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Rheumatology Advance Access originally published online on September 13, 2005
Rheumatology 2005 44(12):1518-1524; doi:10.1093/rheumatology/kei088
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© The Author 2005. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Circulating levels of active transforming growth factor ß1 are reduced in diffuse cutaneous systemic sclerosis and correlate inversely with the modified Rodnan skin score

M. Dziadzio, R. E. Smith, D. J. Abraham, C. M. Black and C. P. Denton

Centre for Rheumatology and Connective Tissue Diseases, Royal Free and University College Medical School, University College, London, UK.

Correspondence to: C. P. Denton, Centre for Rheumatology, Royal Free and University College Medical School, University College London, Rowland Hill Street, London NW3 2PF, UK. E-mail: c.denton{at}medsch.ucl.ac.uk

Objectives. To determine the relationship between clinical features and circulating levels of active transforming growth factor (TGF) ß1 in the major subsets of systemic sclerosis (SSc).

Methods. In a cross-sectional study cases of diffuse cutaneous SSc (dose) (n=27) or limited cutaneous SSc (dose) (n=20) were compared with healthy controls (n=22). Active and total TGFß1 was measured in serum and plasma by a high-sensitivity enzyme-linked immunosorbent assay.

Results. There were no significant differences between levels of total serum TGFß1. However, cases of dcSSc had lower levels of active TGFß1 than cases of lcSSc or controls. In addition, more cases of dcSSc (18/27; 66%, P<0.025) had no detectable active TGFß1 than controls (7/22, 32%) or lcSSc (7/20, 35%). In dcSSc, serum active TGFß1 levels correlated negatively with skin score and positively with disease duration.

Conclusions. Contrary to expectation, levels of active TGFß1 are reduced in dcSSc and this correlates with two variables known to associate with disease activity, shorter duration and more extensive skin sclerosis. This suggests that active TGFß1 may be sequestered in active involved SSc skin and that serum levels are reduced despite strong evidence implicating TGFß isoforms in the pathogenesis of fibrosis. Our findings may have implications for systemic TGFß-trapping therapies in this disease.

KEY WORDS: Scleroderma, Systemic sclerosis, Biological markers, Severity of illness index, Transforming growth factor beta


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