Clopidogrel hypersensitivity: clinical challenges and options for management

Oral antiplatelet agent hypersensitivity and cross-reactivity managed by successful desensitisation

“…Clopidogrel is generally well tolerated but hypersensitivity reactions with pruritic rashes [ 1 ] occur in 6% of patients [ 2 ] while 1.5% requires drug discontinuation. The premature cessation of therapy increases the risk of atherothrombotic complications including death.…”

“…However, ticlopidine is a less well tolerated drug giving toxic side effects of diarrhoea, neutropenia and thrombocytopenic purpura. There have also been reports of cross-reactivity between clopidogrel and ticlopidine [ 4 ], but not cross-reactivity between prasugrel [ 1 ] and ticagrelor [ 3 ].…”

“…Several clinical reports have demonstrated the efficacy of continued drug treatment uninterrupted using short-course corticosteroids and antihistamines [ 1 , 2 ]. However, in the context of severe anaphylactic reactions, such as ours, the continuation of clopidogrel would not be clinically recommended.…”

“…However, upon successful desensitisation, a maintenance daily dose of the drug is required to preserve the desensitised state, irrespective of the underlying mechanism, as interruption of exposure will lead to redevelopment of the drug hypersensitivity. In our case, a published protocol [ 1 , 6 ] was used ( Table 1 ) and performed in a high dependency unit under close supervision with cardiac monitoring.…”

Subacute cutaneous lupus erythematosus: is clopidogrel a trigger?

“…Clopidogrel, a thienopyridine platelet aggregation inhibitor, is used after endovascular stenting procedures. Hypersensitivity reactions occur in approximately 6% of patients, and include leucocytoclastic vasculitis, angio‐oedema, urticaria and Stevens–Johnson syndrome. No reports exist of clopidogrel triggering subacute cutaneous lupus eythematosus (SCLE), although two cases have been reported with the related anti‐platelet drug ticlodipine …”