{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,28]],"date-time":"2026-07-28T03:14:55Z","timestamp":1785208495107,"version":"3.55.0"},"reference-count":39,"publisher":"Akademiai Kiado Zrt.","issue":"9","license":[{"start":{"date-parts":[[2023,3,5]],"date-time":"2023-03-05T00:00:00Z","timestamp":1677974400000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["akjournals.com"],"crossmark-restriction":true},"short-container-title":["OH"],"published-print":{"date-parts":[[2023,3,5]]},"abstract":"<jats:p>A szekunder magas v\u00e9rnyom\u00e1s egyik leggyakoribb oka a primer hyperaldosteronismus.\n                    A primer hyperaldosteronismus a mell\u00e9kvesek\u00e9reg auton\u00f3m\n                    aldoszteron-t\u00faltermel\u00e9s\u00e9vel j\u00e1r; a magas sz\u00e9rum-aldoszteronszint magas\n                    v\u00e9rnyom\u00e1shoz \u00e9s hypokalaemi\u00e1hoz vezethet, kezeletlen\u00fcl pedig sz\u00e1mos\n                    patofiziol\u00f3giai k\u00f6vetkezm\u00e9nyt von maga ut\u00e1n. Diagn\u00f3zisa \u00e9s kezel\u00e9se a beteg\n                    t\u00fcnetmentess\u00e9g\u00e9t vagy ak\u00e1r teljes gy\u00f3gyul\u00e1s\u00e1t eredm\u00e9nyezi, mivel k\u00f3rform\u00e1t\u00f3l\n                    f\u00fcgg\u0151en m\u0171t\u00e9ti \u00faton gy\u00f3gy\u00edthat\u00f3 vagy gy\u00f3gyszeresen kezelhet\u0151. A diagn\u00f3zis\n                    fel\u00e1ll\u00edt\u00e1s\u00e1nak neh\u00e9zs\u00e9gei miatt jelenleg gyakran aluldiagnosztiz\u00e1lt k\u00f3rk\u00e9p. K\u00e9t\n                    leggyakoribb form\u00e1ja az egyoldali aldoszterontermel\u0151 adenoma \u00e9s a bilater\u00e1lis\n                    adrenalis hyperplasia. Az esetek t\u00f6bbs\u00e9g\u00e9ben a betegs\u00e9g kialakul\u00e1sa sporadikus,\n                    de l\u00e9teznek ritka \u00f6r\u00f6kl\u0151d\u0151 form\u00e1i: a familiaris hyperaldosteronismus I\u2013IV. \u00e9s a\n                    primer hyperaldosteronismus g\u00f6rcs\u00f6kkel \u00e9s neurol\u00f3giai abnormalit\u00e1sokkal\n                    szindr\u00f3ma. Az I-es t\u00edpus\u00fa familiaris hyperaldosteronismust a kortizol- \u00e9s\n                    aldoszteron-bioszint\u00e9zis utols\u00f3 l\u00e9p\u00e9s\u00e9t kataliz\u00e1l\u00f3 enzimet k\u00f3dol\u00f3 g\u00e9nek\n                    kiegyenl\u00edtetlen \u00e1tkeresztez\u0151d\u00e9se okozza, m\u00edg a t\u00f6bbi \u00f6r\u00f6kl\u0151d\u0151 k\u00f3rk\u00e9p\n                    kialakul\u00e1s\u00e1\u00e9rt ioncsatorn\u00e1kat k\u00f3dol\u00f3 g\u00e9nek mut\u00e1ci\u00f3i felel\u0151sek. A sporadikus\n                    adenom\u00e1k d\u00f6nt\u0151 r\u00e9sz\u00e9ben a betegs\u00e9g kialakul\u00e1s\u00e1ban kulcsszerepet j\u00e1tsz\u00f3\n                    szomatikus mut\u00e1ci\u00f3k mutathat\u00f3k ki. E szomatikus mut\u00e1ci\u00f3k \u00e1ltal \u00e9rintett g\u00e9nek\n                    k\u00f6z\u00f6tt sz\u00e9p sz\u00e1mmal tal\u00e1lunk az \u00f6r\u00f6kl\u0151d\u0151 form\u00e1kban cs\u00edrasejtes mut\u00e1ci\u00f3k r\u00e9v\u00e9n\n                    \u00e9rintett g\u00e9neket, ami az \u00f6r\u00f6kl\u0151d\u0151 \u00e9s a sporadikus form\u00e1k k\u00f6z\u00f6s\n                    patomechanizmus\u00e1ra utal. \u00d6sszefoglal\u00f3 cikk\u00fcnkben a primer hyperaldosteronismus\n                    genetikai h\u00e1tter\u00e9t, a familiaris \u00e9s sporadikus form\u00e1iban szerepet j\u00e1tsz\u00f3 g\u00e9neket\n                    \u00e9s ezek mut\u00e1ci\u00f3it mutatjuk be, kitekintve ezen ismeretek tudom\u00e1nyos, ter\u00e1pi\u00e1s \u00e9s\n                    diagnosztikus relevanci\u00e1ira is. Orv Hetil. 