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PubMed1982

A comparison of acylated streptokinase-plasminogen complex and streptokinase in healthy volunteers.

The in vivo effects on the fibrinolytic and coagulation system of infusion acylated streptokinase-plasminogen complex (BRL 26921; 5, 7 and 12 mg) or streptokinase (250,000 u) were determined in healthy male volunteers. While this dose of streptokinase resulted in depletion of plasminogen and antiplasmin, and in some cases of fibrinogen and coagulation factors V and VIII, the equivalent 7 mg dose of BRL 26921 had little effect on these parameters. 12 mg BRL 26921 had some systemic effects on the fibrinolytic system. For initial clinical studies a dose of 10 mg BRL 26021 would seem appropriate. Both drugs induced an anamnestic rise in streptokinase antibody, whereas no change in liver function tests were observed. A delayed mild febrile reaction was observed in some subjects following infusion of streptokinase or BRL 26921. Clinical, laboratory, and subjective monitoring revealed no other adverse effects with either drug.

Adult↗
PubMedDate not supplied

Streptokinase in acute myocardial infarction: a multicentric study in an Indian setting. Streptokinase Multicentric Trial Group.

This paper presents the results of a multicentric study on the use of intravenous streptokinase as thrombolytic therapy in acute myocardial infarction. Its aim was to assess the benefits and complications of this therapy in Indian conditions. The study comprised 510 cases from 31 hospitals, employing a common protocol. 1.5 million units of streptokinase was given intravenously to all patients with acute myocardial infarction aged under 76 years, admitted within 8 hours of onset of chest pain. 160 mgms of aspirin was also administered. Use of other drugs was at the discretion of each centre. Parameters studied were reperfusion by enzymatic criteria, complications due to streptokinase and in-hospital mortality. There were 46 deaths overall (9.02%); mortality was lower in those who achieved reperfusion (19/360) as against those who did not (27/150). Complications due to streptokinase were all minor (95 incidents). It is concluded that intravenous thrombolysis with streptokinase in acute myocardial infarction is safe and effective in Indian hospitals of differing sophistication.

Adult↗
PubMed1994

Low anti-streptokinase IgG concentrations following streptokinase-streptodornase treatment of leg ulcer patients.

We have evaluated whether neutralising anti-streptokinase IgG antibodies are produced following streptokinase-streptodornase therapy of leg ulcer patients. Serum anti-streptokinase IgG concentrations in 10 leg ulcer patients were determined before, and 1 week, 2 weeks, and 3 weeks following the treatment. We observed only a negligible increase in neutralizing anti-streptokinase IgG concentrations during the observation period, which was probably of no therapeutical significance.

Humans↗
PubMed2005

Do recipients of kidneys from donors treated with streptokinase develop anti-streptokinase antibodies?

Streptokinase is used for preflush for non-heart-beating donors (NHBDs) in our center. The aim of this study was to evaluate whether the use of thrombolytic streptokinase results in the production of anti-streptokinase antibodies in the recipients after renal transplantation. Recipient sera taken prior to and at 1 and 6 months posttransplant were tested for the presence of antibodies to streptokinase using an enzyme-linked immunosorbent assay assay. No differences were detected between a group of 18 recipients who had kidneys from thrombolytic-treated NHBDs and a further group of 18 who received NHBD kidneys without such treatment.

Antibodies↗
PubMed1997

Incidence and impact on outcome of streptokinase allergy in the GUSTO-I trial. Global Utilization of Streptokinase and t-PA in Occluded Coronary Arteries.

We evaluated allergic reactions in 20,201 patients randomized to the streptokinase arms of The Global Utilization of Streptokinase and t-PA (Tissue Plasminogen Activator) in Occluded Coronary Arteries (GUSTO-I) trial, and tested the hypothesis that patients with streptokinase allergy would exhibit higher mortality. After adjusting for baseline variables and time of death, we found comparable coronary patency, left ventricular function, mortality, and bleeding complications between patients with versus those without streptokinase allergy.

Anaphylaxis↗
PubMed1987

Low dose intra-arterial streptokinase and acylated plasminogen-streptokinase activator complex: a retrospective review of two thrombolytic regimes in recent peripheral arterial ischaemia.

