearance 10.8 +/- 8.8 ml/min, and apparent volume of distribution 1.10 +/- 0.71 l. Streptokinase levels declined progressively during the continuous, prolonged infusion in the patients with venous thromboembolism over 60 hours of treatment. We conclude that there are distinct time-dependent changes in the pharmacokinetics of streptokinase during continuous intravenous infusion and that this phenomenon is likely to be associated with progressively decreasing thrombolytic efficacy.

Adult↗

PubMed1971

The streptokinase-human plasminogen activator complex. Composition and identity of a subcomponent with activator activity.

Reactions between purified plasminogen and streptokinase, labelled with (131)I and (125)I respectively, were investigated by polyacrylamide-gel discontinuous electrophoresis. A molecular complex consisting of both (131)I-labelled plasminogen and (125)I-labelled streptokinase migrated between plasminogen and streptokinase. This complex contained bovine plasminogen activator activity. The relative quantities of (131)I-labelled plasminogen and (125)I-labelled streptokinase in this complex were markedly affected by reaction conditions. A fragment that retained 50% or more of the parent activator activity was released from the complex after exposure to mercaptoethanol. This subcomponent had an estimated molecular weight of 70000, and contained both (131)I-labelled plasminogen and (125)I-labelled streptokinase.

Aminocaproates↗

PubMed1996

Early administration of intrapleural streptokinase in the treatment of multiloculated pleural effusions and pleural empyemas.

In the treatment of multiloculated pleural effusions and empyemas tube thoracostomy often fails and more aggressive surgical therapy is required. Intrapleural administration of fibrinolytics is a valuable alternative. Between October 1994 and December 1995 28 patients (aged 22 to 62 years) with multiloculated pleural effusions were treated with intrapleural instillations of streptokinase after unsuccessful conventional chest tube drainage. Twenty-three pleural effusions were grossly purulent, others were loculated effusions with low pH. The most common cause of the pleural effusions was pneumonia. Duration of illness before hospitalization was 3 to 105 (mean 21.8) days. Treatment with streptokinase was started most commonly one day after chest tube placement. Once a day after clamping the chest tube streptokinase was administered intrapleurally for 10-15 minutes as a solution of 250,000 units in 100 ml normal saline. The tube remained clamped for 3 hours. Two to 8 (mean 3.7) instillations per patient were needed. Twenty-one cases (72.4%) showed excellent resolution of pleural effusion and needed no more therapy. However, one patient died in hospital due to purulent meningitis and bilateral pneumonia. Eight patients needed further surgical treatment, e.g. decortication, in 5 cases together with wedge lung resection. Eleven patients experienced some adverse effects of streptokinase therapy, most frequently chest pain and elevation of body temperature in one case pleural effusion became hemorrhagic, and one patient had nasal bleeding. We conclude that usage of intrapleural streptokinase in the treatment of multiloculated pleural effusions (including pleural empyemas) reduces the need for major surgical interventions in quite a large group of patients.

Adult↗

PubMed1980

[Treatment of the hemolytic-uremic syndrome with streptokinase and heparin (author's transl)].

In a clinical study we treated 16 children, suffering from severe hemolytic-uremic syndrome (HUS), with streptokinase or heparin. All children received the same symptomatic treatment (early dialysis, transfusion of packed red cells). A control group of 10 children was only treated symptomatically. No difference could be shown in clinical grading of severity. We analysed the results of the acute phase and of a follow up study of 1-5 years, which is not yet complete. The results show, that heparin could not improve the prognosis of HUS in comparison to streptokinase or symptomatic treatment. The results of streptokinase treatment were not better than in the control group. In 4 children we saw severe bleeding complications of streptokinase therapy. Accepting the complication rate of a drug and the incidence of chronic renal disease as criterium of the efficacy of drug treatment in severe HUS, streptokinase and heparin are not indicated. We believe, that patients should be managed symptomatically with early dialysis.

Acute Kidney Injury↗

PubMed1983

Western Washington randomized trial of intracoronary streptokinase in acute myocardial infarction.

