A 41-year-old male visited the EMC of our hospital complaining of a sharpening chest pain of his mid sternum lasting for 1 hour. He had previously been diagnosed with ankylosing spondylitis and had been treated with oral meloxicam, sulfasalazine, and methylprednisolone for 10 years. The patient had also been diagnosed with hypertension for 8 years, but did not take any anti-hypertensive medications. EKG revealed ST-segment elevations in the V 2-4 precordial leads. A chest X-ray revealed mild pulmonary congestion and laboratory tests revealed elevated leukocytes, cardiac enzymes, and N-terminal b-natriuretic peptide levels. The patient was subsequently diagnosed with ST elevation myocardial infarction, which we addressed by performing an emergent PCI. Before a coronary angiography was performed, we administrated a loading dose of clopidogrel 600 mg, aspirin 300 mg, and carvedilol. Coronary angiography revealed subtotal occlusion in the proximal left anterior descending artery (LAD). PCI using drug-eluting stents (DESs; Xience prime, Abbott Vascular, Santa Clara, CA, USA, 3.0×38 in proximal to mid LAD lesion, 2.5×15 in the 1st diagonal branch lesion) was performed successfully without any significant complications. A rheumatologist confirmed that the patient was not in the course of active disease, and thus we decided to withhold rheumatologic medications in order to focus on treating the myocardial infarction. The treatment plan for the patient consisted of continued oral methylprednisolone to control ankylosing spondylitis, and we switched clopidogrel to prasugrel, which is known as a more potent thrombus inhibitor, on the 3rd day of admission considering the increased risk of stent thrombosis. Prasugrel was administered with a loading dose of 50 mg daily maintenance dose of 10 mg. The patient was discharged taking aspirin, carvedilol, rosuvastatin, candesartan, furosemide, spironolactone and prasugrel; however, he revisited our outpatient clinic after 5 days complaining of a worsened whole body skin rash with pruritic symptoms (). Blood tests and chest X-rays showed no abnormal findings, and vital signs were within normal limits. Because aspirin was administered without any evidence of skin hypersensitivity or reaction prior to admission, we suspected prasugrel as the cause of the skin reaction. Accordingly, we discontinued prasugrel and switched the patient to clopidogrel (75 mg/d). A punch biopsy of the abdominal skin revealed mild perivascular lymphocytic infiltrations that were compatible with a hypersensitivity skin reaction (). The patient was followed through the outpatient clinic without further complaint of hypersensitivity skin reaction.
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.