| Literature DB >> 26141459 |
Ashlee R Stiles1, Leah Venturoni2, Grace Mucci3, Naser Elbalalesy4, Michael Woontner2, Stephen Goodman2, Jose E Abdenur5,6.
Abstract
2-Ketoadipic aciduria (OMIM 204750), a defect in the catabolic pathway of tryptophan, lysine, and hydroxylysine, is characterized by elevations in 2-ketoadipic, 2-aminoadipic, and 2-hydroxyadipic acids. Patients with the aforementioned biochemical profile have been described with a wide range of clinical presentations, from early-onset developmental delay, epilepsy, ataxia, and microcephaly to completely normal. This broad range of phenotypes has led some to question whether 2-ketoadipic aciduria represents a true disease state or if the biochemical abnormalities found in these patients merely reflect an ascertainment bias. We present four additional individuals from two families, with 2-ketoadipic aciduria with compound heterozygous or homozygous mutations in DHTKD1, three of which remain asymptomatic.Entities:
Keywords: 2-Aminoadipic; 2-Ketoadipic aciduria; 2-Oxoadipic aciduria; DHTKD1; Hydroxylysine; Lysine; Organic acidemia; Tryptophan
Year: 2015 PMID: 26141459 PMCID: PMC5059180 DOI: 10.1007/8904_2015_462
Source DB: PubMed Journal: JIMD Rep ISSN: 2192-8304