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Reactions to alteplase in patients with acute thrombotic stroke CMAJ 2000;163(4):388-9 In response to: W.B. Chodirker See also: We thank William Chodirker for his informed comments. We recognize the distinction between true IgE-mediated anaphylaxis and non-IgE-mediated anaphylactoid reactions. However, Chodirker is correct that in the discussion section of our article [Research]1 the distinction is blurred. To be clear, we do not believe that these reactions represent true anaphylaxis. We postulated that our first patient may have had undiagnosed acquired or hereditary angioedema because she had had 8 previous episodes of angioedema of which only 1 was related to taking an angiotensin-converting-enzyme inhibitor. This diagnosis remains speculative. We understand that true hereditary or acquired angioedema is resistant to antihistamines and corticosteroids. Chodirker is correct to point out that our treatment was based upon the emergent approach to undiagnosed angioedema that does include antihistamines, steroids and epinephrine. Our empirical regimen appears to work in angioedema associated with tissue plasminogen activator but of course we have no control group with which to properly assess efficacy. Given our experience with our first patient, who ultimately died, we remain committed to treating alteplase-associated angioedema because the regimen is generally safe. Finally, although we agree that epidemiological evidence (i.e., a good casecontrol study) is needed to assess the true risk of angioedema with thrombolytic stroke treatment in patients on angiotensin-converting-enzyme inhibitors, we would challenge Chodirker to assess the proposed mechanism for biological plausibility because it is all we have at the moment.
Michael D. Hill Reference
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