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Conference Paper: Endothelial dysfunction is associated with decreased circulating endothelial progenitor cells in pateints with systemic cclerosis
Title | Endothelial dysfunction is associated with decreased circulating endothelial progenitor cells in pateints with systemic cclerosis |
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Authors | |
Issue Date | 2009 |
Publisher | BMJ Publishing Group. The Journal's web site is located at http://ard.bmjjournals.com/ |
Citation | The 2009 ACR/ARHP Annual Scientific Meeting, Philadelphia, PA., 16-21 October 2009. In Annals of the Rheumatic Diseases, 2009, v. 60 n. S10, p. 1710 How to Cite? |
Abstract | Background:
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. |
Persistent Identifier | http://hdl.handle.net/10722/223461 |
ISSN | 2021 Impact Factor: 27.973 2020 SCImago Journal Rankings: 6.333 |
DC Field | Value | Language |
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dc.contributor.author | Mok, TMY | - |
dc.contributor.author | Tse, HF | - |
dc.contributor.author | Lo, Y | - |
dc.contributor.author | Wong, RWS | - |
dc.contributor.author | Lau, WCS | - |
dc.date.accessioned | 2016-02-29T03:03:40Z | - |
dc.date.available | 2016-02-29T03:03:40Z | - |
dc.date.issued | 2009 | - |
dc.identifier.citation | The 2009 ACR/ARHP Annual Scientific Meeting, Philadelphia, PA., 16-21 October 2009. In Annals of the Rheumatic Diseases, 2009, v. 60 n. S10, p. 1710 | - |
dc.identifier.issn | 0003-4967 | - |
dc.identifier.uri | http://hdl.handle.net/10722/223461 | - |
dc.description.abstract | Background: 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.language | eng | - |
dc.publisher | BMJ Publishing Group. The Journal's web site is located at http://ard.bmjjournals.com/ | - |
dc.relation.ispartof | Annals of the Rheumatic Diseases | - |
dc.rights | Annals of the Rheumatic Diseases. Copyright © BMJ Publishing Group. | - |
dc.title | Endothelial dysfunction is associated with decreased circulating endothelial progenitor cells in pateints with systemic cclerosis | - |
dc.type | Conference_Paper | - |
dc.identifier.email | Mok, TMY: temy@hkucc.hku.hk | - |
dc.identifier.email | Tse, HF: hftse@hkucc.hku.hk | - |
dc.identifier.email | Lai, KWH: kwhlai@hku.hk | - |
dc.identifier.email | Lo, Y: yloa@HKUCC.hku.hk | - |
dc.identifier.email | Wong, RWS: rwswong@HKUCC.hku.hk | - |
dc.identifier.email | Lau, WCS: cslau@hku.hk | - |
dc.identifier.authority | Mok, TMY=rp00490 | - |
dc.identifier.authority | Tse, HF=rp00428 | - |
dc.identifier.authority | Lau, WCS=rp01348 | - |
dc.description.nature | abstract | - |
dc.identifier.doi | 10.1002/art.26784 | - |
dc.identifier.hkuros | 160321 | - |
dc.identifier.volume | 60 | - |
dc.identifier.issue | suppl. 10 | - |
dc.identifier.spage | 1710 | - |
dc.identifier.epage | 1710 | - |
dc.publisher.place | United Kingdom | - |
dc.identifier.issnl | 0003-4967 | - |