Clinical and Molecular Characteristics of Neuronal Ceroid Lipofuscinosis in Saudi Arabia.

Consanguinity Inherited metabolic diseases Neuronal ceroid lipofuscinoses Next-generation sequencing Recessive diseases Saudi Arabia

Journal

Pediatric neurology
ISSN: 1873-5150
Titre abrégé: Pediatr Neurol
Pays: United States
ID NLM: 8508183

Informations de publication

Date de publication:
07 Mar 2024
Historique:
received: 04 10 2022
revised: 15 02 2024
accepted: 03 03 2024
medline: 24 4 2024
pubmed: 24 4 2024
entrez: 23 4 2024
Statut: aheadofprint

Résumé

Neuronal ceroid lipofuscinoses (NCLs) represent a heterogeneous group of inherited metabolic lysosomal disorders characterized by neurodegeneration. This study sought to describe the clinical and molecular characteristics of NCLs in Saudi Arabia and determine the most common types in that population. A retrospective review of electronic medical records was conducted for 63 patients with NCL (55 families) from six tertiary and referral centers in Saudi Arabia between 2008 and 2022. Clinical, radiological, and neurophysiological data as well as genetic diagnoses were reviewed. CLN6 was the predominant type, accounting for 45% of cases in 25 families. The most common initial symptoms were speech delay (53%), cognitive decline (50%) and/or gait abnormalities (48%), and seizure (40%). Behavioral symptomatology was observed in 20%, whereas visual impairment was less frequently (9.3%) encountered. Diffuse cerebral and cerebellar atrophy was the predominant finding on brain magnetic resonance imaging. Electroencephalography generally revealed background slowing in all patients with generalized epileptiform discharges in 60%. The most common genotype detected was the p.Ser265del variant found in 36% (20 of 55 families). The most rapidly progressive subtypes were CLN2 and CLN6. Two patients with each died at age five years. The earliest age at which a patient was nonambulatory was two years in a patient with CLN14. This is the largest molecularly confirmed NCL cohort study from Saudi Arabia. Characterizing the natural history of specific NLC types can increase understanding of the underlying pathophysiology and distinctive genotype-phenotype characteristics, facilitating early diagnosis and treatment initiation as well as genetic counseling for families.

Sections du résumé

BACKGROUND BACKGROUND
Neuronal ceroid lipofuscinoses (NCLs) represent a heterogeneous group of inherited metabolic lysosomal disorders characterized by neurodegeneration. This study sought to describe the clinical and molecular characteristics of NCLs in Saudi Arabia and determine the most common types in that population.
METHODS METHODS
A retrospective review of electronic medical records was conducted for 63 patients with NCL (55 families) from six tertiary and referral centers in Saudi Arabia between 2008 and 2022. Clinical, radiological, and neurophysiological data as well as genetic diagnoses were reviewed.
RESULTS RESULTS
CLN6 was the predominant type, accounting for 45% of cases in 25 families. The most common initial symptoms were speech delay (53%), cognitive decline (50%) and/or gait abnormalities (48%), and seizure (40%). Behavioral symptomatology was observed in 20%, whereas visual impairment was less frequently (9.3%) encountered. Diffuse cerebral and cerebellar atrophy was the predominant finding on brain magnetic resonance imaging. Electroencephalography generally revealed background slowing in all patients with generalized epileptiform discharges in 60%. The most common genotype detected was the p.Ser265del variant found in 36% (20 of 55 families). The most rapidly progressive subtypes were CLN2 and CLN6. Two patients with each died at age five years. The earliest age at which a patient was nonambulatory was two years in a patient with CLN14.
CONCLUSIONS CONCLUSIONS
This is the largest molecularly confirmed NCL cohort study from Saudi Arabia. Characterizing the natural history of specific NLC types can increase understanding of the underlying pathophysiology and distinctive genotype-phenotype characteristics, facilitating early diagnosis and treatment initiation as well as genetic counseling for families.

Identifiants

pubmed: 38653183
pii: S0887-8994(24)00079-1
doi: 10.1016/j.pediatrneurol.2024.03.004
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

149-155

Investigateurs

Amal Kentab (A)
H H Muddathir (HH)
M A Salih (MA)
Aziza M Mushiba (AM)
A P Zada (AP)
Mohammed S Bamajboor (MS)
Sadique Zameer (S)
Fahad AlBassam (F)
Adel Mahmoud (A)
A A Alnawfal (AA)
Mushari AlAmr (M)
Maryam Bawazir (M)
Ahmed Al Rumayyan (A)
Waleed Al-Twaijri (W)
Muhammed Talal Alrifai (MT)
Sumayah Al Hajjaj (S)

Informations de copyright

Copyright © 2024 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare the following competing interests: Mohammed M. Saleh, Abdulrahim M. Hamhom, Ali AlOtaibi, Malak AlGhamdi, Yousef Housawi, Yaser I. Aljadhai, Seham Alameer, Mohammed Almannai, Lamyaa Ali Jad, Ali H. AlWadie, Sadia Tabassum, Abdulaziz Alsaman, Ali AlAsmari, Fuad Al Mutairi, Hamad Althiyab, Fahad A. Bashiri, Suzan AlHumaidi, Majid Alfadhel, and Aqeela AlHashim have no conflicts of interest to declare. Jonathan W. Mink is in receipt of research funding from Theranexus, Inc, Neurogene Inc, the National Institute of Neurological Disorders and Stroke, and the Eunice Kennedy Shriver National Institute of Child Health and Human Development; is a consultant for the Beyond Batten Disease Foundation, Amicus, Inc, Polaryx, Inc, and TEVA, Inc; is a member of Data and Safety Monitoring Board for PTC Therapeutics and Passage Bio; and is a Trial Steering Committee for Applied Therapeutics. Eissa A. Faqeih is in receipt of a research grant from the Intramural Research Fund for an extended project to study common genetic diseases in Saudi Arabia (Demography of Recessive Diseases in KSA; Grant #019-052).

