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PubMed2003

Inclusion body myositis--sensory dysfunction revealed with quantitative determination of somatosensory thresholds.

In order to evaluate sensory function in inclusion body myositis (IBM), nine patients were subjected to sensibility screening and quantitative determination of somatosensory thresholds. Data were compared with results from electrophysiological examination and muscle biopsy. On sensibility screening all but one of the IBM patients had abnormal findings in hands and/or feet mostly affecting thermal sensibility. Vibratory thresholds were abnormal in five and thermal thresholds in four of the patients. Mean vibratory thresholds were significantly (P < 0.05) higher in the IBM patients when compared with the controls. Significantly increased heat pain thresholds were found in hands and feet when compared with the controls while thermal thresholds were normal. Nerve conduction velocities were decreased in three patients, EMG showed both myopathic and neuropathic abnormalities in six patients. Eight patients had neuropathic abnormalities on muscle biopsy. The sensory dysfunction found suggests an affection of peripheral nerves in IBM mainly affecting large diameter myelinated nerve fibres corroborating earlier findings of a peripheral neuropathy in IBM.

Aged↗

PubMed2001

Inclusion body myositis associated with hepatitis C virus infection.

The case of a 77-year-old woman with hepatitis C virus infection with a 5-year history of muscle weakness and mild disturbance of gait is reported. Steroid therapy did not improve her symptoms. She developed HCV-related liver cirrhosis and hepatocellular carcinoma, and muscle biopsy revealed inclusion body myositis. Immunohistochemistry showed that the nonstructural region of HCV and 8-hydroxy-2'-deoxyguanosine, a marker of DNA damage by reactive oxygen species, were present in striated muscle cells of this patient.

Aged↗

PubMedDate not supplied

Myositis autoantibody inhibits histidyl-tRNA synthetase: a model for autoimmunity.

In autoimmune disorders such as rheumatoid arthritis and systemic lupus erythematosus (SLE), autoantibodies are generated against a variety of macromolecules. Myositis is a human autoimmune disease characterized by weakness and wasting of muscle. In American studies, antibodies directed against soluble cellular constituents were detected by immunodiffusion in about 60% of cases; the commonest of these, found in 25% of patients, was antibody to the Jo-1 antigen. An antibody system referred to as PL-1 was recognized at a similar frequency in a series of patients studied at Hammersmith Hospital, London. We show here that this system is identical with the Jo-1 system and demonstrate that the antigen is a polypeptide of molecular weight (Mr) 50,000. The protein is immunoprecipitated with tRNA His and appears to be histidyl-tRNA synthetase. The identity of the Jo-1 antigen, the first of the RNA-associated antigens familiar in autoimmune disease to be characterized as a specific enzyme, suggests a model for virus involvement in autoantibody generation.

Amino Acyl-tRNA Synthetases↗

PubMed2006

Sporadic inclusion body myositis--diagnosis, pathogenesis and therapeutic strategies.

Sporadic inclusion body myositis (sIBM) presents with a characteristic clinical phenotype of slow-onset weakness and atrophy, affecting proximal and distal limb muscles and facial and pharyngeal muscles. Histologically, sIBM is characterized by chronic myopathic features, lymphocytic infiltrates invading non-vacuolated fibers, vacuolar degeneration, and accumulation of amyloid-related proteins. The cause of sIBM is unclear, but two processes-one autoimmune and the other degenerative-appear to occur in parallel. In contrast to dystrophies, in sIBM the autoinvasive CD8(+) T cells are cytotoxic and antigen-driven, invading muscle fibers expressing major histocompatibility complex class I antigen and costimulatory molecules. The concurrent degenerative features include vacuolization, filamentous inclusions and intracellular accumulations of amyloid-beta-related molecules. Although viruses have not been amplified from the muscle fibers, at least 12 cases of sIBM have been seen in association with retroviral infections, indicating that a chronic persistent viral infection might be a potential triggering factor. Emerging data imply that continuous upregulation of cytokines and major histocompatibility complex class I on the muscle fibers causes an endoplasmic reticulum stress response, resulting in intracellular accumulation of misfolded glycoproteins and activation of the transcription factor NFkappaB, leading to further cytokine activation. In spite of the brisk, antigen-driven T-cell infiltrates, sIBM does not respond to immunotherapies. New therapies using monoclonal antibodies against lymphocyte signaling pathways might prove helpful in arresting disease progression.

