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Takako Araki, Ning-Ai Liu, Yukiko Tone, Daniel Cuevas-Ramos, Roy Heltsley, Masahide Tone, and Shlomo Melmed

Introduction ACTH-dependent Cushing’s syndrome and consequent hypercortisolemia leads to critical metabolic and cardiovascular complications ( Chrousos 2009 , Nieman et al . 2015 , Raff & Carroll 2015 ). The high ACTH levels that induce

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R van der Pas, W W de Herder, L J Hofland, and R A Feelders

Introduction Cushing's syndrome (CS) is characterized by chronic overproduction of cortisol resulting in significant morbidity and, when untreated, an increased mortality ( Lindholm et al . 2001 , Newell-Price et al . 2006 , Dekkers et al

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Andrea Gutierrez Maria, Christina Tatsi, Annabel Berthon, Ludivine Drougat, Nikolaos Settas, Fady Hannah-Shmouni, Jerome Bertherat, Fabio R Faucz, and Constantine A Stratakis

) ( Almeida & Stratakis 2011 ). RIα, Cα and Cβ defects have been implicated in corticotrophin (ACTH)-independent, adrenocortical Cushing‘s syndrome (CS) ( Stratakis 2014 , Espiard et al. 2018 , Hannah-Shmouni & Stratakis 2020 ). PRKAR1A mutations cause

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Evgenia Gourgari, Maya Lodish, Meg Keil, Robert Wesley, Suvimol Hill, Paraskevi Xekouki, Charalampos Lyssikatos, Elena Belyavskaya, Sierra Maria De La Luz, and Constantine A Stratakis

Dear Editor, Cushing's syndrome (CS) is a rare disease in children it is associated with weight gain and stunting of their linear growth ( McArthur et al . 1980 , Magiakou et al . 1994 a , Stratakis 2012 ). In this study, we assessed growth in

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Carole Guerin, David Taieb, Giorgio Treglia, Thierry Brue, André Lacroix, Frederic Sebag, and Frederic Castinetti

Introduction Hypercortisolism or Cushing's syndrome (CS) is a rare condition; effective treatments are necessary because of an increased morbidity and mortality if left untreated. CS can be due to: i) an excess of adrenocorticotrophin (ACTH

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Dimitra A Vassiliadi and Stylianos Tsagarakis

secretion that compensates for enzymatic defects of cortisol synthesis as in patients with congenital adrenal hyperplasia (CAH). Kirschner et al. (1964) described an unusual form of Cushing’s syndrome (CS), characterized by the constellation of long

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E Louiset, K Isvi, J M Gasc, C Duparc, B Cauliez, A Laquerrière, J M Kuhn, and H Lefebvre

hyperplasias (AIMAHs) and adenomas responsible for Cushing's syndrome ( Bertherat et al . 2005 , Contesse et al . 2005 ). In these lesions, 5-HT is abnormally detected in clusters of steroidogenic cells that harbor therefore a mixed, i.e. both steroidogenic

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Sisi Liu, Emmanouil Saloustros, Annabel Berthon, Matthew F Starost, Isabelle Sahut-Barnola, Paraskevi Salpea, Eva Szarek, Fabio R Faucz, Antoine Martinez, and Constantine A Stratakis

Introduction Primary pigmented nodular adrenocortical disease (PPNAD) leads to adrenocorticotropin hormone (ACTH)-independent Cushing's syndrome (CS) ( Carney et al . 1985 , Stratakis 2007 ) and is caused typically by inactivating mutations of

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Y de Keyzer, D Vieau, A Picon, and X Bertagna

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Fady Hannah-Shmouni, Annabel Berthon, Fabio R Faucz, Juan Medina Briceno, Andrea Gutierrez Maria, Andrew Demidowich, Mirko Peitzsch, Jimmy Masjkur, Fidéline Bonnet-Serrano, Anna Vaczlavik, Jérôme Bertherat, Martin Reincke, Graeme Eisenhofer, and Constantine A Stratakis

Introduction Primary bilateral macronodular adrenocortical hyperplasia (PBMAH) is a rare form of adrenocorticotropic hormone (ACTH)-independent Cushing's syndrome (CS), responsible for <1% of endogenous hypercortisolemia ( Stratakis