Acquired von Willebrand disease (AvWD) is an acquired bleeding disorder which may suddenly become manifest in individuals, usually in the absence of a personal or family history of bleedings and frequently in association with monoclonal gammopathies, lymphoproliferative, myeloproliferative and autoimmune disorders. In a minority of the cases AvWD may develop in association with drugs or solid tumours. Pathogenetic mechanisms involve autoantibodies directed against von Willebrand factor (vWF) resulting in a rapid clearance of vWF from the circulation and/or inactivation of plasma vWF; absorption or adsorption of plasma vWF to malignant cells; drug-induced or cell-mediated proteolysis of plasma vWF; acquired decrease in synthesis of vWF and/or release of vWF from storage sites; or precipitation of plasma vWF. Treatment options include--whenever possible--treatment of the underlying disorder or symptomatic treatment aimed at replacing the loss of vWF by either infusion of vWF-rich concentrates or administration of desmopressin (DDAVP). In selected cases with anti-vWF antibodies, administration of high-dose intravenous gammaglobulin, plasma exchange or extracorporeal immunoadsorption may be successful.
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http://dx.doi.org/10.1016/s0950-3536(98)80051-6 | DOI Listing |
PLoS One
January 2025
Institute of Medical Biochemistry, Center for Molecular Biology of Inflammation, University of Muenster, Muenster, Germany.
Weibel-Palade bodies (WPB) are secretory organelles exclusively found in endothelial cells and among other cargo proteins, contain the hemostatic von-Willebrand factor (VWF). Stimulation of endothelial cells results in exocytosis of WPB and release of their cargo into the vascular lumen, where VWF unfurls into long strings of up to 1000 µm and recruits platelets to sites of vascular injury, thereby mediating a crucial step in the hemostatic response. The function of VWF is strongly correlated to its structure; in order to fulfill its task in the vascular lumen, VWF has to undergo a complex packing/processing after translation into the ER.
View Article and Find Full Text PDFEur J Clin Invest
January 2025
Department of Thromboembolic Disorders, Institute of Cardiology, Jagiellonian University Medical College, Krakow, Poland.
Background: The role of a prothrombotic state in atrial fibrillation (AF) progression to permanent arrythmia (PerAF) is unclear. Formation of denser and poorly lysable fibrin clots has been observed in AF patients also with sinus rhythm in association with higher stroke risk. We investigated whether altered fibrin clot properties and other prothrombotic state markers may contribute to AF transition to PerAF.
View Article and Find Full Text PDFJ Surg Res
January 2025
Center for Injury Science, University of Alabama at Birmingham, Birmingham, Alabama.
Introduction: Previous studies suggested that type O blood may be associated with increased mortality and/or thrombotic complications among trauma patients. The purpose of this analysis was to evaluate the relationship between endogenous blood type, mortality, and complications among patients receiving massive transfusions, using data from the Pragmatic Randomized Optimal Platelet and Plasma Ratios trial.
Materials And Methods: This was a secondary analysis of the Pragmatic Randomized Optimal Platelet and Plasma Ratios trial that included patients with the reported blood type (A, AB, B, or O) data.
Blood Adv
January 2025
Department of Internal Medicine, Division of Thrombosis and Hemostasis, Einthoven Laboratory for Vascular and Regenerative Medicine, Leiden University Medical Center, Leiden, The Netherlands.
Treatment options for the bleeding disorder von Willebrand disease type 2B (VWD2B) are insufficient and fail to address the negative effects of circulating mutant von Willebrand factor (VWF). The dominant-negative nature of VWD2B makes functionally defective VWF an interesting therapeutic target. Previous in vitro studies have demonstrated the feasibility of allele-selective silencing of mutant VWF using small interfering RNAs (siRNAs) targeting common single nucleotide polymorphisms (SNPs) in the human VWF gene, an approach that can be applied irrespective of the disease-causing VWF mutation.
View Article and Find Full Text PDFThromb Haemost
January 2025
Hemostasis and Erythropathology Laboratory, Hematopathology, Pathology Department, Centre de Diagnòstic Biomèdic (CDB), Hospital Clínic de Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain.
Background: V617F-mutated myeloproliferative neoplasms (MPN) exhibit abnormal proliferation of bone marrow progenitors and increased risk of thrombosis, specifically in splanchnic veins (SVT). The contribution of the endothelium to the development of the prothrombotic phenotype was explored.
Material And Methods: Plasma and serum samples from V617F MPN patients with (n=26) or without (n=7) thrombotic debut and different treatments, were obtained (n=33).
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