Soluble form of vascular cell adhesion molecule-1 in systemic lupus erythematosus and discoid lupus erythematosus

The clinical symptoms of systemic lupus erythematosus (SLE) such as lupus nephritis, erythematous lesions and systemic vasculitis are caused by circulating immune complexes and anti-nuclear antibodies. These antibodies are primarily responsible for causing damage to the blood vessels especially through DNA-anti-DNA antibody complexes. Recent studies have indicated the importance of cell adhesion between vascular endothelium and activated leukocytes. Furthermore, soluble adhesion molecules have been reported to bind to their respective ligands after the stimulation of endothelial cells with various cytokines [ 1,2]. Recently the significance of soluble vascular cell adhesion molecule1 (sVCAM1) was reported by several investigators [3-51. Serum levels of sVCAM-1 were directly related to the severity of clinical disease activity; this suggests that immune complex formation and the up-regulation of adhesion molecules are intimately connected in SLE, and are included in the pathogenesis of this disease [4]. Of special interest is whether or not sVCAM-1 is a specific and sensitive marker for monitoring the disease course of SLE. In order to examine the role of the soluble forms of three adhesion molecules commonly localized on the vascular endothelium, we have determined the serum levels of sVCAM1, intercellular adhesion molecule-l (sICAM-1) and E-selectin (SE-selectin) in patients with discoid LE (DLE) as well as SLE. Thirty patients with SLE (4 males, 26 females; age range 14-64 years, average age 38.0 years), 10 patients with DLE (6 males, 4 females; age range 41-68 years, average age 55.2 years), 12 patients with psoriasis vulgaris as clinical control (8 males, 4 females, age range 31-43 years, average age 35.7 years) and 26 normal controls (10 males, 16 females; age range 20-68 years. average age 31.9 years) were studied. Sera from the SLE patients included 17 active cases and 13 inactive cases.