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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
9
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pubmed:dateCreated |
2010-10-28
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pubmed:abstractText |
ADAMTS13 deficiency causes accumulation of unusually large von Willebrand factor molecules, which cross-link platelets in the circulation or on the endothelial surface. This process of intravascular agglutination leads to the microangiopathy thrombotic thrombocytopenic purpura (TTP). Most TTP patients have acquired anti-ADAMTS13 autoantibodies that inhibit enzyme function and/or clear it from the circulation. However, the reason for ADAMTS13 deficiency is not always easily identified in a subset of patients.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1538-7836
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pubmed:author |
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pubmed:copyrightInfo |
© 2010 International Society on Thrombosis and Haemostasis.
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pubmed:issnType |
Electronic
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pubmed:volume |
8
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2053-62
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pubmed:meshHeading |
pubmed-meshheading:20553378-ADAM Proteins,
pubmed-meshheading:20553378-Adult,
pubmed-meshheading:20553378-Autoantibodies,
pubmed-meshheading:20553378-Autoimmunity,
pubmed-meshheading:20553378-Blotting, Western,
pubmed-meshheading:20553378-Fibrinolysin,
pubmed-meshheading:20553378-Humans,
pubmed-meshheading:20553378-Male,
pubmed-meshheading:20553378-Mutation,
pubmed-meshheading:20553378-Protein Structure, Tertiary,
pubmed-meshheading:20553378-Purpura, Thrombotic Thrombocytopenic,
pubmed-meshheading:20553378-Remission Induction,
pubmed-meshheading:20553378-alpha-2-Antiplasmin
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pubmed:year |
2010
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pubmed:articleTitle |
Inactivation of ADAMTS13 by plasmin as a potential cause of thrombotic thrombocytopenic purpura.
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pubmed:affiliation |
Laboratory for Thrombosis Research, Katholieke Universiteit Leuven Campus Kortrijk, Kortrijk, Belgium.
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pubmed:publicationType |
Journal Article,
Case Reports,
Research Support, Non-U.S. Gov't
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