Neuroendocrine modulation induced by selective blockade of TNF-alpha in rheumatoid arthritis
| Autor: | Di Comite G, Marinosci A, Di Matteo P, MANFREDI , ANGELO ANDREA M. A., ROVERE QUERINI , PATRIZIA, Baldissera E, Aiello P, CORTI , ANGELO, Sabbadini MG, Cutolo M. |
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| Přispěvatelé: | Di Comite, G, Marinosci, A, Di Matteo, P, Manfredi, ANGELO ANDREA M. A., ROVERE QUERINI, Patrizia, Baldissera, E, Aiello, P, Corti, Angelo, Sabbadini, Mg, Cutolo, M. |
| Jazyk: | angličtina |
| Rok vydání: | 2006 |
| Předmět: |
Adult
medicine.medical_specialty Arthritis General Biochemistry Genetics and Molecular Biology Receptors Tumor Necrosis Factor Etanercept Arthritis Rheumatoid History and Philosophy of Science Internal medicine medicine Adalimumab Chromogranins Humans Receptor Aged biology business.industry Tumor Necrosis Factor-alpha General Neuroscience Chromogranin A Antibodies Monoclonal Middle Aged medicine.disease Neurosecretory Systems Infliximab Endocrinology Rheumatoid arthritis biology.protein Tumor necrosis factor alpha Immunotherapy business medicine.drug |
| Popis: | Tumor necrosis factor-alpha (TNFalpha) 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-alpha, induced by treatment with anti-TNF-alpha monoclonal antibodies (mAbs), on the serum levels of CHGA and on its correlation with TNF-alpha and TNF-alpha receptors (TNFRs) serum levels. Seven patients with RA have been treated with the anti-TNF-alpha mAb, infliximab. We measured the serum levels of TNF-alpha, 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-alpha, 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-alpha pathway, correlated with those of CHGA before treatment (Pearson's coefficient, respectively, 0.59 and 0.53). Treatment with anti-TNF-alpha 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-alpha blockade allows a clinical effect in patients with RA and modifies the correlation between CHGA and TNFRs, suggesting that TNF-alpha and CHGA reciprocally interfere in the pathogenesis of RA, through intermediate adaptors, whose identification warrants further studies. |
| Databáze: | OpenAIRE |
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