Type I Alexander disease: Update and validation of the clinical evolution-based classification.


Journal

Molecular genetics and metabolism
ISSN: 1096-7206
Titre abrégé: Mol Genet Metab
Pays: United States
ID NLM: 9805456

Informations de publication

Date de publication:
03 2023
Historique:
received: 21 11 2022
revised: 06 02 2023
accepted: 07 02 2023
pubmed: 23 2 2023
medline: 7 3 2023
entrez: 22 2 2023
Statut: ppublish

Résumé

Alexander disease (AxD) is a rare progressive leukodystrophy caused by autosomal dominant mutations in the Glial Fibrillary Acidic Protein (GFAP) gene. Three main disease classifications are currently in use, the traditional one defined by the age of onset, and two other based on clinical features at onset and brain MRI findings. Recently, we proposed a new classification, which is based on taking into consideration not only the presenting features, but also data related to the clinical course. In this study, we tried to apply this modified classification system to the cases of pediatric-onset AxD described in literature. A literature review was conducted in PubMed for articles published between 1949 to date. Articles that reported no patient's medical history and the articles about Adult-onset AxD were excluded. We included patients with a confirmed diagnosis of pediatric-onset AxD and of whom information about age and symptoms at onset, developmental milestones and loss of motor and language skills was available. Clinical data from 205 patients affected with pediatric-onset AxD were retrospectively reviewed. Among these, we identified 65 patients, of whom we had enough information about the clinical course and developmental milestones, and we assessed their disease evolutionary trajectories over time. Our results confirm that patients with Type I AxD might be classified into four subgroups (Ia, Ib, Ic, Id) basing on follow up data. In fact, despite the great variability of phenotypes in AxD, there are some shared trajectories of the disease evolution over time.

Sections du résumé

BACKGROUND AND OBJECTIVES
Alexander disease (AxD) is a rare progressive leukodystrophy caused by autosomal dominant mutations in the Glial Fibrillary Acidic Protein (GFAP) gene. Three main disease classifications are currently in use, the traditional one defined by the age of onset, and two other based on clinical features at onset and brain MRI findings. Recently, we proposed a new classification, which is based on taking into consideration not only the presenting features, but also data related to the clinical course. In this study, we tried to apply this modified classification system to the cases of pediatric-onset AxD described in literature.
METHODS
A literature review was conducted in PubMed for articles published between 1949 to date. Articles that reported no patient's medical history and the articles about Adult-onset AxD were excluded. We included patients with a confirmed diagnosis of pediatric-onset AxD and of whom information about age and symptoms at onset, developmental milestones and loss of motor and language skills was available.
RESULTS
Clinical data from 205 patients affected with pediatric-onset AxD were retrospectively reviewed. Among these, we identified 65 patients, of whom we had enough information about the clinical course and developmental milestones, and we assessed their disease evolutionary trajectories over time.
DISCUSSION
Our results confirm that patients with Type I AxD might be classified into four subgroups (Ia, Ib, Ic, Id) basing on follow up data. In fact, despite the great variability of phenotypes in AxD, there are some shared trajectories of the disease evolution over time.

Identifiants

pubmed: 36804850
pii: S1096-7192(23)00170-1
doi: 10.1016/j.ymgme.2023.107540
pii:
doi:

Substances chimiques

Glial Fibrillary Acidic Protein 0

Types de publication

Review Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

107540

Informations de copyright

Copyright © 2023 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare no conflict of interest.

Auteurs

Ylenia Vaia (Y)

Unit of Pediatric Neurology, C.O.A.L.A (Center for diagnosis and treatment of leukodystrophies), V. Buzzi Children's Hospital, Via Castelvetro 32, 20154 Milan, Italy; University of Milan, Via Festa del Perdono, 7, 20122 Milan, Italy.

Eleonora Mura (E)

Unit of Pediatric Neurology, C.O.A.L.A (Center for diagnosis and treatment of leukodystrophies), V. Buzzi Children's Hospital, Via Castelvetro 32, 20154 Milan, Italy; University of Milan, Via Festa del Perdono, 7, 20122 Milan, Italy.

Davide Tonduti (D)

Unit of Pediatric Neurology, C.O.A.L.A (Center for diagnosis and treatment of leukodystrophies), V. Buzzi Children's Hospital, Via Castelvetro 32, 20154 Milan, Italy; Department of Biomedical and Clinical Sciences, University of Milan, Via Giovanni Battista Grassi, 74, 20157 Milan, Italy. Electronic address: davide.tonduti@unimi.it.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH