Tumor necrosis factor induced adhesion molecule serum concentrations in Henoch-Schonlein purpura and pediatric systemic lupus erythematosus

Objective. Animal models of immune complex mediated tissue injury have show n that tumor necrosis factor (TNF) and TNF induced adhesion molecules play an important role in the pathogenesis of tissue damage mediated by IgG, but not in that mediated by IgA, immune complexes. We compared possible differ ences in the behavior of 2 TNF induced adhesion molecules (VCAM-1 and ICAM- 1) in Henoch-Schonlein purpura (HSP), which is characterized by the formati on of IgA immune complexes, versus systemic lupus erythematosus (SLE), whic h is mostly associated with the vascular deposition of IgG immune complexes . Methods. Serum concentrations of soluble (s) VCAM-1 and ICAM-1 were determi ned by ELISA methods in 20 patients with pediatric SLE showing variably act ive disease, 20 active patients with active HSP, and 19 healthy controls. T NF-alpha as well as p55 and p75 soluble receptors (sTNF-R) were simultaneou sly tested by enzyme amplified sensitivity immunoassay in 22 patients (12 S LE, 10 HSP). Results. Serum sVCAM-1 concentration was significantly higher in patients w ith SLE (mean +/- SD, 608 +/- 76 ng/ml), than in patients with HSP (501.9 /- 63.3 ng/ml) and controls (446.8 +/- 139.2 ng/ml) (p < 0.001). In SLE pat ients, sVCAM-1 correlated positively with ESR (r = 0.45, p = 0.02) and nega tively with C4 serum levels (r = -0.57, p = 0.004), platelets (r = -0.38, p = 0.03), and lymphocyte count (r = -0.42, p = 0.03). No differences in sIC AM-1 serum concentrations were detected among SLE, HSP, or control groups. Soluble VCAM, but not sICAM-1, showed a positive correlation with TNF-alpha (r = 0.71, p = 0.01), p55 (r = 0.63, p = 0.02), and p75 (r = 0.7, p = 0.01 ) sTNF-R serum concentrations in SLE, but not in patients with HSP. Conclusion. Our study provides additional evidence of a possible differenti al involvement of TNF and TNF induced adhesion molecules in the pathogenesi s of tissue damage between pediatric SLE and HSP.