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At least 1,063 records · Page 59Linked to original sources
PubMed2001

Randomized pilot trial of betaINF1a (Avonex) in patients with inclusion body myositis.

BACKGROUND: Inclusion body myositis (IBM) is the most common acquired disease of muscle in adults over the age of 50 years. Although there is compelling evidence for the importance of immunologic abnormalities in its pathogenesis, the cause of the disease is not known, and it is considered to be resistant to treatment with corticosteroids and other conventional immunosuppressive agents. beta-Interferon (betaIFN), an immunomodulatory cytokine, is a candidate therapeutic agent for IBM. METHOD: A 24-week, multicenter, randomized, placebo-controlled, parallel-group clinical trial of 30 microg of beta-interferon-1a (betaINF1a) administered IM once a week in 30 patients with IBM was conducted. The primary goal was to establish the safety and tolerability of betaINF1a in IBM. A secondary goal was to obtain preliminary data on the efficacy of betaINF1a by measuring changes from baseline in muscle strength and muscle mass. RESULTS: Twenty-nine of the 30 subjects enrolled completed the study. Two subjects (one in the placebo group, one in the betaINF1a group) experienced severe adverse events. One subject, randomized to receive betaINF1a, died from an ischemic bowel after resection of a colonic mass. No subjects required dosage reductions, and the adverse event profile was similar for the placebo and betaINF1a groups. There were no significant differences in the changes in muscle strength and muscle mass between the placebo and betaINF1a groups at 6 months. CONCLUSIONS: betaINF1a at a dose of 30 microg/week IM is well tolerated in IBM. Further studies are needed to establish its therapeutic usefulness in this inflammatory myopathy.

Adjuvants, Immunologic↗
PubMed2002

Three lipoprotein receptors and cholesterol in inclusion-body myositis muscle.

BACKGROUND: An important aspect of inclusion-body myositis (IBM) vacuolated muscle fibers (VMF) is abnormal accumulation of amyloid-beta precursor protein (AbetaPP) epitopes and its product, amyloid-beta (Abeta), and of phosphorylated tau (p-tau) in the form of paired helical filaments. Lipoprotein receptors and cholesterol are known to play an important role in AbetaPP processing, Abeta production, and tau phosphorylation. METHODS: In 10 IBM and 22 control muscle biopsies the authors immunolocalized low-density lipoprotein receptor (LDLR), very low-density lipoprotein receptor (VLDLR), and low-density lipoprotein receptor-related protein (LRP), and colocalized them with Abeta, p-tau, APOE, and free cholesterol. RESULTS: In each biopsy, virtually all IBM VMF had strong LDLR-immunoreactive inclusions, which colocalized with Abeta, APOE, p-tau, and free cholesterol. VLDLR was increased mainly diffusely, but in approximately 50% of the VMF it was also accumulated in the form of inclusions colocalizing with Abeta, APOE, and free cholesterol, but not with p-tau. LRP inclusions were present in a few VMF. In all myopathies, a subset of regenerating and necrotizing muscle fibers had prominent diffuse accumulation of both LDLR and free cholesterol. At normal neuromuscular junctions (NMJ) postsynaptically, LDLR and VLDLR, but not LRP, were immunoreactive. CONCLUSIONS: 1) Abnormal accumulation of LDLR, VLDLR, LRP, and cholesterol within IBM vacuolated muscle fibers suggests novel roles for them in the IBM pathogenesis. 2) Expression of LDLR and VLDLR at normal NMJ suggests physiologic roles for them in transsynaptic signaling pathways, increased internalization of lipoproteins there, or both. 3) Increased LDLR and free cholesterol in some regenerating and necrotizing muscle fibers suggest a role for them in human muscle fiber growth and repair and necrotic death.

Amyloid beta-Peptides↗
PubMed2002

A pilot randomized trial of oxandrolone in inclusion body myositis.

BACKGROUND: Inclusion body myositis (IBM) remains without effective therapy. As anabolic steroids have myotrophic properties, the authors studied whether a synthetic androgen, oxandrolone, would have efficacy in IBM. METHODS: A double-blind, placebo-controlled, crossover design was used. Patients received oxandrolone or placebo for 12 weeks followed by a minimum 2-month washout period, followed by 12 weeks of the alternative treatment. Maximal voluntary isometric contraction testing (MVICT), manual muscle testing (MMT), and functional performance testing were obtained before and after each treatment period, with the whole-body MVICT score as the primary outcome measure. RESULTS: Of 19 patients enrolled, 16 (14 men, 2 women; median age 68.5 years) had complete data for at least the first treatment period, with 13 completing the entire study. Whole-body MVICT improved by a median of 15.5 kg with drug and 4.1 kg with placebo (p = 0.06), whereas MMT demonstrated a median increase of 2.0 Medical Research Council points with drug and 0.9 point with placebo (p = 0.33). Upper-extremity MVICT demonstrated a significant treatment effect, with strength increasing a median 6.3 kg with drug vs 2.5 kg with placebo (p = 0.006). Stair climbing also increased a median of 1 step on average with drug versus no change with placebo (p < 0.001). Minimal adverse effects occurred. CONCLUSIONS: Oxandrolone had a borderline significant effect in improving whole-body strength and a significant effect in improving upper-extremity strength as measured by MVICT. Given these findings, further study of this drug, possibly in combination with an immunomodulating agent, is warranted.

