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PubMed2004

Myositis: an update on pathogenesis.

PURPOSE OF REVIEW: The etiology and much about the pathogenesis of the inflammatory myopathies remain a mystery. In this review, we investigate recent research efforts to understand the pathogenesis of the diverse entities of polymyositis (PM), dermatomyositis (DM), and inclusion body myositis (IBM), diseases that result from interactions between environmental risk factors and genetic susceptibility. RECENT FINDINGS: Over the past year, there has been considerable progress toward better understanding of IBM, with relatively few developments toward understanding PM and DM. Although these diseases may share some common clinical phenotypic and serologic components, they differ on a molecular and cellular level. SUMMARY: The need for definitive, safer therapies in these diseases makes vital the search for defining detailed pathogenesis of inflammation and muscle fiber damage at the molecular level.

Animals↗
PubMed2005

Statin-induced myositis: a commonly encountered or rare side effect?

PURPOSE OF REVIEW: Statins are well established as first-line agents for cholesterol lowering in cardiovascular disease, with accumulating evidence supporting their initiation and guidelines recommending treatment to lower LDL levels. Although generally well tolerated with few side effects, including headaches and gastrointestinal symptoms, concerns are raised regarding myopathy, which may lead to fatal rhabdomyolysis. This review examines current evidence on statin interactions, mechanism of injury and toxicity. RECENT FINDINGS: Significant myopathy is rare with an incidence of less than 0.5% of patients. Statin side effects may be dose-related, associated with other drug interactions that interfere with statin metabolic pathways through cytochrome p450 pathways or glucuronidation, or related to co-morbidities. Several theories have suggested that statin myotoxicity may be due to intracellular cholesterol depletion, or interference with oxidative phosphorylation pathways. Exact mechanisms are yet to be fully defined. Individuals with mixed dyslipidaemia may require combination therapy to achieve target lipid levels. No large-scale randomized trials have yet reported on the safety of combination therapy, although more recent studies may shed some light when they report. CONCLUSION: As most individuals on statins are 'high-risk' patients, they tend to be on multiple agents for cardiovascular disease which may interact with their statin. Progression of myalgia or myositis to rhabdomyolysis is rare (one in 30-100,000 patient-years of exposure), but if progressive muscle symptoms are ignored then fatalities can occur. When prescribing statins, physicians should be alert to potential risks and educate patients to report any potentially significant symptoms.

Humans↗
PubMed2004

Severe influenza B myocarditis and myositis.

OBJECTIVE: To report an influenza B infection with associated myocarditis and severe skeletal myositis. DESIGN: Case report. SETTING: Cardiac intensive care unit in a university-affiliated children's hospital. PATIENT: A 4-yr-old girl. RESULTS: The patient was successfully supported with extracorporeal membrane oxygenation for profound myocardial dysfunction and a combination of plasmapheresis and continuous venovenous hemodialysis for rhabdomyolysis and acute renal failure. CONCLUSIONS: This case provides a reminder that patients presenting with viral illness or myoglobinuria accompanied by renal failure, with or without associated myocarditis, may be demonstrating symptoms of influenza B.

Child, Preschool↗
PubMed2003

A rare case of Salmonella-mediated sacroiliitis, adjacent subperiosteal abscess, and myositis.

We report the case of a 16-year-old female who was ultimately diagnosed with Salmonella sacroiliitis, adjacent subperiosteal abscess, and myositis of the left iliopsoas, gluteus medius, and obturator internus muscles. Early and accurate recognition of this syndrome and other infectious musculoskeletal syndromes can prove difficult for the emergency physician, as these disease processes require special attention to pain of proportion to physical findings and a high index of suspicion.

Abscess↗
PubMed2005

Diagnosis, pathogenesis and treatment of inclusion body myositis.

