Evidence map›Paper›PMID 40389839›Full record

ReviewJournal of neurodevelopmental disorders2025

Contribution of families using the GenIDA database to the description of MED13L syndrome and literature review.

Roseline Caumes, Pauline Burger, Jean-Louis Mandel, Hélène Béhal, Jamal Ghoumid, Thomas Smol

Abstract readReview
In one paragraph

Review in Journal of neurodevelopmental disorders, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Roseline CaumesUniv. Lille, ULR7364 - RADEME - Maladies RAres du DEveloppement embryonnaire et du Métabolisme, Lille, France.
Pauline BurgerDepartment of Neurogenetics and Translational Medicine, Institute of Genetics and Molecular and Cellular Biology (IGBMC), Université de Strasbourg, INSERM U1258, CNRS UMR7104, Illkirch, France.
Jean-Louis MandelDepartment of Neurogenetics and Translational Medicine, Institute of Genetics and Molecular and Cellular Biology (IGBMC), Université de Strasbourg, INSERM U1258, CNRS UMR7104, Illkirch, France.
Hélène BéhalCHU Lille, Unité Statistique, Evaluation Economique et Data Management (SEED), Lille, France.
Jamal GhoumidUniv. Lille, ULR7364 - RADEME - Maladies RAres du DEveloppement embryonnaire et du Métabolisme, Lille, France.
Thomas SmolUniv. Lille, ULR7364 - RADEME - Maladies RAres du DEveloppement embryonnaire et du Métabolisme, Lille, France. thomas.smol@chu-lille.fr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The GenIDA project aims to improve the understanding and management of rare genetic forms of intellectual disability by fostering collaboration among patients, caregivers, healthcare professionals, and research professionals. Clinical data is provided by patients' families via a structured questionnaire to identify medically relevant insights and better understand the natural history of rare diseases. This study focused on MED13L syndrome, analyzing data from 41 patients in the GenIDA database and comparing it with 102 cases from the scientific literature and 6 new descriptions of patients from our medical center.The GenIDA series confirmed the key features of MED13L syndrome, including global developmental delay, poor speech, intellectual disability, and cardiac defects (OMIM #616789), at frequencies similar to those reported in the literature. The GenIDA series identified a higher prevalence of visual impairment (76%) and highlighted under-recognized musculoskeletal issues, such as foot deformities, which had previously received little attention. This study highlights the value of family-reported data in describing the full phenotype of rare syndromes. A comprehensive review of published cases showed that patients with missense variants have more severe impairments, including increased cardiac defects, global developmental delay, and a higher incidence of epilepsy, than patients with premature truncated variants.These findings highlight the importance of family involvement in rare disease research and the need for further studies to explore genotype-phenotype correlations to improve patient care and outcomes.

Indexed as

Developmental DisabilitiesIntellectual DisabilityMediator ComplexAdolescentChildChild, PreschoolDatabases, FactualFamilyFemaleHumansInfantMalePhenotypeMED13L protein, humanMediator ComplexFamilyIntellectual disabilityMED13LPatient registry

Identifiers

PMID40389839
PMCPMC12087057

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Registered trials

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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.