SEARCH · PubMed Health

Results for “STREPTOKINASE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 253 records · Page 14Linked to original sources

PubMed1989

Heterogeneity of the streptokinase gene in group A streptococci.

A molecular epidemiological study was conducted to determine the distribution of the streptokinase gene in group A streptococcal strains of different M types and in other streptococcal species. Plasmid pNC1, containing only the internal coding sequence of the streptokinase gene from group C streptococcal strain H46A, was used as a DNA probe in colony and Southern hybridization experiments. Only the pathogenic group A, C, and G streptococci contained a streptokinase gene; 12 other Lancefield group strains did not. A total of 134 group A strains, including 61 M types and 6 T types, were tested. Although only 62% (83 of 134) of the strains tested showed positive streptokinase activity by the casein-plasminogen overlay assay, all strains contained the streptokinase gene as evidenced by strong hybridization with the pNC1 probe. Southern blot DNA hybridizations were carried out with 101 strains of group A streptococci. The restriction enzymes HindIII and HaeIII were used to digest the genomic DNA. Six hybridization patterns were observed after HindIII digestion. Double hybridization bands appeared in all of the patterns, which indicated the existence of a highly conserved HindIII site. More complex hybridization results were obtained after HaeIII digestion. Twelve hybridization patterns were observed; three were characterized by a single hybridization band, and nine were characterized by double bands. Variations in hybridization patterns were observed in strains of both the same and different serotypes. The overall results at the gene level indicate that there is considerable heterogeneity among the streptokinases of group A streptococci, consistent with previous findings of immunological and chemical differences among streptokinases of group A streptococci.

DNA Probes↗

PubMed2000

Allele substitution of the streptokinase gene reduces the nephritogenic capacity of group A streptococcal strain NZ131.

To investigate the role of allelic variants of streptokinase in the pathogenesis of acute poststreptococcal glomerulonephritis (APSGN), site-specific integration plasmids were constructed, which contained either the non-nephritis-associated streptokinase gene (skc5) from the group C streptococcal strain Streptococcus equisimilis H46A or the nephritis-associated streptokinase gene (ska1) from the group A streptococcal nephritogenic strain NZ131. The plasmids were introduced by electroporation and homologous recombination into the chromosome of an isogenic derivative of strain NZ131, in which the streptokinase gene had been deleted and which had thereby lost its nephritogenic capacity in a mouse model of APSGN. The introduction of a non-nephritis-associated allelic variant of streptokinase did not rescue the nephritogenic capacity of the strain. The mutant and the wild-type strains produced equivalent amounts of streptokinase. Complementation of the ska deletion derivative with the original ska allele reconstituted the nephritogenicity of wild-type NZ131. The findings support the hypothesis that the role of streptokinase in the pathogenesis of APSGN is related to the allelic variant of the protein.

Alleles↗

PubMed1999

Thrombolysis in acute myocardial infarction: analysis of studies comparing accelerated t-PA and streptokinase.

OBJECTIVES: To compare outcomes from accelerated alteplase (recombinant tissue plasminogen activator, t-PA) and streptokinase use in acute myocardial infarction. METHODS: Review of available studies identified by Medline and other literature searches that met the criteria of being a prospective, randomised clinical trial enrolling over 1000 patients with acute myocardial infarction. The studies had to contain an intervention arm comprising accelerated infusion t-PA, or an intervention arm comprising streptokinase provided accelerated t-PA that was compared in the same trial. Interventions compared were streptokinase 1.5 million units given over one hour compared with accelerated t-PA infusion, with concomitant use of aspirin and heparin, and main outcome measure of 30 day mortality. RESULTS: Four studies met prespecified criteria, these being the GUSTO I, GUSTO IIb Angioplasty Substudy, GUSTO III, and COBALT trials. There was a total study population of 64,387 patients of whom 20,251 received streptokinase, 19,474 received t-PA, with others receiving different treatment. Pooled data show that accelerated t-PA produces a marginal 30 day mortality advantage compared with streptokinase (6.6% v 7.3%, p = 0.02, Bonferroni adjusted p = 0.12, that is borderline significance, relative risk 0.918, 95% confidence interval 0.854 to 0.986). Any benefit is attributable entirely to patients recruited in the United States in the GUSTO I study. There is an increased incidence of stroke with t-PA. CONCLUSIONS: The data do not consistently show a 30 day mortality benefit from using t-PA compared with streptokinase in acute myocardial infarction, but do show increased risk of stroke. Streptokinase can be considered the thrombolytic agent of choice.