Two hundred fifty patients were enrolled in a multicenter, community-based study of the efficacy of intracoronary streptokinase thrombolysis in acute myocardial infarction; 134 were randomly assigned to streptokinase therapy and 116 were controls. All patients underwent left ventricular angiography and coronary arteriography before the random assignment. The mean time from the onset of symptoms to hospitalization was 134 +/- 144 minutes (S.D), and the mean time to random assignment was 276 +/- 185 minutes. Coronary reperfusion was achieved in 68 per cent of the streptokinase-treated group. The overall 30-day mortality was 18 (7.2 per cent); there were five deaths in the streptokinase-treated group (3.7 per cent) and 13 in the control group (11.2 per cent, P less than 0.02). Fifteen of the 18 deaths occurred in patients with anterior infarction. Intracoronary streptokinase therapy resulted in a nearly threefold reduction in the 30-day mortality after hospitalization for acute myocardial infarction.

Adult↗

PubMed1995

Cost effectiveness of thrombolytic therapy with tissue plasminogen activator as compared with streptokinase for acute myocardial infarction.

BACKGROUND: Patients with acute myocardial infarction who were treated with accelerated tissue plasminogen activator (t-PA) (given over a period of 1 1/2 hours rather than the conventional 3 hours, and with two thirds of the dose given in the first 30 minutes) had a 30-day mortality that was 15 percent lower than that of patients treated with streptokinase in the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO) study. This was equivalent to an absolute decrease of 1 percent in 30-day mortality. We sought to assess whether the use of t-PA, as compared with streptokinase, is cost effective. METHODS: Our primary, or base-case, analysis of cost effectiveness used data from the GUSTO study and life expectancy projected on the basis of the records of survivors of myocardial infarction in the Duke Cardiovascular Disease Database. In the primary analysis, we assumed that there were no additional treatment costs due to the use of t-PA after the first year and that the comparative survival benefit of t-PA was still evident one year after enrollment. RESULTS: One year after enrollment, patients who received t-PA had both higher costs ($2,845) and a higher survival rate (an increase of 1.1 percent, or 11 per 1000 patients treated) than streptokinase-treated patients. On the basis of the projected life expectancy of each treatment group, the incremental cost-effectiveness ratio--with both future costs and benefits discounted at 5 percent per year--was $32,678 per year of life saved. The use of t-PA was least cost effective in younger patients and most cost effective in older patients. At all ages, the use of t-PA in patients with anterior infarctions yielded more favorable cost-effectiveness values. In our secondary analyses, the cost-effectiveness values were most sensitive to a lowering of the projected long-term survival benefits of t-PA and to moderate or greater increases in the projected medical costs for patients in the t-PA group after the first year. In contrast, our results were not sensitive to even very unfavorable assumptions about the additional costs associated with the higher rate of disabling stroke that was noted in patients treated with t-PA in the GUSTO study. CONCLUSIONS: The cost effectiveness of treatment with accelerated t-PA rather than streptokinase compares favorably with that of other therapies whose added medical benefit for dollars spent is judged by society to be worthwhile.

Adult↗

PubMed1984

Streptokinase: cloning, expression, and excretion by Escherichia coli.

Genomic DNA from Streptococcus equisimilis strain H46A was cloned in Escherichia coli by using the bacteriophage lambda replacement vector L47 and an in vitro packaging system. A casein/plasminogen overlay technique was used to screen the phage bank for recombinants carrying the streptokinase gene ( skc ). The gene was present with a frequency of 1 in 836 recombinants, and 10 independent clones containing skc were isolated and physically characterized. One recombinant clone was used to subclone skc in E. coli plasmid vectors. Plasmid pMF2 [10.4 kilobases (kb)] consisting of pACYC184 with a 6.4-kb H46A DNA fragment in the EcoRI site and pMF5 (6.9 kb) carrying a 2.5-kb fragment in the Pst I site of pBR322 were among the recombinant plasmids determining streptokinase production in three different E. coli host strains. Expression of skc was independent of its orientation in either vector, indicating that its own promoter was present and functional in E. coli. However, expression in pBR322 was more efficient in one orientation than in the other, suggesting that one or both of the bla gene promoters contributed to skc expression. Several lines of evidence, including proof obtained by the immunodiffusion technique, established the identity of E. coli streptokinase. Testing cell-free culture supernatant fluids, osmotic shock fluids, and sonicates of osmotically shocked cells for streptokinase activity revealed the substance to be present in all three principal locations, indicating that E. coli cells were capable of releasing substantial amounts of streptokinase into the culture medium.

