High serum APRIL levels strongly correlate with disease severity in pediatric atopic eczema.

BACKGROUND: Expression of the tumor necrosis factor (TNF) family member APRIL (a proliferation-inducing ligand) is low in normal tissues but is elevated in various autoimmune diseases. OBJECTIVES: This study explored serum APRIL in children with atopic eczema (AE) during flare and quiescence. METHODS: A case-control study including 50 patients with AE and 40 control subjects was conducted. The severity of AE was assessed according to each of the Leicester Sign Score (LSS), the Simple Scoring System (SSS), the SCORing of Atopic Dermatitis (SCORAD) index, and the Objective SCORAD. Serum measurements of APRIL, total immunoglobulin E, and lactate dehydrogenase were obtained in all subjects. Data were obtained during both flare and quiescence in AE subjects. Data were analyzed using the Mann-Whitney U-test and Pearson's correlation coefficient. P-values of <0.05 were considered to indicate statistical significance. RESULTS: Serum APRIL levels were significantly elevated in children with AE in comparison with control subjects during both flare and quiescence (P < 0.0001 for both). Serum APRIL levels during AE flare and quiescence were positively correlated (P < 0.001). Serum APRIL levels and scores on each of the LSS, SSS, and SCORAD showed significant positive correlations (P < 0.01 for all). CONCLUSIONS: Serum APRIL levels were significantly elevated in children with AE during both flare and quiescence. This confirms the importance of APRIL in the pathophysiology of pediatric AE. Serum APRIL is a reliable marker of the severity of AE in children. APRIL may be a new target in the treatment of AE.

Up regulation of serum tumor necrosis factor-related apoptosis inducing ligand in juvenile-onset systemic lupus erythematosus: relations with disease activity, antibodies to double -stranded DNA, nephritis and neutropenia.

OBJECTIVES: Apoptosis is induced by binding of death receptor ligands, members of the tumor necrosis factor (TNF) superfamily, to their cognate receptors. It is suggested that TNF-related apoptosis inducing ligand (TRAIL) is involved in pathogenesis of juvenile-onset systemic lupus erythematosus (JSLE). This study aimed to assess TRAIL concentrations in sera of JSLE children and to determine their potential relationship with disease activity, anti-double-stranded DNA (anti-dsDNA) levels, neutropenia and renal involvement. METHODS: Circulating levels of TRAIL were measured by enzyme-linked immunosorbent assay (ELISA) in serum samples obtained from 40 JSLE patients (20 with active and 20 with inactive disease) and 20 controls. RESULTS: The mean (SEM) serum TRAIL concentration in JSLE was 1750.7 (440.2) pg/mL. Serum TRAIL concentrations in patients were higher than those in controls (P < 0.01). Serum TRAIL concentrations for children with inactive disease (1854.8 [485.4] pg/mL) and those with activity (1646.6 [390.6] pg/mL) were statistically comparable. JSLE children with positive anti-dsDNA antibodies had significantly higher TRAIL levels (mean = 1846 [456] vs. 1455 [325] pg/mL; P < 0.05). Serum TRAIL concentrations were significantly higher in classes III and IV nephritis compared to classes I and II nephritis (1970 [512] vs. 1330 [331] pg/mL; P < 0.01). Serum TRAIL concentrations in patients with neutropenia were higher than those without neutropenia (1805 [505] vs. 1516 [400] pg/mL; P = 0.042) and in controls (P = 0.024). CONCLUSIONS: Our data indicate that an increased level of TRAIL is a feature of JSLE that correlates with disease activity, anti-dsDNA titers neutropenia and lupus nephritis.