CSF 5-Methyltetrahydrofolate Serial Monitoring to Guide Treatment of Congenital Folate Malabsorption Due to Proton-Coupled Folate Transporter (PCFT) Deficiency.

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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.

Published: September 2015

AI Article Synopsis

  • Hereditary folate malabsorption is a genetic disorder that leads to folate deficiency, causing megaloblastic anemia, immunodeficiency, seizures, and cognitive issues, particularly affecting the central nervous system (CNS).
  • A 7-year-old girl with this condition has a mutation in the SLC46A1 gene, preventing proper folate transport, resulting in extremely low levels of folate in her blood and cerebrospinal fluid (CSF), leading to serious health problems.
  • Treatment with folinic acid has shown to be effective, helping alleviate symptoms and improve folate levels in the CNS, emphasizing the importance of early diagnosis and intervention in managing this condition.

Article Abstract

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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4582027PMC
http://dx.doi.org/10.1007/8904_2015_445DOI Listing

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