Skip Navigation


Rheumatology Advance Access originally published online on May 13, 2008
Rheumatology 2008 47(7):972-975; doi:10.1093/rheumatology/ken100
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Supplementary Data
Right arrow All Versions of this Article:
47/7/972    most recent
ken100v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Wipff, J.
Right arrow Articles by Allanore, Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wipff, J.
Right arrow Articles by Allanore, Y.
Related Collections
Right arrow Systemic Sclerosis
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2008. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Disturbed angiogenesis in systemic sclerosis: high levels of soluble endoglin

J. Wipff1,2,*, J. Avouac1,2,*, D. Borderie3, D. Zerkak1, H. Lemarechal3, A. Kahan1, C. Boileau2,4 and Y. Allanore1,2

1Department of Rheumatology A, Paris Descartes University, Medical Faculty, Cochin Hospital, 2INSERM U781, Paris Descartes University, Necker Hospital, 3Department of Biochemistry A, Cochin Hospital, Paris and 4Department of Biochemistry, UVSQ, Medical Faculty, A, Paré Hospital, Boulogne-Billancourt, France.

Correspondence to: Y. Allanore, Service de Rhumatologie A, Hôpital Cochin, 27 Rue du Faubourg St Jacques, 75014 Paris, France. E-mail: yannick.allanore{at}cch.aphp.fr


   Abstract

Objective. SSc is a CTD characterized by early generalized microangiopathy with disturbed angiogenesis. Soluble endoglin (sENG), a serum anti-angiogenic protein, has recently been described as a major actor in pre-eclampsia, another severe vascular disease with abnormal angiogenesis. The aim of this study was to investigate, in a cross-sectional study, sENG levels together with other serum vascular markers.

Methods. Serum levels of sENG were assessed by ELISA in consecutive SSc patients and controls matched for age and sex. We also measured by ELISA serum levels of VEGF and asymmetric dimethylarginine (ADMA), as respective markers of angiogenesis and endothelial dysfunction.

Results. We included 235 unrelated subjects: 187 SSc patients and 48 controls. Higher concentrations of sENG (P = 0.002) and sVEGF (P < 0.0001) were found in SSc patients compared with controls whereas there was no difference for ADMA. In multivariate analysis, sENG levels were significantly increased in SSc patients with cutaneous ulcerations (P = 0.0003), positive for ACAs (P = 0.009) and with abnormal diffusing capacity for carbon monoxide divided by alveolar volume (P = 0.03). Soluble ENG levels negatively correlated with ADMA, but no relationship was found between sENG and sVEGF.

Conclusion. This study shows increased values of sENG in a large SSc cohort and a relevant association with a vascular phenotype. The predictive value of the biomarker sENG and its potential role on cellular endothelial disturbances remain to be determined.

KEY WORDS: Systemic sclerosis, Soluble endoglin, Asymmetric dimethylarginine, Soluble vascular endothelial growth factor


*J Wipff and J Avouac equally contributed to this work.

Submitted 19 October 2007; revised version accepted 8 February 2008.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.