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Neuroendocrine Modulation Induced by Selective Blockade of TNF‐α in Rheumatoid Arthritis
Author(s) -
DI COMITE GABRIELE,
MARINOSCI ALESSANDRO,
DI MATTEO PAOLA,
MANFREDI ANGELO,
ROVEREQUERINI PATRIZIA,
BALDISSERA ELENA,
AIELLO PATRIZIA,
CORTI ANGELO,
SABBADINI MARIA GRAZIA
Publication year - 2006
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1351.041
Subject(s) - blockade , rheumatoid arthritis , modulation (music) , tumor necrosis factor alpha , medicine , neuroscience , pharmacology , endocrinology , receptor , biology , physics , acoustics
Tumor necrosis factor‐α (TNFα) is a main actor in the pathogenesis of rheumatoid arthritis (RA), interacting with other molecules in complex mechanisms. The neuroendocrine system is known to be involved and Chromogranin A (CHGA) serum levels are elevated in patients with RA. We evaluated the effect of the selective blockade of TNF‐α, induced by treatment with anti‐TNF‐α monoclonal antibodies (mAbs), on the serum levels of CHGA and on its correlation with TNF‐α and TNF‐α receptors (TNFRs) serum levels. Seven patients with RA have been treated with the anti‐TNF‐α mAb, infliximab. We measured the serum levels of TNF‐α, its receptors (tumor necrosis factor receptor‐I [TNFR‐I] and tumor necrosis factor receptor‐II [TNFR‐II]), and CHGA before and during the treatment. We also measured, as a control, the serum levels of CHGA, TNF‐α, and soluble TNFRs in 14 patients who were being treated with infliximab, adalimumab, or etanercept and in 20 matching negative controls. The serum levels of TNFR‐I and TNFR‐II, which are a sensitive marker for the TNF‐α pathway, correlated with those of CHGA before treatment (Pearson's coefficient, respectively, 0.59 and 0.53). Treatment with anti‐TNF‐α mAb provided a significant clinical response in all patients and the correlation between CHGA and TNFR‐I and TNFR‐II was no more evident during treatment (respectively, −0.09 and −0.07). TNF‐α blockade allows a clinical effect in patients with RA and modifies the correlation between CHGA and TNFRs, suggesting that TNF‐α and CHGA reciprocally interfere in the pathogenesis of RA, through intermediate adaptors, whose identification warrants further studies.