| Literature DB >> 27306358 |
Shwetha Chiplunkar1,2, Parayil Sankaran Bindu3,4, Madhu Nagappa2,5, Cheminikara Bineesh5, Periyasamy Govindaraj2,5, Narayanappa Gayathri2,6, M M Srinivas Bharath2,7, Hanumanthapura R Arvinda8, Pavagada S Mathuranath5, Sanjib Sinha5, Arun B Taly2,5.
Abstract
Huppke -Brendel syndrome is a new addition to the evolving spectrum of copper metabolism defects. It is an autosomal recessive disorder characterized by congenital cataract, impaired hearing, and developmental delay with low copper and ceruloplasmin. It is caused by defects in SLC33A1 that codes for acetyl CoA transporter protein. Reports on variation in this gene causing human disease is extremely scarce and the metabolic link between this gene and copper metabolism is yet to be identified. Here we report a seven months old infant with Huppke-Brendel Syndrome. In addition to the already reported features, he also had hypo pigmented hair and hypogonadism. His magnetic resonance imaging revealed hypo myelination and cerebellar hypoplasia. Clinical exome sequencing revealed a homozygous two base pair deletion, c.542_543delTG (p.Val181GlyfsTer6) in exon 1 of the SLC33A1. This report expands the phenotypic and genotypic spectrum of Huppke Brendel syndrome.Entities:
Keywords: Acetyl co a transporter; Ceruloplasmin; Congenital cataract; Copper; Hypo- myelination; SLC33A1
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Year: 2016 PMID: 27306358 DOI: 10.1007/s11011-016-9854-6
Source DB: PubMed Journal: Metab Brain Dis ISSN: 0885-7490 Impact factor: 3.584