Cloning, Molecular↗

PubMedDate not supplied

Thrombus localization by using streptokinase containing vesicular systems.

Our research focused on the preparation of vesicular drug delivery systems, such as liposomes, noisomes, and sphingosomes, for achieving slow release of entrapped proteins in the circulation to increase half-life, to mask immunogenic properties, and to protect against loss of enzymatic activity. We prepared, characterized, and monitored the biodistribution of three types of vesicular systems (liposomes, niosomes, and sphingosomes) containing streptokinase. For biodistribution stuides, radiolabelled streptokinase dispersions were injected into the ear vein of female rabbits in the weight of 2.5-3 kg weight. Following the application, rabbits were sacrificed, then organs of these animals were removed and radioactivity of organs was measured by well-type gamma counter. The comparison of the biodistribution results of the free streptokinase with the streptokinase vesicles showed that incorporation of the enzyme into the vesicles changed the biodistribution of the drug and by the entrapment of the streptokinase in the vesicles, thrombus uptake and imaging quality were improved.

Animals↗

PubMed1990

Effects of streptokinase, urokinase, and recombinant tissue plasminogen activator on platelet aggregability and stability of platelet aggregates.

STUDY OBJECTIVE: The aim of the study was to evaluate the effects of streptokinase, urokinase and recombinant tissue plasminogen activator (TPA) on platelet aggregability and metabolism and the stability of preformed platelet aggregates. DESIGN: The experiments (n = 15 for each condition) were performed on citrated plasma or on platelet suspensions in phosphate buffered saline, both with a standardised platelet count of 250 x 10(9).litre-1. SUBJECTS: were healthy volunteers. MEASUREMENTS AND MAIN RESULTS: With both ADP (1 mumol.litre-1) and collagen (1 mg.litre-1) as aggregating agents, streptokinase at greater than or equal to 10(5) units.litre-1 led to reduction in the rate of platelet aggregation. With collagen and in most instances with ADP, this was associated with a decreased extent of aggregation, though in five out of 30 cases with ADP as aggregating agent, a conversion from reversible to irreversible aggregation occurred with streptokinase. Urokinase inhibited platelet aggregation at greater than or equal to 3 x 10(5) units.litre-1 with both aggregating agents. TPA inhibited aggregation at greater than or equal to 1 mg.litre-1 with ADP and at greater than or equal to 3.3 mg.litre-1 with collagen as aggregating agent. The inhibitory effect was still present when the platelets were suspended in saline. Platelet synthesis of thromboxane on stimulation with collagen, and of c-AMP on stimulation with prostaglandin E1, was markedly reduced by either agent. The stability of platelet aggregates, as assessed photometrically during a 90 min exposure to stirring stress, increased when streptokinase or urokinase was added to platelet rich plasma, but remained uninfluenced with TPA. CONCLUSIONS: Urokinase and TPA inhibited platelet aggregability uniformly and in a dose dependent manner. Streptokinase inhibited platelet aggregation in most instances, but led to a stimulation of aggregation in a minority of cases. These effects of the thrombolytic agents on platelets might have an influence on the occurrence of bleeding and of reocclusion after thrombolytic therapy.

Adenosine Diphosphate↗

PubMed1993

Raised levels of antistreptokinase antibody and neutralization titres from 4 days to 54 months after administration of streptokinase or anistreplase.

