Evidence map›Paper›PMID 22231380›Full record

ReviewJournal of inherited metabolic disease2012

Update on clinical aspects and treatment of selected vitamin-responsive disorders II (riboflavin and CoQ 10).

Rita Horvath

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of inherited metabolic disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

32 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Fatal multiple acyl-CoA dehydrogenase deficiency caused byWorld journal of clinical cases · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Clinical Diagnosis and Treatment of Leigh Syndrome Based onAntioxidants (Basel, Switzerland) · 2021
    Review
  9. Review
  10. Article
  11. Article
  12. Primary coenzyme Q10 deficiency due to COQ8A gene mutations.Molecular genetics & genomic medicine · 2020
    Article
  13. Review
  14. JIMD reports · 2020
    Article
  15. Article
  16. Advances in drug therapy for mitochondrial diseases.Annals of translational medicine · 2020
    Review
  17. Review
  18. Review
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Rita HorvathInstitute of Genetic Medicine, Newcastle University, Central Parkway, Newcastle upon Tyne, NE1 3BZ, UK. rita.horvath@ncl.ac.uk
Newcastle University · GB

Funding

Medical Research Council G1000848Wellcome Trust 096919
6 · The paper itself

Abstract

Riboflavin and ubiquinone (Coenzyme Q(10), CoQ(10)) deficiencies are heterogeneous groups of autosomal recessive conditions affecting both children and adults. Riboflavin (vitamin B(2))-derived cofactors are essential for the function of numerous dehydrogenases. Genetic defects of the riboflavin transport have been detected in Brown-Vialetto-Van Laere and Fazio-Londe syndromes (C20orf54), and haploinsufficiency of GPR172B has been proposed in one patient to cause persistent riboflavin deficiency. Mutations in the electron tranferring fravoprotein genes (ETFA/ETFB) and its dehydrogenase (ETFDH) are causative for multiple acyl-CoA dehydrogenase deficiency. Mutations in ACAD9, encoding the acyl-CoA dehydrogenase 9 protein were recently reported in mitochondrial disease with respiratory chain complex I deficiency. All these conditions may respond to riboflavin therapy. CoQ(10) is a lipid-soluble component of the cell membranes, where it functions as a mobile electron and proton carrier, but also participates in other cellular processes as a potent antioxidant, and by influencing pyrimidine metabolism. The increasing number of molecular defects in enzymes of the CoQ(10) biosynthetic pathways (PDSS1, PDSS2, COQ2, COQ6, COQ9, CABC1/ADCK3) underlies the importance of these conditions. The clinical heterogeneity may reflect blocks at different levels in the complex biosynthetic pathway. Despite the identification of several primary CoQ(10) deficiency genes, the number of reported patients is still low, and no true genotype-phenotype correlations are known which makes the genetic diagnosis still difficult. Additionally to primary CoQ(10) deficiencies, where the mutation impairs a protein directly involved in CoQ(10) biosynthesis, we can differentiate secondary deficiencies. CoQ(10) supplementation may be beneficial in both primary and secondary deficiencies and therefore the early recognition of these diseases is of utmost importance.

Indexed as

Genetic Association StudiesHumansMultiple Acyl Coenzyme A Dehydrogenase DeficiencyMutationRiboflavinRiboflavin DeficiencyUbiquinoneVitaminscoenzyme Q10RiboflavinUbiquinoneVitamins

Identifiers

PMID22231380
OpenAlexW2027828752

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.