RGD Reference Report - Plasma levels of tissue factor and soluble E-selectin in sickle cell disease: relationship to genotype and to inflammation. - Rat Genome Database

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Plasma levels of tissue factor and soluble E-selectin in sickle cell disease: relationship to genotype and to inflammation.

Authors: Mohan, JS  Lip, GY  Wright, J  Bareford, D  Blann, AD 
Citation: Mohan JS, etal., Blood Coagul Fibrinolysis. 2005 Apr;16(3):209-14.
RGD ID: 11341683
Pubmed: PMID:15795541   (View Abstract at PubMed)

BACKGROUND: Microvascular occlusion, the pathophysiological hallmark of sickle cell disease (SCD), is a complex multifactorial process with alterations in coagulation, endothelial function and inflammation. However, relationships between these process in the two most common genotypes, HbSS and HbSC, are unknown. We hypothesized differences in the hypercoagulable state [as assessed by tissue factor (TF), fibrinogen and D-dimer], endothelial function [markers soluble E-selectin (sE-sel) and von Willebrand factor (vWf)], and inflammation [markers interleukin-6 (IL-6) and high-sensitivity C-reactive protein (hsCRP)] in these two SCD genotypes. Citrated plasma TF, sE-sel, vWf, fibrinogen and fibrin D-dimer, and serum IL-6 and hsCRP (enzyme-linked immunosorbent assay/Clauss) were measured in 64 patients with SCD (27 with HbSS disease) and 42 AA subjects matched for age and ethnic origin. TF (P = 0.0014), sE-sel (P = 0.001) and, as expected, vWf, D-dimer, and hsCRP (all P < or = 0.01), but not fibrinogen or IL-6, were raised in the SCD patients compared with the AA subjects. However, only vWf and, as expected, D-dimer (all P < or = 0.01) were higher in HbSS disease than in HbSC disease. Raised plasma TF and sE-sel in SCD compared with HbAA subjects may contribute to the increased risk of thrombotic disease in this group. Raised vWf in HbSS compared with HbSC may be important in determining pathophysiology in these two genotypes. Positive correlations between IL-6 and TF in both HbSC and HbSS disease leads us to speculate that inflammation may be important in coagulation activation in these patients, or vice versa. However, lack of correlation of sE-sel with inflammatory markers implies that other mechanisms are responsible for increased levels of this marker of endothelial activation.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
F3Ratsickle cell anemia  ISOF3 (Homo sapiens)protein:increased expression:plasmaRGD 
F3Mousesickle cell anemia  ISOF3 (Homo sapiens)protein:increased expression:plasmaRGD 
F3Humansickle cell anemia  IEP protein:increased expression:plasmaRGD 

Objects Annotated

Genes (Rattus norvegicus)
F3  (coagulation factor III, tissue factor)

Genes (Mus musculus)
F3  (coagulation factor III)

Genes (Homo sapiens)
F3  (coagulation factor III, tissue factor)


Additional Information