Thrombolytic therapy was used for 57 patients with acute and sub-acute lower limb arterial ischaemia. In the first 34 patients a new thrombolytic agent, acylated plasminogen-streptokinase complex (BRL 26921) was assessed. Following this, 23 patients received low dose intra-arterial streptokinase. The two thrombolytic regimes have been analysed retrospectively. There were differences observed between the two groups in the type of patients treated and in the severity of limb ischaemia. Of the patients receiving BRL 26921, five (15%) had complete, and three (9%) partial lysis of the occluding thrombus. Serious bleeding occurred in six (18%) and minor bleeding in ten (29%) patients. After 30 days, twelve patients (35%) had limb salvage and eleven (32%) had died. Fifteen patients (65%) receiving intra-arterial streptokinase had lysis of the occluding thrombus. Minor bleeding was observed in three patients (13%). After 30 days, 15 (65%) had limb salvage and three (13%) had died. Patients receiving BRL 26921 had a significantly greater reduction in plasma fibrinogen and plasminogen concentrations during treatment which may have accounted for the bleeding complications. At the dose used, BRL 26921 had no demonstrable fibrinogen sparing effect. Improved lysis rates with fewer bleeding complications might be achieved by reducing the dose of BRL 26921. Low dose intra-arterial streptokinase has been confirmed as a safe, effective method of thrombolysis in recent peripheral arterial ischaemia.

Aged↗
PubMed1993

The incidence and mechanism of hypotension following thrombolytic therapy for acute myocardial infarction with streptokinase-containing agents--lack of relationship to pretreatment streptokinase resistance.

The incidence, amplitude, mechanism and relationship to prior exposure to streptococcal antigen of blood pressure changes to streptokinase-containing thrombolytic agents were investigated in 125 patients treated with either 1.5 x 10(6) IU streptokinase over 60 min or 30 U anistreplase over 5 min, within 6 h of onset of acute myocardial infarction. Twenty-one of 52 patients with anterior and 34 of 73 with inferior myocardial infarction had a hypotensive response. There were no significant differences in the incidence, duration or amplitude of hypotension between the two treatment groups. The maximum mean fall in systolic blood pressure was 16.9 mmHg (95% confidence limits, CL 12.2 to 24.5 mmHg), and the maximum mean fall in diastolic blood pressure was 13.7 mmHg (CL 10.3 to 17.1 mmHg), starting 4 min after start of therapy and resolving within 34 min. Blood pressure changes were well tolerated. Hypotension was not related to pretreatment streptokinase resistance titre, or anti-SK IgG concentration, to changes in plasma fibrinogen, B-beta 15-42 peptide, D-dimer--as indices of thrombin activation and fibrin (-ogen) breakdown--to plasma viscosity. The blood pressure changes following treatment with streptokinase-containing thrombolytic agents in acute myocardial infarction are frequent but well tolerated. The mechanism of hypotension remains unclear, but is not related to prior exposure to streptococcal antigen.

Anistreplase↗
PubMed1990

The proliferative response of peripheral blood mononuclear cells to streptokinase. A study of patients receiving a single intravenous infusion of purified streptokinase.

In vitro proliferative PBM responses were investigated for 26 patients with and 5 patients without acute myocardial infarction. All patients were initially treated with streptokinase (1.5 MIU infused for 1 hour). Five weeks after the disease increased responses to streptokinase, PPD and PHA were seen; but only for streptokinase had original nonresponders become responders (7 out of 14 nonresponders). The increased responsiveness to streptokinase could be detected five days after antigen infusion, and CD-2 positive cells constituted a major part of the proliferating PBM population. The responses after antigen infusion varied within a wide range both for patients with and without myocardial infarction.

Adult↗
PubMed1987

Evaluation of 2 intravenous thrombolytic agents (anisoylated plasminogen streptokinase activator complex versus streptokinase) in patients with acute myocardial infarction.

