ArticleJIMD reports2017
Leigh-Like Syndrome Due to Homoplasmic m.8993T>G Variant with Hypocitrullinemia and Unusual Biochemical Features Suggestive of Multiple Carboxylase Deficiency (MCD).
Article in JIMD reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- Targeted Therapies for Leigh Syndrome: Systematic Review and Steps Towards a 'Treatabolome'.Journal of neuromuscular diseases · 2021Pooled it
- [Decreased plasma citrulline is a biochemical marker in newborn screening forZhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026Review
- Hypocitrullinemia as an Early Diagnostic Biomarker for MT-ATP6 Mitochondrial Diseases.Journal of molecular neuroscience : MN · 2025Article
- Leigh Syndrome: A Comprehensive Review of the Disease and Present and Future Treatments.Biomedicines · 2025Review
- Article
- Leigh Syndrome: Spectrum of Molecular Defects and Clinical Features in Russia.International journal of molecular sciences · 2023Article
- Milder Phenotype of Homoplasmic Versus Heteroplasmic m.8344A>G Variant in the Same Family: A Case Report.Cureus · 2022Article
- Mutational Analysis and mtDNA Haplogroup Characterization in Three Serbian Cases of Mitochondrial Encephalomyopathies and Literature Review.Diagnostics (Basel, Switzerland) · 2021Article
- [Genetic analysis of newborns with abnormal metabolism of 3-hydroxyisovalerylcarnitine].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2019Article
- Recent topics: the diagnosis, molecular genesis, and treatment of mitochondrial diseases.Journal of human genetics · 2019Review
- Biochemical signatures mimicking multiple carboxylase deficiency in children with mutations in MT-ATP6.Mitochondrion · 2019Article
- Clinical Application of Genome and Exome Sequencing as a Diagnostic Tool for Pediatric Patients: a Scoping Review of the Literature.Genetics in medicine : official journal of the American College of Medical Genetics · 2019Article
- Vaccination triggering onset of m.8993T > G associated Leigh syndrome.Molecular genetics and metabolism reports · 2018Article
- The role of the clinician in the multi-omics era: are you ready?Journal of inherited metabolic disease · 2018Article
- 8-year retrospective analysis of intravenous arginine therapy for acute metabolic strokes in pediatric mitochondrial disease.Molecular genetics and metabolism · 2018Article
- [Leigh syndrome caused by the mitochondrial m.8993T>G mutation with hypocitrullinemia: a report of four cases and literature review].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatricsReview
- Prospective diagnosis of MT-ATP6-related mitochondrial disease by newborn screening.Molecular genetics and metabolismArticle
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 7 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Leigh syndrome (LS), or subacute necrotizing encephalomyelopathy, is a genetically heterogeneous, relentlessly progressive, devastating neurodegenerative disorder that usually presents in infancy or early childhood. A diagnosis of Leigh-like syndrome may be considered in individuals who do not fulfil the stringent diagnostic criteria but have features resembling Leigh syndrome.We describe a unique presentation of Leigh-like syndrome in a 3-year-old boy with elevated 3-hydroxyisovalerylcarnitine (C5-OH) on newborn screening (NBS). Subsequent persistent plasma elevations of C5-OH and propionylcarnitine (C3) as well as fluctuating urinary markers were suggestive of multiple carboxylase deficiency (MCD). Normal enzymology and mutational analysis of genes encoding holocarboxylase synthetase (HLCS) and biotinidase (BTD) excluded MCD. Biotin uptake studies were normal excluding biotin transporter deficiency. His clinical features at 13 months of age comprised psychomotor delay, central hypotonia, myopathy, failure to thrive, hypocitrullinemia, recurrent episodes of decompensation with metabolic keto-lactic acidosis and an episode of hyperammonemia. Biotin treatment from 13 months of age was associated with increased patient activity, alertness, and attainment of new developmental milestones, despite lack of biochemical improvements. Whole exome sequencing (WES) analysis failed to identify any other variants which could likely contribute to the observed phenotype, apart from the homoplasmic (100%) m.8993T>G variant initially detected by mitochondrial DNA (mtDNA) sequencing.Hypocitrullinemia has been reported in patients with the m.8993T>G variant and other mitochondrial disorders. However, persistent plasma elevations of C3 and C5-OH have previously only been reported in one other patient with this homoplasmic mutation. We suggest considering the m.8993T>G variant early in the diagnostic evaluation of MCD-like biochemical disturbances, particularly when associated with hypocitrullinemia on NBS and subsequent confirmatory tests. An oral biotin trial is also warranted.
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