Improved biochemical and neurodevelopmental profiles with high-dose hydroxocobalamin therapy in cobalamin C defect

J Inherit Metab Dis. 2025 Jan;48(1):e12787. doi: 10.1002/jimd.12787. Epub 2024 Aug 17.

Abstract

Cobalamin C (Cbl-C) defect causes methylmalonic acidemia, homocystinuria, intellectual disability and visual impairment, despite treatment adherence. While international guidelines recommend parenteral hydroxocobalamin (OH-Cbl) as effective treatment, dose adjustments remain unclear. We assessed OH-Cbl therapy impact on biochemical, neurocognitive and visual outcomes in early-onset Cbl-C patients treated with different OH-Cbl doses over 3 years. Group A (n = 5), diagnosed via newborn screening (NBS), received high-dose OH-Cbl (median 0.55 mg/kg/day); Group B1 (n = 3), NBS-diagnosed, received low-dose OH-Cbl (median 0.09 mg/kg/day); Group B2 (n = 12), diagnosed on clinical bases, received low-dose OH-Cbl (median 0.06 mg/kg/day). Biochemical analyses revealed better values of homocysteine, methionine and methylmalonic acid in Group A compared to Group B1 (p < 0.01, p < 0.05 and p < 0.01, respectively) and B2 (p < 0.001, p < 0.01 and p < 0.001, respectively). Neurodevelopmental assessment showed better outcome in Group A compared to low-dose treated Groups B1 and B2, especially in Developmental Quotient, Hearing and Speech and Performance subscales without significant differences between Group B2 and Group B1. Maculopathy was detected in 100%, 66% and 83% of patients in the three groups, respectively. This study showed that "high-dose" OH-Cbl treatment in NBS-diagnosed children with severe early-onset Cbl-C defect led to a significant improvement in the metabolic profile and in neurocognitive outcome, compared to age-matched patients treated with a "low-dose" regimen. Effects on maculopathy seem unaffected by OH-Cbl dosage. Our findings, although observed in a limited number of patients, may contribute to improve the long-term outcome of Cbl-C patients.

Keywords: biochemical improvement; cobalamin C defect; high‐dose hydroxocobalamin therapy; neurodevelopmental outcome.

MeSH terms

  • Amino Acid Metabolism, Inborn Errors / drug therapy
  • Child
  • Child, Preschool
  • Female
  • Homocysteine / blood
  • Homocystinuria* / drug therapy
  • Humans
  • Hydroxocobalamin* / administration & dosage
  • Hydroxocobalamin* / therapeutic use
  • Infant
  • Infant, Newborn
  • Male
  • Methionine
  • Methylmalonic Acid
  • Neonatal Screening*
  • Treatment Outcome
  • Vitamin B 12 / administration & dosage
  • Vitamin B 12 Deficiency / congenital
  • Vitamin B 12 Deficiency / drug therapy

Substances

  • Hydroxocobalamin
  • Methylmalonic Acid
  • Vitamin B 12
  • Homocysteine
  • Methionine

Supplementary concepts

  • Methylmalonic acidemia
  • Methylmalonic acidemia with homocystinuria