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| 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 | |
| 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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