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| http://dx.doi.org/10.1016/j.thromres.2021.02.008 | DOI Listing |
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Single-Nucleotide Polymorphisms in Thrombotic Thrombocytopenic Purpura: A Genetic Predisposition to Immune Thrombotic Thrombocytopenic Purpura.
Cureus
December 2024
Hematology and Oncology, University of Texas MD Anderson Cancer Center, Galveston, USA.
There are two main classifications for thrombotic thrombocytopenic purpura (TTP): immune and hereditary. The majority of TTP cases are immune in nature and are due to inhibitor autoantibodies against ADAMTS13. Hereditary TTP is caused by biallelic pathogenic variants in the ADAMTS13 gene.
View Article and Find Full Text PDFA novel automated chemiluminescent enzyme immunoassay for ADAMTS-13 activity enables accompanying measurements of the inhibitory autoantibodies.
J Thromb Haemost
December 2024
Department of Hematology, Nara Medical University, Kashihara, Japan; Department of Blood Transfusion Medicine, Nara Medical University, Kashihara, Japan. Electronic address:
Article Synopsis
- TTP is a serious condition linked to low activity of the ADAMTS-13 enzyme, with traditional testing methods being slow and labor-intensive.
- A new automated chemiluminescent enzyme immunoassay (CLEIA) has been developed, which is sensitive and quick, allowing results in just 17 minutes.
- The CLEIA showed excellent agreement with conventional assays in accurately measuring ADAMTS-13 activity and detecting inhibitory antibodies, making it a reliable option for diagnosing and monitoring TTP in hospitals.
Navigating the Nexus: Lenalidomide-Associated Thrombotic Thrombocytopenic Purpura.
Cureus
June 2024
Internal Medicine, Piedmont Athens Regional Medical Center, Athens, USA.
Thrombotic thrombocytopenic purpura (TTP) is a life-threatening thrombotic microangiopathy (TMA) marked by thrombocytopenia, microangiopathic hemolytic anemia, and microvascular thrombosis leading to end-organ damage. While TTP commonly results from hereditary or acquired ADAMTS13 deficiency, its association with lenalidomide is notably rare. The link between lenalidomide and TMA is unclear and requires more studies, given the high mortality risk associated with TTP.
View Article and Find Full Text PDFWeibel-Palade bodies: function and role in thrombotic thrombocytopenic purpura and in diarrhea phase of STEC-hemolytic uremic syndrome.
Pediatr Nephrol
January 2025
Department of Physiology, Radboud University Centre, Nijmegen, the Netherlands.
Vascular endothelial cells are equipped with numerous specialized granules called Weibel-Palade bodies (WPBs). They contain a cocktail of proteins that can be rapidly secreted (3-5 min) into the vascular lumen after an appropriate stimulus such as thrombin. These proteins are ready without synthesis.
View Article and Find Full Text PDFRisk factors of death or chronic renal replacement therapy requirements in patients with thrombotic microangiopathies without ADAMTS-13 deficiency.
Eur J Haematol
October 2024
Fundació Institut d'Investigació Sanitària Illes Balears (IdISBa), Hospital Universitario Son Espases, Palma de Mallorca, Balearic Islands, Spain.
Thrombotic microangiopathy (TMA), characterized by microangiopathic hemolytic anemia, thrombocytopenia, and multisystem organ dysfunction, is a life-threatening disease. Patients with TMA who do not exhibit a severe ADAMTS-13 deficiency (defined as a disintegrin-like and metalloprotease with thrombospondin type 1 motif no. 13 activity ≥10%: TMA-13n) continue to experience elevated mortality rates.
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