PURPOSE OF REVIEW: We provide an update of progress gained from research into sporadic inclusion body myositis (s-IBM). RECENT FINDINGS: Most research on s-IBM has focused on the inflammatory reaction or the accumulation of pathological proteins in vacuolated muscle fibres. The inflammatory reaction is characterized by clonal expansions of lymphocytes, predominantly CD8 cytotoxic T cells, which invade and destroy muscle fibres. That costimulatory molecules have been identified demonstrates that muscle fibres can act as antigen presenting cells, and the expression of various chemokines in muscle indicates their importance in the immunopathogenesis of s-IBM. The region of interest for a susceptibility gene in the major histocompatibility complex has been narrowed, and for the first time it has been demonstrated that a chronic viral infection can trigger the inflammatory process leading to s-IBM. The nature of the accumulated material associated with the vacuoles has been extensively investigated over the past few years. Amyloid-beta and phosphorylated tau protein in intracellular inclusions are a characteristic finding in s-IBM, which may lead to calcium dyshomeostasis and endoplasmic reticulum stress. The proteasomal system is upregulated, including immunoproteasomes. 'Molecular misreading' leading to ubiquitin mRNA mutations and accumulation of pathological ubiquitin in muscle fibres may be associated with proteasomal dysfunction. There is still no efficient treatment for s-IBM, but the effects of new, more specific immunotherapies have begun to be explored. SUMMARY: Recent findings indicate that both inflammatory reaction and abnormal protein accumulation are important for the pathogenesis in s-IBM. The link between them continues to await elucidation.

Humans↗
PubMedDate not supplied

Myositis ossificans masquerading as sepsis.

An unusual case of myositis ossificans about the shoulder in an 11-year-old girl is presented. The purpose in describing this case is twofold: (a) to illustrate the difficulty in making the diagnosis when it presents in an unusual clinical fashion and (b) to demonstrate the potential use of the computed tomography scan as an aid in diagnosing the condition at a relatively early stage in its course.

Arthritis, Infectious↗
PubMed1990

Inclusion body myositis in French patients. A clinicopathological evaluation.

In order to establish the frequency of inclusion body myositis (IBM) in a European neuropathological unit and to evaluate the specificity of IBM pathology, we reviewed the 850 muscle biopsies performed in our laboratory over the past 7 years. Clinical histopathological and ultrastructural evaluation of all cases showing rimmed vacuoles, a constant histopathological feature of IBM, was done and the diagnosis of IBM was assessed using the clinico-pathological criteria of Calabrese, Mitsumoto & Chou (1987). Among the nine cases showing rimmed vacuoles, five were classified as IBM (group 1), either definite (3/5) or probable (2/5), and four suffered from a chronic denervating process of muscle (group 2). The overall frequency of IBM (0.6% of all muscle biopsies) was similar to that reported by North American authors. IBM represented 16% of adult idiopathic inflammatory myopathies investigated in our laboratory. Clinical and histopathological findings in group 1 were homogeneous and distinctive. Muscle biopsy was consistent with an inflammatory myopathy in all patients in group 1 and with a non-inflammatory denervating process in 3/4 patients in group 2. Typical intrasarcoplasmic inclusions were detected by electron microscopy in 3/5 cases in group 1 and 1/4 in group 2, which raises questions about the specificity of the 16-18 nm tubulofilaments. Failure to demonstrate inclusions in two patients with otherwise typical IBM, was probably related to the paucity of rimmed vacuoles observed in these cases.

Adult↗
PubMed1990

Presence of inclusion body myositis-like filaments in oculopharyngeal muscular dystrophy. Ultrastructural study of 10 cases.

Ten cases of oculopharyngeal muscular dystrophy (OPMD) were examined ultrastructurally. Two very different types of filamentous inclusions were observed: (1) Nuclear inclusions composed of 8.5 nm external diameter tubular filaments organized in palisades and similar to those described by Tomé and Fardeau (1980). They have not yet been reported in other muscle diseases. Their presence in 100% of our cases confirms they are the morphological hallmark of OPMD. (2) 16-18 nm external diameter tubular filaments. These were similar to the inclusions observed in inclusion body myositis (IBM) and morphologically very different from the first type. They were randomly dispersed or arranged in bundles near cytoplasmic debris and whorls of membranes. They were found in cytoplasm. Only once were they observed in a nucleus. These inclusions have been described in IBM but also in other diseases. They were found in 80% of our OPMD cases.

