Subsequently increased levels of PMPs after platelet activation and the increased possibility of thrombosis. This is in consideration of the role of platelets in Von Willebrand and platelet-rich thrombus formation in TTP, and Īccording to studies in recent years, identifying the procoagulant properties of microparticles and their role in thromboticĮvents in different diseases, plasma levels of PMPs in TTP patients serves as a useful diagnostic biomarker of patients’ clinical Since microparticles also carry a part of the cytoplasm during their formation, they inherently contain a number of cytokines,Ĭhemokines, enzymes, growth factors, and signaling proteins. Phospholipid expression on the surface of microparticles provides a suitable surface for coagulation enzymes and thus playsĪ role in activation of the coagulation cascade and thrombin generation. Elevation of other types of microparticles are also observed in diabetes, sickle cell anemia, hemolytic anemia, sepsis, and autoimmune diseases such as rheumatoid arthritis. With many diseases such as heparin-induced thrombosis (HIT), immune thrombocytopenic purpura (ITP), TTP, uremia, malignancies, and other thrombocytopenic disorders and cardiovascular disease. Increase of platelet microparticles expressing CD41, CD62p, CD63 and P-selectin (which represents platelet activity) is associated Much researches have shown that platelet microparticles induce angiogenesis and blood vessel regeneration. Or from megakaryocytes that expresses CD41 but are negative for platelet activity markers such as CD63 and CD62p. Many studies have reported that about 70- to 90% of plasma microparticles in healthy individuals are derived from platelets In recent years, it has beenĬlear that the use of rituximab (anti-CD20 antibody) in TTP could be effective in acquired TTP and other antibody-mediated Other treatment choices are immunosuppressive agents such as methylprednisolone and rituximab. The first choice and most important treatment for TTP patients is plasma exchange (PEX), which should be initiated immediately. About 90% of acute episodes of TTP occur in adulthood more often in women (sex ratio of about 3F/1M). Microangiopathic hemolytic anemia, neurologic findings, fever, and renal impairment. Systems such as those in the brain and kidney that lead to thrombotic thrombocytopenic purpura with a classic pentad: thrombocytopenia, In the absence of ADAMTS13, the ultra-large multimers of VWF are not cleaved, causing platelet-rich thrombus in microvascular Approximately 95% of TTP cases, however, are acquired TTP caused by autoantibody In the ADAMTS 13 gene and is relatively rare. There are two types of TTP in the current terminology: congenital and acquired. Role in platelet adhesion and aggregation at high shear rates in microvessels. Von Willebrand Factor is a plasma protein that plays an essential Of a ultra-large multimers of ‘Von Willebrand Factor (VWF)’. With thrombospondin type 1 repeats As well as member 13 (ADAMTS13) deficiency-the metalloprotease responsible for cleavage The known pathological mechanism of TTP involves an A disintegrin and metalloprotease In the absence of plasma exchange, it has high mortality rate (more than 90%), while by proper treatment with plasma exchange Thrombotic Thrombocytopenic Purpura is a rare microangiopathic hemolytic anemia with an annual incidence rate of six cases Previous Section Next Section Introduction
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