Evidence map›Paper›PMID 27450367›Full record

ArticleJIMD reports2017

Leigh-Like Syndrome Due to Homoplasmic m.8993T>G Variant with Hypocitrullinemia and Unusual Biochemical Features Suggestive of Multiple Carboxylase Deficiency (MCD).

Shanti Balasubramaniam, B Lewis, D M Mock, H M Said, M Tarailo-Graovac, A Mattman, C D van Karnebeek, D R Thorburn, R J Rodenburg, J Christodoulou

Erratum issuedOpen access · goldAbstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. [Decreased plasma citrulline is a biochemical marker in newborn screening forZhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. [Genetic analysis of newborns with abnormal metabolism of 3-hydroxyisovalerylcarnitine].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2019
    Article
  10. Review
  11. Article
  12. 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 · 2019
    Article
  13. Article
  14. The role of the clinician in the multi-omics era: are you ready?Journal of inherited metabolic disease · 2018
    Article
  15. Article
  16. Review
  17. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 7 institutions in 4 countries.

Shanti BalasubramaniamMetabolic Unit, Department of Rheumatology and Metabolic Medicine, Princess Margaret Hospital, Perth, WA, Australia. saras329@hotmail.com.
B LewisPathWest Laboratories WA, Princess Margaret Hospital, Perth, WA, Australia.
D M MockDepartment of Biochemistry and Molecular Biology, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
H M SaidDepartment of Medicine, University of California School of Medicine Irvine, Irvine, CA, USA.
M Tarailo-GraovacCentre for Molecular Medicine, Department of Medical Genetics, Child and Family Research Institute, University of British Columbia, Vancouver, BC, Canada.
A MattmanAdult Metabolic Diseases Clinic, Division of Endocrinology and Metabolism, Vancouver General Hospital, UBC, Vancouver, BC, Canada.
C D van KarnebeekCentre for Molecular Medicine, Department of Pediatrics, Child and Family Research Institute, University of British Columbia, Vancouver, BC, Canada.
D R ThorburnMurdoch Childrens Research Institute and Victorian Clinical Genetics Services, Royal Children's Hospital, Melbourne, VIC, Australia.
R J RodenburgRadboud Center for Mitochondrial Medicine, Radboud University Medical Centre, Nijmegen, The Netherlands.
J ChristodoulouMurdoch Childrens Research Institute and Victorian Clinical Genetics Services, Royal Children's Hospital, Melbourne, VIC, Australia.
Child and Family Research Institute · CAPrincess Margaret Hospital for Children · AURoyal Children's Hospital · AURadboud University Medical Center · NLUniversity of Arkansas for Medical Sciences · USUniversity of California, Irvine · USVancouver General Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

AcylcarnitinesCitrullineLeigh syndromemtDNA mutationNewborn screening (NBS)

Identifiers

PMID27450367
PMCPMC5413447
OpenAlexW2502456218

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.