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 57-year-old man with significant history of ischaemic heart disease underwent elective percutaneous coronary intervention to the proximal left anterior descending artery with insertion of two drug-eluting stents in February 2014. He was commenced on dual antiplatelet therapy with the addition of clopidogrel to his regular aspirin. His other past medical history included hypertension and hypercholesterolaemia. He had no previous history of drug allergy or atopy.\nEleven days after commencement of clopidogrel he developed a generalised urticarial rash including his scalp and palms, with associated peripheral paraesthesia. He was treated with antihistamines and his clopidogrel was changed to ticagrelor.\nThirty-six hours after the introduction of ticagrelor, he represented with facial angioedema associated with left sided chest pain and dysphagia without respiratory compromise. Following the cessation of ticagrelor, the symptoms resolved with intramuscular adrenaline and intravenous corticosteroids and he was discharged home after a period of observation.\nFurther cardiology consultation recommended the trial of prasugrel under close supervision. Within two hours, he developed an urticarial reaction involving the hands, feet and groin, which initially resolved with antihistamine. After the third dose of prasugrel, he experienced chest, left arm and abdominal discomfort, with periorbital and lip angioedema. Although haemodynamically stable, he was diaphoretic and required oxygen therapy. Again, he improved with intramuscular adrenaline, intravenous f luid and oral and intravenous antihistamines. All investigations were unremarkable including the tryptase level which was only collected 36 hours post symptom onset.\nThe idea of trialling a fourth antiplatelet agent, ticlopidine, was briefly considered. Given his reaction to three antiplatelet agents, and after reviewing the molecular structure of all four drugs (), as well as available literature on clopidogrel sensitisation and its cross-reactivity towards ticlopidine and prasugrel, there was significant concern about the risk of similar but more severe and rapid onset hypersensitivity reaction. The patient ultimately underwent clopidogrel desensitisation with prednisolone cover. He successfully completed the programme without complication and was maintained on strict daily dose afterwards. He continues to take clopidogrel without adverse effects four months post desensitisation.