{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T20:49:59Z","timestamp":1791924599558,"version":"4.3.4"},"reference-count":78,"publisher":"The Endocrine Society","issue":"9","license":[{"start":{"date-parts":[[2020,6,9]],"date-time":"2020-06-09T00:00:00Z","timestamp":1591660800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK106618"],"award-info":[{"award-number":["DK106618"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000968","name":"American Heart Association","doi-asserted-by":"publisher","award":["17SDG33660447"],"award-info":[{"award-number":["17SDG33660447"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2020,9,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Context and Objective<\/jats:title>\n                    <jats:p>Posture-responsive and posture-unresponsive aldosterone-producing adenomas (APAs) account for approximately 40% and 60% of APAs, respectively. Somatic gene mutations have been recently reported to exist in approximately 90% of APAs. This study was designed to characterize the biochemical, histopathologic, and genetic properties of these 2 types of APA.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Plasma levels of aldosterone and hybrid steroids (18-oxocortisol and 18-hydroxycortisol) were measured by liquid chromatography-tandem mass spectrometry. Immunohistochemistry for CYP11B2 (aldosterone synthase) and CYP17A1 (17\u03b1-hydroxylase) and deoxyribonucleic acid sequencing (Sanger and next-generation sequencing) were performed on APA tissue collected from 23 posture-unresponsive and 17 posture-responsive APA patients.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Patients with posture-unresponsive APA displayed higher (P &amp;lt; 0.01) levels of hybrid steroids, recumbent aldosterone and cortisol, larger (P &amp;lt; 0.01) zona fasciculata (ZF)-like tumors with higher (P &amp;lt; 0.01) expression of CYP17A1 (but not of CYP11B2) than patients with posture-responsive APA (most of which were not ZF-like). Of 40 studied APAs, 37 (92.5%) were found to harbor aldosterone-driving somatic mutations (KCNJ5 = 14 [35.0%], CACNA1D = 13 [32.5%], ATP1A1 = 8 [20.0%], and ATP2B3 = 2 [5.0%]), including 5 previously unreported mutations (3 in CACNA1D and 2 in ATP1A1). Notably, 64.7% (11\/17) of posture-responsive APAs carried CACNA1D mutations, whereas 56.5% (13\/23) of posture-unresponsive APAs harbored KCNJ5 mutations.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>The elevated production of hybrid steroids by posture-unresponsive APAs may relate to their ZF-like tumor cell composition, resulting in expression of CYP17A1 (in addition to somatic gene mutation-driven CYP11B2 expression), thereby allowing production of cortisol, which acts as the substrate for CYP11B2-generated hybrid steroids.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1210\/clinem\/dgaa367","type":"journal-article","created":{"date-parts":[[2020,6,9]],"date-time":"2020-06-09T14:16:08Z","timestamp":1591712168000},"page":"e3224-e3235","source":"Crossref","is-referenced-by-count":29,"title":["Biochemical, Histopathological, and Genetic Characterization of Posture-Responsive and Unresponsive APAs"],"prefix":"10.1210","volume":"105","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2281-6855","authenticated-orcid":false,"given":"Zeng","family":"Guo","sequence":"first","affiliation":[{"name":"Endocrine Hypertension Research Centre, University of Queensland Diamantina Institute, Greenslopes and Princess Alexandra Hospitals , Brisbane,","place":["Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kazutaka","family":"Nanba","sequence":"additional","affiliation":[{"name":"Department of Molecular and Integrative Physiology, University of Michigan , Ann Arbor, MI,","place":["US"]},{"name":"Department of Endocrinology and Metabolism, National Hospital Organization Kyoto Medical Center , Kyoto,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aaron","family":"Udager","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Michigan Medical School , Ann Arbor, MI,","place":["US"]},{"name":"Michigan Center for Translational Pathology , Ann Arbor, MI,","place":["US"]},{"name":"Rogel Cancer Center, University of Michigan , Ann Arbor, MI,","place":["US"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brett C","family":"McWhinney","sequence":"additional","affiliation":[{"name":"Department of Chemical Pathology, Pathology Queensland, Queensland Health, Brisbane ,","place":["Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jacobus P J","family":"Ungerer","sequence":"additional","affiliation":[{"name":"Department of Chemical Pathology, Pathology Queensland, Queensland Health, Brisbane ,","place":["Australia"]},{"name":"School of Biomedical Sciences, University of Queensland , Brisbane,","place":["Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin","family":"Wolley","sequence":"additional","affiliation":[{"name":"Endocrine Hypertension Research Centre, University of Queensland Diamantina Institute, Greenslopes and Princess Alexandra Hospitals , Brisbane,","place":["Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Moe","family":"Thuzar","sequence":"additional","affiliation":[{"name":"Endocrine Hypertension Research Centre, University of Queensland Diamantina Institute, Greenslopes and Princess Alexandra Hospitals , Brisbane,","place":["Australia"]},{"name":"Department of Endocrinology, Princess Alexandra Hospital , Brisbane,","place":["Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard D","family":"Gordon","sequence":"additional","affiliation":[{"name":"Endocrine Hypertension Research Centre, University of Queensland Diamantina Institute, Greenslopes and Princess Alexandra Hospitals , Brisbane,","place":["Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William E","family":"Rainey","sequence":"additional","affiliation":[{"name":"Department of Molecular and Integrative Physiology, University of Michigan , Ann Arbor, MI,","place":["US"]},{"name":"Division of Metabolism, Endocrine, and Diabetes, Department of Internal Medicine, University of Michigan , Ann Arbor, MI,","place":["US"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4317-8584","authenticated-orcid":false,"given":"Michael","family":"Stowasser","sequence":"additional","affiliation":[{"name":"Endocrine Hypertension Research Centre, University of Queensland Diamantina Institute, Greenslopes and Princess Alexandra Hospitals , Brisbane,","place":["Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"80","published-online":{"date-parts":[[2020,6,9]]},"reference":[{"issue":"11","key":"2026041420194575600_CIT0001","doi-asserted-by":"crossref","first-page":"2293","DOI":"10.1016\/j.jacc.2006.07.059","article-title":"A prospective study of the prevalence of primary aldosteronism in 1,125 hypertensive 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