{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T05:17:18Z","timestamp":1783487838931,"version":"3.55.0"},"reference-count":19,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2006,6,30]],"date-time":"2006-06-30T00:00:00Z","timestamp":1151625600000},"content-version":"vor","delay-in-days":29,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of the New York Academy of Sciences"],"published-print":{"date-parts":[[2006,6]]},"abstract":"<jats:p><jats:bold><jats:sc>Abstract:\u2002<\/jats:sc><\/jats:bold>  <jats:bold>Tumor necrosis factor\u2010\u03b1 (TNF\u03b1) 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\u2010\u03b1, induced by treatment with anti\u2010TNF\u2010\u03b1 monoclonal antibodies (mAbs), on the serum levels of CHGA and on its correlation with TNF\u2010\u03b1 and TNF\u2010\u03b1 receptors (TNFRs) serum levels. Seven patients with RA have been treated with the anti\u2010TNF\u2010\u03b1 mAb, infliximab. We measured the serum levels of TNF\u2010\u03b1, its receptors (tumor necrosis factor receptor\u2010I [TNFR\u2010I] and tumor necrosis factor receptor\u2010II [TNFR\u2010II]), and CHGA before and during the treatment. We also measured, as a control, the serum levels of CHGA, TNF\u2010\u03b1, 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\u2010I and TNFR\u2010II, which are a sensitive marker for the TNF\u2010\u03b1 pathway, correlated with those of CHGA before treatment (Pearson's coefficient, respectively, 0.59 and 0.53). Treatment with anti\u2010TNF\u2010\u03b1 mAb provided a significant clinical response in all patients and the correlation between CHGA and TNFR\u2010I and TNFR\u2010II was no more evident during treatment (respectively, \u22120.09 and \u22120.07). TNF\u2010\u03b1 blockade allows a clinical effect in patients with RA and modifies the correlation between CHGA and TNFRs, suggesting that TNF\u2010\u03b1 and CHGA reciprocally interfere in the pathogenesis of RA, through intermediate adaptors, whose identification warrants further studies.<\/jats:bold> <\/jats:p>","DOI":"10.1196\/annals.1351.041","type":"journal-article","created":{"date-parts":[[2006,7,19]],"date-time":"2006-07-19T19:35:49Z","timestamp":1153337749000},"page":"428-437","source":"Crossref","is-referenced-by-count":31,"title":["Neuroendocrine Modulation Induced by Selective Blockade of TNF\u2010\u03b1 in Rheumatoid Arthritis"],"prefix":"10.1111","volume":"1069","author":[{"given":"GABRIELE","family":"DI COMITE","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"ALESSANDRO","family":"MARINOSCI","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"PAOLA","family":"DI MATTEO","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"ANGELO","family":"MANFREDI","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"PATRIZIA","family":"ROVERE\u2010QUERINI","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"ELENA","family":"BALDISSERA","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"PATRIZIA","family":"AIELLO","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"ANGELO","family":"CORTI","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"MARIA GRAZIA","family":"SABBADINI","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2006,6,30]]},"reference":[{"key":"e_1_2_5_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/0306-4522(92)90222-N"},{"key":"e_1_2_5_3_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra021405"},{"key":"e_1_2_5_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(01)00459-7"},{"key":"e_1_2_5_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.tim.2003.10.001"},{"key":"e_1_2_5_6_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.15.3.237"},{"key":"e_1_2_5_7_2","doi-asserted-by":"publisher","DOI":"10.1096\/fj.03-0922fje"},{"key":"e_1_2_5_8_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.2002.tb04495.x"},{"key":"e_1_2_5_9_2","doi-asserted-by":"publisher","DOI":"10.1093\/rheumatology\/keh530"},{"key":"e_1_2_5_10_2","doi-asserted-by":"publisher","DOI":"10.1038\/nature01661"},{"key":"e_1_2_5_11_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199005033221805"},{"key":"e_1_2_5_12_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1999.tb07649.x"},{"key":"e_1_2_5_13_2","doi-asserted-by":"publisher","DOI":"10.1186\/ar121"},{"key":"e_1_2_5_14_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM200011303432202"},{"key":"e_1_2_5_15_2","doi-asserted-by":"crossref","first-page":"478","DOI":"10.7326\/0003-4819-130-6-199903160-00004","article-title":"Etanercept therapy in rheumatoid arthritis. 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