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| http://dx.doi.org/10.1055/s-0040-1716379 | DOI Listing |
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[100 years thrombotic thrombocytopenic purpura (TTP) - lessons learned?].
Dtsch Med Wochenschr
November 2024
Klinik für Innere Medizin I - Abteilung für Hämatologie und Hämostaseologie, Medizinische Universität Wien, Österreich.
100 years ago Dr. Eli Moschcowitz described the first case of thrombotic thrombocytopenic purpura. For many decades there were no recognized treatment options, and the mortality rate was extremely high.
View Article and Find Full Text PDFThe Phenomenon of Thrombotic Microangiopathy in Cancer Patients.
Int J Mol Sci
August 2024
Department of Obstetrics, Gynecology and Perinatal Medicine, I.M. Sechenov First Moscow State Medical University (Sechenov University), Trubetskaya Str. 8-2, 119991 Moscow, Russia.
Article Synopsis
- - Thrombotic microangiopathy (TMA) is a group of disorders where small blood vessel clotting causes organ damage, including conditions like thrombotic thrombocytopenic purpura (TTP) and hemolytic-uremic syndrome (HUS), each with unique causes and impacts on health.
- - In TMA, inflammation leads to endothelial damage and activates platelet and coagulation processes, often linked to low ADAMTS13 enzyme levels, particularly in cancer patients undergoing chemotherapy, which raises thrombotic risk by increasing the VWF/ADAMTS13 ratio.
- - Treatment focuses on diagnosing the specific cause and may include therapies to inhibit complement activation, supportive care, and plasmapheresis
Caplacizumab in pediatric immune thrombotic thrombocytopenic purpura: the UK TTP Registry experience.
Blood Adv
September 2024
Department of Haematology, University College London Hospitals National Health Service Foundation Trust, London, United Kingdom.
Pediatric thrombotic thrombocytopenic purpura (TTP) is an ultrarare disease. Immune TTP (iTTP) is driven by anti-ADAMTS13 autoantibodies causing an imbalanced von Willebrand factor (VWF):ADAMTS13 axis, and rarer still in children, but potentially life-threatening. Caplacizumab is licensed for iTTP treatment in adults and adolescents aged ≥12 years who weigh ≥40 kg.
View Article and Find Full Text PDFRemoval of endothelial surface-associated von villebrand factor suppresses accelerate datherosclerosis after myocardial infarction.
J Transl Med
May 2024
Cardiovascular Division and Robert M. Berne Cardiovascular Research Center, University of Virginia, Box 801394, 415 Lane Rd, Charlottesville, VA, 22908, USA.
Background: Thromboinflammation involving platelet adhesion to endothelial surface-associated von Willebrand factor (VWF) has been implicated in the accelerated progression of non-culprit plaques after MI. The aim of this study was to use arterial endothelial molecular imaging to mechanistically evaluate endothelial-associated VWF as a therapeutic target for reducing remote plaque activation after myocardial infarction (MI).
Methods: Hyperlipidemic mice deficient for the low-density lipoprotein receptor and Apobec-1 underwent closed-chest MI and were treated chronically with either: (i) recombinant ADAMTS13 which is responsible for proteolytic removal of VWF from the endothelial surface, (ii) N-acetylcysteine (NAC) which removes VWF by disulfide bond reduction, (iii) function-blocking anti-factor XI (FXI) antibody, or (iv) no therapy.
Concurrent myocardial infarction in the setting of thrombotic thrombocytopenic purpura secondary to systemic lupus erythematosus: A case report.
Clin Case Rep
April 2024
Department of Internal Medicine, School of Medicine Lorestan University of Medical Sciences Khorramabad Iran.
Key Clinical Message: In acute thrombotic thrombocytopenic purpura (TTP), apart from urgent treatment, assessing the patient's medical history, especially conditions like systemic lupus erythematosus that could trigger TTP, is crucial. Rarely, TTP patients may experience cardiac conditions as severe as a myocardial infarction.
Abstract: A 45-year-old woman manifested severe and acute thrombotic thrombocytopenic purpura (TTP) of unknown origin.
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