Invited commentary to: ADAMTS13 deficiency is associated with abnormal distribution of von Willebrand factor multimers in patients with COVID-19 by Tiffany Pascreau et al. Letter to the Editors-in-Chief, Thrombosis Research

Lämmle, Bernhard; Rossmann, Heidi

doi:10.1016/j.thromres.2021.02.030

Cited by 2 publications

(1 citation statement)

References 28 publications

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“…COVID-19 patients with severe in ammatory reaction have high blood C5a serum levels, indicating vigorous complement activation that resulted in systemic TMA [13] . Recent studies [14,15] have also found a signi cant increasement of the VWF:Ag/ADAMTS13 ratio secondary to COVID-19 infection, which can explain the decrease of ADAMTS13 level in out report.…”

Section: Discussionmentioning

confidence: 77%

AHUS mistaken for TTP associated with COVID-19: a case report

Wang

Cong

et al. 2023

Preprint

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Thrombotic thrombocytopenic purpura (TTP) and atypical hemolytic uremic syndrome (aHUS) are both thrombotic microangiopathies that share several clinical traits including microangiopathic hemolytic anemia, thrombocytopenia, and organic damage. There is inherent opportunity for misdiagnosis. As thrombocytopenia and thrombus are strongly related to COVID-19, it may be more difficult to tell an aHUS from a TTP when COVID-19 is present. Thus, we describe a patient presenting with severe COVID-19 who was misdiagnosed with TTP but in the end corrected to aHUS. We suggest that perform detection to ADAMTS-13 activity and complement gene mutation as soon as possible is necessary.

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Section: Discussionmentioning

confidence: 77%

AHUS mistaken for TTP associated with COVID-19: a case report

Wang

Cong

et al. 2023

Preprint

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Low-density lipoprotein promotes microvascular thrombosis by enhancing von Willebrand factor self-association

Chung

Platten

Ozawa

et al. 2023

Blood

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Von Willebrand factor (VWF) mediates primary hemostasis and thrombosis in response to hydrodynamic forces. We previously showed that high shear promoted self-association of VWF into hyperadhesive strands, which can be attenuated by high density lipoprotein (HDL) and apolipoprotein(apo) A-I. Here, we show that low density lipoprotein (LDL) binds VWF under shear and enhances self-association. Vortexing VWF in tubes resulted in its loss from the solution and deposition onto tube surfaces, which was prevented by HDL. At a stabilizing HDL concentration of 1.2 mg/ml, increasing concentrations of LDL progressively increased VWF loss, the effect correlating with the LDL/HDL ratio and not the absolute concentration of the lipoproteins. Similarly, HDL diminished deposition of VWF in a post-in-channel microfluidic device, whereas LDL increased both the rate and extent of strand deposition, with both purified VWF and plasma. Hypercholesterolemic human plasma also displayed accelerated VWF accumulation in the microfluidic device. The initial rate of accumulation correlated linearly with the LDL/HDL ratio. In Adamts13-/- and Adamts13-/-LDLR-/-mice, high LDL levels enhanced VWF and platelet adhesion to the myocardial microvasculature, reducing cardiac perfusion, impairing systolic function, and producing early signs of cardiomyopathy. In wild-type mice, high plasma LDL concentrations also increased the size and persistence of VWF-platelet thrombi in ionophore-treated mesenteric microvessels, exceeding even that seen in similarly treated ADAMTS13-deficient mice that did not receive LDL infusion. We propose that targeting the interaction of VWF with itself and with LDL may improve the course of thrombotic microangiopathies, atherosclerosis, and other disorders with defective microvascular circulation.

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Invited commentary to: ADAMTS13 deficiency is associated with abnormal distribution of von Willebrand factor multimers in patients with COVID-19 by Tiffany Pascreau et al. Letter to the Editors-in-Chief, Thrombosis Research

Cited by 2 publications

References 28 publications

AHUS mistaken for TTP associated with COVID-19: a case report

AHUS mistaken for TTP associated with COVID-19: a case report

Low-density lipoprotein promotes microvascular thrombosis by enhancing von Willebrand factor self-association

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