Female↗

PubMed1992

Streptokinase induced defibrination assessed by thrombin time: effects on residual coronary stenosis and left ventricular ejection fraction.

OBJECTIVE: To evaluate laboratory markers of defibrination early after thrombolytic therapy and to determine their relation to residual stenosis and left ventricular ejection fraction measured angiographically before discharge from hospital. DESIGN: Prospective analysis of defibrination after streptokinase measured by fibrinogen assay and thrombin time to provide a comparison of these coagulation variables for predicting angiographic responses to treatment in patients with acute myocardial infarction. SETTING: The coronary care unit of a district general hospital. PATIENTS: 44 patients with acute myocardial infarction treated by streptokinase infusion, all of whom underwent paired blood sampling before and one hour after streptokinase and cardiac catheterisation at a median of six (interquartile range 3-9) days later. MAIN OUTCOME MEASURES: Assay of thrombin time and plasma fibrinogen concentrations one hour after streptokinase infusion. Relations between these coagulation variables and residual stenosis in the infarct related coronary artery and left ventricular ejection fraction. Separate analyses are presented for all patients (n = 44) and those with patency of the infarct related artery (n = 35). RESULTS: Streptokinase infusion produced profound defibrination in every patient as shown by changes in thrombin time and circulating fibrinogen. Thrombin time after streptokinase infusion correlated significantly with both residual stenosis (r = -0.43, p < 0.005) and left ventricular ejection fraction (r = 0.38, p < 0.02). The importance of these correlations was emphasised by the interquartile group comparison which showed that a thrombin time > or = 49 seconds predicted a residual stenosis of 74% and an ejection fraction of 65%, compared with 90% and 49% for a thrombin time < or = 31 seconds (p < 0.01). When the analysis was restricted to patients with patency of the infarct related artery, the correlation between thrombin time and residual stenosis remained significant and group comparisons continued to show that patients in the highest quartile range had more widely patent arteries and better preservation of ejection fraction. Analysis of the fibrinogen data, on the other hand, showed insignificant or only marginally significant correlations with these angiographic variables. CONCLUSIONS: Early after streptokinase infusion for acute myocardial infarction, the level of defibrination measured by thrombin time has an important influence on residual coronary stenosis and left ventricular ejection fraction at discharge from hospital, values above 49 seconds being associated with the best angiographic result.

Aged↗

PubMed1994

Intrapleural streptokinase in the management of empyema.

BACKGROUND: Significant morbidity and mortality result from the ineffective evacuation of empyema. Failure of conventional first line treatment with closed intercostal tube drainage and antibiotic therapy may result in fibrin deposition and loculated empyema. Enzymatic debridement using intrapleural instillation of streptokinase is a non-invasive therapeutic option which may obviate the need for surgical intervention. METHODS: Eleven adults with multiloculated post-pneumonic empyemas who had failed to respond satisfactorily to intercostal tube drainage and antibiotic therapy were treated with intrapleural streptokinase between November 1992 and January 1994. A small catheter was inserted under ultrasound guidance into a loculation within the pleural space. Aliquots of 250,000 units of streptokinase in 100 ml normal saline were instilled into the pleural cavity and the tube clamped for four hours. Response was assessed by clinical outcome, measurement of drain output after unclamping, and subsequent pleural ultrasound, chest radiography, or both. RESULTS: Streptokinase enhanced drainage in all patients. Complete resolution of the empyema with re-expansion of the underlying lung was effected in eight patients, all of whom remain well. Further resolution of minimal pleural thickening was shown on subsequent chest radiographs. Two patients with considerably thickened visceral pleura following empyema drainage underwent successful decortication. The other, with myocarditis and a pyopneumothorax, underwent surgery for non-resolution of the pneumothorax but died perioperatively from cardiac failure. The number of streptokinase instillations per patient ranged from two to six (median three), and the volume of empyema fluid drained per patient ranged from 100 ml to 4870 ml (median 900 ml). Streptokinase was well tolerated in all patients. CONCLUSIONS: Intrapleural streptokinase is an effective adjunct in the management of complicated empyema and may reduce the need for surgery.