2023; 164(9): 332\u2013338.<\/jats:p>","DOI":"10.1556\/650.2023.32730","type":"journal-article","created":{"date-parts":[[2023,3,5]],"date-time":"2023-03-05T17:06:55Z","timestamp":1678036015000},"page":"332-338","update-policy":"https:\/\/doi.org\/10.1556\/policypage.crossmark.crossref.2","source":"Crossref","is-referenced-by-count":1,"title":["A primer hyperaldosteronismus genetik\u00e1ja"],"prefix":"10.1556","volume":"164","author":[{"given":"B\u00e1lint","family":"V\u00e9kony","sequence":"first","affiliation":[{"name":"Semmelweis Egyetem, \u00c1ltal\u00e1nos Orvostudom\u00e1nyi Kar, Endokrinol\u00f3giai Tansz\u00e9k Budapest Magyarorsz\u00e1g"},{"name":"Semmelweis Egyetem, \u00c1ltal\u00e1nos Orvostudom\u00e1nyi Kar, Belgy\u00f3gy\u00e1szati \u00e9s Onkol\u00f3giai Klinika Budapest, Kor\u00e1nyi S. u. 2\/a, 1083 Magyarorsz\u00e1g"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P\u00e9ter","family":"Igaz","sequence":"additional","affiliation":[{"name":"Semmelweis Egyetem, \u00c1ltal\u00e1nos Orvostudom\u00e1nyi Kar, Endokrinol\u00f3giai Tansz\u00e9k Budapest Magyarorsz\u00e1g"},{"name":"Semmelweis Egyetem, \u00c1ltal\u00e1nos Orvostudom\u00e1nyi Kar, Belgy\u00f3gy\u00e1szati \u00e9s Onkol\u00f3giai Klinika Budapest, Kor\u00e1nyi S. u. 2\/a, 1083 Magyarorsz\u00e1g"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"425","reference":[{"key":"ref0","doi-asserted-by":"publisher","first-page":"329","DOI":"10.1161\/01.CIR.101.3.329","article-title":"Part I: definition and etiology","volume":"101","author":"Carretero OA","year":"2000","unstructured":"1 Carretero OA, Oparil S. 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A screening test to identify aldosterone-producing adenoma by measuring plasma renin activity: results in hypertensive patients. Arch Intern Med. 1981; 141: 1589-1593.","journal-title":"Arch Intern Med"},{"key":"ref3","doi-asserted-by":"publisher","first-page":"1892","DOI":"10.1097\/HJH.0b013e32833d2192","article-title":"The aldosterone-renin ratio based on the plasma renin activity and the direct renin assay for diagnosing aldosterone-producing adenoma","volume":"28","author":"4 Rossi","year":"2010","unstructured":"4 Rossi GP, Barisa M, Belfiore A, et al. The aldosterone-renin ratio based on the plasma renin activity and the direct renin assay for diagnosing aldosterone-producing adenoma. 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Lancet Diabetes Endocrinol. 