Adrenoleukodystrophy: the most frequent genetic cause of Addison’s disease
Abstract
Research Articles| November 17 2004 Adrenoleukodystrophy: The Most Frequent Genetic Cause of Addison's Disease Subject Area: Endocrinology , Women's and Children's Health Patrick Aubourg; Patrick Aubourg Department of Paediatric Endocrinology, Saint Vincent de Paul Hospital, Paris; Medical School of Paris V-René Descartes University, and INSERM Unit 342, Paris, France Search for other works by this author on: This Site PubMed Google Scholar Jean-Louis Chaussain Jean-Louis Chaussain Department of Paediatric Endocrinology, Saint Vincent de Paul Hospital, Paris; Medical School of Paris V-René Descartes University, and INSERM Unit 342, Paris, France Search for other works by this author on: This Site PubMed Google Scholar Hormone Research (2003) 59 (Suppl. 1): 104–105. https://doi.org/10.1159/000067833 Article history Published Online: November 17 2004 Content Tools Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation Patrick Aubourg, Jean-Louis Chaussain; Adrenoleukodystrophy: The Most Frequent Genetic Cause of Addison's Disease. Hormone Research 1 January 2003; 59 (Suppl. 1): 104–105. https://doi.org/10.1159/000067833 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsHormone Research in Paediatrics Search Advanced Search Article PDF first page preview Close Modal 2004Copyright / Drug Dosage / DisclaimerCopyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements. You do not currently have access to this content.
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In X-ALD related PAI, mineralocorticoid function can remain unaffected.
“While PAI is commonly associated with deficits in both glucocorticoid and mineralocorticoid functions, it’s worth noting that in cases of X-ALD related PAI, the mineralocorticoid function can remain unaffected (9, 10).”
From X-linked adrenoleukodystrophy and primary adrenal insufficiency (2023) · cites this paper as [10]
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X-linked adrenoleukodystrophy and primary adrenal insufficiency
Cappa, M., Todisco, T., & Bizzarri, C. (2023) · Frontiers in Endocrinology · doi:10.3389/fendo.2023.1309053 · Cited by 28 · see citing works
- Authors
- Aubourg, P., & Chaussain, J.-L.
- Affiliations
- Inserm (FR)
- Venue
- Hormone Research in Paediatrics
- Publisher
- S. Karger AG
- Published
- 2003
- Volume
- 59
- Issue
- 1
- Pages
- 104-105
- ISSN
- 1663-2818 (ISSN-L)
- 1663-2826
- OpenAlex
- W2036949250
- Cited by
- 19
- References
- 0
- Citations by year
- 2023: 2 · 2021: 1 · 2019: 1 · 2017: 1 · 2015: 1 · 2013: 3
- FWCI
- 1.30
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Hormone Research in Paediatrics (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Metabolism and Genetic Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Sexual Differentiation and Disorders
- Keywords
- adrenoleukodystrophy, Addison's disease, genetic etiology, ABCD1 gene, leukodystrophy, pediatric endocrinology, adrenal cortex dysfunction, fatty acid oxidation disorders, inborn errors of metabolism
- MeSH terms
- Addison Disease, Adrenoleukodystrophy, Female, Humans, Male
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