Standardization and comparison of nonautomated assays to measure the collagen binding activity of von Willebrand factor

Oliveira, Larissa Maira Moura de; Amorim, MM; Corsini, Camila Amormino; Neto, C. C. A.; Chaves, Daniel Gonçalves

doi:10.1111/ijlh.12874

Cited by 3 publications

(2 citation statements)

References 27 publications

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“…The latter were studied with SDS–agarose gel electrophoresis (0.8% agarose, stacking gel −1.5% agarose, running gel), as previously detailed . The deficiency of high‐molecular‐weight multimers of VWF was defined by the VWF:Act/VWF:Ag ratio < 0.6, that has been shown to reflect a loss of high‐molecular‐weight multimers, as in the case of type 2A or 2B von Willebrand disease . FVIII levels were measured by an ELISA method (Diagnostica Stago).…”

Section: Methodsmentioning

confidence: 99%

Increased von Willebrand factor levels in polycythemia vera and phenotypic differences with essential thrombocythemia

Sacco

Ranalli

Lancellotti

et al. 2020

Research and Practice in Thrombosis and Haemostasis

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Background Acquired von Willebrand factor (VWF) deficiency was described in Philadelphia‐negative myeloproliferative neoplasms, especially in essential thrombocythemia (ET). VWF phenotype in contemporary patients with polycythemia vera (PV) remains less explored. Objectives To characterize the VWF phenotype in PV and to compare VWF phenotype in PV with matched healthy subjects and ET patients. Patients/Methods We studied 48 PV patients, treated according to current recommendations (hematocrit ≤ 45%, on low‐dose aspirin prophylaxis); 48 healthy and 41 subjects with ET, all sex, age, and blood group matched. We measured VWF antigen, activity, multimeric pattern, ADAMTS‐13, and factor VIII (FVIII) antigen. Results In patients with PV, VWF antigen and activity were significantly higher than in healthy subjects (antigen: 119[96‐137] vs 93[79‐107] IU/dL; activity: 114[95‐128] vs 90[79‐107] IU/dL, respectively, medians and interquartile, P < 0.01), with normal multimeric distribution. ADAMTS‐13 levels were similar between patients with PV and healthy subjects. FVIII levels were higher in PV than in healthy subjects (141[119‐169] versus 98[88‐123] IU/dL, respectively, P < 0.01). By multivariable analysis, JAK2‐p.V617F allelic burden, erythrocyte count, and male sex significantly predicted VWF antigen and activity levels. As compared to patients with ET, patients with PV showed similar VWF antigen levels but approximately 40% higher activity (79[49‐104] vs 112[93‐125] IU/dL, respectively, P < 0.01). Conclusions Patients with PV show increased VWF and FVIII levels, predicted by JAK2‐p.V617F burden and erythrocyte count. At variance with ET, acquired VWF defect was not observed in PV. High VWF/FVIII levels may sustain the thrombotic diathesis of PV and may be investigated as biomarkers for risk stratification.

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Section: Methodsmentioning

confidence: 99%

Increased von Willebrand factor levels in polycythemia vera and phenotypic differences with essential thrombocythemia

Sacco

Ranalli

Lancellotti

et al. 2020

Research and Practice in Thrombosis and Haemostasis

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“…VWF:Ag, VWF:RCo, and VWF:CB were elevated in both cirrhotic groups, with 24/54 AD patients showing presence of ultra-large VWF multimers, with this also associated with low ADAMTS13 activity and high CRP levels. Oliveira et al 280 compared three nonautomated VWF:CB assays, two by ELISA and the other by flow cytometry. The ELISA assays could differentiate 2A and 2M VWD.…”

Section: A History Of the Von Willebrand Factor Collagen-binding Assaymentioning

confidence: 99%

The Role of the von Willebrand Factor Collagen-Binding Assay (VWF:CB) in the Diagnosis and Treatment of von Willebrand Disease (VWD) and Way Beyond: A Comprehensive 36-Year History

Favaloro

2023

Semin Thromb Hemost

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The von Willebrand factor (VWF) collagen binding (VWF:CB) assay was first reported for use in von Willebrand diagnostics in 1986, by Brown and Bosak. Since then, the VWF:CB has continued to be used to help diagnose von Willebrand disease (VWD) (correctly) and also to help assign the correct subtype, as well as to assist in the monitoring of VWD therapy, especially desmopressin (DDAVP). However, it is important to recognize that the specific value of any VWF:CB is predicated on the use of an optimized VWF:CB, and that not all VWF:CB assays are so optimized. There are some good commercial assays available, but there are also some “not-so-good” commercial assays available, and these may continue to give the VWF:CB “a bad reputation.” In addition to VWD diagnosis and management, the VWF:CB found purpose in a variety of other applications, from assessing ADAMTS13 activity, to investigation into acquired von Willebrand syndrome (especially as associated with use of mechanical circulatory support or cardiac assist devices), to assessment of VWF activity in disease states in where an excess of high-molecular-weight VWF may accumulate, and lead to increased (micro)thrombosis risk (e.g., coronavirus disease 2019, thrombotic thrombocytopenic purpura). The VWF:CB turns 37 in 2023. This review is a celebration of the utility of the VWF:CB over this nearly 40-year history.

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ADAMTS-13–VWF axis in sickle cell disease patients

et al. 2021

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Standardization and comparison of nonautomated assays to measure the collagen binding activity of von Willebrand factor

Abstract: The ELISA test demonstrated better performance to detect VWF-collagen binding activity in healthy individuals and VWD patients. This test could differentiate 2A and 2M subtypes using a feasible protocol that can be easily implemented.

Cited by 3 publications

References 27 publications

Increased von Willebrand factor levels in polycythemia vera and phenotypic differences with essential thrombocythemia

Increased von Willebrand factor levels in polycythemia vera and phenotypic differences with essential thrombocythemia

The Role of the von Willebrand Factor Collagen-Binding Assay (VWF:CB) in the Diagnosis and Treatment of von Willebrand Disease (VWD) and Way Beyond: A Comprehensive 36-Year History

ADAMTS-13–VWF axis in sickle cell disease patients

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