2021; 9: 876-892.","journal-title":"Lancet Diabetes Endocrinol"},{"key":"ref6","doi-asserted-by":"publisher","first-page":"797","DOI":"10.1161\/HYPERTENSIONAHA.111.175083","article-title":"Prevalence and characteristics of familial hyperaldosteronism: the PATOGEN study (Primary Aldosteronism in TOrino-GENetic forms)","volume":"58","author":"7 Mulatero","year":"2011","unstructured":"7 Mulatero P, Tizziani D, Viola A, et al. Prevalence and characteristics of familial hyperaldosteronism: the PATOGEN study (Primary Aldosteronism in TOrino-GENetic forms). Hypertension 2011; 58: 797-803.","journal-title":"Hypertension"},{"key":"ref7","doi-asserted-by":"publisher","first-page":"887","DOI":"10.1161\/HYPERTENSIONAHA.121.16498","article-title":"Genetics of primary aldosteronism","volume":"79","author":"8 Scholl","year":"2022","unstructured":"8 Scholl UI. Genetics of primary aldosteronism. Hypertension 2022; 79: 887-897.","journal-title":"Hypertension"},{"key":"ref8","unstructured":"9 Sutherland DJ, Ruse JL, Laidlaw JC. Hypertension, increased aldosterone secretion and low plasma renin activity relieved by dexamethasone. Can Med Assoc J. 1966; 95: 1109-1119."},{"key":"ref9","doi-asserted-by":"publisher","first-page":"262","DOI":"10.1038\/355262a0","article-title":"A chimaeric 11 beta-hydroxylase\/aldosterone synthase gene causes glucocorticoid-remediable aldosteronism and human hypertension","volume":"355","author":"10 Lifton","year":"1992","unstructured":"10 Lifton RP, Dluhy RG, Powers M, et al. A chimaeric 11 beta-hydroxylase\/aldosterone synthase gene causes glucocorticoid-remediable aldosteronism and human hypertension. Nature 1992; 355: 262-265.","journal-title":"Nature"},{"key":"ref10","doi-asserted-by":"publisher","first-page":"1889","DOI":"10.1210\/jc.2015-4061","article-title":"The management of primary aldosteronism: case detection, diagnosis, and treatment: an endocrine society clinical practice guideline","volume":"101","author":"11 Funder","year":"2016","unstructured":"11 Funder JW, Carey RM, Mantero F, et al. The management of primary aldosteronism: case detection, diagnosis, and treatment: an endocrine society clinical practice guideline. J Clin Endocrinol Metab. 2016; 101: 1889-1916.","journal-title":"J Clin Endocrinol Metab"},{"key":"ref11","doi-asserted-by":"publisher","first-page":"283","DOI":"10.1111\/j.1440-1681.1991.tb01446.x","article-title":"Clinical and pathological diversity of primary aldosteronism, including a new familial variety","volume":"18","author":"12 Gordon","year":"1991","unstructured":"12 Gordon RD, Stowasser M, Tunny TJ, et al. 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JAMA Netw Open 2020; 3: e2016209.","DOI":"10.1001\/jamanetworkopen.2020.16209"},{"key":"ref33","doi-asserted-by":"publisher","first-page":"2739","DOI":"10.1172\/JCI91733","article-title":"Macrolides selectively inhibit mutant KCNJ5 potassium channels that cause aldosterone-producing adenoma","volume":"127","author":"34 Scholl","year":"2017","unstructured":"34 Scholl UI, Abriola L, Zhang C, et al. Macrolides selectively inhibit mutant KCNJ5 potassium channels that cause aldosterone-producing adenoma. J Clin Invest. 2017; 127: 2739-2750.","journal-title":"J Clin Invest"},{"key":"ref34","doi-asserted-by":"publisher","first-page":"351","DOI":"10.1146\/annurev-biochem-060308-103103","article-title":"Regulation of mRNA translation and stability by microRNAs","volume":"79","author":"35 Fabian","year":"2010","unstructured":"35 Fabian MR, Sonenberg N, Filipowicz W. Regulation of mRNA translation and stability by microRNAs. 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