p.Val452Ile mutation of the SLC25A13 gene in a Turkish patient with citrin deficiency.
p.Val452Ile mutation of the SLC25A13 gene in a Turkish patient with citrin deficiency.
复制标题
土耳其柑橘缺乏症患者的 SLC25A13 基因 p.Val452Ile 突变。
DOI:
10.24953/turkjped.2017.03.012
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发表时间:
2017
期刊:
影响因子:
--
通讯作者:
Neslihan Önenli
中科院分区:
文献类型:
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作者:
Berna Şeker;D. Kör;Gökhan Tümgör;S. Ceylaner;Neslihan Önenli
Şeker-Yılmaz B, Kör D, Tümgör G, Ceylaner S, Önenli-Mungan N. p.Val452Ile mutation of the SLC25A13 gene in a Turkish patient with citrin deficiency. Turk J Pediatr 2017; 59: 311-314. Citrin deficiency is an autosomal recessive metabolic disorder, which is caused by pathogenic mutations in the SLC25A13 gene on chromosome 7q21.3, as the causative gene that encodes the liver type aspartate/glutamate carrier isoform 2 (AGC2). One of the main clinical presentations is neonatal intrahepatic cholestatic hepatitis caused by citrin deficiency. We report a Turkish child presented with prolonged neonatal jaundice associated with elevated plasma citrulline and galactosuria. NICCD was suspected at this point and mutation study of SLC25A13 showed that she was homozygous for the missense NM_014251.2:c.1354G > A (NP_055066.1:p.Val452Ile) (dbSNP: rs143877538) mutation. Dramatic response was observed to the dietary treatment with medium-chain triglycerides containing formula, ursodeoxycholic acid and fat-soluble vitamin supplementation. The minor allele frequency of this variant was given as nearly as 0.01 in the South Asian population; it seems like a disease causing variant. This is the first report of this variant in the Turkish and European population.