Effect of rapid desensitization on platelet inhibition and basophil activation in patients with aspirin hypersensitivity and coronary disease

To determine antiplatelet efficacy after desensitization in patients with a history of aspirin hypersensitivity.

We conducted a case–control study to evaluate the efficacy of aspirin 1 day (D1) and 6–8 weeks (W6–8) after desensitization. We also assessed ex vivo basophil reactivity to aspirin after desensitization. Cases were patients with coronary artery disease (CAD) and documented history of aspirin hypersensitivity who underwent rapid successful oral desensitization to aspirin. Controls were patients with stable CAD without hypersensitivity and receiving aspirin. Among 56 cases, 27 received aspirin for acute coronary syndromes and 29 were treated for stable CAD. Aspirin was effective (defined as light transmission aggregometry induced by arachidonic acid ≤20%) at D1 in 86% of cases (P = 0.045 vs. controls) and in 95% at W6–8, vs. 100% of controls (P = 0.39). Urinary excretion of thromboxane B₂ diminished substantially in cases (P < 0.0001, D0 vs. W6–8) but remained higher than in controls (P = 0.03). Platelet reactivity (defined by platelet P-selectin expression, activated glycoprotein IIb/IIIa inhibitors, and platelet-monocyte aggregates) was similar in cases between D0 and D1 but decreased at W6–8. Basophil activation (quantified by upregulation of CD203c in response to aspirin) was higher in cases at W6–8 than in controls (P = 0.0002).

Thus, following rapid desensitization, aspirin achieves rapid biological efficacy, which is slightly lower at D1, but becomes indistinguishable from chronically treated patients at W6–8. Persistent basophil activation several weeks after desensitization suggests infraclinical hypersensitivity and the need to continue aspirin to maintain desensitization.