LETTER TO THE EDITOR
Aspirin "allergy" and resistance
Julian L. Ambrus, MD, PhD, FACP
State University of NY at Buffalo, Buffalo General Hospital/Kaleida Health System, 100 High Street, Building E; Room 320, Buffalo, New York 14203
Clara M. Ambrus, MD, PhD, FACP and
Selina Akhter, MD, MA
(Email: jlambrus{at}netscape.net).
In a recent article, Gum et al.(1) discussed aspirin resistance, and Eikelboom et al. (2) wrote an editorial comment regarding this topic. We have seen several patients who reported that they seemed to have "allergic" reactions to aspirin. These "allergic" reactions consisted primarily of asthma-type attacks. Careful study revealed that these patients are not "allergic" to aspirin in the classical way; inhibition of cyclo-oxygenases by 325 mg of aspirin shifts the arachidonic acid cascade to the lipo-oxygenase branch (Fig. 1). This results in the production of more leukotreine C4, D4, and E4, which together are the "slow-reacting substance of anaphylaxis" and powerful bronchoconstrictors. These patients then refuse to take aspirin and claim that they are "resistant" to and have "allergies" to aspirin.
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Figure 1 The arachidonic acid cascade and its lipo-oxygenase branch, determinants of aspirin side effects.
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On the other hand, when patients are given only 81 mg of aspirin, cyclo-oxygenase production recovers rapidly, including prostaglandin i2 synthesis, which is platelet-aggregation inhibitory and a vasodilator. Inhibition of the platelet-aggregation inducer thromboxane A2 appears to persist for several hours. It is generally accepted that low-dose aspirin (81 mg one time daily) should be recommended as a preventive agent for cardiovascular episode in patients who are not resistant to aspirin by the criteria discussed by Gum et al. (1) and Eikelboom et al. (2). A simple method used by our group to establish aspirin resistance (3) is based on the determination of aggregated platelets in the circulation and its resolution by one week of aspirin therapy. This simple method can even be used as a bedside procedure. It may be a screening method used before introducing the spectrum of tests discussed by Eikelboom et al. (2). It is our impression that clopidogrel (75 mg one time daily) alone or in combination with aspirin (81 mg one time daily) is effective in possibly resistant patients. Data are being collected for eventual statistical evaluation.
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References
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- Gum PA, Kottke-Marchant K, Welsh PA, White J, Topol EJ. A prospective, blinded determination of the natural history of aspirin resistance among stable patients with cardiovascular disease J Am Coll Cardiol 2003;41:961-965.[Abstract/Free Full Text]
- Eikelboom JW, Hankey GJ. Aspirin resistancea new independent predictor of vascular events?. J Am Coll Cardiol 2003;41:966-968.[Free Full Text]
- Ambrus JL, Anain JM, Anain SM, et al. The effects of pentoxifylline (Trental) on circulating platelet aggregates and platelet aggregation patterns in patients with chronic obstructive arteriosclerotic disease Clin Hemorrheol 1990;10:225-230.
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