Adult↗

PubMed1985

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.

Animals↗

PubMedDate not supplied

Comparative effects of tissue plasminogen activator, streptokinase, and staphylokinase on cerebral ischemic infarction and pulmonary clot lysis in hamster models.

BACKGROUND: The effects of alteplase (rtPA), streptokinase, and staphylokinase (rSak) on focal cerebral ischemia (FCI) and on pulmonary clot lysis (PCL) were studied in hamsters. METHODS AND RESULTS: ++FCI was produced by ligation of the left middle cerebral artery (MCA) and common carotid artery (CCA) and a 10-minute occlusion of the right CCA. FCI was measured after 24 hours by 2,3, 5-triphenyltetrazolium chloride staining. (125)I-fibrin-labeled plasma clots were injected via the jugular vein, and clot lysis was determined from residual radioactivity at 90 minutes. Study drugs were given intravenously over 60 minutes. FCI increased from 1.2 (0. 27 to 2.3) mm(3) (median and 17th to 83rd percentile range, n=24) in controls to 19 to 27 mm(3) with thrombolytic agent, with maximal rates at 0.13+/-0.05 mg/kg rtPA, 0.23+/-0.09 mg/kg streptokinase, and 0.037+/-0.025 mg/kg rSak. PCL increased from 18+/-2% (mean+/-SEM, n=27) in controls to approximately 85% with thrombolytics, with maximal rates at 0.12+/-0.03 mg/kg rtPA, 0.17+/-0.05 mg/kg streptokinase, and 0.018+/-0.002 mg/kg rSak. All agents caused maximal FCI and PCL rates at similar doses without alpha(2)-antiplasmin and fibrinogen depletion. Injection of 6 mg/kg human plasminogen combined with streptokinase caused a "systemic fibrinolytic state" with fibrinogen depletion. Maximal rates of FCI were obtained with 0.097+/-0.077 mg/kg streptokinase (P=0.26 versus streptokinase alone) and of PCL with 0.010+/-0.002 mg/kg (P=0.006 versus streptokinase alone). CONCLUSIONS: Thrombolytic agents cause similar dose-related extension of FCI after MCA ligation and PCL, irrespective of the agent or systemic plasmin generation.

Animals↗

PubMed1985

A comparison of the thrombolytic and hemorrhagic effects of tissue-type plasminogen activator and streptokinase in rabbits.

Tissue-type plasminogen activator (t-PA) is a promising thrombolytic agent because it can produce thrombolysis without inducing a plasma proteolytic state. It is uncertain if this potentially important feature renders t-PA less hemorrhagic than other plasminogen activators. We have compared the hemorrhagic and thrombolytic effects of t-PA and streptokinase in rabbits. Streptokinase, 4000 U/kg/hr over 4 hr, failed to produce significant thrombolysis and 8000 U/kg/hr streptokinase over 4 hr produced only 28 +/- 6% thrombolysis. Both streptokinase regimens were associated with a plasmin-mediated plasma proteolytic state and both streptokinase regimens produced a significant increase in hemorrhage that was evident within 15 min of beginning the infusion and was progressive over the 4 hr of drug administration. In contrast, t-PA in a dose of 7500 U/kg/hr produced 35 +/- 6% thrombolysis, but it did not produce a plasmin-mediated plasma proteolytic state or a significant increase in hemorrhage over the 4 hr of infusion. t-PA in a dose of 15,000 U/kg/hr produced 85 +/- 4% thrombolysis but was associated with a plasmin-mediated proteolytic state and produced significant bleeding which, in contrast to streptokinase-induced bleeding, was delayed in onset. Therefore, t-PA induced less hemorrhage than streptokinase at doses that produced more effective thrombolysis. Bleeding with both thrombolytic agents was associated with a plasmin-mediated proteolytic state.

Animals↗

PubMed1988

Intravenous streptokinase for acute myocardial infarction. Effects on global and regional systolic function.

