{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,1]],"date-time":"2026-06-01T16:52:46Z","timestamp":1780332766996,"version":"3.54.1"},"reference-count":36,"publisher":"Springer Science and Business Media LLC","issue":"4","license":[{"start":{"date-parts":[[2012,8,15]],"date-time":"2012-08-15T00:00:00Z","timestamp":1344988800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/2.0\/"},{"start":{"date-parts":[[2012,8,15]],"date-time":"2012-08-15T00:00:00Z","timestamp":1344988800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/2.0\/"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Arthritis Res Ther"],"abstract":"<jats:title>Abstract<\/jats:title><jats:sec>\n                        <jats:title>Introduction<\/jats:title>\n                        <jats:p>In this study, we evaluated the activity of the neuroendocrine axes in patients with polymyalgia rheumatica (PMR) before and after tumor necrosis factor (TNF)-\u03b1-blocking etanercept treatment, which previously has been shown to reduce interleukin 6 (IL-6) and C-reactive protein (CRP) markedly in PMR.<\/jats:p>\n                     <\/jats:sec><jats:sec>\n                        <jats:title>Methods<\/jats:title>\n                        <jats:p>Plasma samples were collected from 10 glucocorticoid-na\u00efve patients with PMR and 10 matched controls before and after etanercept treatment (25 mg biweekly for 2 weeks). The primary end points were pre- and posttreatment levels of adrenocorticotropic hormone (ACTH), cortisol, adrenaline, thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH), prolactin, and insulin-like growth factor 1 (IGF-1).<\/jats:p>\n                     <\/jats:sec><jats:sec>\n                        <jats:title>Results<\/jats:title>\n                        <jats:p>Before TNF-\u03b1-blocking treatment, plasma TNF-\u03b1, ACTH, and cortisol levels were higher in patients versus controls (<jats:italic>P<\/jats:italic> &lt; 0.05 and <jats:italic>P<\/jats:italic> &lt; 0.001, respectively); during TNF-\u03b1 blockade in patients, levels of both hormones decreased (<jats:italic>P<\/jats:italic> &lt; 0.05 and <jats:italic>P<\/jats:italic> &lt; 0.01, respectively), whereas levels in controls increased (<jats:italic>P<\/jats:italic> &lt; 0.05), abolishing the pretreatment differences. Pretreatment adrenaline levels were more than twice as high in patients than in controls (<jats:italic>P<\/jats:italic> &lt; 0.01); after treatment in patients, levels had decreased (<jats:italic>P<\/jats:italic> &lt; 0.05) but remained higher versus controls (<jats:italic>P<\/jats:italic> &lt; 0.05). Levels of the other hormones never differed significantly between groups (<jats:italic>P<\/jats:italic> &gt; 0.05).<\/jats:p>\n                     <\/jats:sec><jats:sec>\n                        <jats:title>Conclusions<\/jats:title>\n                        <jats:p>In PMR, TNF-\u03b1 may increase the activities of the hypothalamic-pituitary-adrenal and the hypothalamic-sympthoadrenomedullary axes. Secretion of TSH, FSH, prolactin, and IGF-1 is not clearly changed in PMR.<\/jats:p>\n                     <\/jats:sec><jats:sec>\n                        <jats:title>Trial registration<\/jats:title>\n                        <jats:p>ClinicalTrials.gov (<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"uri\" xlink:href=\"http:\/\/www.clinicaltrials.gov\/ct2\/show\/NCT00524381\">NCT00524381<\/jats:ext-link>).<\/jats:p>\n                     <\/jats:sec>","DOI":"10.1186\/ar4017","type":"journal-article","created":{"date-parts":[[2012,8,15]],"date-time":"2012-08-15T12:13:57Z","timestamp":1345032837000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Activity of the neuroendocrine axes in patients with polymyalgia rheumatica before and after TNF-\u03b1 blocking etanercept treatment"],"prefix":"10.1186","volume":"14","author":[{"given":"Frederik Flindt","family":"Kreiner","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Henrik","family":"Galbo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2012,8,15]]},"reference":[{"key":"3769_CR1","doi-asserted-by":"publisher","first-page":"261","DOI":"10.1056\/NEJMra011913","volume":"347","author":"C Salvarani","year":"2002","unstructured":"Salvarani C, Cantini F, Boiardi L, Hunder GG: Polymyalgia rheumatica and giant-cell arteritis. 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