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Conference Paper: Endothelial dysfunction is associated with decreased circulating endothelial progenitor cells in patients with systemic sclerosis

TitleEndothelial dysfunction is associated with decreased circulating endothelial progenitor cells in patients with systemic sclerosis
Authors
KeywordsMedical sciences
Rheumatology
Issue Date2009
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0004-3591/
Citation
The 2009 ACR/ARHP Annual Scientific Meeting, Philadelphia, PA., 16-21 October 2009. In Arthritis & Rheumatism, 2009, v. 60 suppl. 10 How to Cite?
AbstractBACKGROUND: The role of circulating bone marrow derived endothelial progenitor cells (EPCs) for vascular repair in scleroderma (SSc) remains unclear. PURPOSE: To examine endothelial dysfunction in SSc patients and to correlate findings with biochemical markers of endothelial injury, circulating EPC count, disease activity and organ involvement. METHODS: Endothelial dependent and independent vasodilation responses were assessed by changes in flow mediated dilation (FMD%) and nitroglycerin challenge (NTG%) in the brachial artery respectively in SSc patients compared to age- and sex- matched controls. Serum levels of vascular endothelial growth factor (VEGF) and soluble vascular cell adhesion molecule (sVCAM)-1 were measured by ELISA. Enumeration of circulating CD133/VEGFR2+ EPCs was performed by flow cytometry. RESULTS: Median FMD% (4.8% vs. 7.8%, P<0.001) and NTG% (17.0% vs. 21.4%, P=0.002) were found to be significantly lower in SSc patients (n=52) than controls (n=52), especially in patients with limited disease (lSSc). Median circulating EPC count was significantly lower in lSSc patients (23.0/ml) compared to controls (73.0/ml) (P<0.001). This was accompanied by higher level of sVCAM-1 in these patients compared to those with diffuse disease (P=0.01). Lower circulating EPC count was found to be associated with high disease activity (P=0.04), abnormal forced vital capacity (P=0.003), longer disease duration (P=0.04), total skin score>20 (P=0.03) and lSSc subset (P<0.001). Multivariate analysis identified disease duration as the only independent predictor for circulating EPC count (P=0.04). CONCLUSION: Endothelial dysfunction was demonstrated in SSc and correlated with biochemical markers of endothelial injury. Lower circulating EPCs might contribute to deficient vascular repair in SSc patients.
DescriptionThis journal supplement is the Abstracts of the 2009 ACR/ARHP Annual Scientific Meeting http://www.blackwellpublishing.com/acrmeeting/
Open Access Journal
Persistent Identifierhttp://hdl.handle.net/10722/129835
ISSN
2015 Impact Factor: 8.955
2015 SCImago Journal Rankings: 3.206

 

DC FieldValueLanguage
dc.contributor.authorMok, TMYen_US
dc.contributor.authorTse, HFen_US
dc.contributor.authorLo, Yen_US
dc.contributor.authorWong, RWSen_US
dc.contributor.authorLau, WCSen_US
dc.date.accessioned2010-12-23T08:42:46Z-
dc.date.available2010-12-23T08:42:46Z-
dc.date.issued2009en_US
dc.identifier.citationThe 2009 ACR/ARHP Annual Scientific Meeting, Philadelphia, PA., 16-21 October 2009. In Arthritis & Rheumatism, 2009, v. 60 suppl. 10en_US
dc.identifier.issn0004-3591-
dc.identifier.urihttp://hdl.handle.net/10722/129835-
dc.descriptionThis journal supplement is the Abstracts of the 2009 ACR/ARHP Annual Scientific Meeting http://www.blackwellpublishing.com/acrmeeting/-
dc.descriptionOpen Access Journal-
dc.description.abstractBACKGROUND: The role of circulating bone marrow derived endothelial progenitor cells (EPCs) for vascular repair in scleroderma (SSc) remains unclear. PURPOSE: To examine endothelial dysfunction in SSc patients and to correlate findings with biochemical markers of endothelial injury, circulating EPC count, disease activity and organ involvement. METHODS: Endothelial dependent and independent vasodilation responses were assessed by changes in flow mediated dilation (FMD%) and nitroglycerin challenge (NTG%) in the brachial artery respectively in SSc patients compared to age- and sex- matched controls. Serum levels of vascular endothelial growth factor (VEGF) and soluble vascular cell adhesion molecule (sVCAM)-1 were measured by ELISA. Enumeration of circulating CD133/VEGFR2+ EPCs was performed by flow cytometry. RESULTS: Median FMD% (4.8% vs. 7.8%, P<0.001) and NTG% (17.0% vs. 21.4%, P=0.002) were found to be significantly lower in SSc patients (n=52) than controls (n=52), especially in patients with limited disease (lSSc). Median circulating EPC count was significantly lower in lSSc patients (23.0/ml) compared to controls (73.0/ml) (P<0.001). This was accompanied by higher level of sVCAM-1 in these patients compared to those with diffuse disease (P=0.01). Lower circulating EPC count was found to be associated with high disease activity (P=0.04), abnormal forced vital capacity (P=0.003), longer disease duration (P=0.04), total skin score>20 (P=0.03) and lSSc subset (P<0.001). Multivariate analysis identified disease duration as the only independent predictor for circulating EPC count (P=0.04). CONCLUSION: Endothelial dysfunction was demonstrated in SSc and correlated with biochemical markers of endothelial injury. Lower circulating EPCs might contribute to deficient vascular repair in SSc patients.-
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0004-3591/-
dc.relation.ispartofArthritis & Rheumatismen_US
dc.rightsArthritis & Rheumatism. Copyright © John Wiley & Sons, Inc.-
dc.subjectMedical sciences-
dc.subjectRheumatology-
dc.titleEndothelial dysfunction is associated with decreased circulating endothelial progenitor cells in patients with systemic sclerosisen_US
dc.typeConference_Paperen_US
dc.identifier.emailMok, TMY: temy@hkucc.hku.hken_US
dc.identifier.emailTse, HF: hftse@hkucc.hku.hken_US
dc.identifier.emailLo, Y: yloa@hkucc.hku.hken_US
dc.identifier.emailWong, RWS: rwswong@hkucc.hku.hken_US
dc.identifier.emailLau, WCS: cslau@hku.hken_US
dc.identifier.authorityMok, TMY=rp00490en_US
dc.identifier.authorityTse, HF=rp00428en_US
dc.identifier.authorityLau, WCS=rp01348en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1002/art.27423-
dc.identifier.hkuros177401en_US
dc.identifier.volume60en_US
dc.identifier.issuesuppl. 10-
dc.publisher.placeUnited States-

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