Clopidogrel-Associated Thrombotic Thrombocytopenic Purpura following Endovascular Treatment of Spontaneous Carotid Artery Dissection

Abstract

Thrombotic thrombocytopenic purpura (TTP) is a life-threatening multisystem disease secondary to platelet aggregation. We present a patient who developed profound thrombocytopenia and anemia 8 days following initiation of therapy with clopidogrel after stent placement for carotid artery dissection. She did not have a disintegrin and metalloproteinase with thrombospondin domain 13 (ADAMTS 13) deficiency. Management included steroids and therapeutic plasma exchange. Clopidogrel has rarely been associated with TTP. Unlike other causes of acquired TTP, the diagnosis of early clopidogrel-associated TTP is largely clinical given the infrequent reduction in ADAMTS 13 activity.

P2X1 receptor blockers reduce the number of circulating thrombocytes and the overall survival of urosepsis with haemolysin-producing Escherichia coli

“…This is primarily true for acetylsalicylic acid, although the actions are not acute and rely mainly on stimulation of antibody formation and inhibition of megakaryocyte function [33]. Moreover, it has also been reported casuistically for P2Y 12 receptor antagonists [34][35][36].…”

Treatment tactics for acute coronary syndrome in primary immune thrombocytopenia

“…Было показано, что ТЦП на фоне применения тиклопидина является проявлением ИТП [40]. По мере появления новых производных тиенопиридинов накапливались данные о развитии ИТП при лечении и другими препаратами из этой группы, в частности клопидогрелем [41,42]. Авторы акцентируют внимание на потенциальной опасности развития данного лекарственного осложнения, которое должно учитываться врачами у всех больных, получающих клопидогрел.…”

Ticagrelor-associated thrombotic thrombocytopenic purpura

“…In most cases, it is secondary to production of autoantibodies that reduce activity of a disintegrin and metalloproteinase with thrombospondin domain 13 (ADAMTS-13), which cleaves von Willebrand factor (vWF). Decrease in vWF degradation induces microvascular thrombosis, hemolytic anemia, and thrombocytopenia ( 3 ). Common laboratory findings include anemia and fragmented red blood cells (schistocytes), reduced platelet count, increased lactate dehydrogenase (LDH) level.…”