Diagnosis, Differential↗

PubMed1999

Dermatomyositis with the features of inclusion body myositis associated with carcinoma of the bladder.

Inclusion body myositis (IBM) is a unique category of inflammatory myopathy. It is characterized histologically by the presence of muscle fibres with rimmed vacuoles and abnormal intracellular accumulations of proteins. We report here a 62-year-old patient with bladder carcinoma, where the signs of IBM overlapped with clinical features of dermatomyositis (DM). A combination of cutaneous changes typical for DM with histological and other features of IBM is exceedingly rare, and has not been previously addressed in dermatological literature. To the best of our knowledge this is also the first description of the association of DM/IBM with internal malignancy.

Carcinoma, Transitional Cell↗

PubMed2004

The spectrum of myositis ossiticans in haemophilia.

Myositis ossificans (MO) refers to non-neoplastic heterotopic soft tissue ossification that can have several aetiologies. Broadly it can be classified into three categories based on aetiology [1]. MO traumatica, the most common form occurs secondary to acute or chronic trauma. MO can also be associated with neurological disorders and in rare cases is congenital. The latter (progressive MO) is a genetic disorder in which congenital osseous abnormalities are associated with progressive soft tissue calcification. Despite an increased tendency to soft tissue bleeds, MO has been rarely reported in haemophilia. We treated three adolescents with haemophilia and MO of varying degrees of severity and outcome.

Adolescent↗

PubMed1996

Limited T-cell receptor V gene usage in inclusion body myositis.

Inclusion body myositis (IBM) is a chronic, progressive inflammatory myopathy. The inflammatory infiltrates are dominated by T cells, which frequently invade muscle fibres. The present study was performed to characterize the usage of the variable (V) segment of the T-cell receptor of muscle infiltrating cells in IBM. Using the reverse transcriptase polymerase chain reaction (RT-PCR) technique the authors analysed the expression of 22 V alpha and 24 V beta families in muscle tissue from six patients with IBM displaying intense inflammatory cell infiltration. The following V alpha/V beta families appeared in at least 50% of the patients: V alpha 1, 5, 7, 15, 16, 17, 20, 21, 22 and V beta 3, 5.2, 8, 12, 14, 22. In all patients V alpha 7, 16 and V beta 8 were expressed in muscle tissue. Furthermore, in two of the patients peripheral blood lymphocytes (PBL) were investigated in parallel. There was a restricted usage of V alpha and V beta families in muscle in comparison to PBL, indicating a selective homing or local proliferation of T lymphocytes in the inflammatory lesions in IBM.

Adult↗

PubMed2003

Inclusion body myositis: clonal expansions of muscle-infiltrating T cells persist over time.

Inclusion body myositis (IBM) is a chronic inflammatory myopathy. The muscle histology is characterized by infiltration of T cells, which invade and apparently destroy muscle fibres. This study was performed to investigate whether predominant clones of muscle-infiltrating T cells are identical in different muscles and whether they persist over time in IBM. By reverse transcriptase-polymerase chain reaction, 25 T-cell receptor (TCR) variable beta (Vbeta) chain families and the complementarity-determining region 3 (CDR3) of the TCR were analysed in two different muscle biopsies of four patients with IBM. In two of the patients, the muscle biopsies were obtained from different muscles at one time point, whereas in two patients, the second biopsy was obtained 9 years after the first biopsy. T cells expressing predominant Vbeta families were analysed for clonality by fragment length analysis of the CDR3. Predominant Vbeta families were analysed by DNA sequencing to identify identical clones. Immunohistochemical staining of Vbeta families was performed to study the distribution of T cells expressing identified predominant Vbeta families. The muscle-infiltrating lymphocytes showed restricted expression of TCR Vbeta families. DNA sequencing proved that clonally expanded T cells were identical in different muscles and persisted 9 years after the first biopsy. Immunohistochemical analysis with Vbeta family-specific antibodies demonstrated the endomysial localization of these T cells in inflammatory cell infiltrates. Our results show that in IBM there is clonal restriction of TCR expression in muscle-infiltrating lymphocytes. Identical T-cell clones predominate in different muscles, and these clones persist for many years. These results indicate an important, continuous, antigen-driven inflammatory reaction in IBM.