The Western Washington Intravenous Streptokinase Trial randomized 368 patients with acute myocardial infarction to receive either intravenous streptokinase or standard therapy. The ventriculograms and coronary angiograms obtained in 170 patients 10.4 +/- 7.4 days after infarction were analyzed to evaluate the effects of thrombolytic therapy on global and regional systolic function. Streptokinase treatment resulted in a higher patency rate of the infarct-related artery (68.5%) than did standard therapy (44.8%) (p = 0.003). Ejection fraction was higher in streptokinase-treated patients (54% vs. 51%, p = 0.056), and the difference was most marked in patients with anterior myocardial infarction (53% vs. 44%, p = 0.03). Regional wall motion was measured by the centerline method and expressed in mean +/- SD motion in 52 normal subjects. There was a trend toward better function of the infarct zone in streptokinase-treated patients (SD, -2.48 vs. -2.70, p = 0.24). Additionally, streptokinase-treated patients had significantly better wall motion of noninfarct areas (SD, 0.36 vs. -0.08, p = 0.02). Treatment effects on function of noninfarct regions were most apparent in the subset of patients with multivessel disease. Thus, intravenous streptokinase preserves left ventricular function in patients with acute myocardial infarction. This benefit includes favorable effects on the function of regions remote from the site of infarction.

Cardiac Catheterization↗

PubMed1991

Multicenter patency trial of intravenous anistreplase compared with streptokinase in acute myocardial infarction. The TEAM-2 Study Investigators.

Thrombolytic therapy has been shown to improve clinical outcome when administered early after the onset of symptoms of acute myocardial infarction; the mechanism of benefit is believed to be reestablishment and maintenance of coronary artery patency. Anistreplase is a second generation thrombolytic agent that is easily administered and has a long duration of action. To compare anistreplase (30 units/2-5 min) and therapy with the Food and Drug Administration-approved regimen of intravenous streptokinase (1.5 million units/60 min), a randomized, double-blind, multicenter patency trial was undertaken in 370 patients less than 76 years of age with electrocardiographic ST segment elevation who could be treated within 4 hours of symptom onset. Coronary patency was determined by reading, in a blinded fashion, angiograms obtained early (90-240 minutes; mean, 140 minutes) and later (18-48 hours; mean, 28 hours) after beginning therapy. Early total patency (defined as Thrombolysis in Myocardial Infarction grade 2 or 3 perfusion) was high after both anistreplase (132/183 = 72%) and streptokinase (129/176 = 73%) therapy, and overall patency patterns were similar, although patent arteries showed "complete" (grade 3) perfusion more often after anistreplase (83%) than streptokinase (72%) (p = 0.03). Similarly, residual coronary stenosis, determined quantitatively by a validated computer-assisted method, was slightly less in patent arteries early after anistreplase (mean stenosis diameter, 74.0%) than streptokinase (77.2%, p = 0.02). In patients with patent arteries without other early interventions, reocclusion risk within 1-2 days was defined angiographically and found to be very low (anistreplase = 1/96, streptokinase = 2/94). Average coronary perfusion grade was greater, and percent residual stenosis was less, at follow-up than on initial evaluation and did not differ between treatment groups. Enzymatic and electrocardiographic evolution was not significantly different in the two groups. Despite rapid injection, anistreplase was associated with only a small (4-5 mm Hg), transient (at 5-10 minutes) mean differential fall in blood pressure. In-hospital mortality rates were comparable for anistreplase and streptokinase (5.9%, 7.1%). Stroke occurred in one (0.5%) and three (1.6%) patients, respectively; one stroke was hemorrhagic. Other serious bleeding events and adverse experiences occurred uncommonly and with similar frequency in the two groups. Thus, for the end points of our study (patency, safety), anistreplase and streptokinase showed overall favorable and relatively comparable outcomes, with a few differences.(ABSTRACT TRUNCATED AT 400 WORDS)

Anistreplase↗

PubMed1996

Streptokinase increases luxury perfusion after stroke.

