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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Haematologica
2016 ; 101
(11
): 1319-1326
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Human neutrophil peptides and complement factor Bb in pathogenesis of acquired
thrombotic thrombocytopenic purpura
#MMPMID27662014
Cao W
; Pham HP
; Williams LA
; McDaniel J
; Siniard RC
; Lorenz RG
; Marques MB
; Zheng XL
Haematologica
2016[Nov]; 101
(11
): 1319-1326
PMID27662014
show ga
Acquired thrombotic thrombocytopenic purpura is primarily caused by the
deficiency of plasma ADAMTS13 activity resulting from autoantibodies against
ADAMTS13. However, ADAMTS13 deficiency alone is often not sufficient to cause
acute thrombotic thrombocytopenic purpura. Infections or systemic inflammation
may precede acute bursts of the disease, but the underlying mechanisms are not
fully understood. Herein, 52 patients with acquired autoimmune thrombotic
thrombocytopenic purpura and 30 blood donor controls were recruited for the
study. The plasma levels of human neutrophil peptides 1-3 and complement
activation fragments (i.e. Bb, iC3b, C4d, and sC5b-9) were determined by
enzyme-linked immunosorbent assays. Univariate analyses were performed to
determine the correlation between each biomarker and clinical outcomes. We found
that the plasma levels of human neutrophil peptides 1-3 and Bb in patients with
acute thrombotic thrombocytopenic purpura were significantly higher than those in
the control (P<0.0001). The plasma levels of HNP1-3 correlated with the levels of
plasma complement fragment Bb (rho=0.48, P=0.0004) and serum lactate
dehydrogenase (rho=0.28, P=0.04); in addition, the plasma levels of Bb correlated
with iC3b (rho=0.55, P<0.0001), sC5b-9 (rho=0.63, P<0.0001), serum creatinine
(rho=0.42, p=0.0011), and lactate dehydrogenase (rho=0.40, P=0.0034),
respectively. Moreover, the plasma levels of iC3b and sC5b-9 were correlated
(rho=0.72, P<0.0001), despite no statistically significant difference of the two
markers between thrombotic thrombocytopenic purpura patients and the control. We
conclude that innate immunity, i.e. neutrophil and complement activation via the
alternative pathway, may play a role in the pathogenesis of acute autoimmune
thrombotic thrombocytopenic purpura, and a therapy targeted at these pathways may
be considered in a subset of these patients.
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