Aged↗
PubMed2004

McArdle's disease diagnosed following statin-induced myositis.

We describe the case of a 69-year-old man with a history of muscular symptoms dating back to his childhood; McArdle's disease (glycogen-storage disease V) was diagnosed following an episode of myositis in which a statin and physical exertion appear to have been precipitating factors. This case demonstrates that the ischaemic lactate-ammonia test still has a place in screening patients with symptoms suggestive of McArdle's disease and emphasizes the importance of carrying out glycogen phosphorylase histochemistry on the skeletal muscle biopsy to confirm the diagnosis. In patients who develop a raised plasma creatine kinase level or muscular symptoms during lipid-lowering therapy, the clinician should be alert to the possibility of an underlying myopathy.

Aged↗
PubMed1993

Inclusion body myositis as a cause of respiratory failure.

Inclusion body myositis (IBM) is a slowly progressive myopathy that has not been reported to affect respiratory muscles. It is often refractory to treatment and a muscle biopsy specimen is necessary for the diagnosis. This is a report of a patient with IBM who quickly progressed to respiratory muscle failure requiring intubation.

Aged↗
PubMed1993

Interstitial lung disease and myositis in a patient with simultaneously occurring sarcoidosis and scleroderma.

A patient initially presented with sarcoidosis in combination with myositis of sarcoid origin and Raynaud's phenomenon. During the course of his disease, he additionally developed scleroderma. Bronchoalveolar lavage, performed because of increase of interstitial markings in the presence of enlarged hilar nodes, showed an increased percentage of granulocytes and a low CD4 to CD8 ratio of lymphocytes, suggesting a change to scleroderma lung disease.

Adult↗
PubMed2004

Skeletal muscle regeneration and Trypanosoma cruzi-induced myositis in rats.

Although Chagas' disease is known to provoke severe acute myositis, information on muscle regeneration is missing. The current paper shows that during T. cruzi infection in rats, skeletal muscle parasitism and the consequent inflammatory process are higher in muscle with a high proportion of type-I myofibres (soleus and diaphragm). Immunohistochemistry showed an acute inflammatory process characterized by ED1+ and ED2+ macrophages, CD8+ lymphocytes, and NK cells. Parasite-nest rupture provoked segmental degeneration of myofibres followed by regeneration. These phenomena were observed at both light and transmission electron microscopy levels. Myofibre regeneration involved activation of satellite cells assessed by the expression of MyoD, a muscle-specific transcription factor. Ultrastructural evidence of fusion of myoblast-like cells with the intact segment of degenerating fibres has been provided. At the chronic phase no signs of fibrosis were found, but sparse and small inflammatory foci were found. Our results argue against the relevant participation of autoimmunity phenomena in both acute and chronic phases and furnish a new view for explaining histopathological findings in human patient muscles.

Animals↗
PubMed1998

[Immunocytochemical analysis of the inflammatory infiltrate in inclusion body myositis and other neuromuscular disorders with rimmed vacuoles].

Among 1400 muscle biopsies, we found 16 cases with rimmed vacuoles whose diagnosis were sporadic inclusion body myositis (IBM) (4 cases), juvenile spinal muscular atrophy (6 cases), distal myopathies (3 cases), limb-girdle muscular dystrophy (2 cases), and peripheral neuropathy (1 case). Monoclonal antibodies reactive for T lymphocytes and subsets, B lymphocytes, macrophages, natural killer cells, immunoglobulins, and complement were used to analyze the inflammatory infiltrate. The analysis was quantitative and according to the site of accumulation (interstitial, endomysial, and perivascular). The immunocytochemical analysis showed CD8+ lymphocytes in the interstitial in most cases, occasionally inside of muscle fibers, and rarely in the perivascular region. The IBM cases had an increased number of CD8+ lymphocytes comparing with the other diseases. CD8+/CD4+ ratio was increased in IBM compared with the other diseases. Macrophages were frequent in IBM, distal myopathy, and one case of limb-girdle muscular dystrophy. Natural killer cells were frequent at interstitial.

Adolescent↗
PubMed2004

[Peripheral neuropathy and myositis in idiopathic hypereosinophilic syndrome: case report].

