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 article1 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 case-control 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.
Signature
Michael D. Hill
Philip A. Barber
Jennifer Takahashi
Andrew M. Demchuk
Thomas E. Feasby
Alastair M. Buchan
Department of Clinical Neurosciences University of Calgary Calgary, Alta.
Reference
- 1.Hill MD, Barber PA, Takahashi J, Demchuk AM, Feasby TE, Buchan AM. Anaphylactoid reactions and angioedema during alteplase treatment of acute ischemic stroke. CMAJ 2000; 162(9):1281-4. [PMC free article] [PubMed]