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L-2(OH) glutaric aciduria

Last edited: 4/14/2026

Overview

Glutaric aciduria type 1 (GA1) is an inherited metabolic disorder characterized by deficiency of the enzyme electron transfer flavoprotein-ubiquinone oxidoreductase (ETF-QO), leading to accumulation of glutaric and related organic acids. This accumulation can cause neurological damage, particularly in early childhood, but can also present with diverse symptoms in adulthood 1.

Diagnosis

  • Key Diagnostic Criteria: Elevated urinary glutaric acid (>4 mmol/mol creatinine) and 3-hydroxyglutaric acid (>1 mmol/mol creatinine) 1.
  • Recommended Tests: Urinary organic acid analysis, plasma glutaryl carnitine levels 1.
  • Imaging Findings: MRI may show confluent bilateral symmetric white matter signal abnormalities, Sylvian fissure widening, and cerebral atrophy 1.
  • Management

  • First-Line Treatment: L-carnitine supplementation to mitigate metabolic derangements 1.
  • Adjunctive Treatments: Caloric support with dextrose infusion during critical periods, such as peripartum management 2.
  • Dietary Management: High-caloric, protein-rich diet with essential amino acid supplementation, particularly in cases of malnutrition 3.
  • Special Populations

  • Pregnancy: Ensure adequate caloric intake and carnitine supplementation during delivery to prevent encephalopathic crisis 2.
  • Malnutrition: Address nutritional deficiencies, especially essential amino acids and trace elements like zinc, to manage complications like acrodermatitis enteropathica-like skin lesions 3.
  • Key Recommendations

  • Perform urinary organic acid testing in patients with suspected leukodystrophies to identify treatable metabolic disorders like GA1 (Evidence: Moderate 1).
  • Maintain adequate caloric intake and carnitine supplementation during critical periods, such as pregnancy and delivery, to prevent metabolic crises in GA1 patients (Evidence: Expert opinion 2).
  • Supplement with a high-calorie, protein-rich diet and essential nutrients (e.g., zinc) in GA1 patients experiencing malnutrition to address associated complications (Evidence: Weak 3).
  • References

    1 Badve MS, Bhuta S, Mcgill J. Rare presentation of a treatable disorder: glutaric aciduria type 1. The New Zealand medical journal 2015. link 2 Ituk US, Allen TK, Habib AS. The peripartum management of a patient with glutaric aciduria type 1. Journal of clinical anesthesia 2013. link 3 Niiyama S, Koelker S, Degen I, Hoffmann GF, Happle R, Hoffmann R. Acrodermatitis acidemica secondary to malnutrition in glutaric aciduria type I. European journal of dermatology : EJD 2001. link 4 Shigeoka S, Nakano Y. Characterization and molecular properties of 2-oxoglutarate decarboxylase from Euglena gracilis. Archives of biochemistry and biophysics 1991. link90160-k)

    Original source

    1. [1]
      Rare presentation of a treatable disorder: glutaric aciduria type 1.Badve MS, Bhuta S, Mcgill J The New Zealand medical journal (2015)
    2. [2]
      The peripartum management of a patient with glutaric aciduria type 1.Ituk US, Allen TK, Habib AS Journal of clinical anesthesia (2013)
    3. [3]
      Acrodermatitis acidemica secondary to malnutrition in glutaric aciduria type I.Niiyama S, Koelker S, Degen I, Hoffmann GF, Happle R, Hoffmann R European journal of dermatology : EJD (2001)
    4. [4]
      Characterization and molecular properties of 2-oxoglutarate decarboxylase from Euglena gracilis.Shigeoka S, Nakano Y Archives of biochemistry and biophysics (1991)

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