Ten patients with symptoms of acute myocardial infarction of less than 6 hours duration were randomised to receive either anisoylated plasminogen streptokinase activator complex [APSAC] (30U) or streptokinase (1,500,000U) intravenously. The aims of the study were to compare the angiographic patency of the infarct-related coronary arteries and to monitor drug safety and tolerance for up to 24 hours. The left anterior descending artery was occluded in 3, the left circumflex in 3 and right coronary artery in 4 patients. Time between onset of pain and treatment ranged from 150 to 330 minutes. At 90 minutes, 8 patients, 3 of 5 (60%) of the APSAC group and all of the streptokinase group, had patent arteries. No significant differences were found in measurements of coagulation. There were no haemorrhagic complications. One patient of the APSAC group had reinfarction 6 hours after treatment and died in cardiogenic shock. APSAC seems safe and is easier to use than streptokinase, and both agents result in patency in the majority of patients, although too few patients were included to allow a valid comparison. However, thrombolysis should be considered only a temporary solution in acute myocardial infarction, associated mainly with 3-vessel disease.

Aged↗
PubMed1987

Intracoronary streptokinase versus intravenous anisoylated plasminogen streptokinase activator complex in the treatment of acute myocardial infarction.

As part of a randomised multicentre study, 16 patients with acute myocardial infarction were treated with either anisoylated plasminogen streptokinase activator complex (APSAC) administered as an intravenous bolus of 30U or 250,000U of streptokinase by the intracoronary route. The reperfusion was documented angiographically during a 90-minute period and possible reocclusion was assessed at 90 minutes and 24 hours after the start of therapy. The percentage of reperfusion obtained in the APSAC group was 83% versus 63% in the streptokinase group. One reocclusion was seen after 24 hours in the APSAC group. Fibrinolytic activity was more pronounced in the APSAC group but there were no major bleeding problems in either group. The administration of 30U of APSAC by an intravenous bolus injection produced results at least as good as those obtained with intracoronary streptokinase and in addition offered the advantage of a simpler and quicker administration.

Adult↗
PubMed1988

Effect of reperfusion on electrocardiographic and enzymatic infarct size: results of a randomized multicenter study of intravenous anisoylated plasminogen streptokinase activator complex (APSAC) versus intracoronary streptokinase in acute myocardial infarction.

The effect of early coronary artery reperfusion on ECG and enzymatic parameters was examined in 240 patients with acute myocardial infarction. These patients had participated in a randomized trial comparing intravenous anisoylated plasminogen streptokinase activator complex (APSAC) (n = 123) and intracoronary streptokinase (n = 117) therapy. Reperfusion occurred in 59 of 115 (51%) patients receiving APSAC and 67 of 111 (60%) patients receiving streptokinase (p = NS). There was greater early resolution of ST segment elevation in the reperfused than in the nonreperfused patients (p less than or equal to 0.003) and more rapid Q wave evolution (p less than or equal to 0.03). Sigma Q was lower in reperfused than in nonreperfused patients at 8 hours (1.41 +/- 1.18 versus 2.11 +/- 2.10 mV; p less than or equal to 0.05) and at 24 hours (1.43 +/- 1.25 mV versus 2.08 +/- 1.88 mV; p less than or equal to 0.02). Time to peak level was shorter in the reperfused patients for creatine kinase (CK) (10.7 +/- 5.5 hours versus 14.9 +/- 5.9 hours; p less than 0.0001) and lactic acid dehydrogenase (LDH) (29.6 +/- 13.6 hours versus 34.4 +/- 10.5 hours; less than or equal to 0.03) enzymes. Peak LDH-1 was lower in the reperfused group (274 +/- 149 U/L versus 341 +/- 173 U/L; p less than or equal to 0.04). Reperfusion at a mean of 3.9 hours after the onset of infarction was associated with more rapid resolution of ST segment elevation, faster Q wave evolution, smaller ECG infarct size, earlier cardiac enzyme release, and smaller enzymatic infarct size than later or no reperfusion.

Anistreplase↗
PubMed1987

Haematological effects of anisoylated plasminogen streptokinase activator complex and streptokinase in patients with acute myocardial infarction. Interim report of the IRS II Study.

