Mapping the genetic landscape of treatable inherited metabolic disorders in a large Middle Eastern biobank.

Inherited metabolic disorders Middle Eastern population VUS reclassification carrier frequency inbreeding coefficient

Journal

Genetics in medicine : official journal of the American College of Medical Genetics
ISSN: 1530-0366
Titre abrégé: Genet Med
Pays: United States
ID NLM: 9815831

Informations de publication

Date de publication:
13 Sep 2024
Historique:
received: 28 03 2024
revised: 10 09 2024
accepted: 10 09 2024
medline: 17 9 2024
pubmed: 17 9 2024
entrez: 17 9 2024
Statut: aheadofprint

Résumé

To date, approximately 1,400 inherited metabolic disorders (IMDs) have been described, some of which are treatable. It is estimated that 2-3% of live births worldwide are affected by treatable IMDs. Roughly 80% of IMDs are autosomal recessive, leading to a potentially higher incidence in regions with high consanguinity. The study utilized genome sequencing (GS) data from 14,060 adult Qatari participants who were recruited by the Qatar Biobank (QBB) and sequenced by the Qatar Genome Program (QGP). The GS data was analysed for 125 nuclear genes known to be associated with 115 treatable IMDs. Our study identified 253 pathogenic/likely pathogenic SNVs associated with 69 treatable IMDs, including 211 known and 42 novel predicted loss-of-function variants. We estimated that approximately 1 in 13 unrelated individuals (8%) carry a heterozygous pathogenic variant for at least one of 46 treatable IMDs. Notably, phenylketonuria/hyperphenylalaninemia and homocystinuria had among the highest carrier frequencies (1 in 68 and 1 in 85, respectively). Population-based studies of treatable IMDs, particularly in globally under-studied populations, can identify high-frequency alleles segregating in the community and inform public health policies, including carrier and newborn screening.

Sections du résumé

BACKGROUND BACKGROUND
To date, approximately 1,400 inherited metabolic disorders (IMDs) have been described, some of which are treatable. It is estimated that 2-3% of live births worldwide are affected by treatable IMDs. Roughly 80% of IMDs are autosomal recessive, leading to a potentially higher incidence in regions with high consanguinity.
METHODOLOGY METHODS
The study utilized genome sequencing (GS) data from 14,060 adult Qatari participants who were recruited by the Qatar Biobank (QBB) and sequenced by the Qatar Genome Program (QGP). The GS data was analysed for 125 nuclear genes known to be associated with 115 treatable IMDs.
RESULTS RESULTS
Our study identified 253 pathogenic/likely pathogenic SNVs associated with 69 treatable IMDs, including 211 known and 42 novel predicted loss-of-function variants. We estimated that approximately 1 in 13 unrelated individuals (8%) carry a heterozygous pathogenic variant for at least one of 46 treatable IMDs. Notably, phenylketonuria/hyperphenylalaninemia and homocystinuria had among the highest carrier frequencies (1 in 68 and 1 in 85, respectively).
CONCLUSION CONCLUSIONS
Population-based studies of treatable IMDs, particularly in globally under-studied populations, can identify high-frequency alleles segregating in the community and inform public health policies, including carrier and newborn screening.

Identifiants

pubmed: 39286960
pii: S1098-3600(24)00202-8
doi: 10.1016/j.gim.2024.101268
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

101268

Investigateurs

Said I Ismail (SI)
Wadha Al-Muftah (W)
Radja Badji (R)
Hamdi Mbarek (H)
Dima Darwish (D)
Tasnim Fadl (T)
Heba Yasin (H)
Maryem Ennaifar (M)
Rania Abdellatif (R)
Fatima Alkuwari (F)
Muhammad Alvi (M)
Yasser Al-Sarraj (Y)
Chadi Saad (C)
Asmaa Althani (A)
Eleni Fethnou (E)
Fatima Qafoud (F)
Eiman Alkhayat (E)
Nahla Afifi (N)
Sara Tomei (S)
Wei Liu (W)
Stephan Lorenz (S)
Najeeb Syed (N)
Hakeem Almabrazi (H)
Fazulur Rehaman Vempalli (FR)
Ramzi Temanni (R)
Tariq Abu Saqri (TA)
Mohammedhusen Khatib (M)
Mehshad Hamza (M)
Tariq Abu Zaid (TA)
Ahmed El Khouly (A)
Tushar Pathare (T)
Shafeeq Poolat (S)
Rashid Al-Ali (R)
Omar Albagha (O)
Souhaila Al-Khodor (S)
Mashael Alshafai (M)
Ramin Badii (R)
Lotfi Chouchane (L)
Xavier Estivill (X)
Khalid A Fakhro (KA)
Hamdi Mbarek (H)
Younes Mokrab (Y)
Jithesh V Puthen (JV)
Karsten Suhre (K)
Zohreh Tatari (Z)

Informations de copyright

Copyright © 2024. Published by Elsevier Inc.

Auteurs

Geethanjali Devadoss Gandhi (G)

Human Genetics Department, Sidra Medicine, Doha, Qatar.

Elbay Aliyev (E)

Human Genetics Department, Sidra Medicine, Doha, Qatar.

Najeeb Syed (N)

Human Genetics Department, Sidra Medicine, Doha, Qatar.

Fazulur Rehaman Vempalli (FR)

Bioinformatics, Genomic Data Science Core Sec, Sidra Medicine, Doha, Qatar.

Chadi Saad (C)

Qatar Genome Program, Qatar Foundation Research Development and Innovation, Doha, Qatar.

Hamdi Mbarek (H)

Qatar Genome Program, Qatar Foundation Research Development and Innovation, Doha, Qatar.

Omayma Al-Saei (O)

Human Genetics Department, Sidra Medicine, Doha, Qatar.

Aljazi Al-Maraghi (A)

Human Genetics Department, Sidra Medicine, Doha, Qatar.

Mona Abdi (M)

Human Genetics Department, Sidra Medicine, Doha, Qatar.

Navaneethakrishnan Krishnamoorthy (N)

Human Genetics Department, Sidra Medicine, Doha, Qatar.

Ramin Badii (R)

Molecular Genetics Laboratory, Hamad Medical Corporation, Doha, Qatar.

Ammira Akil (A)

Human Genetics Department, Sidra Medicine, Doha, Qatar.

Tawfeg Ben-Omran (T)

Division of Genetic & Genomics Medicine, Sidra Medicine, Doha, Qatar; Department of Medical Genetics, Hamad Medical Corporation, Doha, Qatar; Department of Pediatric, Weill Cornell Medical College, Doha, Qatar.

Khalid A Fakhro (KA)

Human Genetics Department, Sidra Medicine, Doha, Qatar; College of Health and Life Sciences, Hamad Bin Khalifa University (HBKU), Doha, Qatar; Department of Genetic Medicine, Weill Cornell Medicine, Qatar, (WCM-Q). Electronic address: kfakhro@sidra.org.

Classifications MeSH