Pillai Nishitha R, Amin Hitha, Gijavanekar Charul, Liu Ning, Issaq Niveen, Broniowska Katarzyna A, Bertuch Alison A, Sutton V Reid, Elsea Sarah H, Scaglia Fernando
Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA.
Texas Children's Hospital, Houston, Texas, USA.
Am J Med Genet A. 2020 Nov;182(11):2781-2787. doi: 10.1002/ajmg.a.61851. Epub 2020 Sep 10.
Riboflavin transporter deficiency (RTD) (MIM #614707) is a neurogenetic disorder with its most common manifestations including sensorineural hearing loss, peripheral neuropathy, respiratory insufficiency, and bulbar palsy. Here, we present a 2-year-old boy whose initial presentation was severe macrocytic anemia necessitating multiple blood transfusions and intermittent neutropenia; he subsequently developed ataxia and dysarthria. Trio-exome sequencing detected compound heterozygous variants in SLC52A2 that were classified as pathogenic and a variant of uncertain significance. Bone marrow evaluation demonstrated megaloblastic changes. Notably, his anemia and neutropenia resolved after treatment with oral riboflavin, thus expanding the clinical phenotype of this disorder. We reiterate the importance of starting riboflavin supplementation in a young child who presents with macrocytic anemia and neurological features while awaiting biochemical and genetic work up. We detected multiple biochemical abnormalities with the help of untargeted metabolomics analysis associated with abnormal flavin adenine nucleotide function which normalized after treatment, emphasizing the reversible pathomechanisms involved in this disorder. The utility of untargeted metabolomics analysis to monitor the effects of riboflavin supplementation in RTD has not been previously reported.
核黄素转运蛋白缺乏症(RTD)(MIM #614707)是一种神经遗传性疾病,其最常见的表现包括感音神经性听力损失、周围神经病变、呼吸功能不全和延髓麻痹。在此,我们报告一名2岁男孩,其最初表现为严重的大细胞性贫血,需要多次输血以及间歇性中性粒细胞减少;随后他出现了共济失调和构音障碍。三联外显子组测序在SLC52A2基因中检测到复合杂合变异,这些变异被分类为致病性变异以及一个意义未明的变异。骨髓评估显示有巨幼细胞改变。值得注意的是,口服核黄素治疗后他的贫血和中性粒细胞减少症得到缓解,从而扩展了该疾病的临床表型。我们重申,在一名出现大细胞性贫血和神经学特征的幼儿中,在等待生化和基因检查结果期间开始补充核黄素的重要性。我们借助非靶向代谢组学分析检测到了多种与黄素腺嘌呤核苷酸功能异常相关的生化异常,这些异常在治疗后恢复正常,强调了该疾病中涉及的可逆病理机制。此前尚未报道非靶向代谢组学分析在监测RTD中核黄素补充效果方面的效用。