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Case Reports
Journal Article
Prasugrel hypersensitivity with respiratory distress and rash.
American Journal of Health-system Pharmacy : AJHP 2016 July 16
PURPOSE: An adverse drug reaction associated with the use of prasugrel for dual antiplatelet therapy after percutaneous coronary intervention (PCI) with stent placement is reported.
SUMMARY: About one week after starting prasugrel use following angioplasty and a stent revision procedure, a 61-year-old woman arrived in the emergency department with wheezing, shortness of breath, a feeling of throat closure, and a widespread erythematous, maculopapular, pruritic rash. She reported that the respiratory symptoms had started to develop the previous day, with the onset of rash occurring about 24 hours after initiation of prasugrel therapy. The patient's symptoms subsided after administration of 0.3 mg epinephrine subcutaneously, diphenhydramine 50 mg i.v., and methylprednisolone 125 mg i.v. Prasugrel was discontinued, and the patient was switched to another P2Y12 inhibitor (ticagrelor) for continued dual antiplatelet therapy. Analysis of the case using the adverse drug reaction probability scale of Naranjo et al. indicated that prasugrel was the probable cause of the hypersensitivity reaction. Hypersensitivity manifesting as a rash has been previously reported in patients receiving prasugrel, a thienopyridine P2Y12 inhibitor. Desensitization may be an option for thienopyridine-allergic patients undergoing PCI with stenting; alternatively, the nonthienopyridine P2Y12 inhibitor ticagrelor may be used in a dual antiplatelet therapy regimen.
CONCLUSION: A patient who had undergone PCI with stenting developed shortness of breath and rash associated with prasugrel therapy. Symptoms abated after supportive therapy and discontinuation of prasugrel, the probable offending agent. Treatment was safely switched to ticagrelor.
SUMMARY: About one week after starting prasugrel use following angioplasty and a stent revision procedure, a 61-year-old woman arrived in the emergency department with wheezing, shortness of breath, a feeling of throat closure, and a widespread erythematous, maculopapular, pruritic rash. She reported that the respiratory symptoms had started to develop the previous day, with the onset of rash occurring about 24 hours after initiation of prasugrel therapy. The patient's symptoms subsided after administration of 0.3 mg epinephrine subcutaneously, diphenhydramine 50 mg i.v., and methylprednisolone 125 mg i.v. Prasugrel was discontinued, and the patient was switched to another P2Y12 inhibitor (ticagrelor) for continued dual antiplatelet therapy. Analysis of the case using the adverse drug reaction probability scale of Naranjo et al. indicated that prasugrel was the probable cause of the hypersensitivity reaction. Hypersensitivity manifesting as a rash has been previously reported in patients receiving prasugrel, a thienopyridine P2Y12 inhibitor. Desensitization may be an option for thienopyridine-allergic patients undergoing PCI with stenting; alternatively, the nonthienopyridine P2Y12 inhibitor ticagrelor may be used in a dual antiplatelet therapy regimen.
CONCLUSION: A patient who had undergone PCI with stenting developed shortness of breath and rash associated with prasugrel therapy. Symptoms abated after supportive therapy and discontinuation of prasugrel, the probable offending agent. Treatment was safely switched to ticagrelor.
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