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ea0029p14 | Adrenal cortex | ICEECE2012

PET-tracers for differential diagnosis in primary hyperaldosteronism – in vitro studies

Heinze B. , Mathe K. , Gabor S. , Lang K. , Zink M. , Allolio B. , Schirbel A. , Hahner S.

Objective: The major diagnostic problem in primary aldosteronism is the differentiation between bilateral hyperplasia and aldosterone producing adenoma which is essential for further treatment. Adrenal vein sampling is regarded as the current gold standard, however it is an invasive, highly examiner-dependent method. Molecular imaging targeting the aldosterone synthase (CYP11B2) which is expressed specifically in aldosterone producing adrenal tissue may be an useful alternativ...

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ea0029p32 | Adrenal cortex | ICEECE2012

KCNJ5 Mutations in European Families with Non-Glucocorticoid Remediable Familial Hyperaldosteronism

Mulatero P. , Tauber P. , Zennaro M. , Monticone S. , Lang K. , Beuschlein F. , Fischer E. , Burrello J. , Pallauf A. , Galmozzi M. , Amar L. , Williams T. , Strom T. , Graf E. , Bandulik S. , Penton D. , Plouin P. , Warth R. , Allolio B. , Jeunemaitre X. , Veglio F. , Reincke M.

Primary Aldosteronism (PA) is the most frequent cause of endocrine hypertension. Three forms of familial hyperaldosteronism (FH) have been described, named FH-I to -III. Recently, a mutation of KCNJ5 has been shown to be associated with FH-III, whereas the cause of FH-II is still unknown. In this study we searched for mutations in KCNJ5 in 46 patients from 21 families with FH, in which FH-I was excluded. We identified a new germline G151E mutation in two PA affected subjects f...

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Endocrine Abstracts

PET-tracers for differential diagnosis in primary hyperaldosteronism – in vitro studies

KCNJ5 Mutations in European Families with Non-Glucocorticoid Remediable Familial Hyperaldosteronism

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