DIFFERENCES IN TUMOR-NECROSIS-FACTOR-ALPHA SOLUBLE RECEPTOR SERUM CONCENTRATIONS BETWEEN PATIENTS WITH HENOCH-SCHONLEIN PURPURA AND PEDIATRIC SYSTEMIC LUPUS-ERYTHEMATOSUS - PATHOGENETIC IMPLICATIONS
M. Gattorno et al., DIFFERENCES IN TUMOR-NECROSIS-FACTOR-ALPHA SOLUBLE RECEPTOR SERUM CONCENTRATIONS BETWEEN PATIENTS WITH HENOCH-SCHONLEIN PURPURA AND PEDIATRIC SYSTEMIC LUPUS-ERYTHEMATOSUS - PATHOGENETIC IMPLICATIONS, Journal of rheumatology, 25(2), 1998, pp. 361-365
Objective, Animal models of immune complex mediated tissue injury have
shown different patterns of proinflammatory cytokine production accor
ding to the subtype of immunoglobulin involved. The IgA immune complex
model differs from the IgG model by the lack of involvement of tumor
necrosis factor (TNF) in the pathogenesis of tissue damage. We investi
gated in age matched patients the possible difference in TNF involveme
nt in a predominantly IgA mediated disease, Henoch-Schonlein purpura (
HSP), in comparison with systemic lupus erythematosus (SLE), in which
vascular injury is mostly associated with local deposition of IgG immu
ne complexes. Methods, Serum concentrations of TNF-alpha and its solub
le receptors (sTNF-R) p55 and p75 were studied in 20 patients with ped
iatric SLE at various degrees of disease activity, in 16 patients with
highly active HSP, and in 15 healthy controls by enzyme amplified sen
sitivity immunoassay. SLE disease activity was evaluated using 2 score
s, the European Consensus Group Study for SLE Disease Activity Criteri
a and the SLE Disease Activity Index. Results, Serum concentrations of
TNF-alpha fell within the normal range in patients with both SLE and
HSP irrespective of disease activity. Conversely, patients with SLE di
splayed increased serum levels of sTNF-R that correlated positively wi
th the degree of disease activity (r = 0.60, p < 0.001; r = 0.71, p <
0.001, for p55 and p75, respectively). In contrast, no difference in t
he serum levels of sTNF-R was found between patients with highly activ
e HSP and controls Conclusion, Our study provides the first circumstan
tial evidence that pediatric SLE and HSP are characterized by differen
tial involvement of TNF in the pathogenesis of tissue damage.