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Genetic analysis of pediatric primary adrenal insufficiency of unknown etiology: 25 years' experience in the UK

Genetic analysis of pediatric primary adrenal insufficiency of unknown etiology: 25 years' experience in the UK
Genetic analysis of pediatric primary adrenal insufficiency of unknown etiology: 25 years' experience in the UK

Context: Although primary adrenal insufficiency (PAI) in children and young people is often due to congenital adrenal hyperplasia (CAH) or autoimmunity, other genetic causes occur. The relative prevalence of these conditions is poorly understood.

Objective: We investigated genetic causes of PAI in children and young people over a 25 year period.

Design Setting and Participants: Unpublished and published data were reviewed for 155 young people in the United Kingdom who underwent genetic analysis for PAI of unknown etiology in three major research centers between 1993 and 2018. We pre-excluded those with CAH, autoimmune, or metabolic causes. We obtained additional data from NR0B1 (DAX-1) clinical testing centers.

Intervention and Outcome Measurements: Genetic analysis involved a candidate gene approach (1993 onward) or next generation sequencing (NGS; targeted panels, exomes) (2013-2018).

Results: A genetic diagnosis was reached in 103/155 (66.5%) individuals. In 5 children the adrenal insufficiency resolved and no genetic cause was found. Pathogenic variants occurred in 11 genes: MC2R (adrenocorticotropin receptor; 30/155, 19.4%), NR0B1 (DAX-1; 7.7%), CYP11A1 (7.7%), AAAS (7.1%), NNT (6.5%), MRAP (4.5%), TXNRD2 (4.5%), STAR (3.9%), SAMD9 (3.2%), CDKN1C (1.3%), and NR5A1/steroidogenic factor-1 (SF-1; 0.6%). Additionally, 51 boys had NR0B1 variants identified through clinical testing. Although age at presentation, treatment, ancestral background, and birthweight can provide diagnostic clues, genetic testing was often needed to define the cause.

Conclusions: PAI in children and young people often has a genetic basis. Establishing the specific etiology can influence management of this lifelong condition. NGS approaches improve the diagnostic yield when many potential candidate genes are involved.

Addison disease, NGS, adrenal, adrenal insufficiency, genetics
2472-1972
Buonocore, Federica
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Maharaj, Avinaash
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Qamar, Younus
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Koehler, Katrin
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Suntharalingham, Jenifer P
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Chan, Li F
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Ferraz-de-Souza, Bruno
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Lin, Lin
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Prasad, Rathi
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Allgrove, Jeremy
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Andrews, Edward T
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Buchanan, Charles R
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Cheetham, Tim D
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Crowne, Elizabeth C
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Davies, Justin H
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Gregory, John W
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Hindmarsh, Peter C
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Hulse, Tony
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Krone, Nils P
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Shah, Pratik
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Shaikh, M Guftar
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Roberts, Catherine
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Clayton, Peter E
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Dattani, Mehul T
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Thomas, N Simon
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Huebner, Angela
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Clark, Adrian J
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Metherell, Louise A
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Achermann, John C
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Buonocore, Federica
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Maharaj, Avinaash
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Qamar, Younus
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Koehler, Katrin
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Suntharalingham, Jenifer P
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Chan, Li F
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Ferraz-de-Souza, Bruno
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Lin, Lin
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Prasad, Rathi
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Allgrove, Jeremy
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Andrews, Edward T
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Buchanan, Charles R
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Cheetham, Tim D
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Crowne, Elizabeth C
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Davies, Justin H
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Gregory, John W
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Hindmarsh, Peter C
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Hulse, Tony
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Krone, Nils P
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Shah, Pratik
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Shaikh, M Guftar
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Roberts, Catherine
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Clayton, Peter E
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Dattani, Mehul T
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Thomas, N Simon
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Huebner, Angela
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Clark, Adrian J
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Metherell, Louise A
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Achermann, John C
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Buonocore, Federica, Maharaj, Avinaash, Qamar, Younus, Koehler, Katrin, Suntharalingham, Jenifer P, Chan, Li F, Ferraz-de-Souza, Bruno, Lin, Lin, Prasad, Rathi, Allgrove, Jeremy, Andrews, Edward T, Buchanan, Charles R, Cheetham, Tim D, Crowne, Elizabeth C, Davies, Justin H, Gregory, John W, Hindmarsh, Peter C, Hulse, Tony, Krone, Nils P, Shah, Pratik, Shaikh, M Guftar, Roberts, Catherine, Clayton, Peter E, Dattani, Mehul T, Thomas, N Simon, Huebner, Angela, Clark, Adrian J, Metherell, Louise A and Achermann, John C (2021) Genetic analysis of pediatric primary adrenal insufficiency of unknown etiology: 25 years' experience in the UK. Journal of the Endocrine Society, 5 (8), [bvab086]. (doi:10.1210/jendso/bvab086).

