PMID- 11127848
OWN - NLM
STAT- MEDLINE
DCOM- 20010426
LR  - 20151119
IS  - 0340-6245 (Print)
IS  - 0340-6245 (Linking)
VI  - 84
IP  - 5
DP  - 2000 Nov
TI  - Systemic endothelial cell markers in primary antiphospholipid syndrome.
PG  - 742-6
AB  - The pathogenic mechanism underlying the prothrombotic tendency of Hughes' or 
      antiphospholipid syndrome (APS) has not been elucidated. Numerous procoagulant 
      mechanisms have been tested including platelet activation, monocyte tissue factor 
      (TF) expression and endothelial cell (EC) activation. There is some evidence for 
      the latter from studies on cultured human umbilical vein endothelial cells 
      (HUVEC). Incubation with antiphospholipid antibodies (aPL) induces EC activation 
      in vitro. We investigated whether there was evidence of EC perturbation in vivo 
      using enzyme-linked immunosorbant assays (ELISAs) for soluble markers of EC 
      dysfunction. Serum and plasma were collected from controls and patients with 
      primary APS and ELISAs performed to quantify soluble vascular cell adhesion 
      molecule (sVCAM), soluble intercellular adhesion molecule-1 (sICAM-1), 
      interleukin-6 (IL-6), endothelin-1 (ET-1), von Willebrand factor (vWF) and 
      soluble tissue factor (sTF). In addition, soluble p-selectin (p-selectin) and 
      vascular endothelial growth factor (VEGF) were measured: the former as a marker 
      of platelet activation, the latter as a potential mediator of TF expression. No 
      significant differences in the levels of blood-borne soluble markers were 
      detected between the patient and control groups except for VEGF and sTF, patients 
      having significantly higher levels of VEGF and sTF than controls (p <0.05). These 
      results suggest plasma soluble tissue factor and VEGF may play a role in the 
      pathogenesis of thrombosis in APS, although the cell of origin of these molecules 
      remains unclear.
FAU - Williams, F M
AU  - Williams FM
AD  - Department of Haematology and Lupus Research, St Thomas' Hospital, London, UK.
FAU - Parmar, K
AU  - Parmar K
FAU - Hughes, G R
AU  - Hughes GR
FAU - Hunt, B J
AU  - Hunt BJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Germany
TA  - Thromb Haemost
JT  - Thrombosis and haemostasis
JID - 7608063
RN  - 0 (Biomarkers)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Endothelial Growth Factors)
RN  - 0 (Lymphokines)
RN  - 0 (P-Selectin)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 0 (Vascular Endothelial Growth Factors)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Antiphospholipid Syndrome/*metabolism/*physiopathology
MH  - *Biomarkers
MH  - Cell Adhesion Molecules
MH  - Endothelial Growth Factors/*metabolism
MH  - Endothelium, Vascular/*metabolism/*physiopathology
MH  - Female
MH  - Humans
MH  - Lymphokines/*metabolism
MH  - Male
MH  - Middle Aged
MH  - P-Selectin/*metabolism
MH  - Platelet Activation
MH  - Vascular Endothelial Growth Factor A
MH  - Vascular Endothelial Growth Factors
EDAT- 2000/12/29 11:00
MHDA- 2001/05/01 10:01
CRDT- 2000/12/29 11:00
PHST- 2000/12/29 11:00 [pubmed]
PHST- 2001/05/01 10:01 [medline]
PHST- 2000/12/29 11:00 [entrez]
AID - 00110742 [pii]
PST - ppublish
SO  - Thromb Haemost. 2000 Nov;84(5):742-6.