{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T01:53:12Z","timestamp":1791337992516,"version":"4.3.1"},"reference-count":0,"publisher":"Oxford University Press (OUP)","issue":"4","content-domain":{"domain":["eje.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2020,4]]},"abstract":"<jats:sec>\n                    <jats:title>Context<\/jats:title>\n                    <jats:p>The human adrenal is the dominant source of androgens in castration-resistant prostate cancer (CRPC) and classic 21-hydroxylase deficiency (21OHD). Abiraterone, derived from the prodrug abiraterone acetate (AA), inhibits the activity of cytochrome P450 17-hydroxylase\/17,20-lyase (CYP17A1), the enzyme required for all androgen biosynthesis. AA treatment effectively lowers testosterone and androstenedione in 21OHD and CRPC patients. The 11-oxygenated androgens are major adrenal-derived androgens, yet little is known regarding the effects of AA administration on 11-oxygenated androgens.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>To test the hypothesis that AA therapy decreases 11-oxygenated androgens.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Design<\/jats:title>\n                    <jats:p>Samples were obtained from 21OHD or CRPC participants in AA or AA plus prednisone (AAP)-treatment studies, respectively.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We employed liquid chromatography-tandem mass spectrometry (LC-MS\/MS) to measure the 11-oxygenated androgens, 11\u03b2-hydroxyandrostenedione, 11-ketoandrostenedione, 11\u03b2-hydroxytestosterone, and 11-ketotestosterone, in plasma or serum samples from six 21OHD and six CRPC patients before and after treatment with AA or AAP, respectively.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>In CRPC patients, administration of AAP (1000 mg\/day AA with prednisone and medical castration) lowered all four 11-oxygenated androgens to below the lower limits of quantitation (&lt;0.1\u20130.3 nmol\/L), equivalent to 64\u201394% reductions from baseline. In 21OHD patients, administration of AA (100\u2013250 mg\/day for 6 days) reduced all 11-oxygenated androgens by on average 56\u201377% from baseline.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>We conclude that AA and AAP therapies markedly reduce the production of the adrenal-derived 11-oxygenated androgens, both in patients with high (21OHD) or normal (CRPC) 11-oxygenated androgens at baseline, respectively. Reduction of 11-oxygenated androgens is an important aspect of AA and AAP pharmacology.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1530\/eje-19-0905","type":"journal-article","created":{"date-parts":[[2020,2,10]],"date-time":"2020-02-10T10:56:12Z","timestamp":1581332172000},"page":"413-421","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-1","source":"Crossref","is-referenced-by-count":70,"title":["Abiraterone acetate treatment lowers 11-oxygenated androgens"],"prefix":"10.1093","volume":"182","author":[{"given":"Connor","family":"Wright","sequence":"first","affiliation":[{"name":"1Division of Metabolism, Diabetes, and Endocrinology, Department of Internal Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patrick","family":"O\u2019Day","sequence":"additional","affiliation":[{"name":"1Division of Metabolism, Diabetes, and Endocrinology, Department of Internal Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohammed","family":"Alyamani","sequence":"additional","affiliation":[{"name":"3Genitourinary Malignancies Research Center, Lerner Research Institute"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nima","family":"Sharifi","sequence":"additional","affiliation":[{"name":"3Genitourinary Malignancies Research Center, Lerner Research Institute"},{"name":"4Department of Urology, Glickman Urological and Kidney Institute"},{"name":"5Department of Hematology and Oncology, Taussig Cancer Institute, Cleveland Clinic, Cleveland, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard J","family":"Auchus","sequence":"additional","affiliation":[{"name":"1Division of Metabolism, Diabetes, and Endocrinology, Department of Internal Medicine"},{"name":"2Department of Pharmacology, University of Michigan, Ann Arbor, Michigan, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","container-title":["European Journal of Endocrinology"],"original-title":[],"link":[{"URL":"https:\/\/eje.bioscientifica.com\/view\/journals\/eje\/182\/4\/EJE-19-0905.xml","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/eje.bioscientifica.com\/view\/journals\/eje\/182\/4\/EJE-19-0905.xml","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,2,14]],"date-time":"2023-02-14T11:14:12Z","timestamp":1676373252000},"score":1,"resource":{"primary":{"URL":"https:\/\/academic.oup.com\/ejendo\/article\/182\/4\/413\/6653975"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2020,4]]},"references-count":0,"journal-issue":{"issue":"4"},"URL":"https:\/\/doi.org\/10.1530\/eje-19-0905","relation":{},"ISSN":["0804-4643","1479-683X"],"issn-type":[{"value":"0804-4643","type":"print"},{"value":"1479-683X","type":"electronic"}],"subject":[],"published":{"date-parts":[[2020,4]]}}}