BACKGROUND AND PURPOSE: Recent acute stroke trials have reported that intravenous streptokinase is associated with an increased risk of adverse outcomes. We aimed to study the effect of streptokinase on the nature of reperfusion and the relation between reperfusion and clinical outcome. METHODS: We studied 24 patients in the Australian Streptokinase Trial with acute middle cerebral cortical infarction using 99mTc-hexamethylpropyleneamine oxime single-photon emission CT. Eleven of the 24 patients were scanned before therapy and again 24 hours later. The remaining 13 were scanned once either before therapy (1 patient) or after therapy (12 patients). All patients had outcome scans after 3 months. Infarct hypoperfusion was measured with a validated volumetric technique. Neurological impairment and functional outcome were assessed with the Canadian Neurological Scale and the Barthel Index, respectively. RESULTS: Fifteen patients received streptokinase and 9 received placebo. There was no difference in early reperfusion between streptokinase and placebo. However, streptokinase was associated with a greater amount of nonnutritional reperfusion than was placebo (P = .04). This luxury perfusion was associated with poor functional outcome (P = .02). CONCLUSIONS: This study suggests that streptokinase augments luxury perfusion after stroke. Luxury perfusion is associated with a worse outcome, which might be due in part to reperfusion injury.

Adult↗

PubMed1993

Intrapleural streptokinase in experimental empyema.

Intrapleural streptokinase has been used in multiloculated empyemas to enhance pleural space drainage, presumably by causing fibrinolysis of the interlocular septae. We evaluated the efficacy and safety of daily administration of 10,000 U intrapleural streptokinase or equal volumes of saline to enhance resolution of experimental empyema in the rabbit pleural space. Seventy-two hours after intrapleural turpentine, 10(8) colony-forming units each of Escherichia coli, Peptostreptococcus anaerobius, and Bacteroides fragilis were injected into the sterile pleural effusion of all animals. Immediately after bacterial inoculation, and daily for 3 days, animals received 10,000 U streptokinase or saline intrapleurally. Animals that achieved a pleural fluid pH < 7.30 and either glucose < 50 mg/dl or LDH > 500 IU/L were included for data analysis. At Day 4 after bacterial inoculation, the streptokinase-treated empyemic rabbits had more pleural fluid (18.8 +/- 5.1 ml) (mean +/- SEM) than did saline-treated control animals (4.8 +/- 1.7 ml) (p = 0.015), fewer interpleural adhesions (8.2 +/- 2.7) than did saline-treated control animals (25.1 +/- 3.6) (p = 0.002), and comparable amounts of visceral and parietal pleural plaque than did saline-treated control animals (p = NS). No evidence of systemic fibrinolysis was observed at 1 h after intrapleural streptokinase administration. We conclude that intrapleural streptokinase decreases interpleural adhesion numbers but fails to reduce the amount of pleural plaque observed in experimental empyema in rabbits. The increases in pleural fluid volume observed after streptokinase administration may be due to mechanisms other than fibrinolytic activity.

Animals↗

PubMed2004

A study of empyema thoracis and role of intrapleural streptokinase in its management.

BACKGROUND: Clinical spectrum, microbiology and outcome of empyema thoracis are changing. Intrapleural instillation of fibrinolytic agents is being increasingly used for management of empyema thoracis. The present study was carried out to describe the clinical profile and outcome of patients with empyema thoracis including those with chronic empyema and to study the efficacy and safety of intrapleural streptokinase in its management. METHODS: Clinical profile, etiological agents, hospital course and outcome of 31 patients (mean age 40 +/- 16 years, M: F 25: 6) with empyema thoracis treated from 1998 to 2003 was analyzed. All patients were diagnosed on the basis of aspiration of frank pus from pleural cavity. Clinical profile, response to therapy and outcome were compared between the patients who received intrapleural streptokinase (n = 12) and those who did not (n = 19). RESULTS: Etiology was tubercular in 42% of the patients (n = 13) whereas the rest were bacterial. Amongst the patients in which organisms could be isolated (n = 13, 42%) Staphylococcus aureus was the commonest (n = 5). Intrapleural streptokinase was instilled in 12 patients. This procedure resulted in increase of drainage of pleural fluid in all patients. Mean daily pleural fluid drainage after streptokinase instillation was significantly higher for patients who received intrapleural streptokinase than those who did not (213 ml vs 57 ml, p = 0.006). Only one patient who was instilled streptokinase eventually required decortication, which had to be done in five patients (16.1%). Mean hospital stay was 30.2 +/- 17.6 days whereas two patients died. CONCLUSIONS: Tubercular empyema is common in Indian patients. Intrapleural streptokinase appears to be a useful strategy to preserve lung function and reduce need for surgery in patients with late stage of empyema thoracis.

