Evidence map›Paper›PMID 37604083›Full record

ReviewMolecular genetics and metabolism2023

Endogenous, non-reducing end glycosaminoglycan biomarkers for the mucopolysaccharidoses: Accurate diagnosis and elimination of false positive newborn screening results.

Jennifer T Saville, Zackary M Herbst, Michael H Gelb, Maria Fuller

Open access · greenAbstract readReview
In one paragraph

Review in Molecular genetics and metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Biomarkers for gene therapy clinical trials of lysosomal storage disorders.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    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

4 authors at 2 institutions in 2 countries.

Jennifer T SavilleGenetics and Molecular Pathology, SA Pathology at Women's and Children's Hospital; Adelaide Medical School, University of Adelaide, Adelaide, 5005 South Australia, Australia.
Zackary M HerbstDepartment of Chemistry, University of Washington, Seattle, WA 98195, USA.
Michael H GelbDepartment of Chemistry, University of Washington, Seattle, WA 98195, USA.
Maria FullerGenetics and Molecular Pathology, SA Pathology at Women's and Children's Hospital; Adelaide Medical School, University of Adelaide, Adelaide, 5005 South Australia, Australia; School of Biological Sciences, University of Adelaide, Adelaide 5005, South Australia, Australia. Electronic address: maria.fuller@adelaide.edu.au.
South Australia Pathology · AUUniversity of Washington · US

Funding

Multiplex Analysis of Inborn Errors of MetabolismR01DK067859 · NIDDK · UNIVERSITY OF WASHINGTON · PI GELB, MICHAEL H · 2003 to 2025
$9.8M
NIDDK NIH HHS R01 DK067859
6 · The paper itself

Abstract

The mucopolysaccharidoses (MPS) are a family of inborn errors of metabolism resulting from a deficiency in a lysosomal hydrolase responsible for the degradation of glycosaminoglycans (GAG). From a biochemical standpoint, excessive urinary excretion of GAG has afforded first-tier laboratory investigations for diagnosis whereas newborn screening programs employ lysosomal hydrolase measurements. Given false positives are not uncommon, second-tier diagnostic testing relies on lysosomal hydrolase measurements following elevated urinary GAG, and newborn screening results are often corroborated with GAG determinations. Molecular genetics requires acknowledgement, as identifying pathogenic variants in the hydrolase genes confirms the diagnosis and allows cascade testing for families, but genetic variants of uncertain significance complicate this paradigm. Initiating cellular, tissue and organ damage that leads to an MPS phenotype is undoubtedly the accumulation of partially degraded GAG, and with mass spectrometry technologies now readily available in the biochemical genetics' laboratory, the ability to properly measure these GAG fragments has been realized. The most common approach involves bacterial lyase/hydrolase digestion of the long chain GAG polymers into their disaccharide units that can be measured by mass spectrometry. Another, less well-known method, the endogenous, non-reducing end method, does not require depolymerization of GAG but rather relies on the mass spectrometric measurement of the naturally produced oligosaccharides that arise from the enzyme deficiency. All MPS can be identified by this one method, and evidence to date shows it to be the only GAG analysis method that gives no false positives when employed as a first-tier laboratory diagnostic test and second-tier newborn screening test.

Indexed as

GlycosaminoglycansMucopolysaccharidosesBiomarkersHumansHydrolasesInfant, NewbornNeonatal ScreeningTandem Mass SpectrometryBiomarkersGlycosaminoglycansHydrolasesBiomarkerDiagnosisGlycosaminoglycansLysosomal storage disorderMucopolysaccharidosesNewborn screening

Identifiers

PMID37604083
PMCPMC12516791
OpenAlexW4385814082

What OpenQuestion holds

Textmetadata
LicenceTDM
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.