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• W2072943314 abstract "The Cochrane Collaboration reviewers of thrombolysis in stroke1Wardlaw JM Warlow CP Counsell C Systematic review of evidence on thrombolytic therapy for acute ischaemic stroke.Lancet. 1997; 350: 607-614Summary Full Text Full Text PDF PubMed Scopus (252) Google Scholar choose to draw conclusions that are not best supported by their data, and thus reinforce recent criticisms of meta-analysis.In presenting their analysis of streptokinase and tissue plasminogen factor (tPA) trials, they seem to dismiss both pharmacological and statistical differences in order to conclude that there is no evidence that tPA is safer than streptokinase. More strangely, they exclude from the streptokinase overview half the MAST-Italy-trial2Multicentre Acute Stroke Trial-Italy (MAST-I) Group.Randomised controlled trial of streptokinase, aspirin, and combination of both in treatment of acute ischaemic stroke.Lancet. 1995; 346: 1509-1514Summary PubMed Google Scholar patients on the grounds of aspirin exposure, despite widespread aspirin use within the remaining trials, and in the absence of statistical evidence of heterogeneity. Indeed, a formal meta-analysis of the data on individual patients from the streptokinase trials available to the investigators fails to show a significant influence of aspirin (TAS-PP group, unpublished data).The primary endpoint of the major recent trials was death and disability combined. On this endpoint, there is heterogeneity neither in the streptokinase trials (x2Multicentre Acute Stroke Trial-Italy (MAST-I) Group.Randomised controlled trial of streptokinase, aspirin, and combination of both in treatment of acute ischaemic stroke.Lancet. 1995; 346: 1509-1514Summary PubMed Google Scholar 2·33, degree freedom 4), nor among the tPA trials (2·38, 2), but the streptokinase trial results differ significantly from those of the tPA trials (15·08, 7, p<0·05). The 95% CI do not overlap, and reveal significant benefit with tPA but not streptokinase (tPA: odds ratio [OR] 0·57 [95% CI 0·45–0·72]; streptokinase: 0·98 [0·78–1·24]).The proposal that further, larger clinical trials including streptokinase are required demands critical evaluation. Case fatality for all streptokinase trials, as presented in their figure 3, is clearly increased (OR 1·43 [1·10–1·88]), whereas that for tPA does not differ significantly from placebo (1·06 [0·80–1·39]). When the MAST-Italy figures are included, streptokinase comes out even less favourably (1·71 [1·35–2·16]), and the lower end of the CI barely touches that for tPA.We agree that further trials and rigorous audit are required to determine whether the benefits of tPA can be translated safely into clinical practice. At present, the use of tPA even in clinical trials should be strongly discouraged. Despite previous enthusiasm in coordinating the Glasgow and MAST-Europe streptokinase trials,3Morris AD Ritchie C Grosset DG Adams FG Lees KR A pilot study of streptokinase for acute cerebral infarction.Q J Med. 1995; 88: 727-731Google Scholar, 4The Multicenter Acute Stroke Trial— Europe Study GroupThrombolytic therapy with streptokinase in acute ischaemic stroke.N Engl J Med. 1996; 335: 145-150Crossref PubMed Scopus (555) Google Scholar we now see no grounds for pursuing the use of streptokinase in ischaemic stroke. We believe that it would be unethical to test streptokinase 1·5 MU further when it clearly increases mortality without reducing disability, and when no such excess hazard has been shown for tPA. The Cochrane Collaboration reviewers of thrombolysis in stroke1Wardlaw JM Warlow CP Counsell C Systematic review of evidence on thrombolytic therapy for acute ischaemic stroke.Lancet. 1997; 350: 607-614Summary Full Text Full Text PDF PubMed Scopus (252) Google Scholar choose to draw conclusions that are not best supported by their data, and thus reinforce recent criticisms of meta-analysis. In presenting their analysis of streptokinase and tissue plasminogen factor (tPA) trials, they seem to dismiss both pharmacological and statistical differences in order to conclude that there is no evidence that tPA is safer than streptokinase. More strangely, they exclude from the streptokinase overview half the MAST-Italy-trial2Multicentre Acute Stroke Trial-Italy (MAST-I) Group.Randomised controlled trial of streptokinase, aspirin, and combination of both in treatment of acute ischaemic stroke.Lancet. 1995; 346: 1509-1514Summary PubMed Google Scholar patients on the grounds of aspirin exposure, despite widespread aspirin use within the remaining trials, and in the absence of statistical evidence of heterogeneity. Indeed, a formal meta-analysis of the data on individual patients from the streptokinase trials available to the investigators fails to show a significant influence of aspirin (TAS-PP group, unpublished data). The primary endpoint of the major recent trials was death and disability combined. On this endpoint, there is heterogeneity neither in the streptokinase trials (x2Multicentre Acute Stroke Trial-Italy (MAST-I) Group.Randomised controlled trial of streptokinase, aspirin, and combination of both in treatment of acute ischaemic stroke.Lancet. 1995; 346: 1509-1514Summary PubMed Google Scholar 2·33, degree freedom 4), nor among the tPA trials (2·38, 2), but the streptokinase trial results differ significantly from those of the tPA trials (15·08, 7, p<0·05). The 95% CI do not overlap, and reveal significant benefit with tPA but not streptokinase (tPA: odds ratio [OR] 0·57 [95% CI 0·45–0·72]; streptokinase: 0·98 [0·78–1·24]). The proposal that further, larger clinical trials including streptokinase are required demands critical evaluation. Case fatality for all streptokinase trials, as presented in their figure 3, is clearly increased (OR 1·43 [1·10–1·88]), whereas that for tPA does not differ significantly from placebo (1·06 [0·80–1·39]). When the MAST-Italy figures are included, streptokinase comes out even less favourably (1·71 [1·35–2·16]), and the lower end of the CI barely touches that for tPA. We agree that further trials and rigorous audit are required to determine whether the benefits of tPA can be translated safely into clinical practice. At present, the use of tPA even in clinical trials should be strongly discouraged. Despite previous enthusiasm in coordinating the Glasgow and MAST-Europe streptokinase trials,3Morris AD Ritchie C Grosset DG Adams FG Lees KR A pilot study of streptokinase for acute cerebral infarction.Q J Med. 1995; 88: 727-731Google Scholar, 4The Multicenter Acute Stroke Trial— Europe Study GroupThrombolytic therapy with streptokinase in acute ischaemic stroke.N Engl J Med. 1996; 335: 145-150Crossref PubMed Scopus (555) Google Scholar we now see no grounds for pursuing the use of streptokinase in ischaemic stroke. We believe that it would be unethical to test streptokinase 1·5 MU further when it clearly increases mortality without reducing disability, and when no such excess hazard has been shown for tPA. Thrombolytic therapy for acute ischaemic strokeAuthors' reply Full-Text PDF" @default.
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• W2072943314 title "Thrombolytic therapy for acute ischaemic stroke" @default.
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