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 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.