Clopidogrel-Associated TTP

Zakarija, Anaadriana; Bandarenko, Nicholas; Pandey, Dilip K.; Auerbach, Amy R.; Raisch, Dennis W.; Kim, Benjamin; Kwaan, Hau C.; McKoy, June M.; Schmitt, Brian P.; Davidson, Charles J.; Yarnold, Paul R.; Gorelick, Philip B.; Bennett, Charles L.

doi:10.1161/01.str.0000109253.66918.5e

Cited by 97 publications

(23 citation statements)

References 16 publications

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“…25 It must be noted, however, that thrombotic thrombocytopenic purpura is still a harmful, albeit very rare, complication of clopidogrel treatment. 29,30 Combined Therapy With Aspirin and Thienopyridines…”

Section: Thienopyridinesmentioning

confidence: 99%

Aspirin and Clopidogrel

Cattaneo

2004

ATVB

370

133

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Abstract-Aspirin and the thienopyridines ticlopidine and clopidogrel are antiplatelet agents that display good antithrombotic activity. In the past few years, the concept of aspirin resistance has been largely emphasized in the medical literature, although its definition is still uncertain. I suggest that "aspirin-resistant" should be considered as a description for those individuals in whom aspirin fails to inhibit thromboxane A 2 production, irrespective of the results of unspecific tests of platelet function, such as the bleeding time, platelet aggregation, or the PFA-100 system. Less well known than aspirin resistance, but certainly better characterized, is the issue of "clopidogrel resistance," which is probably mostly caused by inefficient metabolism of the prodrug clopidogrel to its active metabolite. At present, aspirin and clopidogrel resistance should not be looked for in the clinical setting, because there is no definite demonstration of an association with clinical events conditioning cost-effective changes in patient management. Key Words: aspirin resistance Ⅲ clopidogrel resistance Ⅲ antiplatelet agents Ⅲ cardiovascular diseases Ⅲ cerebrovascular diseases A spirin and the thienopyridines ticlopidine and clopidogrel are inhibitors of platelet aggregation that display good antithrombotic activity. They are used in the prophylaxis of patients undergoing vascular grafting or percutaneous angioplasty, in the medical management of acute coronary syndromes, and in long-term prevention of cardiovascular and cerebrovascular events.Both aspirin and the thienopyridines selectively inhibit a single pathway of platelet activation: aspirin affects the arachidonate-thromboxane A 2 (TxA 2 ) pathway by irreversibly inhibiting cyclo-oxygenase-1 (COX-1) (Figure 1). 1 The thienopyridines affect the adenosine diphosphate (ADP) pathway, by irreversibly blocking the ADP receptor P2Y 12 ( Figure 1). 2 Despite their selective mechanism of action, which does not counteract the many alternative pathways for platelet activation, aspirin and thienopyridines display a good antithrombotic activity. This is explained by the fact that both the arachidonate-TxA 2 pathway and the ADP pathway contribute to the amplification of platelet activation and are essential for the full aggregation and secretion response of platelets to agonists. 2

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Section: Thienopyridinesmentioning

confidence: 99%

Aspirin and Clopidogrel

Cattaneo

2004

ATVB

370

133

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“…However, only in very few cases was the presence of ADAMTS13 inhibitors documented. Time-course analysis suggests that for most cases the duration between initiation of drug therapy and complication of thrombotic microangiopathy was 2 -6 weeks with ticlopidine and ≤ 2 weeks with clopidogrel (59,60).…”

Section: Etiologymentioning

confidence: 99%

ADAMTS13 and microvascular thrombosis

Tsai¹

2006

Expert Review of Cardiovascular Therapy

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SummaryInteraction between platelet and von Willebrand factor (VWF), a circulating adhesive glycoprotein, is essential for hemostasis under the high shear environments of arterioles and capillaries. If unregulated, this interaction may lead to unwarranted platelet thrombosis ADAMTS13 (a disintegrin and metalloprotease with thrombospondin type 1 motif, number 13), a plasma zinc metalloprotease synthesized primarily in the stellate cells of the liver, cleaves shear stress activated VWF, thereby preventing the occurrence of VWF-platelet interaction in the circulation. A profound deficiency of ADAMTS13, due to genetic mutations or autoimmune inhibitors, results in intravascular VWFplatelet aggregation and widespread microvascular thrombosis characteristic of thrombotic thrombocytopenic purpura (TTP). Cloning of ADAMTS13 and structure-function analysis of the enzyme are leading to exciting advances in the diagnosis and therapy of this hitherto mysterious disease.

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“…Plasma therapy is also beneficial in some secondary forms of TTP like ticlopidine or clopidogrel induced TTP or pregnancy associated TTP but its role in chemotherapy associated TTP and bone marrow transplantation associated TTP has not resulted in improved outcome [35,40].…”

Section: Ttp and Adamts-13mentioning

confidence: 99%

Thrombotic Thrombocytopenic Purpura

Saifan¹

2013

J Blood Disord Transfus 2012

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Clopidogrel-Associated TTP

Cited by 97 publications

References 16 publications

Aspirin and Clopidogrel

Aspirin and Clopidogrel

ADAMTS13 and microvascular thrombosis

Thrombotic Thrombocytopenic Purpura

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