Diagnosis and classification of sporadic inclusion body myositis (sIBM)

Catalán, Miguel; Selva-O’Callaghan, Albert; Grau, Josep M.

doi:10.1016/j.autrev.2014.01.016

Cited by 35 publications

(33 citation statements)

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“…Histological data were collected to study inflammation and the presence of ragged-red fibres, COX-negative and SDH-positive fibres, as well as the number of vacuolated muscle cells. Diagnosis of sIBM was considered as definite or probable according to the criteria of the European Neuromuscular Centre [1,25]. Samples from 23 muscle biopsies from sIBM patients and 18 from controls were included following these criteria.…”

Section: Study Population Diagnosis Clinical Data and Sample Collecmentioning

confidence: 99%

“…The histological features observed in muscle biopsies of sIBM patients include: (i) inflammatory changes with predominant CD8+ T-cell infiltrates and the expression of MHC-I antigens by non-necrotic muscle fibres, (ii) different degrees of degenerative changes in muscle fibres and the presence of rimmed vacuoles composed mainly of β-amyloid, phosphorylated tau and caveolin proteins, among others, and (iii) mitochondrial abnormalities characterized by the presence of ragged-red fibres, cytochrome c oxidase (COX)-negative and succinate dehydrogenase (SDH)-positive muscle cells [5,6], all of which are widely associated with mitochondrial dysfunction and ageing [1,2,7]. However, the distribution of these histological features is not homogeneous, and they may not be simultaneously present, particularly in the early stages of the disease.…”

Section: Introductionmentioning

confidence: 99%

“…Sporadic inclusion body myositis (sIBM) is the most common inflammatory myopathy in individuals aged >50 years [1] and one of the most important myopathies associated with ageing [2]. With a male:female ratio of 3:1, it is a rare disease (ORPHA611) and its prevalence varies from 4.7 per million in the Netherlands to 14.9 per million in western Australia [3].…”

Section: Introductionmentioning

confidence: 99%

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Mitochondrial DNA disturbances and deregulated expression of oxidative phosphorylation and mitochondrial fusion proteins in sporadic inclusion body myositis

et al. 2016

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Sporadic inclusion body myositis (sIBM) is one of the most common myopathies in elderly people. Mitochondrial abnormalities at the histological level are present in these patients. We hypothesize that mitochondrial dysfunction may play a role in disease aetiology. We took the following measurements of muscle and peripheral blood mononuclear cells (PBMCs) from 30 sIBM patients and 38 age- and gender-paired controls: mitochondrial DNA (mtDNA) deletions, amount of mtDNA and mtRNA, mitochondrial protein synthesis, mitochondrial respiratory chain (MRC) complex I and IV enzymatic activity, mitochondrial mass, oxidative stress and mitochondrial dynamics (mitofusin 2 and optic atrophy 1 levels). Depletion of mtDNA was present in muscle from sIBM patients and PBMCs showed deregulated expression of mitochondrial proteins in oxidative phosphorylation. MRC complex IV/citrate synthase activity was significantly decreased in both tissues and mitochondrial dynamics were affected in muscle. Depletion of mtDNA was significantly more severe in patients with mtDNA deletions, which also presented deregulation of mitochondrial fusion proteins. Imbalance in mitochondrial dynamics in muscle was associated with increased mitochondrial genetic disturbances (both depletion and deletions), demonstrating that proper mitochondrial turnover is essential for mitochondrial homoeostasis and muscle function in these patients.

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Section: Study Population Diagnosis Clinical Data and Sample Collecmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Mitochondrial DNA disturbances and deregulated expression of oxidative phosphorylation and mitochondrial fusion proteins in sporadic inclusion body myositis

et al. 2016

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“…The most commonly used criteria for the classification of IIMs are those that were proposed by Bohan and Peter in 1975 [1]. From a clinico-pathological perspective, the IIMs fall into six categories: (1) dermatomyositis (DM; juvenile, adult), (2) polymyositis (PM; T-cell mediated, eosinophilic, granulomatous), (3) overlap syndromes (with DM, with PM, with sIBM/hIBM), (4) cancer-associated myositis, (5) inclusion body myositis (IBM), and (6) other forms (focal: orbital myositis, localised nodular myositis, inflammatory pseudotumor; diffuse: macrophagic myofasciitis, necrotizing autoimmune myopathy (NAM), infantile myositis) [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16]. Although this clinico-pathological subdivision has a predictive value in prognosis and in therapy, according to our rising knowledge of the autoantibodies, this system seems to be worn out.…”