Aged↗

PubMed2001

Focal myositis.

Focal myositis is a rare, benign focal inflammation of muscle. The lesion often presents as a mass that may be mistaken for a soft tissue sarcoma. This report describes the MRI and histopathological features of a case and illustrates how the diagnosis may be suspected on the basis of the MR findings.

Adolescent↗

PubMed2003

Eosinophilic major basic protein and interleukin-5 in eosinophilic myositis.

To determine whether eosinophils play a critical role in muscle fiber damage in patients with eosinophilic myositis (EM). We investigated expression of eosinophilic major basic protein (MBP) and interleukin (IL)-5 at the protein and mRNA levels in muscle biopsies from three patients with idiopathic EM. MBP deposits were found on the surface of eosinophils and muscle fibers surrounded by the eosinophils. Reverse transcriptase-polymerase chain reaction analysis showed increased IL-5 expression in EM muscle but not in control muscle. These results suggest that IL-5 induces local accumulation of eosinophils and their release of MBP. The secreted proteins adhere to the muscle fiber membrane, resulting in muscle damage.

Adult↗

PubMed2003

Cystatin C colocalizes with amyloid-beta and coimmunoprecipitates with amyloid-beta precursor protein in sporadic inclusion-body myositis muscles.

Cystatin C (CC), an endogenous cysteine protease inhibitor, is accumulated within amyloid-beta (A beta) amyloid deposits in Alzheimer's disease (AD) brain and was proposed to play a role in the AD pathogenesis. Because the chemo-morphologic muscle phenotype of sporadic inclusion-body myositis (s-IBM) has several similarities with the phenotype of AD brain, including abnormal accumulation of A beta deposits, we studied expression and localization of CC in muscle biopsies of 10 s-IBM, and 16 disease- and five normal-control muscle biopsies. Physical interaction of CC with amyloid-beta precursor protein (A beta PP) was studied by a combined immunoprecipitation/immunoblotting technique in the s-IBM muscle biopsies and in A beta PP-overexpressing cultured human muscle fibers. In all s-IBM muscle biopsies, CC-immunoreactivity either colocalized with, or was adjacent to, the A beta-immunoreactive inclusions in 80-90% of the vacuolated muscle fibers, mostly in non-vacuolated regions of their cytoplasm. Ultrastructurally, CC immunoreactivity-colocalized with A beta on 6-10 nm amyloid-like fibrils and floccular material. By immunoblotting, CC expression was strongly increased in IBM muscle as compared to the controls. By immunoprecipitation/immunoblotting experiments, CC coimmunoprecipitated with A beta PP, both in s-IBM muscle and in A beta PP-overexpressing cultured normal human muscle fibers. Our studies (i) demonstrate for the first time that CC physically associates with A beta PP, and (ii) suggest that CC may play a novel role in the s-IBM pathogenesis, possibly by influencing A beta PP processing and A beta deposition.

Amyloid beta-Peptides↗

PubMed2005

Leg pain due to bilateral focal recurrent myositis in a hemodialysis patient.

Leg pain is a common symptom in dialysis patients. In most cases, the cause is easily identified, but some rare causes have been recognized. We describe a case of focal myositis as the source of recurrent leg pain in a hemodialysis patient. This disease usually is self-limited and has a spontaneously favorable outcome. We review the differential diagnosis of leg pain in this patient population.

Female↗

PubMed2002

Myositis in children with meningococcal disease: a role for tumour necrosis factor-alpha and interleukin-8?

