Thiamine deficiency in childhood with attention to genetic causes: Survival and outcome predictors

Ann Neurol. 2017 Sep;82(3):317-330. doi: 10.1002/ana.24998. Epub 2017 Aug 30.

Abstract

Primary and secondary conditions leading to thiamine deficiency have overlapping features in children, presenting with acute episodes of encephalopathy, bilateral symmetric brain lesions, and high excretion of organic acids that are specific of thiamine-dependent mitochondrial enzymes, mainly lactate, alpha-ketoglutarate, and branched chain keto-acids. Undiagnosed and untreated thiamine deficiencies are often fatal or lead to severe sequelae. Herein, we describe the clinical and genetic characterization of 79 patients with inherited thiamine defects causing encephalopathy in childhood, identifying outcome predictors in patients with pathogenic SLC19A3 variants, the most common genetic etiology. We propose diagnostic criteria that will aid clinicians to establish a faster and accurate diagnosis so that early vitamin supplementation is considered. Ann Neurol 2017;82:317-330.

MeSH terms

  • Adolescent
  • Age of Onset
  • Child
  • Child, Preschool
  • Female
  • Humans
  • Infant
  • Membrane Transport Proteins / genetics
  • Mitochondrial Membrane Transport Proteins
  • Mutation
  • Prognosis
  • Survival Rate
  • Thiamine Deficiency / genetics*
  • Thiamine Deficiency / mortality
  • Young Adult

Substances

  • Membrane Transport Proteins
  • Mitochondrial Membrane Transport Proteins
  • SLC19A3 protein, human
  • SLC25A19 protein, human