Section: Introductionmentioning

confidence: 99%

Four dermatomyositis-specific autoantibodies—anti-TIF1γ, anti-NXP2, anti-SAE and anti-MDA5—in adult and juvenile patients with idiopathic inflammatory myopathies in a Hungarian cohort

Bodoki

Nagy‐Vincze

Griger

et al. 2014

Autoimmunity Reviews

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“…Neck flexors and extensors are frequently affected, and also dysphagia is present in up to 60% of patients with sIBM. The clinical progression is slow and often leads to severe disability (2)(3)(4)(5)(6).…”

mentioning

confidence: 99%

BACE-1, PS-1 and sAPPβ Levels Are Increased in Plasma from Sporadic Inclusion Body Myositis Patients: Surrogate Biomarkers among Inflammatory Myopathies

Catalán-García

Garrabou

Morén

et al. 2015

Mol Med

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Sporadic inclusion body myositis (sIBM) is a rare disease that is difficult to diagnose. Muscle biopsy provides three prominent pathological findings: inflammation, mitochondrial abnormalities and fibber degeneration, represented by the accumulation of protein depots constituted by β-amyloid peptide, among others. We aim to perform a screening in plasma of circulating molecules related to the putative etiopathogenesis of sIBM to determine potential surrogate biomarkers for diagnosis. Plasma from 21 sIBM patients and 20 age-and gender-paired healthy controls were collected and stored at -80°C. An additional population of patients with non-sIBM inflammatory myopathies was also included (nine patients with dermatomyositis and five with polymyositis). Circulating levels of inflammatory cytokines ( were assessed with magnetic bead-based assays, real-time polymerase chain reaction, enzyme-linked immunosorbent assay (ELISA) and high-pressure liquid chromatography (HPLC). Despite remarkable trends toward altered plasmatic expression of inflammatory and mitochondrial molecules (increased IL-6, TNF-α, circulating mtDNA and FGF-21 levels and decreased content in CoQ), only amyloidogenic degenerative markers including BACE-1, PS-1 and sAPPβ levels were significantly increased in plasma from sIBM patients compared with controls and other patients with non-sIBM inflammatory myopathies (p < 0.05). Inflammatory, mitochondrial and amyloidogenic degeneration markers are altered in plasma of sIBM patients confirming their etiopathological implication in the disease. Sensitivity and specificity analysis show that BACE-1, PS-1 and sAPPβ represent a good predictive noninvasive tool for the diagnosis of sIBM, especially in distinguishing this disease from polymyositis. Online address: http://www.molmed.org doi: 10.2119/molmed.2015.00168 Marc Catalán-García, Muscle Research and Mitochondrial Function Laboratory, Cellex, IDIBAPS, Faculty of Medicine, University of Barcelona, Department of Internal Medicine-Hospital Clinic of Barcelona, CELLEX 4B, Villarroel 170, 08036 Barcelona, Catalonia, Spain. Phone: +34-93227-5400, Ext. 2907; Fax: +34-93227-9365; E-mail: macatala@clinic.ub.es. Submitted July 8, 2015; Accepted for publication October 27, 2015; Published Online (www.molmed.org) November 3, 2015. Address correspondence to N O V E L P L A S M A T I C B I O M A R K E R S F O R s I B M D I A G N O S I S8 1 8 | C a t a L á n -G a r C í a E t a L . | M O L M E D 2 1 : 8 1 7 -8 2 3 , 2 0 1 5

show abstract

Diagnosis and classification of sporadic inclusion body myositis (sIBM)

Cited by 35 publications

References 23 publications

Mitochondrial DNA disturbances and deregulated expression of oxidative phosphorylation and mitochondrial fusion proteins in sporadic inclusion body myositis

Mitochondrial DNA disturbances and deregulated expression of oxidative phosphorylation and mitochondrial fusion proteins in sporadic inclusion body myositis

Four dermatomyositis-specific autoantibodies—anti-TIF1γ, anti-NXP2, anti-SAE and anti-MDA5—in adult and juvenile patients with idiopathic inflammatory myopathies in a Hungarian cohort

BACE-1, PS-1 and sAPPβ Levels Are Increased in Plasma from Sporadic Inclusion Body Myositis Patients: Surrogate Biomarkers among Inflammatory Myopathies

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