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TA Brighton

Bio: TA Brighton is an academic researcher from University of New South Wales. The author has contributed to research in topics: Antigen & Thrombocytopenic purpura. The author has an hindex of 1, co-authored 2 publications receiving 179 citations.

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Journal ArticleDOI
01 Jul 1996-Blood
TL;DR: The experience suggests that MAIPA assays are useful in the laboratory assessment of thrombocytopenia, should be performed before therapy, and that some patients with 'nonimmune' thromBocy topenia may have genuine antiplatelet antibodies.

186 citations


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Journal ArticleDOI
21 Apr 2011-Blood
TL;DR: This review identified the need for additional studies in many key areas of the therapy of ITP such as comparative studies of "front-line" therapy for ITP, the management of serious bleeding in patients withITP, and studies that will provide guidance about which therapy should be used as salvage therapy for patients after failure of a first-line intervention.

1,601 citations

Journal ArticleDOI
TL;DR: The authors of this up-to-date review discuss the current understanding of pathophysiology and, in particular, the way in which autoantibodies against platelets are generated.
Abstract: Immune thrombocytopenic purpura, which may lead to bleeding, is typically caused by antibodies directed against the platelet glycoprotein IIb/IIIa complex. Since the management of the disorder is different for children and adults, the authors of this up-to-date review provide separate sections on the two age groups. Along with advances in management, they also discuss the current understanding of pathophysiology and, in particular, the way in which autoantibodies against platelets are generated.

1,255 citations

Journal Article
TL;DR: This guideline aims to assess available diagnostic tests and therapies, and attempts to provide a rational approach to the diagnosis and treatment in adults, children and in pregnancy.
Abstract: Idiopathic thrombocytopenic purpura (ITP) is an autoimmune disorder characterized by persistent thrombocytopenia (peripheral blood platelet count < 150 · 10 ⁄ l) due to autoantibody binding to platelet antigen(s) causing their premature destruction by the reticuloendothelial system, and in particular the spleen (Woods et al, 1984a,b). Although the basic underlying pathophysiology of ITP has been known for 50 years (Harrington et al, 1951), the literature shows that the investigation and management of patients with thrombocytopenia vary widely, and is not evidence-based, due to a lack of clinical trials and quality research. Despite major advances in our understanding of the molecular basis of many blood disorders, the diagnosis of ITP remains one of exclusion; there are currently no robust clinical or laboratory parameters that are able to establish the diagnosis of ITP with accuracy. This guideline aims to assess available diagnostic tests and therapies, and attempts to provide a rational approach to the diagnosis and treatment in adults, children and in pregnancy. Although natural history data are becoming available (Cohen et al, 2000; Djulbegovic & Cohen, 2001; Portielje et al, 2001), there are few randomized trials in ITP and many of the recommendations, like those of the American Society of Hematology (ASH) Panel (George et al, 1996), are based on expert opinion.

711 citations

Journal ArticleDOI
TL;DR: The recent insights into the molecular and cellular pathways that are involved in IVIG-mediated immunosuppression are covered, with a particular focus on IVIG as a therapy for IgG-dependent autoimmune diseases.
Abstract: Intravenous immunoglobulin (IVIG) preparations comprise pooled IgG antibodies from the serum of thousands of donors and were initially used as an IgG replacement therapy in immunocompromised patients. Since the discovery, more than 30 years ago, that IVIG therapy can ameliorate immune thrombocytopenia, the use of IVIG preparations has been extended to a wide range of autoimmune and inflammatory diseases. Despite the broad efficacy of IVIG therapy, its modes of action remain unclear. In this Review, we cover the recent insights into the molecular and cellular pathways that are involved in IVIG-mediated immunosuppression, with a particular focus on IVIG as a therapy for IgG-dependent autoimmune diseases.

679 citations