{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,19]],"date-time":"2026-03-19T20:50:41Z","timestamp":1773953441538,"version":"3.50.1"},"reference-count":0,"publisher":"Oxford University Press (OUP)","issue":"3","content-domain":{"domain":["eje.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2021,3]]},"abstract":"<jats:sec>\n<jats:title>Objective<\/jats:title>\n<jats:p>While vitamin D regulates immune cells, little is known about it in autoimmune Addison\u2019s disease (AAD). We investigated the vitamin D status in AAD patients from five European populations to assess its deficiency. In addition, we studied two case-control cohorts for vitamin D metabolism and pathway genes.<\/jats:p>\n<\/jats:sec>\n<jats:sec>\n<jats:title>Design<\/jats:title>\n<jats:p>Cross-sectional study.<\/jats:p>\n<\/jats:sec>\n<jats:sec>\n<jats:title>Methods<\/jats:title>\n<jats:p>A total of 1028 patients with AAD from Germany (<jats:italic>n<\/jats:italic> = 239), Italy (<jats:italic>n<\/jats:italic> = 328), Norway (<jats:italic>n<\/jats:italic> = 378), UK (<jats:italic>n<\/jats:italic> = 44) and Poland (<jats:italic>n<\/jats:italic> = 39) and 679 controls from Germany (<jats:italic>n<\/jats:italic> = 301) and Norway (<jats:italic>n<\/jats:italic> = 378) were studied for 25(OH)D<jats:sub>3<\/jats:sub> (primary objective).<jats:sub\/> Secondary objectives (1,25(OH)<jats:sub>2<\/jats:sub>D<jats:sub>3<\/jats:sub> and pathway genes) were examined in case-controls from Germany and Norway correlating 25(OH)D<jats:sub>3<\/jats:sub> and single nucleotide polymorphisms within genes encoding the vitamin D receptor (VDR), 1-\u03b1-hydroxylase (CYP27B1), 25-hydroxylase (CYP2R1), 24-hydroxylase (CYP24A1) and vitamin D binding protein (GC\/DBP).<\/jats:p>\n<\/jats:sec>\n<jats:sec>\n<jats:title>Results<\/jats:title>\n<jats:p>Vitamin D deficiency (25(OH)D<jats:sub>3<\/jats:sub> 10\u201320 ng\/mL) was highly prevalent in AAD patients (34\u201357%), 5\u201322% were severely deficient (&lt;10 ng\/mL), 28\u201338% insufficient (20\u201330 ng\/mL) and only 7\u201314% sufficient (&gt;30 ng\/mL). Lower 25(OH)D<jats:sub>3<\/jats:sub> and 1,25(OH)<jats:sub>2<\/jats:sub>D<jats:sub>3<\/jats:sub> levels were observed both in Norwegian and German AAD (<jats:italic>P<\/jats:italic>\u2009=\u20090.03\/0.003 and <jats:italic>P<\/jats:italic>\u2009=\u20091 \u00d7 10<jats:sup>-5<\/jats:sup>\/&lt; 1 \u00d7 10<jats:sup>-7<\/jats:sup><jats:sub>,<\/jats:sub> respectively) the former was associated with <jats:italic>CYP2R1<\/jats:italic> (rs1553006) genotype G. Whereas controls achieved sufficient median 25(OH)D<jats:sub>3<\/jats:sub> in summers (21.4 to 21.9 ng\/mL), AAD patients remained largely deficient (18.0 to 21.2 ng\/mL) and synthesize less 1,25(OH)<jats:sub>2<\/jats:sub>D<jats:sub>3<\/jats:sub>.<\/jats:p>\n<\/jats:sec>\n<jats:sec>\n<jats:title>Conclusion<\/jats:title>\n<jats:p>Vitamin D deficiency and insufficiency are highly prevalent in AAD patients. The vitamin D status of AAD may be influenced by genetic factors and suggests individual vitamin D requirements throughout the year.<\/jats:p>\n<\/jats:sec>","DOI":"10.1530\/eje-20-0956","type":"journal-article","created":{"date-parts":[[2021,1,12]],"date-time":"2021-01-12T22:58:16Z","timestamp":1610492296000},"page":"373-381","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-7","source":"Crossref","is-referenced-by-count":5,"title":["Vitamin D status and pathway genes in five European autoimmune Addison\u2019s disease cohorts"],"prefix":"10.1093","volume":"184","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6767-8057","authenticated-orcid":true,"given":"Marissa","family":"Penna-Martinez","sequence":"first","affiliation":[{"name":"1Division of Endocrinology, Diabetes