Successful clopidogrel desensitization after drug-eluting stent implantation.

A 55-year-old male was admitted with a recent non-ST-elevation myocardial infarction (NTEMI) and taken to the catheterization laboratory for further management. Culprit lesions were identified in the distal right coronary artery and ramus intermedius, requiring 2 paclitaxel-eluting stents (Taxus(R), Boston Scientific Corp., Natick, Massachusetts) and a bare-metal stent, respectively. The patient was started on ticlopidine therapy due to a history of clopidogrel- associated skin rash. One day after ticlopidine initiation, the patient developed pruritus and a maculopapular rash of the trunk area. The patient was discharged briefly on aspirin and cilostazol therapy with readmission plans for clopidogrel desensitization. A modified protocol was successfully utilized to desensitize the patient.

Case report on clopidogrel rash after coronary placement of a paclitaxol-coated stent.

Antiplatelet agents are indicated after coronary stenting to prevent stent thrombosis and these should not be inadvertently discontinued after stenting. Adverse effects from the use of these drugs may require use of alternative agents.

Clopidogrel desensitization protocol for the treatment of thienopyridine hypersensitivity.

The antiplatelet agent clopidogrel has become a mainstay of treatment of patients with acute coronary syndromes and strokes, and to reduce ischemic complications after percutaneous coronary and peripheral interventions. As the use of this agent has become more widespread, hypersensitivity reactions to clopidogrel have been increasingly recognized. This problem can be difficult to manage, especially in patients who are in need of or have recently undergone intracoronary stenting, as therapeutic alternatives are limited. Our previously published experience shows that desensitization can allow clopidogrel to be used safely in these patients. The protocol is simple, rapid, and can be conducted by a team of cardiology and allergy-immunology specialists. This article outlines the procedural details of the protocol.

Relation between impaired antiplatelet response to clopidogrel and possible pleiotropic effects.

BACKGROUND: The study was designed to determine whether impaired antiplatelet response to clopidogrel but not to aspirin may be responsible for loss of pleiotropic effects of the drug. METHODS: Study included 34 consecutive patients with STEMI undergoing primary percutaneous coronary intervention (PCI) with stent implantation treated with aspirin (loading dose 300 mg followed by 75 mg/day) and clopidogrel (loading dose 600 mg followed by 75 mg/day). On the basis of Platelet Function Analyzer (PFA)-100 test which measured closure times (CT) in test with collagen/epinephrine (CEPI-CT) or collagen/adenosine diphosphate (CADP-CT) patients were stratified after 7 days from admission as full aspirin or clopidogrel responders (CEPI-CT or CADP-CT = 300 sec., respectively) and non-full aspirin or clopidogrel responders (CEPI-CT or CADP-CT < 300 sec., respectively). High sensitivity C-reactive protein (hs-CRP) was measured at baseline and after 7 days of treatment. RESULTS: All patients received comparable statin treatment. Median and interquartile ranges (IQR) of hs-CRP increased significantly from 2.5 mg/L (0.4-44.8) at baseline to 8.05 mg/L (1.4-33.9) at day 7 (P = .002) in non-full clopidogrel responders subgroup and only slightly in the full clopidogrel responders subgroup (2.45 mg/L, IQR 0.4-48.3 vs. 4.2 mg/L, IQR 1.9-17.5) (P = .3) remaining within reference intervals. On the contrary median and IQR of hs-CRP increased significantly in both non-full aspirin responders (2.4 mg/L, IQR 1.3-3.3 vs. 5.8 mg/L, IQR 3.2-14.8, P = .01) and full aspirin responders (2.9 mg/L, IQR 2.0-3.7 vs. 5.6 mg/L, IQR 4.3-12.9, P = .04). CONCLUSIONS: Impaired antiplatelet response to clopidogrel but not to aspirin may contribute to smaller anti-inflammatory response in patients with ST-elevation myocardial infarction.

Desensitization for the management of clopidogrel hypersensitivity: initial clinical experience.

Platelet activation and aggregation play an important role in the pathogenesis of arterial thrombosis in coronary, cerebral and peripheral vascular beds. The antiplatelet agent clopidogrel has become a mainstay of treatment for patients with acute coronary syndromes and stroke, and to reduce ischemic complications after percutaneous coronary and peripheral interventions. There are, however, increasing numbers of reports of hypersensitivity reactions to clopidogrel. We present here a protocol for clopidogrel desensitization in isolated cutaneous reactions. Eight patients have completed the protocol successfully. Three subsequently underwent coronary intervention, and all are currently tolerating a daily clopidogrel dose a median of 7.5 months after desensitization. Desensitization may allow for the safe use of clopidogrel in patients with a history of prior cutaneous hypersensitivity reactions.

Drug-induced thrombotic microangiopathy.

Drug-associated thrombotic thrombocytopenic purpura and hemolytic uremic syndrome (TTP/HUS) has been recognized for several years. The most commonly implicated drugs are mitomycin-C, cyclosporine, quinine, and ticlopidine. As with idiopathic cases of TTP/HUS, basic science discoveries in the late 1990s now suggest that the likely mechanisms by which these agents lead to a thrombotic microangiopathy (TMA) include either an immune-mediated phenomenon involving the ADAMTS13 metalloprotease or direct endothelial toxicity. This article reviews the current understanding of the pathogenesis, the clinical and laboratory features, and the recommended treatments, prognosis, and outcomes of drug-associated TMA.