Serum autoantibodies profile and increased levels of circulating intercellular adhesion molecule-1: a reflection of the immunologically mediated systemic vasculopathy in rheumatic diseases?

The clinical manifestation of systemic vasculitis may be postulated as a consequence of immune response abnormalities in the course of connective tissue diseases (CTD). The aim of this study was to elucidate the significance of the different autoantibodies and soluble intercellular adhesion molecule 1 (sICAM-1) being shed into the circulation in the diagnosis of vasculitis in rheumatic diseases. Sera of 86 patients with rheumatic diseases (54 with rheumatoid arthritis (RA) and 32 with CTD) were analyzed for the concentrations of sICAM-1 levels by the enzyme-linked immunosorbent assay (ELISA). Control sera were obtained from 30 healthy individuals. Anti-nuclear antibodies (ANA), anti-double-stranded DNA (anti-dsDNA) antibodies and anti-proteinase 3 (PR-3) antibodies (cytoplasmic specific anti-neutrophil cytoplasmic autoantibodies, cANCA) were assessed by the ELISA method. Fifty out of the 86 patients had systemic lesions. A pathological picture of the vascular loop under nailfold capillary microscopy was found in 84 patients. In 19 patients the microvascular changes were advanced, in 35 moderate and in 30 mild. All patients with articular manifestations had pathological changes under capillary microscopy. Patients with advanced changes under capillary microscopy had longer disease durations than patients with a mild intensity of vasculitis. The serum concentrations of sICAM-1 were significantly increased in RA and CTD patients compared with 30 controls (in both cases p<0.001). Moreover, RA and CTD patients with systemic vasculitis showed significantly higher levels of sICAM-1 than those without vascular involvement (p<0.001 and p<0.005 respectively). ANA were observed in significantly elevated concentration among RA and CTD patients with the systemic damage compared with patients without organ injury (p<0.001 and p<0.05 respectively). Also, cANCA levels were two-fold higher, but only among CTD patients with systemic damage (p<0.05). Serum concentrations of sICAM-1 were elevated in the patients showing the presence of ANA antibodies (p<0.05). Significant correlations between ANA level and disease duration and hemoglobin concentration were observed. The concentrations of cANCA correlated with those of rheumatoid factor and of dsDNA with patient age. We conclude that systemic lesions in the course of RA and CTD are accompanied by the microvascular injury observed under nailfold capillary microscopy. Our data suggest that sICAM-1, ANA and cANCA serum levels may reflect the extent of the vascular involvement in RA and CTD patients.