Evidence map›Paper›PMID 29891879›Full record

ArticleEuropean journal of human genetics : EJHG2018

Uniparental isodisomy as a cause of recessive Mendelian disease: a diagnostic pitfall with a quick and easy solution in medium/large NGS analyses.

Florian Erger, Karin Burau, Michael Elsässer, Katharina Zimmermann, Ute Moog, Christian Netzer

Open access · bronzeAbstract read
In one paragraph

Article in European journal of human genetics : EJHG, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 24% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

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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

6 authors at 3 institutions in 1 country.

Florian ErgerInstitute of Human Genetics, University of Cologne, Cologne, Germany. florian.erger@uk-koeln.de.ORCID http://orcid.org/0000-0002-2768-1702
Karin BurauInstitute of Human Genetics, Heidelberg University, Heidelberg, Germany.
Michael ElsässerDepartment of Prenatal Medicine, Heidelberg University Women's Hospital, Heidelberg, Germany.
Katharina ZimmermannInstitute of Human Genetics, University of Cologne, Cologne, Germany.
Ute MoogInstitute of Human Genetics, Heidelberg University, Heidelberg, Germany.
Christian NetzerInstitute of Human Genetics, University of Cologne, Cologne, Germany.
Heidelberg University · DEUniversity of Cologne · DETH Köln - University of Applied Sciences · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Complete uniparental isodisomy (iUPD)-the presence of two identical chromosomes in an individual that originate from only a single parental homolog-is an underestimated cause of recessive Mendelian disease in humans. Correctly identifying iUPD in an index patient is of enormous consequence to correctly counseling the family/couple, as the recurrence risk for siblings is reduced from 25% to usually <1%. In medium/large-scale NGS analyses, we found that complete iUPD can be rapidly and straightforwardly inferred from a singleton dataset (index patient only) through a simple chromosome- and genotype-filtering step in <1 min. We discuss the opportunities of iUPD detection in medium/large-scale NGS analyses by example of a case of CHRNG-associated multiple pterygium syndrome due to complete maternal iUPD. Using computer simulations for several detection thresholds, we validate and estimate sensitivity, specificity, positive (PPV), and negative predictive values (NPV) of the proposed screening method for reliable detection of complete iUPD. When screening for complete iUPD, our models suggest that a >85% proportion of homozygous calls on a single chromosome with ≥30 sufficiently interspaced called variants results in a sensitivity of 97.9% and specificity of 99.7%. The PPV is 95.1%, the NPV 99.9%. When this threshold is exceeded for a chromosome on which a patient harbors an apparently homozygous disease-associated variant, it should be sufficient cause to discuss iUPD as a plausible or probable mechanism of disease in the genetic analysis report, even when parental segregation has not (yet) been performed.

Indexed as

Aborted FetusAdultDiagnostic ErrorsFemaleGenes, RecessiveGenetic TestingHumansMalePrenatal DiagnosisSequence Analysis, DNAUniparental Disomy

Identifiers

PMID29891879
PMCPMC6117279
OpenAlexW2808148909

What OpenQuestion holds

Textmetadata
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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.