Evidence map›Paper›PMID 24070816›Full record

ArticleNeuromuscular disorders : NMD2013

'Double trouble': diagnostic challenges in Duchenne muscular dystrophy in patients with an additional hereditary skeletal dysplasia.

Sandra Donkervoort, Alice Schindler, Carolina Tesi-Rocha, Allison Schreiber, Meganne E Leach, Jahannaz Dastgir, Ying Hu, Ami Mankodi, Kathryn R Wagner, Neil R Friedman and 1 more

Abstract readCase Reports
In one paragraph

Article in Neuromuscular disorders : NMD, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.1field-weighted citation impact, top 43% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Step-by-Step Double-Trouble OBAIRH and DMD Diagnosis in a One-Year-Old Boy.International journal of molecular sciences · 2023
    Article
  4. Article
  5. Article
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

11 authors at 5 institutions in 1 country.

Sandra DonkervoortNational Institutes of Health, National Institute of Neurological Disorders and Stroke, Neurogenetics Branch, Bethesda, MD, United States.
Alice Schindler
Carolina Tesi-Rocha
Allison Schreiber
Meganne E Leach
Jahannaz Dastgir
Ying Hu
Ami Mankodi
Kathryn R Wagner
Neil R Friedman
Carsten G Bönnemann
National Institutes of Health · USCleveland Clinic · USNational Institute of Neurological Disorders and Stroke · USChildren's National · USKennedy Krieger Institute · US

Funding

Molecular and Clinical Manifestations of Matrix and Aggregate MyopathiesZIANS003129 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI BÖNNEMANN, CARSTEN · 2011 to 2025
$52.8M
Studies Of Hereditary Neurological Disease: Disease Gene IdentificationZIANS002974 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI FISCHBECK, KENNETH · 2009 to 2023
$9.8M
Intramural NIH HHS Z99 NS999999Intramural NIH HHS ZIA NS003129
6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) is caused by mutations in Dystrophin and affects 1 in 3600-6000 males. It is characterized by progressive weakness leading to loss of ambulation, respiratory insufficiency, cardiomyopathy, and scoliosis. We describe the unusual phenotype of 3 patients with skeletal dysplasias in whom an additional diagnosis of DMD was later established. Two unrelated boys presented with osteogenesis imperfecta due to point mutations in COL1A1 and were both subsequently found to have a 1 bp frameshift deletion in the Dystrophin gene at age 3 and age 15 years, respectively. The third patient had a diagnosis of pseudoachondroplasia caused by a mutation in the COMP gene and was found to have a deletion of exons 48-50 in Dystrophin at age 9. We discuss the atypical presentation caused by the concomitant presence of 2 conditions affecting the musculoskeletal system, emphasizing aspects that may confound the presentation of a well-characterized disease like DMD. Additional series of patients with DMD and a secondary inherited condition are necessary to establish the natural history in this "double trouble" population. The recognition and accurate diagnosis of patients with two independent genetic disease processes is essential for management, prognosis, genetic risk assessment, and discussion regarding potential therapeutic interventions.

Indexed as

Bone Diseases, DevelopmentalMuscular Dystrophy, DuchenneAdolescentCartilage Oligomeric Matrix ProteinChildChild, PreschoolCollagen Type ICollagen Type I, alpha 1 ChainDystrophinExonsHumansMaleMuscle, SkeletalPhenotypeSequence DeletionTomography, X-Ray ComputedCartilage Oligomeric Matrix ProteinCollagen Type ICollagen Type I, alpha 1 ChainDystrophinTSP5 protein, humanDouble troubleDuchenne muscular dystrophyGenetic counselingOstoegenesis imperfecta

Identifiers

PMID24070816
PMCPMC5030769
OpenAlexW2077547871

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.