Streptokinase and anistreplase are antigenic and their administration often leads to antibody formation. These can cause allergic reactions and/or neutralization of streptokinase with resulting suboptimal treatment. Currently, streptokinase re-administration is considered appropriate for up to 5 days and from 1 year after a previous dose. Antistreptokinase antibody and neutralization titres (NT) were measured in three groups of patients to determine if this practice is appropriate: 1. (early)--36 patients whose titres were measured for at least 5 days after thrombolysis; 2. (late)--57 patients who received thrombolysis 12-54 months previously; 3. (controls)--182 consecutive suspected myocardial infarction patients (without previous exposure to thrombolysis). Results were as follows (mean +/- SEM): 1. (early)--the antibody and/or NT were raised by day 4 in 19.4% of the patients. One patient could have neutralized 1.97 million units (MU) of streptokinase by day 4. (Day 4--antibody 1:39 +/- 11, NT 0.19 +/- 0.05 MU; day 5--1:136 +/- 41 and NT 0.7 +/- 0.43 MU respectively.) 2. (late)--23 patients (40%) had either antibody titres > or = 1:160 and/or NT > 1.5 MU. (12-23 months--antibody 1:243 +/- 43, NT 0.63 +/- 0.15 MU; 24-35 months--1:98 +/- 31 and 0.69 +/- 0.22 MU; 36-54 months--1:87 +/- 14 and 0.54 +/- 0.12 MU.) All titres were significantly higher than the controls (antibody 1:25 +/- 3, NT 0.14 +/- 0.01 MU, P < 0.01). After streptokinase or antistreplase, antibodies are raised from 4 days to at least 54 months. It would seem prudent to avoid their re-administration during this time interval.

Anistreplase↗

PubMed1997

Streptokinase vs alteplase in massive pulmonary embolism. A randomized trial assessing right heart haemodynamics and pulmonary vascular obstruction.

OBJECTIVE: The aim of the study was to test the efficacy of recombinant tissue plasminogen activator and streptokinase in massive pulmonary embolism, the primary endpoints being haemodynamic improvement and thrombus lysis, and the secondary endpoints efficacy and safety. DESIGN: Fifty patients with massive pulmonary embolism were randomly allocated either to a 100 mg 2 h infusion of recombinant tissue plasminogen activator followed by a 20 IU.kg-1.h-1 infusion of heparin, or to a 100,000 IU.h-1 12 h infusion of streptokinase after a initial bolus of 250,000 IU over 15 min, followed by heparin infusion of 10 IU.kg-1.h-1. Total pulmonary resistance and right ventricular ejection fraction were monitored over a 12 h period. Pulmonary vascular obstruction was assessed at 24 to 48 h and 10 days after thrombolytic therapy. RESULTS: Thrombolysis occurred more rapidly with recombinant tissue plasminogen activator than with streptokinase, but without any significant difference in terms of right heart haemodynamics at 12 h or in improvement of pulmonary vascular obstruction at 24-48 h or at 10 days. There was no significant difference in bleeding complication rates and no patients suffered intracranial haemorrhage. CONCLUSION: These results proved that, when the full dose of streptokinase has been given over 12 h, its efficacy is as good as that of 2 h of recombinant tissue plasminogen. A further trial aimed at comparing recombinant tissue plasminogen activator and streptokinase infused over a 2 h period is needed to determine whether a similar efficacy can be obtained.

Aged↗

PubMedDate not supplied

Augmentation of streptokinase-induced thrombolysis by heparin and prostacyclin.

The ability of heparin and prostacyclin to improve streptokinase-induced recanalization was examined in open-chest dogs subjected to thrombotic occlusion of the left circumflex coronary artery. Vessel injury was produced by electrical stimulation of the intimal surface at the site of a noncircumferential fixed stenosis. Animals were divided into three treatment groups as follows: group 1 received intracoronary streptokinase alone (75,000 units/80 min starting 30 min postocclusion; n = 8); group 2 received streptokinase plus heparin (300 units/kg i.v. at 20 min postocclusion; n = 7); group 3 received streptokinase plus heparin plus prostacyclin (500 ng/kg/min, intracoronary, given intermittently during reperfusion; n = 7). Overall, the groups did not differ with respect to preocclusion coronary blood flow (27 +/- 1 ml/min; +/- SEM), the duration of streptokinase infusion required to achieve reflow (15 +/- 2 min), and the percentage of animals recanalized (85%). They did differ in the average rate of reflow, which was greater in group 2 (16 +/- 2 ml/min) and group 3 (20 +/- 4 ml/min) as compared with group 1 (6 +/- 1 ml/min; p less than 0.05). The intermittent reocclusions which persisted during reperfusion in group 1 and 2 dogs were diminished during the periodic infusions of prostacyclin. Thrombus mass at the site of injury was comparable among groups. In contrast, distal circumflex thrombi, about twice the weight of the proximal mass, were observed in all group 1 dogs and were undetectable in group 2 and 3 animals. Transient improvements in contractile force during reperfusion were observed only with groups 2 and 3.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