Best Practice for Identification of Classical 21-Hydroxylase Deficiency Should Include 21 Deoxycortisol Analysis with Appropriate Isomeric Steroid Separation.

21-deoxycortisol best practice congenital adrenal hyperplasia interferences isobaric steroids liquid chromatography–tandem mass spectrometry method validation newborn screening

Journal

International journal of neonatal screening
ISSN: 2409-515X
Titre abrégé: Int J Neonatal Screen
Pays: Switzerland
ID NLM: 101665400

Informations de publication

Date de publication:
16 Oct 2023
Historique:
received: 30 07 2023
revised: 18 09 2023
accepted: 09 10 2023
medline: 24 10 2023
pubmed: 24 10 2023
entrez: 24 10 2023
Statut: epublish

Résumé

There are mixed reports on the inclusion and use of 21 deoxycortisol (21DF) as the primary decision marker for classical 21-hydroxylase deficiency. We hypothesize that this may be due to insufficient recognition of the presence and chromatographic separation of isomeric steroids. The aim of this study was to determine the comparative utility of 21DF for screening and diagnosis of CAH due to classical 21-hydroxylase deficiency using a second-tier LC-MS/MS method that included the separation of isomeric steroids to 17OHP and 21DF. For each baby sample, one 3.2 mm dried blood spot was eluted in a methanolic solution containing isotopically matched internal standards. Data were interrogated by univariate and receiver operator characteristic analysis. Steroid profile results were generated for 924 non-CAH baby samples (median gestational age 37 weeks, range 22 to 43 weeks) and 17 babies with 21-hydroxylase deficiency. The ROC curves demonstrated 21DF to have the best sensitivity and specificity for the diagnosis of classical 21-hydroxylase deficiency with an AUC = 1.0. The heatmap showed the very strong correlation (r = 0.83) between 17OHP and 21DF. Our data support 21DF as a robust marker for CAH due to 21-hydroxylase deficiency. We recommend that 21DF be incorporated into routine newborn screening panels as part of the second-tier LC-MS/MS method, follow-up plasma steroid panels, and external quality assurance material.

Identifiants

pubmed: 37873849
pii: ijns9040058
doi: 10.3390/ijns9040058
pmc: PMC10594498
pii:
doi:

Types de publication

Journal Article

Langues

eng

Références

Ann Clin Biochem. 1994 Nov;31 ( Pt 6):561-5
pubmed: 7880075
J Paediatr Child Health. 2006 Oct;42(10):652-4
pubmed: 16972976
J Steroid Biochem Mol Biol. 2018 May;179:88-103
pubmed: 28962971
J Clin Endocrinol Metab. 2021 Oct 21;106(11):e4487-e4496
pubmed: 34171085
Ann Lab Med. 2015 Nov;35(6):578-85
pubmed: 26354345
Trends Endocrinol Metab. 2004 Sep;15(7):311-5
pubmed: 15350602
J Clin Endocrinol Metab. 2020 Aug 1;105(8):
pubmed: 32525982
Ann Lab Med. 2019 May;39(3):263-270
pubmed: 30623618
J Clin Endocrinol Metab. 2022 Nov 25;107(12):3341-3352
pubmed: 36071550
Int J Neonatal Screen. 2020 Jan 28;6(1):6
pubmed: 33073005
J Endocr Soc. 2017 Feb 10;1(3):186-201
pubmed: 29264476
Pediatr Dev Pathol. 2005 May-Jun;8(3):397-401
pubmed: 16010485
Int J Neonatal Screen. 2020 Aug 28;6(3):
pubmed: 33239597
J Pediatr. 2022 Mar;242:213-219.e1
pubmed: 34780778
Clin Chem Lab Med. 2022 Dec 02;61(3):e64-e66
pubmed: 36457285
Genet Med. 2021 Jun;23(6):1143-1150
pubmed: 33442021
Horm Res Paediatr. 2019;91(6):416-420
pubmed: 31450227
Medicina (Kaunas). 2021 Sep 29;57(10):
pubmed: 34684072
Int J Neonatal Screen. 2020 Aug 12;6(3):63
pubmed: 33117905
J Clin Endocrinol Metab. 2002 Sep;87(9):4106-10
pubmed: 12213856
J Clin Endocrinol Metab. 2004 Dec;89(12):6087-91
pubmed: 15579762
Bioanalysis. 2010 Aug;2(8):1397-403
pubmed: 21083340
Clin Biochem. 2014 Oct;47(15):5-15
pubmed: 25086367
Horm Res Paediatr. 2015;84(5):311-8
pubmed: 26397944
Int J Neonatal Screen. 2021 Jun 29;7(3):
pubmed: 34209888
Int J Neonatal Screen. 2020 Aug 14;6(3):
pubmed: 33239590
Pediatr Res. 2004 Nov;56(5):701-5
pubmed: 15371568
Horm Res. 2008;69(5):266-75
pubmed: 18259105
J Steroid Biochem Mol Biol. 2019 Apr;188:77-85
pubmed: 30557606
Clin Chem Lab Med. 2018 Sep 25;56(10):1685-1697
pubmed: 29397022
Steroids. 2011 Dec 11;76(13):1437-42
pubmed: 21839763

Auteurs

Ronda F Greaves (RF)

Victorian Clinical Genetics Services, Murdoch Children's Research Institute, Parkville, VIC 3052, Australia.
Department of Paediatrics, University of Melbourne, Parkville, VIC 3052, Australia.

Monish Kumar (M)

Victorian Clinical Genetics Services, Murdoch Children's Research Institute, Parkville, VIC 3052, Australia.

Nazha Mawad (N)

Victorian Clinical Genetics Services, Murdoch Children's Research Institute, Parkville, VIC 3052, Australia.

Alberto Francescon (A)

Victorian Clinical Genetics Services, Murdoch Children's Research Institute, Parkville, VIC 3052, Australia.

Chris Le (C)

Victorian Clinical Genetics Services, Murdoch Children's Research Institute, Parkville, VIC 3052, Australia.

Michele O'Connell (M)

Department of Paediatrics, University of Melbourne, Parkville, VIC 3052, Australia.
Department of Endocrinology, The Royal Children's Hospital, Parkville, VIC 3052, Australia.

James Chi (J)

Victorian Clinical Genetics Services, Murdoch Children's Research Institute, Parkville, VIC 3052, Australia.

James Pitt (J)

Victorian Clinical Genetics Services, Murdoch Children's Research Institute, Parkville, VIC 3052, Australia.
Department of Paediatrics, University of Melbourne, Parkville, VIC 3052, Australia.

Classifications MeSH