| Literature DB >> 30159852 |
Tina Shirzadeh1, Amir Hossein Saeidian2,3, Hamideh Bagherian1, Shadab Salehpour4,5, Aria Setoodeh6,7, Mohammad Reza Alaei4, Leila Youssefian2,3,8, Ashraf Samavat9, Andrew Touati10, Mohammad-Sadegh Fallah1, Hassan Vahidnezhad2,11, Morteza Karimipoor11, Sarah Azadmehr1, Marzieh Raeisi12,13, Ameneh Bandehi Sarhadi1, Fatemeh Zafarghandi Motlagh1, Mojdeh Jamali1, Zahra Zeinali1, Maryam Abiri14, Sirous Zeinali15,16.
Abstract
Phenylketonuria (PKU) is an inborn error of amino acid metabolism caused by mutations in the phenylalanine hydroxylase (PAH) gene, characterized by intellectual deficit and neuropsychiatric complications in untreated patients with estimated frequency of about one in 10,000 to 15,000 live births. PAH deficiency can be detected by neonatal screening in nearly all cases with hyperphenylalaninemia on a heel prick blood spot. Molecular testing of the PAH gene can then be performed in affected family members. Herein, we report molecular study of 635 patients genetically diagnosed with PKU from all ethnicities in Iran. The disease-causing mutations were found in 611 (96.22%) of cases. To the best of our knowledge, this is the most comprehensive molecular genetics study of PKU in Iran, identifying 100 distinct mutations in the PAH gene, including 15 previously unreported mutations. Interestingly, we found unique cases of PKU with uniparental disomy, germline mosaicism, and coinheritance with another Mendelian single-gene disorder that provides new insights for improving the genetic counseling, prenatal diagnosis (PND), and/or pre-implantation genetic diagnosis (PGD) for the inborn error of metabolism group of disorders.Entities:
Keywords: Consanguinity; Genetic counseling; Metabolism; Phenylketonuria
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Year: 2018 PMID: 30159852 DOI: 10.1007/s10545-018-0228-6
Source DB: PubMed Journal: J Inherit Metab Dis ISSN: 0141-8955 Impact factor: 4.982