OBJECTIVES: Myalgia is under-recognized in meningococcal disease (MCD). In septic shock, myositis is thought to be mediated by pro-inflammatory cytokines such as tumour necrosis factor-alpha (TNF-alpha), interleukin-8 (IL-8) and interleukin-6 (IL-6) but this has never previously been studied in MCD. We aimed to demonstrate whether muscle damage mediated via TNF-alpha and other pro-inflammatory cytokines occurs in MCD, as estimated by creatine kinase skeletal muscle isoenzyme (CK-MM) and cardiac isoenzyme (CK-MB) concentrations. METHODS: A total of 68 children, median age 2.7 years, with a diagnosis of MCD were prospectively studied. Severity of disease was measured using the Glasgow Meningococcal Septicaemia Prognostic Score (GMSPS). Severe disease was defined as a GMSPS of > or =8. TNF-alpha, IL-8, IL-6 and IL-1Ra concentrations were determined on samples taken on admission. RESULTS: CK-MM correlated significantly with TNF-alpha, IL-8 and GMSPS. There was no significant correlation between CK-MB and TNF-alpha or IL-6, but CK-MB correlated with GMSPS and IL-8. Fifty-six percent of children with MCD had evidence of muscle damage as manifested by elevated CK-MM. CONCLUSIONS: TNF-alpha and IL-8 may be potential mediators in the pathophysiology of skeletal muscle damage in MCD.

Adolescent↗

PubMed1999

Myositis ossificans of the hand.

We present a case of myositis ossificans of the hand and review the clinical, radiological, and histological presentation, as well as the appropriate therapeutic management.

Adult↗

PubMed1978

[Non-traumatic myositis ossificans circumscripta (author's transl)].

The clinical, pathological and radiological features and the differential diagnosis of the very rare condition of non-traumatic myositis ossificans circumscripta are illustrated by one patient. The characteristic radiological appearances make a correct diagnosis of this localised, non-malignant process possible.

Adolescent↗

PubMed2006

[Immunogenic myositis].

Immunogenic inflammatory myopathies are a heterogeneous group of acquired muscle disorders. Clinical and morphological characteristics are on one side muscle weakness, on the other side inflammatory infiltrates in muscle biopsy. Three main groups of different pathogenesis and course can be subdivided: The treatment of inflammatory myopathies is predominantly based on empiric data. Baseline drugs are Corticosteroids and Immunosuppressives. High dose intravenous Immunoglobulins (IVIG) are an important additional therapeutic possibility, especially in inclusion body myositis.

Adult↗

PubMed1980

[Ultrastructural and clinical studies in "inclusion body myositis" (author's transl)].

A non-hereditary slowly progressive neuromuscular disease occuring in a 39-year-old male, consisting of an asymmetrical wasting of the muscles of the shanks, is reported. Neither clinical nor electromyographic criteria can safely distinguish whether a primary neurogenic or a primary myogenic process is causally involved. The initial rise in serum CPK-activity indicates a myopathic origin. The lightmicroscopic aspect of the muscle-biopsy shows a muscular atrophy which resembles a primary neurogenic pattern with grouped clusters of atrophic fibers as well as a myopathic or rather myositic tissue-pattern with randomly scattered atrophic fibers. In addition there are numerous vacuoles which are equivalent to concentric lamellae of dense material in electronmicroscopy. Numerous fibrillary inclusions as well in the cytoplasm as in the cell-nucleus correspond to typical alterations in the so-called "inclusion body myositis". The disease is critically discussed as a nosological entity among neuromuscular disorders.

Adult↗

PubMed1980

[Myositis ossificans progressiva (M.o.p.)--a morphological and biochemical study (author's transl)].

In a two-year-old girl suffering from myositis ossificans progressiva a biopsy specimen from a soft tissue tumor was examined by electron microscopy and by collagen electrophoresis (SDS-Polyacrylamide Gel Electrophoresis). Electron microscopic findings of the biopsy specimen showed that the collagen appeared to be similar to type II collagen which can be found for example in hyaline cartilage however collagen electrophoresis revealed neither any certain signs of type II collagen nor any different proportion of type I and type III collagen compared to a healthy child.

Biopsy↗