Auteurs

Mohammed M Saleh (MM)

Section of Medical Genetics, Children's Specialist Hospital, King Fahad Medical City, Riyadh, Saudi Arabia.

Abdulrahim M Hamhom (AM)

Department of Pediatric Neurology, National Neuroscience Institute, King Fahad Medical City, Riyadh, Saudi Arabia.

Ali Al-Otaibi (A)

Department of Pediatric Neurology, National Neuroscience Institute, King Fahad Medical City, Riyadh, Saudi Arabia.

Malak AlGhamdi (M)

Unit of Medical Genetics, Department of Pediatrics, College of Medicine, King Saud University Medical City, King Saud University, Riyadh, Saudi Arabia.

Yousef Housawi (Y)

Section of Medical Genetics, Pediatric Department, King Fahad Specialist Hospital, Dammam, Saudi Arabia.

Yaser I Aljadhai (YI)

Department of Neuroimaging and Intervention, Medical Imaging Administration, King Fahad Medical City, Riyadh, Saudi Arabia.

Seham Alameer (S)

Department of Pediatric, Ministry of the National Guard-Health Affairs, King Abdullah International Medical Research Center, King Saud bin Abdulaziz University for Health Sciences, Jeddah, Saudi Arabia.

Mohammed Almannai (M)

Genetics and Precision Medicine Department (GPM), King Abdullah Specialized Children's Hospital (KASCH), King Abdulaziz Medical City, Ministry of National Guard Health Affairs (MNG-HA), Riyadh, Saudi Arabia.

Lamyaa A Jad (LA)

Department of Pediatric Neurology, National Neuroscience Institute, King Fahad Medical City, Riyadh, Saudi Arabia.

Ali H Alwadei (AH)

Department of Pediatric Neurology, National Neuroscience Institute, King Fahad Medical City, Riyadh, Saudi Arabia.

Sadia Tabassum (S)

Department of Pediatric Neurology, National Neuroscience Institute, King Fahad Medical City, Riyadh, Saudi Arabia.

Abdulaziz Alsaman (A)

Department of Pediatric Neurology, National Neuroscience Institute, King Fahad Medical City, Riyadh, Saudi Arabia.

Ali AlAsmari (A)

Section of Medical Genetics, Children's Specialist Hospital, King Fahad Medical City, Riyadh, Saudi Arabia.

Fuad Al Mutairi (F)

Genetics and Precision Medicine Department (GPM), King Abdullah Specialized Children's Hospital (KASCH), King Abdulaziz Medical City, Ministry of National Guard Health Affairs (MNG-HA), Riyadh, Saudi Arabia; King Saud Bin Abdulaziz University for Health Sciences (KSAU-HS), Ministry of National Guard Health Affairs (MNG-HA), Riyadh, Saudi Arabia.

Hamad Althiyab (H)

Genetics and Precision Medicine Department (GPM), King Abdullah Specialized Children's Hospital (KASCH), King Abdulaziz Medical City, Ministry of National Guard Health Affairs (MNG-HA), Riyadh, Saudi Arabia.

Fahad A Bashiri (FA)

Division of Pediatric Neurology, Department of Pediatrics, College of Medicine, King Saud University Medical City, King Saud University, Riyadh, Saudi Arabia.

Suzan AlHumaidi (S)

Section of Medical Genetics, Children's Hospital, King Saud Medical City, Riyadh, Saudi Arabia.

Majid Alfadhel (M)

Genetics and Precision Medicine Department (GPM), King Abdullah Specialized Children's Hospital (KASCH), King Abdulaziz Medical City, Ministry of National Guard Health Affairs (MNG-HA), Riyadh, Saudi Arabia; King Saud Bin Abdulaziz University for Health Sciences (KSAU-HS), Ministry of National Guard Health Affairs (MNG-HA), Riyadh, Saudi Arabia; Medical Genomics Research Department, King Abdullah International Medical Research Center, Ministry of National Guard Health Affairs (MNG-HA), Riyadh, Saudi Arabia.

Jonathan W Mink (JW)

Department of Neurology, University of Rochester, Rochester, New York.

Aqeela AlHashim (A)

Department of Pediatric Neurology, National Neuroscience Institute, King Fahad Medical City, Riyadh, Saudi Arabia.

Eissa A Faqeih (EA)

Section of Medical Genetics, Children's Specialist Hospital, King Fahad Medical City, Riyadh, Saudi Arabia. Electronic address: efaqeih@kfmc.med.sa.

Classifications MeSH