and Metabolism, Department of Internal Medicine I, University Hospital Frankfurt, Goethe-University, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gesine","family":"Meyer","sequence":"additional","affiliation":[{"name":"1Division of Endocrinology, Diabetes and Metabolism, Department of Internal Medicine I, University Hospital Frankfurt, Goethe-University, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8485-2248","authenticated-orcid":true,"given":"Anette Boe","family":"Wolff","sequence":"additional","affiliation":[{"name":"2Department of Clinical Science and KG Jebsen Center for Autoimmune Disorders, University of Bergen, Bergen, Norway"},{"name":"7Department of Medicine, Haukeland University Hospital, Bergen, Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Beate","family":"Skinningsrud","sequence":"additional","affiliation":[{"name":"3Department of Medical Genetics, Oslo University Hospital and University of Oslo, Oslo, Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Corrado","family":"Betterle","sequence":"additional","affiliation":[{"name":"4Department of Medicine (DIMED), University of Padua School of Medicine, Padua, Italy"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alberto","family":"Falorni","sequence":"additional","affiliation":[{"name":"5Department of Internal Medicine, University of Perugia, Perugia, Italy"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"William","family":"Ollier","sequence":"additional","affiliation":[{"name":"6Faculty of Science and Engineering, Manchester Metropolitan University, Manchester, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dag","family":"Undlien","sequence":"additional","affiliation":[{"name":"3Department of Medical Genetics, Oslo University Hospital and University of Oslo, Oslo, Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Eystein","family":"Husebye","sequence":"additional","affiliation":[{"name":"2Department of Clinical Science and KG Jebsen Center for Autoimmune Disorders, University of Bergen, Bergen, Norway"},{"name":"7Department of Medicine, Haukeland University Hospital, Bergen, Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Simon","family":"Pearce","sequence":"additional","affiliation":[{"name":"8Translational & Clinical Research Institute, Newcastle University, Newcastle, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anna L","family":"Mitchell","sequence":"additional","affiliation":[{"name":"8Translational & Clinical Research Institute, Newcastle University, Newcastle, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Klaus","family":"Badenhoop","sequence":"additional","affiliation":[{"name":"1Division of Endocrinology, Diabetes and Metabolism, Department of Internal Medicine I, University Hospital Frankfurt, Goethe-University, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","container-title":["European Journal of Endocrinology"],"original-title":[],"link":[{"URL":"https:\/\/eje.bioscientifica.com\/view\/journals\/eje\/184\/3\/EJE-20-0956.xml","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/eje.bioscientifica.com\/downloadpdf\/journals\/eje\/184\/3\/EJE-20-0956.xml","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,2,14]],"date-time":"2023-02-14T16:15:36Z","timestamp":1676391336000},"score":1,"resource":{"primary":{"URL":"https:\/\/academic.oup.com\/ejendo\/article\/184\/3\/373\/6653856"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2021,3]]},"references-count":0,"journal-issue":{"issue":"3"},"URL":"https:\/\/doi.org\/10.1530\/eje-20-0956","relation":{},"ISSN":["0804-4643","1479-683X"],"issn-type":[{"value":"0804-4643","type":"print"},{"value":"1479-683X","type":"electronic"}],"subject":[],"published":{"date-parts":[[2021,3]]}}}