Aged↗
PubMed2004

Tau aggregates are abnormally phosphorylated in inclusion body myositis and have an immunoelectrophoretic profile distinct from other tauopathies.

Sporadic inclusion body myositis (s-IBM) is the most frequent progressive acquired inflammatory myopathy in people older than 50 years. Abnormal aggregates of 'Alzheimer's proteins', including tau proteins, have been previously demonstrated in s-IBM. In the present study, we have investigated by immunohistochemistry and immunoblotting analysis the presence of tau proteins in muscle biopsy samples from patients with s-IBM and other myopathies with rimmed vacuoles, using newly developed antibodies raised against tau protein epitopes found in Alzheimer's disease brain. Tau immunoreactivity was shown in rimmed vacuoles or inclusions, preferentially with antibodies directed against phosphorylated carboxy-terminal epitopes of tau proteins. Cytoplasmic reactivity was also demonstrated in atrophic, nonvacuolated fibres, as well as in non-necrotic fibres invaded by inflammatory cells. Abnormally phosphorylated tau aggregates were also found in other compartments of the muscle fibre in s-IBM and other myopathies. Tau immunoblotting showed an electrophorectic profile of a doublet within the range of 60-62 kDa isovariants, which was different from tauopathies of the central nervous system. Finally, the unique pattern of immunoreactivity of s-IBM samples towards anti-tau antibodies is a new clue to a possible distinct subclass of peripheral tauopathy, different from the tauopathies of the central nervous system.

Adult↗
PubMed1976

Mast cell sensitizing antibodies in experimental myositis.

Mast cell sensitizing antibodies, direct mast cell degranulation and positive delayed skin tests were detected in guinea pigs and rats during experimental paralysis provoked by inoculation with acetylcholine receptors from the Electrophorus electricus. The animals also developed fluorescent antibodies to the sarcolemma, and massive myositis with histological changes in muscles similar to those characterizing clinical polymyositis.

Acetylcholine↗
PubMed2004

Two major histocompatibility complex haplotypes influence susceptibility to sporadic inclusion body myositis: critical evaluation of an association with HLA-DR3.

Previous studies of sporadic inclusion body myositis (sIBM) have shown a strong association with HLA-DR3 and other components of the 8.1 ancestral haplotype (AH) (HLA-A1, B8, DR3), where the susceptibility locus has been mapped to the central major histocompatibility complex (MHC) region between HLA-DR and C4. Here, the association with HLA-DR3 and other genes in the central MHC and class II region was further investigated in a group of 42 sIBM patients and in an ethnically similar control group (n = 214), using single-nucleotide polymorphisms and microsatellite screening. HLA-DR3 (marking DRB1*0301 in Caucasians) was associated with sIBM (Fisher's test). However, among HLA-DR3-positive patients and controls, carriage of HLA-DR3 without microsatellite and single-nucleotide polymorphism alleles of the 8.1AH (HLA-A1, B8, DRB3*0101, DRB1*0301, DQB1*0201) was marginally less common in patients. Patients showed no increase in carriage of the 18.2AH (HLA-A30, B18, DRB3*0202, DRB1*0301, DQB1*0201) or HLA-DR3 without the central MHC of the 8.1AH, further arguing against HLA-DRB1 as the direct cause of susceptibility. Genes between HLA-DRB1 and HOX12 require further investigation. BTL-II lies in this region and is expressed in muscle. Carriage of allele 2 (exon 6) was more common in patients. BTL-II(E6)*2 is characteristic of the 35.2AH (HLA-A3, B35, DRB1*01) in Caucasians and HLA-DR1, BTL-II(E6)*2, HOX12*2, RAGE*2 was carried by several patients. The 8.1AH and 35.2AH may confer susceptibility to sIBM independently or share a critical allele.

