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Inflammation-associated ADAMTS13 deficiency promotes formation of ultra-large von Willebrand factor.

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Inflammation-associated ADAMTS13 deficiency promotes formation of ultra-large von Willebrand factor. / Bockmeyer, Clemens L; Claus, Ralf A; Budde, Ulrich; Kentouche, Karim; Schneppenheim, Reinhard; Lösche, Wolfgang; Reinhart, Konrad; Brunkhorst, Frank M.

In: HAEMATOLOGICA, Vol. 93, No. 1, 1, 2008, p. 137-140.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Bockmeyer, CL, Claus, RA, Budde, U, Kentouche, K, Schneppenheim, R, Lösche, W, Reinhart, K & Brunkhorst, FM 2008, 'Inflammation-associated ADAMTS13 deficiency promotes formation of ultra-large von Willebrand factor.', HAEMATOLOGICA, vol. 93, no. 1, 1, pp. 137-140. https://doi.org/10.3324/haematol.11677

APA

Bockmeyer, C. L., Claus, R. A., Budde, U., Kentouche, K., Schneppenheim, R., Lösche, W., Reinhart, K., & Brunkhorst, F. M. (2008). Inflammation-associated ADAMTS13 deficiency promotes formation of ultra-large von Willebrand factor. HAEMATOLOGICA, 93(1), 137-140. [1]. https://doi.org/10.3324/haematol.11677

Vancouver

Bockmeyer CL, Claus RA, Budde U, Kentouche K, Schneppenheim R, Lösche W et al. Inflammation-associated ADAMTS13 deficiency promotes formation of ultra-large von Willebrand factor. HAEMATOLOGICA. 2008;93(1):137-140. 1. https://doi.org/10.3324/haematol.11677

Bibtex

@article{35a4990bd4664dc2a64b9025519ecd96,
title = "Inflammation-associated ADAMTS13 deficiency promotes formation of ultra-large von Willebrand factor.",
abstract = "In a prospective, longitudinal study, we investigated the association between decreased ADAMTS13 activity and impaired hemostasis, as well as organ dysfunctions in patients with systemic inflammation due to extracorporeal cardiopulmonary circuit or with severe sepsis. Similar to negative acute phase proteins, ADAMTS13 activity declined stepwise according to the extent of inflammatory responses. A marked imbalance between ADAMTS13 activity and VWF antigen level was associated with the appearance of ultra-large VWF multimers in plasma, with organ dysfunction and lethality. Our data support the view that systemic inflammation results in an ADAMTS13 deficiency which activates hemostasis.",
author = "Bockmeyer, {Clemens L} and Claus, {Ralf A} and Ulrich Budde and Karim Kentouche and Reinhard Schneppenheim and Wolfgang L{\"o}sche and Konrad Reinhart and Brunkhorst, {Frank M}",
year = "2008",
doi = "10.3324/haematol.11677",
language = "Deutsch",
volume = "93",
pages = "137--140",
journal = "HAEMATOLOGICA",
issn = "0390-6078",
publisher = "Ferrata Storti Foundation",
number = "1",

}

RIS

TY - JOUR

T1 - Inflammation-associated ADAMTS13 deficiency promotes formation of ultra-large von Willebrand factor.

AU - Bockmeyer, Clemens L

AU - Claus, Ralf A

AU - Budde, Ulrich

AU - Kentouche, Karim

AU - Schneppenheim, Reinhard

AU - Lösche, Wolfgang

AU - Reinhart, Konrad

AU - Brunkhorst, Frank M

PY - 2008

Y1 - 2008

N2 - In a prospective, longitudinal study, we investigated the association between decreased ADAMTS13 activity and impaired hemostasis, as well as organ dysfunctions in patients with systemic inflammation due to extracorporeal cardiopulmonary circuit or with severe sepsis. Similar to negative acute phase proteins, ADAMTS13 activity declined stepwise according to the extent of inflammatory responses. A marked imbalance between ADAMTS13 activity and VWF antigen level was associated with the appearance of ultra-large VWF multimers in plasma, with organ dysfunction and lethality. Our data support the view that systemic inflammation results in an ADAMTS13 deficiency which activates hemostasis.

AB - In a prospective, longitudinal study, we investigated the association between decreased ADAMTS13 activity and impaired hemostasis, as well as organ dysfunctions in patients with systemic inflammation due to extracorporeal cardiopulmonary circuit or with severe sepsis. Similar to negative acute phase proteins, ADAMTS13 activity declined stepwise according to the extent of inflammatory responses. A marked imbalance between ADAMTS13 activity and VWF antigen level was associated with the appearance of ultra-large VWF multimers in plasma, with organ dysfunction and lethality. Our data support the view that systemic inflammation results in an ADAMTS13 deficiency which activates hemostasis.

U2 - 10.3324/haematol.11677

DO - 10.3324/haematol.11677

M3 - SCORING: Zeitschriftenaufsatz

VL - 93

SP - 137

EP - 140

JO - HAEMATOLOGICA

JF - HAEMATOLOGICA

SN - 0390-6078

IS - 1

M1 - 1

ER -