coagulation activation <<

"Markers of **hemolysis** are associated with coagulation activation"

Haematologica, Vol 93, Issue 1, 20-26

Red Cell Disorders

Coagulation activation and inflammation in sickle cell disease-
associated pulmonary hypertension
Kenneth I. Ataga1,, Charity G. Moore1, Cheryl A. Hillery2, Susan
Jones1, Herbert C. Whinna3, Dell Strayhorn1, Cathy Sohier4, Alan
Hinderliter1, Leslie V. Parise5, Eugene P. Orringer1
1 Department of Medicine, University of North Carolina, Chapel Hill
2 Department of Pediatrics, Medical College of Wisconsin, Milwaukee
3 Department of Pathology and Laboratory Medicine, University of North
Carolina, Chapel Hill
4 McLendon Clinical Laboratories, University of North Carolina
Hospitals, Chapel Hill and
5 Department of Biochemistry and Biophysics, University of North
Carolina, Chapel Hill, USA

Correspondence: Kenneth I. Ataga, MBBS, Division of Hematology/
Oncology, University of North Carolina at Chapel Hill, CB# 7305, 3009
Old Clinic Bldg Chapel Hill, NC 27599-7305, USA. E-mail:
kataga@med.unc.edu

Background: Pulmonary hypertension (PHT) is common in sickle cell
disease (SCD). The purpose of this study was to determine whether
markers of coagulation activation and inflammation are associated with
PHT in SCD.

Design and Methods: This cross-sectional study was performed using a
cohort of patients followed at an adult Sickle Cell Clinic. Pulmonary
artery systolic pressure was determined by Doppler echocardiography,
and the diagnosis of PHT was defined using age, sex and body mass
index-adjusted reference ranges. Clinical laboratory examinations,
including hematologic studies and biochemical tests, as well as
various measures of coagulation activation, endothelial activation and
inflammation, were conducted on SCD subjects and on healthy, race-
matched control subjects without SCD.

Results: Patients with SCD (n=76) had higher plasma levels of markers
of coagulation (thrombin-antithrombin complex, prothrombin fragment
F1+2, D-dimer) and endothelial (soluble vascular endothelial cell
adhesion molecule, sVCAM) activation compared with control subjects
(n=6). SCD patients with PHT (n=26) had significantly higher levels of
sVCAM compared with those patients without PHT (n=50). Although PHT
patients showed increased plasma measures of coagulation activation,
the differences were not statistically significant when compared to
those of patients without PHT. HbSS patients with PHT also had a trend
towards higher levels of other inflammatory cytokines (interleukins 6,
8 and 10) than HbSS patients without PHT. There was a modest negative
correlation between hemoglobin and plasma measures of coagulation and
endothelial activation, and modest positive correlations between
markers of hemolysis and plasma measures of coagulation and
endothelial activation.

Conclusions: SCD patients with PHT have higher levels of markers of
endothelial activation and other inflammatory markers than patients
without PHT. A trend towards an increased level of markers of
coagulation activation was observed in SCD patients with PHT compared
with that in patients without PHT. Markers of hemolysis are associated
with coagulation activation and endothelial dysfunction in SCD
patients. Clinical trials of anticoagulants and anti-inflammatory
agents are warranted in SCD patients with PHT.

Key words: sickle cell disease, coagulation activation, endothelial
activation, inflammation, pulmonary hypertension.
doi:10.3324/haematol.11763
Copyright © 2008 by Ferrata Storti Foundation This Article

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