Relevant bibliographies by topics / FVIII clearance

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'FVIII clearance'

Author: Grafiati
Published: 9 March 2023
Last updated: 31 July 2025

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Journal articles on the topic "FVIII clearance"

1

Hulshof, Anne-Marije, Lilian Antunes Heck, Ferdows Atiq, et al. "Whole Genome Sequencing to Elucidate Genetic Modifiers of FVIII Clearance Heterogeneity in Patients with Hemophilia a." Blood 144, Supplement 1 (2024): 3958. https://doi.org/10.1182/blood-2024-204546.

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Introduction: Significant inter-individual variation in FVIII clearance has been described in patients with haemophilia A (HA). The mechanisms underlying this heterogeneity remain poorly defined. Importantly, previous GWAS studies in healthy populations have described associations between SNPs and plasma FVIII and VWF levels.Furthermore, specific lectin and scavenger clearance receptors have been shown to regulate FVIII clearance in vivo. Methods: In vivo clearance of rFVIII (Advate) was assessed in 49 adult patients with HA using MyPKFit. Age, ABO blood group, plasma VWF:Ag and VWF propeptide
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Swystun, Laura L., Colleen Notley, Kate Sponagle, Paula D. James, and David Lillicrap. "Regulation Of Factor VIII Clearance By Mannose-Binding Lectins." Blood 122, no. 21 (2013): 2340. http://dx.doi.org/10.1182/blood.v122.21.2340.2340.

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Abstract The coagulation factors von Willebrand factor (FVIII) and factor VIII (FVIII) circulate in the plasma in a non-covalent complex. VWF acts as a carrier for FVIII and protects it from proteolysis and accelerated clearance. However, in the absence of VWF, the molecular mechanisms that regulate FVIII clearance are largely uncharacterized. The glycosylation of FVIII may regulate its interaction with lectin clearance receptors such as the asialoglycoprotein receptor and siglec-5. The FVIII polypeptide is modified by the addition of 24 N-linked glycans and 7 O-linked glycans. The majority of
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Makogonenko, Evgeny M., Andrey G. Sarafanov, Natalya M. Ananyeva, Klaus-Peter Radtke, Dudley K. Strickland, and Evgueni L. Saenko. "B Domain of Coagulation Factor VIII Regulates Exposure of Its Heparin-Binding Site." Blood 106, no. 11 (2005): 1014. http://dx.doi.org/10.1182/blood.v106.11.1014.1014.

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Abstract B domain of coagulation factor VIII (fVIII) was previously considered to be dispensable for fVIII function. Recently, it was found that the B domain is important for fVIII intracellular interaction with its chaperon and likely involved in fVIII clearance via asialoglycoprotein receptor. At the same time, the major clearance mechanism of fVIII involves initial interaction with heparan sulfate proteoglycans (HSPGs) followed by internalization via low-density lipoprotein receptor-related protein (LRP), member of low-density lipoprotein receptor (LDLR) family (Saenko et al, 1999; Sarafano
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Bukkems, Laura H., Jessica M. Heijdra, Nico C. B. de Jager, et al. "Population pharmacokinetics of the von Willebrand factor–factor VIII interaction in patients with von Willebrand disease." Blood Advances 5, no. 5 (2021): 1513–22. http://dx.doi.org/10.1182/bloodadvances.2020003891.

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Abstract Recent studies have reported that patients with von Willebrand disease treated perioperatively with a von Willebrand factor (VWF)/factor VIII (FVIII) concentrate with a ratio of 2.4:1 (Humate P/Haemate P) often present with VWF and/or FVIII levels outside of prespecified target levels necessary to prevent bleeding. Pharmacokinetic (PK)-guided dosing may resolve this problem. As clinical guidelines increasingly recommend aiming for certain target levels of both VWF and FVIII, application of an integrated population PK model describing both VWF activity (VWF:Act) and FVIII levels may im
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5

Pipe, Steven W., Robert R. Montgomery, Kathleen P. Pratt, Peter J. Lenting, and David Lillicrap. "Life in the shadow of a dominant partner: the FVIII-VWF association and its clinical implications for hemophilia A." Blood 128, no. 16 (2016): 2007–16. http://dx.doi.org/10.1182/blood-2016-04-713289.

