{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,20]],"date-time":"2026-05-20T00:20:07Z","timestamp":1779236407019,"version":"3.51.4"},"reference-count":18,"publisher":"Oxford University Press (OUP)","issue":"5","content-domain":{"domain":["eje.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2013,11]]},"abstract":"<jats:sec><jats:title>Objective<\/jats:title><jats:p>Adrenal vein sampling (AVS) is a technically demanding procedure required for the identification of suitable candidates for unilateral adrenalectomy in primary aldosteronism. Recently, somatic<jats:italic>KCNJ5<\/jats:italic>K<jats:sup>+<\/jats:sup>-channel mutations in aldosterone-producing adenoma (APA) patients have been shown to influence steroid gradients during AVS. These and other recently identified genetic modifiers (<jats:italic>ATP1A1<\/jats:italic>and<jats:italic>ATP2B3<\/jats:italic>) might affect the final diagnosis and treatment of the affected patients.<\/jats:p><\/jats:sec><jats:sec><jats:title>Design<\/jats:title><jats:p>Fifty-nine patients with APAs who had undergone successful AVS (adrenal vein cortisol:peripheral cortisol ratio \u22652) and had undergone a mutation analysis of their tumor tissue were studied. The mutation status of the APAs was as follows: 19<jats:italic>KCNJ5<\/jats:italic>mutations, eight ATPase mutations (five<jats:italic>ATP1A1<\/jats:italic>and three<jats:italic>ATP2B3<\/jats:italic>), and 32 patients with none of these mutations.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>The lateralization index (ratio of aldosterone:cortisol on the side of the adenoma to aldosterone to cortisol on the contralateral side) and the contralateral suppression index (ratio of aldosterone:cortisol on the contralateral side to aldosterone to cortisol in the periphery) were calculated for the<jats:italic>KCNJ5<\/jats:italic>-mutated, ATPase-mutated, and the<jats:italic>KCNJ5<\/jats:italic>\/ATPase mutation-negative APA patients.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The lateralization indices of the ATPase mutation carriers had a median of 19.9 compared with a median of 16.0 in the<jats:italic>KCNJ5<\/jats:italic>mutation carriers and that of 20.5 in the<jats:italic>KCNJ5<\/jats:italic>\/ATPase mutation-negative patients. The contralateral suppression indices of the ATPase-mutated patients had a median of 0.1 compared with a median of 0.4 in the<jats:italic>KCNJ5<\/jats:italic>mutation carriers and that of 0.2 in the<jats:italic>KCNJ5<\/jats:italic>\/ATPase mutation-negative patients. The differences between the genetic groups were not statistically significant.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>We did not find evidence for a clinically important impact of mutation status on steroid gradients during AVS.<\/jats:p><\/jats:sec>","DOI":"10.1530\/eje-13-0551","type":"journal-article","created":{"date-parts":[[2013,8,15]],"date-time":"2013-08-15T07:34:48Z","timestamp":1376552088000},"page":"657-663","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-1","source":"Crossref","is-referenced-by-count":21,"title":["Lack of influence of somatic mutations on steroid gradients during adrenal vein sampling in aldosterone-producing adenoma patients"],"prefix":"10.1093","volume":"169","author":[{"given":"Andrea","family":"O\u00dfwald","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Evelyn","family":"Fischer","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christoph","family":"Degenhart","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marcus","family":"Quinkler","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Martin","family":"Bidlingmaier","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anna","family":"Pallauf","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Katharina","family":"Lang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thomas","family":"Mussack","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Klaus","family":"Hallfeldt","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Felix","family":"Beuschlein","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Martin","family":"Reincke","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","reference":[{"issue":"11","key":"1_18469473","doi-asserted-by":"publisher","first-page":"2217","DOI":"10.1097\/00004872-200411000-00026","volume":"22","author":"Eide","year":"2004","journal-title":"Journal of hypertension","ISSN":"https:\/\/id.crossref.org\/issn\/0263-6352","issn-type":"print"},{"issue":"1","key":"2_42351771","doi-asserted-by":"publisher","first-page":"7","DOI":"10.1530\/EJE-11-1013","volume":"167","year":"2012","journal-title":"European Journal of Endocrinology","ISSN":"https:\/\/id.crossref.org\/issn\/0804-4643","issn-type":"print"},{"issue":"4","key":"3_33857276","doi-asserted-by":"publisher","first-page":"1125","DOI":"10.1210\/jc.2008-2116","volume":"94","year":"2009","journal-title":"Journal of Clinical Endocrinology &amp; 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