Adolescent↗

PubMed1990

Effect of intravenous streptokinase on early mortality in patients with suspected acute myocardial infarction. A meta-analysis by anatomic location of infarction .

PURPOSE: To determine the effect of intravenous streptokinase on early mortality in patients with suspected acute anterior and acute inferior myocardial infarctions. DATA IDENTIFICATION: A literature search of English-language studies on the use of intravenous streptokinase in the treatment of suspected acute myocardial infarction for the period 1966 to 1989 using Medlars II and the bibliographies of relevant articles. In a number of instances, additional details on early mortality by location of myocardial infarction were provided by the authors. STUDY SELECTION: Of 140 originally identified articles, 6 that specifically met our inclusion criteria were selected: randomized trials that used intravenous streptokinase in a dose of 1.5 million units, with or without additional agents, compared with a group that differed only by the absence of streptokinase. Trials were selected by review of the methods section without regard for the results. DATA EXTRACTION: Data were extracted independently by two observers using specific methodologic criteria for infarct location and early mortality. After they conferred, the observers agreed completely on the data. RESULTS OF DATA SYNTHESIS: Among the 9155 patients with suspected acute anterior myocardial infarction, the mortality rate in the control group was 17.4%. In contrast, patients treated with streptokinase had a 12.5% mortality. The mean risk difference was -4.8% (95% CI, -7.5% to -2.1%) and the summary risk ratio was 0.72 (CI, 0.65 to 0.79). A total of 9650 patients with suspected inferior infarction had a mortality rate in the control group of 7.6% [corrected]. The mortality for streptokinase-treated patients was 6.6%. The mean risk difference was -0.8% (CI, -1.8% to 0.2%) and the summary risk ratio was 0.87 (CI, 0.76 to 1.01). CONCLUSIONS: Intravenous streptokinase clearly confers a protective effect against early mortality in patients with suspected acute anterior myocardial infarction. The magnitude of this effect is on the order of a 5% absolute reduction in risk of death by 21 to 35 days. For these patients, 21 need to be treated to save 1 additional life. For patients with suspected acute inferior infarction, the benefit of treatment on reducing early mortality is of smaller magnitude and less certain. These patients have an estimated absolute reduction of early mortality of approximately 1%, which would require treating 125 patients to save 1 additional life.

Humans↗

PubMed1975

Pharmacokinetics of radioiodinated streptokinase.

The pharmacokinetics of radioiodinated streptokinase have been investigated in mice and dogs in order to explore further its potential usefulness as a radiopharmaceutical to detect thrombi and neoplasms. The purified streptokinase used in these studies showed no alteration in its physical or enzymatic properties following radioiodination. In the mouse, radioiodinated streptokinase accumulated rapidly in the liver and at 4 hr, large amounts of free iodine were detected in the plasma. The plasma clearance curve in dogs was biexponential showing that 70% of the protein-bound radioactivity was cleared with a half-life of 1525 min while the remaining 30% was cleared with a half-life of 6080 min. Seventy percent of the plasma radioactivity appeared as free iodine after 4 hr. No change in clearance was obtained by preloading animals with unlabeled streptokinase. Based primarily on the rapid plasma clearance, deiodination, and possible limitations of effectiveness of preloading with unlabeled streptokinase, the results of these studies are in accord with the conclusion that radioiodinated streptokinase may have restricted usefulness as a radiopharmaceutical for detecting thrombi and neoplasms. The full extent of its potential usefulness, however, awaits the provision of further in vivo and in vitro studies directed at testing a covalently modified enzyme that retains streptokinase activity but whose immunologic properties have been altered so that the enzyme is not as rapidly cleared from the plasma.

Animals↗

PubMedDate not supplied

Efficacy, safety and tolerability of streptokinase in multiloculated empyema.