86 patients with a first myocardial infarction presenting within 6 hours of the onset of symptoms were randomly allocated to treatment with intravenous streptokinase or anisoylated plasminogen streptokinase activator complex (APSAC). Plasma concentrations of fibrinogen, plasminogen, alpha 2-antiplasmin and fibrinogen degradation products and thrombin and prothrombin times, were measured before the injection of the thrombolytic drug and every 3 hours during the first 24 hours. APSAC and streptokinase produced identical and important systemic effects. APSAC produced a slightly smaller decrease in fibrinogen concentrations. The duration of this systemic activity was about the same for the 2 drugs (congruent to 24 hours).

Anistreplase↗
PubMed2004

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).

UNLABELLED: The Streptokinase (SK) regimen (1.5 MU/60 minutes) has remained unchanged for the past 20 years in patients with ST-segment elevation acute myocardial infarction (STEMI) due to fear of hypotension (a specific effect of this thrombolytic agent) and of hemorrhagic complications. OBJECTIVE: To evaluate the influence of the Streptokinase-induced hypotension (SK-hTA) on the rate of coronary reperfusion (CR), incidence of cardiogenic shock (CS), 30-day mortality and incidence of stroke in patients (pts.) with STEMI. The SK-hTA was defined as decrease of the systolic blood pressure with at least 20% within the first 20 min. after the start of the SK infusion. METHODS: A group of 837 pts. (age 20-90) with thrombolytic treatment, with three "accelerated" SK regimens within the first 6 hours after the onset of STEMI and enrolled in the Romanian open, prospective, non-randomised study for accelerated SK in STEMI (ASK-ROMANIA) have been included. The SK regimens consisted in infusing of the standard dose of 1.5 M.U. either in 30 min. (regimen SK1.5/30, 173 pts).) or in 20 min. (regimen SK1.5/20, 377 pts.) or of the half dose (0.75 M.U.) in 10 min. followed by a new infusion of 0.75 M.U. after 50 min. only if no bed-side signs of CR have been recorded (regimen SK 0.75/10, 287 pts.). The speed of the SK infusion was maintained in all pts. experiencing SK-hTA. All pts. received aspirin and heparin or enoxaparin if not contraindicated. Three noninvasive CR criteria have been used: 1. Rapid cessation of the chest pain. 2. Rapid decrease of the ST segment elevation by more than 50% of the initial value. 3. Rapid increase of the CK and CK-MB with a peak within the first 12 hrs. RESULTS: SK-hTA appeared in 372 pts. (44.55%) at 9+/-5 min after the start of the SK infusion. In this subgroup the rate of CR was 74.46%, non-significantly higher than the one of 68.81% registered in pts. without SK-hTA (p=0.071). SK-hTA disappeared in all patients after 16+/-6 minutes without a specific therapy. Fourteen pts. with SK-hTA (3.76%) and 16 pts. without SK-hTA (3.44%) developed CS after thrombolysis ( non-significant difference). The global in-hospital mortality was 10.21% in pts. with SK-hTA and 9.89% in pts. without this side effect (non-significant difference). The incidences of hemorrhagic and ischemic strokes were 0.26% (1 patient) respectively 0.52% (2 pts.) in the SK-hTA subgroup and 0.43% (2 pts.) respectively 0.64% (3 pts.) in the subgroup without SK-hTA. CONCLUSIONS: 1. Despite a very high incidence (44.55%) the SK-hTA has not a detrimental effect in pts. treated with accelerated SK regimens for STEMI. 2. Streptokinase can be rapidly administered without an increased risk.

Adult↗
PubMed1995

Drug eruptions and isotypic antibody responses to streptokinase after infusions of anisoylated plasminogen-streptokinase complex (APSAC, anistreplase).

