458 Increased adhesion molecule levels in systemic lupus erythematosus: relationships with severity of illness, autoimmunity and cortisol levels

<h3>Background and aims</h3> To delineate disorders in adhesion molecules in systemic lupus erythematosus (SLE) and to assess whether cortisol, nuclear autoantibody (ANA) titers and the metabolic syndrome (MetS) are associated with adhesion molecules in SLE. <h3>Methods</h3> 48 healthy individuals and 171 SLE patients were enrolled. Disease activity was determined by SLEDAI (SLE Disease Activity Index) score. Adhesion molecules and cortisol levels were evaluated. <h3>Results</h3> Platelet endothelial cell adhesion molecule 1 (PECAM-1), Vascular cell adhesion molecule 1 (VCAM-1), E-selectin, P-selectin and Plasminogen activator inhibitor type-1 (PAI-1) were significantly higher in SLE patients. These significant differences could not be explained by the drug treatment. Mycophenolate treatment significantly decreased intercellular adhesion molecule 1 (ICAM-1) and increased E-selectin levels. Binary logistic regression analysis showed that PECAM-1 and PAI-1 predicted SLE with a sensitivity of 86.5% and a specificity of 81.3%. ANA was significantly and positively associated with PECAM-1, VCAM-1, E-selectin, and PAI-1, whilst cortisol was negatively associated with PCAM-1 and ICAM-1. There were significant associations between MetS and E-selectin and PAI-1. 18.2% of the variance in SLEDAI score was explained by increased PECAM-1 values and DNA titers and the MetS. <h3>Conclusions</h3> Our data confirm that adhesion molecules play a role in the pathophysiology of SLE and show that increased adhesion molecule levels, especially PECAM-1, can be used as an external validating criterion for the diagnosis SLE. MetS, ANA, and cortisol modulate the adhesion molecule concentrations but do not explain the increased levels in SLE Increased levels of adhesion molecules are a new drug target in SLE.