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, Jahrgang 93, Nr. 1, 1, 2008, S. 137-140.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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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 -