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Abstract A normal hemostatic response to vascular injury requires both factor VIII (FVIII) and von Willebrand factor (VWF). In plasma, VWF and FVIII normally circulate as a noncovalent complex, and each has a critical function in the maintenance of hemostasis. Furthermore, the interaction between VWF and FVIII plays a crucial role in FVIII function, immunogenicity, and clearance, with VWF essentially serving as a chaperone for FVIII. Several novel recombinant FVIII (rFVIII) therapies for hemophilia A have been in clinical development, which aim to increase the half-life of FVIII (∼12 hours) an
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6

Blasko, Eric, Lilley Leong, Derek S. Sim, et al. "Reduced Polyethylene Glycol-Conjugated B-Domain–Deleted Factor VIII (PEG-BDD-FVIII) Clearance: Selective Peg Steric Modulation without Affecting Potency." Blood 124, no. 21 (2014): 1471. http://dx.doi.org/10.1182/blood.v124.21.1471.1471.

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Abstract Prophylactic factor VIII (FVIII) replacement therapy in hemophilia A requires intravenous administration up to every other day due to the short half-life of FVIII in plasma. Plasma half-life extension of FVIII by polyethylene glycol (PEG) conjugation is thought to be mediated by decreasing hepatic clearance of FVIII. BAY 94-9027 is a rationally designed B-domain–deleted (BDD) FVIII molecule, in which a single 60-kDa PEG molecule was attached to a specific amino acid (1804) to increase its circulating half-life and reduce the exposure to epitopes reported to cause immunogenicity in the
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7

James, Andra H., Peter Kouides, Barbara A. Konkle, and Claire S. Philipp. "Transient Decrease in Factor VIII Following Delivery: Clearance or Consumption?" Blood 118, no. 21 (2011): 2286. http://dx.doi.org/10.1182/blood.v118.21.2286.2286.

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Abstract Abstract 2286 Background: Von Willebrand factor (VWF) and factor VIII (FVIII) levels increase during pregnancy and return to baseline by one month postpartum (PP). Understanding the normal levels during this period has implications for the management of women with bleeding disorders. As part of a larger study of von Willebrand disease (VWD) postpartum, we obtained VWF ristocetin cofactor (VWF:RCo), VWF antigen (VWF:Ag) and FVIII levels on 26 women without a known bleeding disorder to establish normal ranges during the PP period. Methods: Subjects were enrolled during the last trimeste
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8

Ogiwara, Kenichi, Laura L. Swystun, Ilinca Georgescu, et al. "Clearance and Genetic Variability of Von Willebrand Factor Are Major Determinants of the Pharmacokinetic Behavior of Factor VIII Concentrates in the Treatment of Pediatric Hemophilia A." Blood 124, no. 21 (2014): 473. http://dx.doi.org/10.1182/blood.v124.21.473.473.

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Abstract Background: Although Factor VIII (FVIII) concentrates are now routinely used for the prophylactic treatment of hemophilia A (HA), the optimal doses and intervals between administrations are difficult to predict because of variable pharmacokinetics of FVIII (FVIII-PK) between patients. Previous studies in HA have revealed a close relationship between FVIII-PK and the FVIII carrier protein, von Willebrand factor (VWF). A large genome-wide association study from the CHARGE consortium highlighted several novel loci associated with plasma levels of VWF and FVIII in normal subjects, and the
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9

Lenting, Peter J., Vincent Muczynski, Gabriel Aymé, Cecile V. Denis, and Olivier D. Christophe. "Von Willebrand Factor Interaction with FVIII: Development of Long Acting FVIII Therapies." Blood 128, no. 22 (2016): SCI—8—SCI—8. http://dx.doi.org/10.1182/blood.v128.22.sci-8.sci-8.

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Abstract Coagulation factor VIII (FVIII) and von Willebrand factor (VWF) both play a centrol role in hemostasis, illustrated by the severe bleeding disorders associated with their functional absence. Despite their different functionalities in hemostasis and being products from two different genes, both proteins circulate in a tight, non-covalently linked complex. The physiological concequences of complex formation are many, including stabilization of FVIII heterodimeric structure, protection of FVIII from protelytic degradation, and modulation of FVIII immunogenicity. Another relevant issue re
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10

Schambeck, C. M. "Das Janusgesicht der Einzelfaktoren." Hämostaseologie 27, no. 04 (2007): 268–72. http://dx.doi.org/10.1055/s-0037-1617092.