Record type: Article

Abstract

Context: Although primary adrenal insufficiency (PAI) in children and young people is often due to congenital adrenal hyperplasia (CAH) or autoimmunity, other genetic causes occur. The relative prevalence of these conditions is poorly understood.

Objective: We investigated genetic causes of PAI in children and young people over a 25 year period.

Design Setting and Participants: Unpublished and published data were reviewed for 155 young people in the United Kingdom who underwent genetic analysis for PAI of unknown etiology in three major research centers between 1993 and 2018. We pre-excluded those with CAH, autoimmune, or metabolic causes. We obtained additional data from NR0B1 (DAX-1) clinical testing centers.

Intervention and Outcome Measurements: Genetic analysis involved a candidate gene approach (1993 onward) or next generation sequencing (NGS; targeted panels, exomes) (2013-2018).

Results: A genetic diagnosis was reached in 103/155 (66.5%) individuals. In 5 children the adrenal insufficiency resolved and no genetic cause was found. Pathogenic variants occurred in 11 genes: MC2R (adrenocorticotropin receptor; 30/155, 19.4%), NR0B1 (DAX-1; 7.7%), CYP11A1 (7.7%), AAAS (7.1%), NNT (6.5%), MRAP (4.5%), TXNRD2 (4.5%), STAR (3.9%), SAMD9 (3.2%), CDKN1C (1.3%), and NR5A1/steroidogenic factor-1 (SF-1; 0.6%). Additionally, 51 boys had NR0B1 variants identified through clinical testing. Although age at presentation, treatment, ancestral background, and birthweight can provide diagnostic clues, genetic testing was often needed to define the cause.

Conclusions: PAI in children and young people often has a genetic basis. Establishing the specific etiology can influence management of this lifelong condition. NGS approaches improve the diagnostic yield when many potential candidate genes are involved.

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Accepted/In Press date: 3 May 0002
Published date: 11 May 2021
Additional Information: Financial Support: This research was funded in whole, or in part, by the Wellcome Trust (grants 098513/Z/12/Z and 209328/Z/17/Z). For the purpose of Open Access, the author has applied a CC BY public copyright license to any Author Accepted Manuscript version arising from this submission. JCA also has research support from Great Ormond Street Hospital Children’s Charity (grant V2518) and the National Institute for Health Research, Great Ormond Street Hospital Biomedical Research Centre (grant IS-BRC-1215–20012). LAM is supported by funding from Barts Charity (grant MGU0438) and the Medical Research Council (MRC; Project Grant MR/K020455/1). LFC received funding from the MRC (G0802796), IFCAH, BSPED, and Barts Charity (MGU0458). RP is supported by funding from the MRC (Project Grant MR/T02402X/1). The views expressed are those of the authors and not necessarily those of the National Health Service, National Institute for Health Research, or Department of Health. KK and AH are supported by funding from the German Research Foundation (grants KO 3588/2-1, HU 895/3-3, 3–4, 3–5, 4-1, 5-1, 5-2 and 314061271 CRC-TRR205).
Keywords: Addison disease, NGS, adrenal, adrenal insufficiency, genetics

Identifiers

Local EPrints ID: 453425
URI: http://eprints.soton.ac.uk/id/eprint/453425
ISSN: 2472-1972
PURE UUID: 03efd812-a70c-49e4-8ec2-2c3d0fb3eb74

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Date deposited: 14 Jan 2022 17:39
Last modified: 16 Mar 2024 14:30

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Contributors

Author: Federica Buonocore
Author: Avinaash Maharaj
Author: Younus Qamar
Author: Katrin Koehler
Author: Jenifer P Suntharalingham
Author: Li F Chan
Author: Bruno Ferraz-de-Souza
Author: Lin Lin
Author: Rathi Prasad
Author: Jeremy Allgrove
Author: Edward T Andrews
Author: Charles R Buchanan
Author: Tim D Cheetham
Author: Elizabeth C Crowne
Author: Justin H Davies
Author: John W Gregory
Author: Peter C Hindmarsh
Author: Tony Hulse
Author: Nils P Krone
Author: Pratik Shah
Author: M Guftar Shaikh
Author: Catherine Roberts
Author: Peter E Clayton
Author: Mehul T Dattani
Author: N Simon Thomas
Author: Angela Huebner
Author: Adrian J Clark
Author: Louise A Metherell
Author: John C Achermann

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