A 50-year-old male with past medical history of ischemic heart disease and prasugrel hypersensitivity in the form of generalized rash underwent elective PCI with one drug-eluting stent (DES) to the left anterior descending artery (LAD). He was subsequently started on dual antiplatelet therapy with aspirin 81 mg daily and ticagrelor 90 mg twice a day.\nTwo days following discharge, the patient was complaining of severe shortness of breath with minimal exertion, and occasionally at rest. He denied any fevers, chills, productive cough, orthopnea, paroxysmal nocturnal dyspnea or lower limb edema. The patient’s dyspnea was heavily investigated with basic labs, cardiac biomarkers, imaging of the chest, and repeat transthoracic echocardiogram. All results came back within normal limits. The patient’s dyspnea was deemed secondary to ticagrelor use and the drug was discontinued, with subsequent improvement of his symptoms. Given his history of prasugrel hypersensitivity and current intolerance to ticagrelor, the patient was started on clopidogrel. Three days later, he presented to the emergency department (ED) with a rash that started on his chest and spread to his arms and face (Figure ).\nThe patient was diagnosed with cutaneous hypersensitivity to clopidogrel. Given the patient’s need for dual antiplatelet therapy and previously documented prasugrel hypersensitivity as well as intolerance to ticagrelor, shifting to any of them was not an option.\nReviewing the literature, three management strategies have been described for clopidogrel hypersensitivity, including switching to another agent, implementing a desensitization protocol, and a six-day course of steroids without clopidogrel discontinuation. A shared decision was made to implement the latter approach however with a slow taper over a three-week period. The patient was started on oral prednisone 30 mg twice a day for five days, followed by a decrease of 5 mg/day every three days for 15 days. On his one-week follow-up, the patient was well-tolerating clopidogrel with complete resolution of his symptoms and no significant side effects from steroids. The patient showed no side effects related to steroids on his one-month follow-up.
A 68-year-old male developed pruritic and exanthematous eruptions over a 24-hour period. He had a history of angina for the past 6 months, and he underwent elective percutaneous coronary intervention in the left anterior descending artery and left circumflex artery on June 24, 2015. Three drug-eluting stents were inserted (2 paclitaxel eluting stents, YINYI Biomedical Materials R&D Center Co., Ltd., Liaoning, China; and 1 sirolimus eluting stent, Lepu Medical Technology Co., Ltd., Beijing, China). All 3 stents were made of 316L stainless steel. Moreover, he also had a previous history of hypertension and hypercholesterolaemia. He had no history of prior drug allergy.\nDrugs included aspirin, ticagrelor, bisoprolol, and rosuvastatin. He has taken aspirin, bisoprolol, and rosuvastatin for the last 5 months, showing a good tolerance. After taking ticagrelor for 2 days, he developed pruritic and maculopapular rash on his bilateral costal margin, which was then generalized to the trunk (predominantly affected the chest and abdomen). His extremities were not affected, with no angioedema, no fever, and no arthralgia.\nThe laboratory test result showed an elevation in the leukocyte count (11.4 ×109/L) and in the neutrophil count (8.21 ×109/L). The lymphocyte count was 1.72 ×109/L and the eosinophil count was 0.58 ×109/L. The liver function test results were as follows: alanine aminotransferase, 14 U/L; aspartate aminotransferase, 27 U/L; total protein, 61.9 g/L; albumin, 40.2 g/L; total bilirubin, 36.8 µmol/L; direct bilirubin, 5.59 µmol/L; γ-glutamyltranspetidase, 61 U/L; total bile acid, 0.9 µmol/L; and lactate dehydrogenase, 380 U/L.\nHe showed to have a hypersensitive reaction to ticagrelor, and he was treated with antihistamines. Ticagrelor was switched to clopidogrel. Soon thereafter, his rash was gradually improved.\nHowever, 10 days later, he developed severe chest pain and received emergency coronary angiogram. Subacute definite stent thrombosis was confirmed, and thrombectomy was performed. After the procedure, a platelet function test was conducted, revealing a low response to clopidogrel.\nTo achieve therapeutic platelet aggregation inhibition, ticagrelor was reused under close supervision. Within approximately 2 hours, he developed generalized maculopapular rash in the whole trunk, which was resolved with intravenous corticosteroids. Ticagrelor was discontinued to avoid further hypersensitive reaction. Our patient showed delayed-type hypersensitivity reaction from the use of ticagrelor, represented in the form of generalized maculopapular rashes. Ticagrelor desensitization might not be appropriate for this patient.\nSwitching to other kinds of P2Y12 receptor antagonist antiplatelet drug was considered. Drugs that are structurally different from ticagrelor may be a good substitute for those with ticagrelor hypersensitivity. The chemical class of ticagrelor is cyclopentyl-triazolo-pyrimidine, and the other chemical class consists of thienopyridines (clopidogrel, prasugrel, ticlopidine) []. This patient presented a low response to clopidogrel and had suffered subacute in-stent thrombosis. Currently, prasugrel has not been approved for use in China. Ticlopidine has been associated with toxic side effects, such as rash, severe neutropenia, diarrhea, and thrombocytopenic purpura. Therefore, antithrombotic therapy was significantly difficult in this patient.\nThe patient ultimately received aspirin and warfarin as an antithrombotic treatment. He was given subcutaneous injection of low molecular weight heparin for 7 days. The regulated dose of warfarin was maintained in between 2 and 3 of the international normalized ratio (INR). During the follow-up period, our patient did not report any discomfort.