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Increased titres of IgM anti-heparan sulfate antibody in Behçet's disease

C. Briani, A. Doria, R. Marcolongo, S. Tognon, S. Ruggero, E. Toffanin, M. Ermani, A. Ghirardello, S. Zampieri, G. Semenzato

Department of Neurosciences, University of Padova, Padova, Italy

CER2854
2006 Vol.24, N°5 ,Suppl.42 - PI 0104, PF 0107
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Rheumatology Article

 

Abstract

OBJECTIVES:
Endothelial dysfunction is crucial in Behçet`s disease (BD) pathogenesis, and measures of endothelial damage are potential markers of BD activity. Heparan sulfate (HS) is the most abundant proteoglycan in the endothelial cells, and anti-HS antibodies have been reported in subjects with vascular damage, due to vasculitis/vasculopathy. The aim of our study was to measure serum anti-HS antibodies in patients with BD and to determine whether their presence correlates with disease activity or clinical manifestations.
METHODS:
Thirty-two patients with BD (21 men, 11 women) (median age 36.81±12.0 years) were considered. Of these, 13 had clinically active disease at the time of study. The mean disease duration was 7.31± 8.2 years (median 6 years). Anti-HS antibodies were measured by ELISA. As controls, sera from 40 sex- and age-matched healthy subjects, and 78 age-matched patients with systemic lupus erythematosus (SLE) were studied.
RESULTS:
Anti-HS IgM antibody titres were significantly higher in BD patients compared to healthy subjects (p=0.016) and SLE controls (p=0.0008). No differences in anti-HS IgG antibody titres were observed among the 3 groups. Using categorical data, increased titres of IgM anti-HS antibodies were significantly more frequent in patients with BD vs patients with SLE (p=0.02). The presence of the antibodies, of either isotype, did not correlate with disease duration, disease activity or clinical manifestations.
CONCLUSIONS:
BD patients have increased IgM anti-HS antibody titres compared to healthy and SLE controls. These antibodies did not correlate with disease activity or discrete clinical features, but might be relevant for pathogenic mechanisms of the disease.

PMID: 17067438 [PubMed]