BACKGROUND: Empyema thoracis is a common illness with significant morbidity and mortality. Standard treatment of Empyema includes tube drainage and antibiotics. But the tube drainage often fails if the fluid is loculated. Intrapleural Streptokinase has been used in multiloculated empyemas with good success rate. We evaluated the efficacy and safety of intra-pleural Streptokinase in loculated empyemas. METHODS: A total of 15 patients admitted in Pulmonology unit with multiloculated empyemas whose drainage via drainage tube was less than 100 ml during the last 24 hours were included in the study. Aliquots of 250,000 units of Streptokinase in 100 ml of normal saline were instilled into the pleural cavity and the tube clamped for 3 hours. Response was assessed by clinical outcome, measurement of drain output after unclamping and subsequent chest radiography and serial chest ultrasounds. RESULTS: Streptokinase enhanced drainage in all patients with complete resolution of Empyema in 13 patients. Two patients with thickened visceral pleura following empyema drainage were referred to thoracic surgeon for decortication. The number of instillations of Streptokinase per patient ranged from 1 to 3 and the volume of drained empyema fluid ranged from 60 ml to 600 ml per patient. Streptokinase was well tolerated in all patients. CONCLUSION: Intrapleural Streptokinase is a safe and effective means of increasing the tube drainage in multiloculated Empyema without causing systemic fibrinolysis.

Adolescent↗

PubMed1991

Streptokinase immunogenicity in thrombolytic therapy for acute myocardial infarction.

The major drawback in implementing thrombolytic therapy with streptokinase in cases of acute myocardial infarction (AMI) stems from its antigenicity. To evaluate the dimensions of this problem, the immune response following thrombolytic therapy with streptokinase was prospectively studied in 16 patients with AMI. Streptokinase was given to 12 patients once and to 4 patients twice within 4-14 days. No clinical immune responses were observed following treatment. The specific antistreptokinase immune responses subsequent to streptokinase administration were monitored. The cellular immune response, reflected by the 3H-thymidine uptake of streptokinase-stimulated peripheral blood mononuclear cells, was three times higher than that of the controls. The antistreptokinase circulating IgG antibody level, measured by an enzyme-linked immunosorbent assay, was 8 times higher than that of the controls. No antistreptokinase circulating IgE antibodies could be detected and no decrease in complement concentration was noted. The profile and magnitude of the immune response of patients who had received two treatments were similar to those of patients who had received a single treatment only. Our data suggest that thrombolytic therapy with streptokinase in AMI elicits a characteristic profile of antistreptokinase immune responses, in vitro, not necessarily associated with parallel clinical immune responses. An early repeat treatment with streptokinase was not accompanied by clinical or exacerbated in vitro immune responses.

Antibody Formation↗

PubMed1989

Randomised double-blind trial of recombinant pro-urokinase against streptokinase in acute myocardial infarction. PRIMI Trial Study Group.

In a prospective, double-blind, randomised trial, 401 patients with a first acute myocardial infarction were treated within 4 h of onset of symptoms with 80 mg recombinant pro-urokinase or single-chain urokinase plasminogen activator (rscu-PA; proposed INN saruplase) intravenously given as a 20 mg bolus followed by 60 mg infusion for 60 min (198 patients), or 1.5 million IU streptokinase infused over 60 min (203 patients). The first two angiograms were taken at 60 min and at 90 min. Angiography was repeated at 24-36 h. Patency rates at 60 min were 71.8% for rscu-PA and 48.0% for streptokinase (p less than 0.001) and at 90 min they were 71.2% and 63.9%, respectively (p = 0.15). At 24-36 h 6/121 patients treated with rscu-PA and 5/114 patients treated with streptokinase showed reocclusion of the vessel. At the end of the thrombolytic infusion (60 min) fibrinogen concentration had decreased to 0.44 (0.23-1.27) g/l (median, 1st and 3rd quartile) in patients treated with rscu-PA and to 0.17 (0.06-0.27) g/l in patients treated with streptokinase (p less than 0.001). Concentrations of fibrin(ogen) degradation products rose to 96 (24-240) mg/l after rscu-PA and to 240 (192-360) mg/l after streptokinase (p less than 0.001). Bleeding complications were less common in the rscu-PA than in the streptokinase group (p less than 0.01). Thus intravenous rscu-PA led to higher patency rate, earlier reperfusion, less disturbance of haemostasis, and fewer bleeding complications than did intravenous administration of streptokinase.

Adult↗