| Literature DB >> 25504888 |
Miriam Erlacher1, Sarah Catharina Grünert, Annamaria Cseh, Robert Steinfeld, Ulrich Salzer, Ekkehart Lausch, Ulrike Nosswitz, Gregor Dückers, Tim Niehues, Stephan Ehl, Charlotte Marie Niemeyer, Carsten Speckmann.
Abstract
Mutations in SLC46A1 result in a defect of the proton coupled folate transporter (PCFT) and are the basis of hereditary folate malabsorption (HFM). Patients with HFM frequently present with neurodevelopmental delay and megaloblastic anemia. Some cases may be complicated by additional lymphopenia and immunodeficiency. We report a patient with a new homozygous mutation in the SLC46A1 gene. The boy presented with early-onset pancytopenia and secondary immunodeficiency. We provide clinical and molecular observations that extend the phenotypic description of HFM and highlight diagnostic as well as therapeutic pitfalls in this rare condition.Entities:
Keywords: bone marrow failure; congenital (not HIV); hematology; immunodeficiency; immunology; infections in imunocompromised host non-malignant
Mesh:
Year: 2014 PMID: 25504888 DOI: 10.1002/pbc.25364
Source DB: PubMed Journal: Pediatr Blood Cancer ISSN: 1545-5009 Impact factor: 3.167