Evidence map›Paper›PMID 28053302›Full record

ArticleThe American journal of case reports2017

Polymyositis without Beneficial Response to Steroid Therapy: Should Miyoshi Myopathy be a Differential Diagnosis?

Renata Siciliani Scalco, Paulo José Lorenzoni, David S Lynch, William Alves Martins, Heinz Jungbluth, Ros Quinlivan, Jefferson Becker, Henry Houlden

Open access · hybridAbstract readCase Reports
In one paragraph

Article in The American journal of case reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

3 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. 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

8 authors at 5 institutions in 2 countries.

Renata Siciliani ScalcoMRC Centre for Neuromuscular Diseases and Division of Molecular Neuroscience, University College London (UCL) Institute of Neurology, London, United Kingdom.
Paulo José LorenzoniService of Neuromuscular Disorders, Division of Neurology, Department of Internal Medicine, Universidade Federal do Paraná (UFPR), Curitiba, Brazil.
David S LynchMRC Centre for Neuromuscular Diseases and Division of Molecular Neuroscience, University College London (UCL) Institute of Neurology, London, United Kingdom.
William Alves MartinsDepartment of Neurology, Pontifical Catholic University of Rio Grande do Sul (PUCRS), Porto Alegre, Brazil.
Heinz JungbluthDepartment of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology and Neuroscience, King's College London (KCL), London, United Kingdom.
Ros QuinlivanMRC Centre for Neuromuscular Diseases and Division of Molecular Neuroscience, University College London (UCL) Institute of Neurology, London, United Kingdom.
Jefferson BeckerDepartment of Neurology, Pontifical Catholic University of Rio Grande do Sul (PUCRS), Porto Alegre, Brazil.
Henry HouldenMRC Centre for Neuromuscular Diseases and Division of Molecular Neuroscience, University College London (UCL) Institute of Neurology, London, United Kingdom.
MRC Prion Unit · GBPontifícia Universidade Católica do Rio Grande do Sul · BRKing's College London · GBUniversidade Federal do Paraná · BRUniversity College London · GB

Funding

Medical Research Council G0802760Medical Research Council G1001253Medical Research Council G108/638Medical Research Council MR/J004758/1
6 · The paper itself

Abstract

BACKGROUND Miyoshi myopathy (MM) is an autosomal-recessive muscle disorder caused by mutations in the DYSF gene. Clinical features and histopathological changes in dysferlinopathies may mimic inflammatory myopathies and a high degree of clinical suspicion is required to guide the genetic investigation. CASE REPORT We report the case of a 16-year-old male who presented with severe bilateral calf pain and elevated CK levels (15 000 IU/l) who was on prolonged steroid therapy prompted by the clinical suspicion of inflammatory myopathy. Three years into his illness, he was referred for neuromuscular evaluation presenting with untreatable muscle pain and progressive weakness. The diagnosis of "refractory polymyositis" was revisited. Targeted exome sequencing revealed homozygous pathogenic mutations in the DYSF gene, confirming a diagnosis of Miyoshi myopathy. CONCLUSIONS Our case illustrates that severe muscle pain may be the initial feature of Miyoshi myopathy and should be considered in the differential diagnosis of inflammatory myopathies. Although the described patient reported partial clinical improvement in muscle pain, steroid treatment is not an effective therapy for dysferlinopathy patients and it did not prevent disease progression. In addition, we confirm the utility of next-generation sequencing approaches to myopathies, particularly in complex or unusual cases when muscle biopsy is not available.

Indexed as

MutationAdolescentBiomarkersDiagnosis, DifferentialDisease ProgressionDistal MyopathiesDysferlinHumansMaleMembrane ProteinsMuscle ProteinsMuscle, SkeletalMuscular AtrophyMyalgiaPolymyositisBiomarkersDysferlinDYSF protein, humanMembrane ProteinsMuscle Proteins

Identifiers

PMID28053302
PMCPMC5228759
OpenAlexW2569679339

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.