Butyrophilins↗
PubMed1995

Streptococcal myositis and tissue necrosis with intramuscular administration of diclofenac (Voltaren).

The authors describe a fatal case of a group A beta-haemolytic streptococci infection. The symptoms seemed to have been initiated by minor skin trauma; intramuscular injections of diclofenac (Voltaren) and metoclopramide (Primperan) after which the patient developed extensive muscle necrosis. The clinical course was rapid and he died within 48 hours after the first injection from circulatory collapse, probably due to overwhelming septicaemia with group A beta-haemolytic streptococci. Streptococcal myositis is a rare and extremely serious complication of skin trauma. Muscle necrosis is also a known but rare side effect of intramuscular administration of drugs (the "Nicolau syndrome") in which non-steroid anti-inflammatory drugs are often implicated. The case is discussed in the context of this specific syndrome.

Adult↗
PubMed1976

Myositis ossificans progressiva with parathyroid hyperplasia and polycystic ovary.

A report was made on an autopsy case of myositis ossificans progressiva in a girl who died at the age of 8 year and 11 months. The first symptom appeared as right wryneck ten days after birth. Parathyroid hyperplasia and polycystic ovary with high level of serum parathyroid hormone, FSH and LH were confirmed at autopsy. Parathyroid hyperactivity might be a secondary response to the continuous stimulation by increased peripheral consumption of calcium ions due to relentlessly progressive ossification in fibrous connective tissue.

Child↗
PubMed2006

Calcifying haematoma mimicking a soft tissue sarcoma and myositis ossificans.

We describe a case of calcifying haematoma in a 78-year-old war veteran with a mass in his right lower leg. The likely differential diagnosis of myositis ossificans and soft tissue sarcoma was worked up. We discuss some of the difficulties of diagnosis despite having computed tomography and magnetic resonance imaging examinations and the unexpected final diagnosis of calcifying haematoma that was made on incisional biopsy.

Aged↗
PubMed1997

Myositis ossificans complicating severe Guillain-Barré syndrome.

We report myositis ossificans occurring in a 13-year-old boy with severe and rapidly progressive Guillain-Barré syndrome. This complication should be considered when severe musculoskeletal pain is experienced by such patients. Disodium etidronate may be of benefit in this condition.

Adolescent↗
PubMed2006

Neprilysin participates in skeletal muscle regeneration and is accumulated in abnormal muscle fibres of inclusion body myositis.

Neprilysin (NEP, EP24.11), a metallopeptidase originally shown to modulate signalling events by degrading small regulatory peptides, is also an amyloid-beta- (Abeta) degrading enzyme. We investigated a possible role of NEP in inclusion body myositis (IBM) and other acquired and hereditary muscle disorders and found that in all myopathies NEP expression was directly associated with the degree of muscle fibre regeneration. In IBM muscle, NEP protein was also strongly accumulated in Abeta-bearing abnormal fibres. In vitro, during the experimental differentiation of myoblasts, NEP protein expression was regulated at the post-transcriptional level with a rapid increase in the early stage of myoblast differentiation followed by a gradual reduction thereafter, coincident with the progression of the myogenic programme. Treatment of differentiating muscle cells with the NEP inhibitor dl-3-mercapto-2-benzylpropanoylglycine resulted in impaired differentiation that was mainly associated with an abnormal regulation of Akt activation. Therefore, NEP may play an important role during muscle cell differentiation, possibly through the regulation, either directly or indirectly, of the insulin-like growth factor I-driven myogenic programme. In IBM muscle increased NEP may be instrumental in (i) reducing the Abeta accumulation in vulnerable fibres and (ii) promoting a repair/regenerative attempt of muscle fibres possibly through the modulation of insulin-like growth factor I-dependent pathways.

Aged↗