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ZusammenfassungDas Wissen um eine Blutungsneigung infolge Einzelfaktorenmangel ist Allgemeingut. Das Gegenteil – eine Thromboseneigung infolge hoher Einzelfaktorenspiegel – scheint nicht überraschend, doch erst in jüngster Zeit wurde ein Zusammenhang zwischen dem Spiegel von Einzelfaktoren und dem Risiko für venöse Thromboembolien beschrieben. Gut dokumentiert ist die Rolle hoher Faktor- VIII(FVIII)-Spiegel. Das Risiko für ein erstmaliges Thromboseereignis ist ähnlich hoch wie das Risiko infolge einer APC-Resistenz. Ein familiärer Hintergrund wurde für hohe FVIII-Spiegel beschrieben. Veränderu
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Dissertations / Theses on the topic "FVIII clearance"

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AGOSTI, PASQUALE. "POTENTIAL GENE VARIANTS INFLUENCING FVIII LEVELS: THE ROLE OF LDL RECEPTOR ON FVIII CLEARANCE." Doctoral thesis, Università degli Studi di Milano, 2022. http://hdl.handle.net/2434/924042.

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Background Genetic variants in the LDL receptor (LDLR) gene have been associated with higher LDL cholesterol levels, premature atherosclerotic cardiovascular disease (ASCVD) and increased cardiovascular risk. However, the increased arterial thrombotic risk observed in LDLR carriers is partly independent from the lipoprotein levels and could be related to the LDLR modulation of FVIII levels. Indeed, a role of LDLR in FVIII clearance has been shown and LDLR variants have been associated with higher FVIII levels. To date, it is not clear which are the LDLR variants involved in FVIII clearance a
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Book chapters on the topic "FVIII clearance"

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Kubisz, Peter, Pavol Holly, and Jan Stasko. "Bleeding in Patients with Antiphospholipid Antibodies." In Antiphospholipid Syndrome - Recent Advances in Basic and Clinical Aspects [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97856.

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The antiphospholipid antibodies (aPL) are commonly associated with thrombotic events and obstetric complications. However, apart from the bleeding complications of antithrombotic therapy, the acquired coagulopathy caused by the aPL, particularly by lupus anticoagulant and anticardiolipin antibodies, might be occasionally manifested as a hemorrhagic syndrome with various clinical severity. Bleeding symptoms vary from mild (mucocutaneous) up to life-threatening (gastrointestinal, intracranial). The bleeding may be the first manifestation of aPL or appear concomitantly with thrombosis. The underl
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2

Pulido Flores, Mariem, Ángel Gabriel Vargas Ruiz, Oscar Jaime Moreno García, and Elena Tuna Aguilar. "The Importance of Searching for Acquired von Willebrand Syndrome in Chronic Myeloproliferative Neoplasms." In Coagulation Disorders - Innovative Developments in Diagnostic and Therapeutic Approaches [Working Title]. IntechOpen, 2025. https://doi.org/10.5772/intechopen.1006940.

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Acquired von Willebrand syndrome is an entity unknown and misdiagnosed in most cases. It is a bleeding disorder presented with mild to moderate hemorrhagic symptoms secondary to lymphoproliferative disorders (and known as the most frequent cause of acquired von Willebrand syndrome), cardiovascular disease, myeloproliferative neoplasms (essential thrombocythemia, polycythemia vera, and chronic myeloid leukemia), autoimmune disease or solid neoplasms. The most known mechanisms of a von Willebrand antigen diminished consist of an increased degradation or clearance of circulating VWF. This occurs
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Conference papers on the topic "FVIII clearance"

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De Angelis, V., M. Zambon, L. Toffolo, C. Donada, G. L. Molaro, and R. Zuin. "ACTIVATION OF FACTOR VII IS RELATED TO BLEEDING TENDENCY IN LIVER CIRRHOSIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644800.

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Coagulation abnormalities are among the number of potential risk factors toinitiate the bleeding episodes from gastrcr-esophageal varices in liver cirrhosis. The impairment of liver clearance of activated coagulation factors, the release of thromboplastin-like activity from the necrotic liver cells and the hemodynamic changes due to expanded bollaterals may all contribute to activate the coagulation cascade.However, little is known about the mechanisms leading to this activation. Activated Factor VII (FVIIa) is known totrigger both intrinsec and extrinsec coagulation pathway. Therefore, we mea
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