ArticleJournal of thrombosis and haemostasis : JTH2024
Mechanism underlying severe deficiency of plasma ADAMTS-13 activity in immune thrombotic thrombocytopenic purpura.
Article in Journal of thrombosis and haemostasis : JTH, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Human monoclonal and polyclonal anti-ADAMTS13 antibodies in immune thrombotic thrombocytopenic purpura: variable mechanisms of inhibition.Journal of thrombosis and haemostasis : JTH · 2026Article
- ADAMTS-13 R1206K variant exhibits an open conformation and an enhanced proteolytic activity toward von Willebrand factor.Journal of thrombosis and haemostasis : JTH · 2026Article
- The landscape of ADAMTS13-related tests in thrombotic thrombocytopenic purpura: a review.Frontiers in medicine · 2026Review
- Preventative and therapeutic effects of a novel humanized anti-glycoprotein Ibα fragment of antigen-binding region in a murine model of thrombotic thrombocytopenic purpura.Journal of thrombosis and haemostasis : JTH · 2025Article
- Arginine Methylation by PRMT1 Affects ADAMTS13 Secretion and Enzymatic Activity.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Mechanistic insight into multiple antibody binding to ADAMTS13 in immune thrombotic thrombocytopenic purpura.Research and practice in thrombosis and haemostasis · 2024Article
- A comparative study of anti-ADAMTS-13 antibody dynamics in immune-mediated thrombotic thrombocytopenic purpura.Research and practice in thrombosis and haemostasis · 2024Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
backgroundImmune-mediated thrombotic thrombocytopenic purpura is caused by autoantibodies against ADAMTS-13, a plasma enzyme that cleaves von Willebrand factor. However, the mechanism resulting in severe deficiency of plasma ADAMTS-13 activity remains controversial.
objectivesTo determine the mechanism of autoantibody-mediated severe deficiency of plasma ADAMTS13 activity in immune-mediated thrombotic thrombocytopenic purpura.
methodsFluorescence resonance energy transfer-VWF73 was used to determine plasma ADAMTS-13 activity. Enzyme-linked immunosorbent assay (ELISA) was used to determine anti-ADAMTS-13 immunoglobulin G. ELISA and capillary electrophoresis-based Western blotting were employed to assess plasma ADAMTS-13 antigen.
resultsWe showed that plasma ADAMTS-13 antigen levels varied substantially in the samples collected on admission despite all showing plasma ADAMTS-13 activity of <10 IU/dL (or <10% of normal level) using either ELISA or Western blotting. More severe deficiency of plasma ADAMTS-13 antigen (<10%) was detected in admission samples by ELISA than by capillary Western blotting. There was a significant but moderate correlation between plasma ADAMTS-13 activity and ADAMTS-13 antigen by either assay method, suggesting that severe deficiency of plasma ADAMTS-13 activity is not entirely associated with low levels of ADAMTS-13 antigen.
conclusionWe conclude that severe deficiency of plasma ADAMTS-13 activity primarily resulted from antibody-mediated inhibition, but the accelerated clearance of plasma ADAMTS-13 antigen via immune complexes may also contribute significantly to severe deficiency of plasma ADAMTS-13 activity in a subset of patients with acute immune-mediated thrombotic thrombocytopenic purpura.
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