BACKGROUND: Anisoylated plasminogen-streptokinase complex (APSAC, anistreplase) is a thrombolytic agent (131 kd) used for treatment of myocardial infarction. Like its principal antigenic determinant, streptokinase, APSAC has been reported to cause a variety of allergic reactions. OBJECTIVE: This study was intended to determine any association between isotypic antibody responses to streptokinase and observed allergic reactions to APSAC. METHODS: We measured sequential IgM, IgG, IgA, and IgE antistreptokinase serum levels in 21 patients who received APSAC or tissue-type plasminogen activator in a prospective, double-blind study. RESULTS: Of 11 patients who received APSAC, four had maculopapular rashes and one had urticaria; those with maculopapular rashes had significantly higher rises in serum IgM, IgG, IgA, and IgE antistreptokinase levels. We could not, however, define a temporal relationship between rises in antistreptokinase levels of a particular isotype and the onset of maculopapular rashes. The patient who had urticaria had no antistreptokinase responses but had also received several other potentially causal drugs. None of 10 patients who received tissue-type plasminogen activator had allergic reactions or significant rises in serum antistreptokinase levels. CONCLUSION: The more vigorous panisotypic antistreptokinase responses observed in patients who received APSAC and had maculopapular rashes may reflect generalized immune system activation that included other immune responses (such as cell-mediated hypersensitivity) that were responsible for these reactions.

Aged↗
PubMed1983

Streptokinase and anisoylated streptokinase plasminogen complex. Their action on haemostasis in human volunteers.

A new fibrinolytic agent, BRL 26921, a member of the novel class of thrombolytic agents; the acyl enzymes, has been compared with streptokinase. It has been shown that this new agent, which can bind to fibrin before releasing activator, does not result in clinically significant destruction of the haemostatic system when compared to an equivalent dose of streptokinase.

Adult↗
PubMed1984

Comparison of the hypotensive effects of streptokinase-(human) plasmin activator complex and BRL 26921 (p-anisoylated streptokinase-plasminogen activator complex) in the dog after high dose, bolus administration.

In view of current interest in the possibility of rapid, high-dose administration of thrombolytic agents by the intravenous route in patients with coronary thrombosis (AMI), a study of this technique was carried out in the dog. Streptokinase-(human) plasmin activator complex (SK-Pm) and BRL 26921 (p-anisoylated streptokinase-(human) plasminogen activator complex) were each given at equivalent doses (28,500 IU/kg and 800 micrograms/kg respectively) to groups of beagle dogs by rapid injection over 10 sec and their effects on blood pressure, plasmin formation and kallikrein production were compared over the next 3h. SK-Pm produced, within 1-3 min, a pronounced hypotensive effect that was kinetically related to a rapid and steep rise in systemic plasmin and kallikrein concentrations. BRL 26921 had no hypotensive effect, the rise in plasmin production was slower and the rate and extent of kallikrein formation was significantly less than in the SK-Pm group.

Animals↗
PubMed2002

Anti-streptokinase titers and response to streptokinase treatment in Pakistani patients.

In order to investigate whether anti-streptokinase (anti-SK) antibody titers have any effect on response to standard dose (1.5 million units) streptokinase (SK) therapy in patients with acute myocardial infarction, anti-SK titers in plasma were determined in 97 such patients. These patients were classified as "responders" or "non-responders" on the basis of a criteria which involved resolution of chest pain in less than 90 min after the start of thrombolysis, greater than 50% reduction of ST segment elevation in two contiguous leads showing maximum elevations in a 12-lead tracing, reperfusion arrythmias and slope of increase in creatine kinase over a 90-min period after initiation of thrombolysis. Anti-SK antibody levels in plasma were determined in these patients as well as in 50 normal healthy subjects by dissolution of clot method. Mean+/-S.D. anti-SK levels among responders, non-responders and normal healthy subjects were found to be 0.21+/-0.12, 0.25+/-0.22 and 0.21+/-0.15 million units, respectively. A comparison of these mean values by one-way ANOVA revealed no statistical difference (P=0.68). However, when compared with the reported values for a Western population, these values were found to be significantly higher (P<0.03). Whereas, compared to the reported values for an Indian population, these were significantly lower (P<0.0001). 42% of patients appeared to have responded to SK treatment, while 21% were found to be non-responders. There was no association between response to SK and anti-SK titers in these patients suggesting that the standard dose of SK (1.5 million units) may be quite appropriate for the Pakistani population requiring SK treatment for the first time.

Antibodies, Bacterial↗