Evidence map›Paper›PMID 18500572›Full record

ArticleJournal of inherited metabolic disease2008

Congenital disorder of glycosylation type Ix: review of clinical spectrum and diagnostic steps.

E Morava, H Wosik, J Kárteszi, M Guillard, M Adamowicz, J Sykut-Cegielska, K Hadzsiev, R A Wevers, D J Lefeber

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In one paragraph

Article in Journal of inherited metabolic disease, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 37 citations in OpenAlex.

  1. Putative role of TMEM165 in congenital cardiomyopathies.Frontiers in molecular neuroscience · 2025
    Review
  2. Frontiers in genetics · 2025
    Article
  3. Article
  4. Review
  5. Congenital nephrotic syndrome in an infant with ALG1-congenital disorder of glycosylation.Pediatrics international : official journal of the Japan Pediatric Society · 2016
    Article
  6. Article
  7. Article
  8. Article
  9. How to find and diagnose a CDG due to defective N-glycosylation.Journal of inherited metabolic disease · 2011
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Glycosylation diseases: quo vadis?Biochimica et biophysica acta · 2009
    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

9 authors at 5 institutions in 3 countries.

E MoravaLaboratory of Paediatrics and Neurology, Department of Paediatrics, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands. E.Morava@cukz.umcn.nl
H Wosik
J Kárteszi
M Guillard
M Adamowicz
J Sykut-Cegielska
K Hadzsiev
R A Wevers
D J Lefeber
Radboud University Nijmegen · NLUniversity of Pecs · HUUniversity of Warsaw · PLMedical University of Lodz · PLRadboud University Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Congenital disorder of glycosylation type I (CDG I) represent a rapidly growing group of inherited multisystem disorders with 13 genetically established subtypes (CDG Ia to CDG Im), and a high number of biochemically unresolved cases (CDG Ix). Further diagnostic effort and prognosis counselling are very challenging in these children. In the current study, we reviewed the clinical records of 10 CDG Ix patients and compared the data with 13 CDG Ix patients published in the literature in search for specific symptoms to create clinical subgroups. The most frequent findings were rather nonspecific, including developmental delay and axial hypotonia. Several features were found that are uncommon in CDG syndrome, such as elevated creatine kinase or arthrogryposis. Distinct ophthalmological abnormalities were observed including optic nerve atrophy, cataract and glaucoma. Two subgroups could be established: one with a pure neurological presentation and the other with a neurological-multivisceral form. The first group had a significantly better prognosis. The unique presentation of microcephaly, seizures, ascites, hepatomegaly, nephrotic syndrome and severe developmental delay was observed in one child diagnosed with CDG Ik. Establishing clinical subgroups and increasing the number of patients within the subgroups may lead the way towards the genetic defect in children with a so far unsolved type of the congenital disorders of glycosylation. Raising awareness for less common, non-CDG specific clinical features such as congenital joint contractures, movement disorders or ophthalmological anomalies will encourage clinicians to think of CDG in its more unusual presentation. Clinical grouping also helps to determine the prognosis and provide better counselling for the families.

Indexed as

Abnormalities, MultipleAtrophyBlood Coagulation DisordersCataractCongenital Disorders of GlycosylationGlycosylationHumansOptic Nerve

Identifiers

PMID18500572
OpenAlexW2012067142

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.