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  1. Annual review of medicine
  2. Year: 2015, Volume: 66
  3. Year: 2015, Volume: 66, Issue: Unspecified
  4. ADAMTS13 and von Willebrand Factor in Thrombotic Thrombocytopenic Purpura
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Year: 2016, Volume: 67
Year: 2015, Volume: 66
Year: 2015, Volume: 66, Issue: Unspecified
T Cell–Mediated Hypersensitivity Reactions to Drugs
Understanding HIV Latency: The Road to an HIV Cure
The Gut Microbial Endocrine Organ: Bacterially-Derived Signals Driving Cardiometabolic Diseases
ADAMTS13 and von Willebrand Factor in Thrombotic Thrombocytopenic Purpura
Neuroblastoma: Molecular Pathogenesis and Therapy
Regulation of Tumor Metastasis by Myeloid-derived Suppressor Cells
Ketamine and Rapid-Acting Antidepressants: A Window into a New Neurobiology for Mood Disorder Therapeutics
Year: 2014, Volume: 65
Year: 2013, Volume: 64
Year: 2012, Volume: 63
Year: 2011, Volume: 62
Year: 2010, Volume: 61
Year: 2009, Volume: 60
Year: 2008, Volume: 59
Year: 2006, Volume: 57
Year: 2004, Volume: 55
Year: 1994, Volume: 45

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ADAMTS13 and von Willebrand Factor in Thrombotic Thrombocytopenic Purpura

Content Provider PubMed Central
Author Zheng, X. Long
Abstract Pathogenesis of thrombotic thrombocytopenic purpura (TTP) was a mystery for over half a century until the discovery of ADAMTS13. ADAMTS13 is primarily synthesized in the liver, and its main function is to cleave von Willebrand factor (VWF) anchored on the endothelial surface, in circulation, and at the sites of vascular injury. Deficiency of plasma ADAMTS13 activity (<10%) resulting from mutations of the ADAMTS13 gene or autoantibodies against ADAMTS13 causes hereditary or acquired (idiopathic) TTP. ADAMTS13 activity is usually normal or modestly reduced (>20%) in other forms of thrombotic microangiopathy secondary to hematopoietic progenitor cell transplantation, infection, and disseminated malignancy or in hemolytic uremic syndrome. Plasma infusion or exchange remains the initial treatment of choice to date, but novel therapeutics such as recombinant ADAMTS13 and gene therapy are under development. Moreover, ADAMTS13 deficiency has been shown to be a risk factor for the development of myocardial infarction, stroke, cerebral malaria, and preeclampsia.
Related Links http://dx.doi.org/10.1146/annurev-med-061813-013241
Ending Page 225
Page Count 15
Starting Page 211
File Format PDF
ISSN 00664219
e-ISSN 1545326X
Journal Annual review of medicine
Volume Number 66
Language English
Publisher Date 2015-01-14
Access Restriction Open
Subject Keyword Biochemistry, Genetics and Molecular Biology(all) Medicine(all) Research in Higher Education
Content Type Text
Resource Type Article
Subject Medicine Biochemistry, Genetics and Molecular Biology
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