ArticleBMJ open2014
A retrospective cohort study identifying the principal pathological features useful in the diagnosis of inclusion body myositis.
Article in BMJ open, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 48 papers, 2 of them syntheses that pooled it.
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Who cites it
48 citing papers in PubMed, 2 syntheses or guidelines pooled it, 96 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition).Autophagy · 2016Guideline
- The NORAD-Pumilio regulatory axis in the evolution of inclusion body myositis.Journal of neuropathology and experimental neurology · 2026Article
- Alpha-Synuclein as a Potential Biomarker for Inclusion Body Myositis in Blood and Muscle.Neuropathology and applied neurobiology · 2025Article
- Intramyocardial fatty infiltration lesion in sporadic inclusion body myositis: a case report.The international journal of cardiovascular imaging · 2025Article
- Loss of TDP-43 Splicing Repression Occurs in Myonuclei of Inclusion Body Myositis Patients.Annals of neurology · 2025Article
- Inclusion body myositis and immunosenescence: current evidence and future perspectives.Rheumatology (Oxford, England) · 2025Review
- The clinical features, muscle pathology, and role of autophagy in anti-Ku-positive patients.Frontiers in immunology · 2025Article
- Seeding-competent TDP-43 persists in human patient and mouse muscle.Science translational medicine · 2024Article
- Current biomarkers in inclusion body myositis.Journal of neuromuscular diseases · 2024Review
- Anti-Ku + myositis: an acquired inflammatory protein-aggregate myopathy.Acta neuropathologica · 2024Article
- Seeding competent TDP-43 persists in human patient and mouse muscle.bioRxiv : the preprint server for biology · 2024Article
- Article
- Amplifying the Heat Shock Response Ameliorates ALS and FTD Pathology in Mouse and Human Models.Molecular neurobiology · 2023Article
- From data to diagnosis: how machine learning is revolutionizing biomarker discovery in idiopathic inflammatory myopathies.Briefings in bioinformatics · 2023Review
- Protein Aggregates and Aggrephagy in Myopathies.International journal of molecular sciences · 2023Review
- Inclusion body myositis and associated diseases: an argument for shared immune pathologies.Acta neuropathologica communications · 2022Review
- Inclusion body myositis: Update on the diagnostic and therapeutic landscape.Frontiers in neurology · 2022Review
- Inflammatory myopathies: update on diagnosis, pathogenesis and therapies, and COVID-19-related implications.Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology · 2020Review
- Spinal Cord and Motor Neuron TDP-43 Pathology in a Sporadic Inclusion Body Myositis Patient.Journal of neuropathology and experimental neurology · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
objectiveThe current pathological diagnostic criteria for sporadic inclusion body myositis (IBM) lack sensitivity. Using immunohistochemical techniques abnormal protein aggregates have been identified in IBM, including some associated with neurodegenerative disorders. Our objective was to investigate the diagnostic utility of a number of markers of protein aggregates together with mitochondrial and inflammatory changes in IBM.
designRetrospective cohort study. The sensitivity of pathological features was evaluated in cases of Griggs definite IBM. The diagnostic potential of the most reliable features was then assessed in clinically typical IBM with rimmed vacuoles (n=15), clinically typical IBM without rimmed vacuoles (n=9) and IBM mimics-protein accumulation myopathies containing rimmed vacuoles (n=7) and steroid-responsive inflammatory myopathies (n=11).
settingSpecialist muscle services at the John Radcliffe Hospital, Oxford and the National Hospital for Neurology and Neurosurgery, London.
resultsIndividual pathological features, in isolation, lacked sensitivity and specificity. However, the morphology and distribution of p62 aggregates in IBM were characteristic and in a myopathy with rimmed vacuoles, the combination of characteristic p62 aggregates and increased sarcolemmal and internal major histocompatibility complex class I expression or endomysial T cells were diagnostic for IBM with a sensitivity of 93% and specificity of 100%. In an inflammatory myopathy lacking rimmed vacuoles, the presence of mitochondrial changes was 100% sensitive and 73% specific for IBM; characteristic p62 aggregates were specific (91%), but lacked sensitivity (44%).
conclusionsWe propose an easily applied diagnostic algorithm for the pathological diagnosis of IBM. Additionally our findings support the hypothesis that many of the pathological features considered typical of IBM develop later in the disease, explaining their poor sensitivity at disease presentation and emphasising the need for revised pathological criteria to supplement the clinical criteria in the diagnosis of IBM.
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