Torres A, Newton S A, Crompton B, Borzutzky A, Neufeld E J, Notarangelo L, Berry G T
Department of Pediatrics, Division of Pediatric Neurology, Boston Medical Center, Boston University Medical School, Boston, MA, USA.
Department of Neurology, Divisions of Hematology and Genetics and Genomics, The Manton Center for Orphan Disease Research, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
JIMD Rep. 2015;24:91-6. doi: 10.1007/8904_2015_445. Epub 2015 May 26.
Hereditary folate malabsorption is characterized by folate deficiency with impaired folate transport into the central nervous system (CNS). This disease is characterized by megaloblastic anemia of early appearance, combined immunodeficiency, seizures, and cognitive impairment. The anemia and immunologic disease are responsive but neurological signs are refractory to folic-acid treatment. We report a 7-year-old girl who has congenital folate deficiency and SLC46A1 gene mutation who is unable to transport folate from her gut to the circulatory system and consequently from the blood to the cerebrospinal fluid (CSF). As a result she developed undetectable 5-methyltetrahydrofolate levels in her plasma and CSF and became immunocompromised and quite ill. Intramuscular treatment with 5-formyltetrahydrofolate (folinic acid) was therapeutic at her presentation and has been successful preventing other signs and symptoms of hereditary folate malabsorption even at relatively low CSF levels. Although difficult, early detection and diagnosis of cerebral folate deficiency are important because folinic acid at a pharmacologic dose may normalize outcome in PCFT gene defects, as well as bypass autoantibody-blocked folate receptors and enter the cerebrospinal fluid by way of the reduced folate carrier. This route elevates the 5-methyltetrahydrofolate level within the central nervous system and can prevent the neuropsychiatric disorder. CSF levels of 5-methyltetrahydrofolate between 18 and 46 nmol/L may be sufficient to eradicate CNS disease.
遗传性叶酸吸收不良的特征是叶酸缺乏,同时叶酸向中枢神经系统(CNS)的转运受损。这种疾病的特点是早期出现巨幼细胞贫血、联合免疫缺陷、癫痫发作和认知障碍。贫血和免疫性疾病对治疗有反应,但神经学症状对叶酸治疗无效。我们报告了一名7岁女孩,她患有先天性叶酸缺乏和SLC46A1基因突变,无法将叶酸从肠道转运到循环系统,进而无法从血液转运到脑脊液(CSF)。结果,她的血浆和脑脊液中5-甲基四氢叶酸水平检测不到,免疫功能受损且病情严重。在她就诊时,肌内注射5-甲酰四氢叶酸(亚叶酸)具有治疗效果,即使在脑脊液水平相对较低时,也成功预防了遗传性叶酸吸收不良的其他体征和症状。尽管困难,但早期发现和诊断脑叶酸缺乏很重要,因为药理剂量的亚叶酸可能使PCFT基因缺陷的预后正常化,还能绕过自身抗体阻断的叶酸受体,并通过还原型叶酸载体进入脑脊液。这条途径可提高中枢神经系统内的5-甲基四氢叶酸水平,并能预防神经精神障碍。脑脊液中5-甲基四氢叶酸水平在18至46 nmol/L之间可能足以根除中枢神经系统疾病。