Immediate hypersensitivity and delayed hypersensitivity to Clopidogrel

Gutiérrez-Fernández, D; Fuentes-Vallejo, M S; Rueda-Ygueravides, M.D.; Fernández, Antonio Foncubierta; León‐Jiménez, Antonio

doi:10.1157/13110317

Cited by 10 publications

(4 citation statements)

References 5 publications

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“…Proposed mechanisms include direct mast cell activation, complement system activation, immune complex deposition, T-cell activation and IgE-mediated hypersensitivity 12. Hypersensitivity to metabolites of clopidogrel rather than clopidogrel itself has also been suggested as a possibility.…”

Section: Discussionmentioning

confidence: 99%

Leucocytoclastic vasculitis as a late complication of clopidogrel therapy

et al. 2013

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We describe a case of leucocytoclastic vasculitis manifested as exanthematous rash in a 57-year-old woman on long-term therapy with clopidogrel. The diagnosis was confirmed by skin biopsy. The patient was managed symptomatically with oral antihistaminics and topical steroids in consultation with dermatologists. Clopidogrel therapy was discontinued on suspicion of drug-induced vasculitis. The rash resolved completely within 2 weeks of withdrawal of clopidogrel, satisfying criteria for a probable adverse drug reaction. Leucocytoclastic vasculitis is an unusual adverse effect of clopidogrel therapy and even rarer as a late complication.

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Section: Discussionmentioning

confidence: 99%

Leucocytoclastic vasculitis as a late complication of clopidogrel therapy

et al. 2013

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“…The reaction does not appear to be related to the clopidogrel dose [7]. However, it is not clear whether the immune response is related to the parent clopidogrel compound or to its metabolites [18].…”

Section: Mechanism Of Clopidogrel Hypersensitivitymentioning

confidence: 97%

“…Screening for type I hypersensitivity is possible with a skin prick or intradermal challenge [7]. Such testing has been employed to confirm type I clopidogrel hypersensitivity reactions [12,18].…”

Section: Mechanism Of Clopidogrel Hypersensitivitymentioning

confidence: 99%

Management Strategies for Clopidogrel Hypersensitivity

Beavers

Carris

Ruf

2015

Drugs

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Clopidogrel is a cornerstone of dual antiplatelet therapy. Hypersensitivity reactions potentially limit the use of this treatment and present a significant clinical challenge. The authors have developed recommendations for the management of clopidogrel hypersensitivity with consideration for the etiology, pathophysiology, and critical evaluation of potential management strategies. The clopidogrel hypersensitivity reaction is complex in mechanism and presents generally around day 5 of treatment. Generalized reactions are most common, but the reaction may also be localized or systemic. Screening patients for hypersensitivity is not always possible because the type IV delayed reaction is not detected reliably by conventional skin prick, intradermal challenge, or patch testing. Proposed strategies for management of clopidogrel hypersensitivity include treatment of the reaction with corticosteroids, clopidogrel desensitization, substituting an alternative P2Y12 inhibitor, or clopidogrel avoidance. The safety, efficacy, and cost of each potential strategy must be considered when managing a patient with clopidogrel hypersensitivity.

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“…In another case with a desquamating exanthema, prick, intradermal and patch tests with Clopidogrel were negative; however, an oral challenge test reproduced an exanthematous reaction [84].…”

Section: Immediate Hypersensitivity Reactionsmentioning

confidence: 93%

Hypersensitivity Reactions to Anticoagulant Drugs

Scherer¹,

Tsakiris²,

Bircher³

2008

CPD

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Drugs with anticoagulant activity, including heparins, hirudins, coumarins, and platelet aggregation inhibitors belong to the most widely used drugs. Hypersensitivity reactions from these agents are rare. However, due to their widespread use, they may have a considerable impact on patient safety and treatment. Accurate diagnosis of potentially life-threatening adverse events and identification of alternatives is mandatory. We review hypersensitivity reactions caused by the different groups of anticoagulant agents and discuss the pathophysiological mechanisms, diagnostic possibilities and management options. According to patients histories the most common hypersensitivity reaction is intolerance to acetylsalicylic acid (ASA). Also localized erythematous plaques, occurring to subcutaneous application of heparins are rather common. Other hypersensitivity reactions are rare but may be life-threatening, e.g. skin necrosis due to heparin-induced thrombocytopenia. Rarely anaphylactoid reactions have been observed to ASA, heparin, and hirudin. Skin and provocation tests with immediate and late readings are the most reliable diagnostic tools for heparin- or hirudin-induced urticaria/anaphylaxis or heparin-induced delayed plaques. Provocation tests may be used to identify safe alternatives. In cases of necrosis from heparins or coumarins, all in vivo tests are contraindicated. Most in vitro tests are not universally available, and with the exception of platelet aggregation tests, they have a low sensitivity. In some anticoagulant-associated hypersensitivity reactions detailed allergologic investigation may help to identify safe treatment alternatives. Typically, several tests are needed, and therefore the test procedures are time consuming.

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Immediate hypersensitivity and delayed hypersensitivity to Clopidogrel

Cited by 10 publications

References 5 publications

Leucocytoclastic vasculitis as a late complication of clopidogrel therapy

Leucocytoclastic vasculitis as a late complication of clopidogrel therapy

Management Strategies for Clopidogrel Hypersensitivity

Hypersensitivity Reactions to Anticoagulant Drugs

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