We describe a case of idiopathic hypereosinophilic syndrome manifested by an axonal sensory-motor polyneuropathy (ASMP) and signals of myositis. A 20 year old woman began with progressive gait impairment with drops and presented with subacute lower limb edema associated with paresthesis and cramps. She showed hypotonia in the lower limbs, absence of knee and ankle jerks, steppage gait, and decreased sensation on both legs. Examinations of stools were negative. Blood examination showed 7700 leukocytes with 24% (1848/mm(3)) eosinophils. Electrodiagnostic studies showed axonal lesion in sensory and motor nerves. Muscle biopsy showed type 2 muscle fibers atrophy with discrete inflammatory cells, predominantly lymphocytic in perivascular and interstitial locations. She was treated with prednisone and all the symptoms subsided after two months.

Adult↗
PubMed1997

Recognition and management of myositis.

Polymyositis and dermatomyositis are severe inflammatory muscle disorders of unknown cause, with possible life-threatening complications. Prognosis and response to therapy may be predicted not only from the clinical and pathological diagnostic group to which a patient belongs, but also from the patient's myositis-specific antibody status, extraskeletal muscle involvement, and the interval between onset of muscle weakness and the start of the treatment. Corticosteroids are the mainstay of treatment, providing recovery of normal muscular function in about 60% of patients. However, adequate dose, duration of therapy and gradual tapering of corticosteroids are required to produce favourable biochemical and clinical outcomes. In patients refractory to or intolerant of corticosteroids, additional therapy, often involving an immunosuppressive agent or intravenous immunoglobulin, is required. The potential roles of plasmapheresis and total body irradiation must be balanced by their inconclusive efficacies and adverse effects.

Animals↗
PubMed2001

Severe inclusion body myositis with interstitial pneumonia.

We report a patient with a severe inclusion body myositis (IBM). His illness was unusual in terms of a rapid progression, high creatine kinase levels, and complication with interstitial pneumonia. He responded well to immunosuppressive agents such as corticosteroids, cyclosporin A, cyclophosphamide, and immunoglobulin. The present patient indicates the wide range of the disease, and that immunosuppressive agents may be useful for treatment of IBM.

Aged↗
PubMed1976

Myositis ossificans circumscripta: a benign lesion with a malignant differential diagnosis.

Localized areas of active myositis ossificans, occurring without a clear history of antecedent trauma, have been referred to as a "pseudo-malignant osseous tumor of soft tissue." This lesion may be mistaken both roentgenographically and pathologically for a malignancy. The roentgenographic signs which favor a diagnosis of non-neoplastic heterotopic bone formation include a lucent zone between the lesion and the adjacent bone, an intact underlying cortex, diaphyseal location, dense calcification in the periphery, and loss of volume on serial films.

Adolescent↗
PubMed2006

Genetically augmenting Abeta42 levels in skeletal muscle exacerbates inclusion body myositis-like pathology and motor deficits in transgenic mice.

The pathogenic basis of inclusion body myositis (IBM), the leading muscle degenerative disease afflicting the elderly, is unknown, although the histopathological features are remarkably similar to those observed in Alzheimer's disease. One leading hypothesis is that the buildup of amyloid-beta (Abeta) peptide within selective skeletal muscle fibers contributes to the degenerative phenotype. Abeta is a small peptide derived via endoproteolysis of the amyloid precursor protein (APP). To determine the pathogenic effect of augmenting Abeta42 levels in skeletal muscle, we used a genetic approach to replace the endogenous wild-type presenilin-1 (PS1) allele with the PS1(M146V) allele in MCK-APP mice. Although APP transgene expression was unaltered, Abeta levels, particularly Abeta42, were elevated in skeletal muscle of the double transgenic (MCK-APP/PS1) mice compared to the parental MCK-APP line. Elevated phospho-tau accumulation was found in the MCK-APP/PS1 mice, and the greater activation of GSK-3beta and cdk5 were observed. Other IBM-like pathological features, such as inclusion bodies and inflammatory infiltrates, were more severe and prominent in the MCK-APP/PS1 mice. Motor coordination and balance were more adversely affected and manifested at an earlier age in the MCK-APP/PS1 mice. The data presented here provide experimental evidence that Abeta42 plays a proximal and critical role in the muscle degenerative process.

Amyloid beta-Peptides↗
PubMed1992

Myositis ossificans in childhood.

Myositis ossificans is a benign, localized, ossifying lesion of soft tissues that is rarely reported in young children. This paper describes two cases found in a search of the surgical biopsy files of the Adelaide Children's Hospital over the 30 yr period from 1962 to 1991, in boys both aged 7 yrs. Diagnosis was assisted by combined clinical, radiological and histopathological information (including an adequate well-orientated biopsy in Case 1 that demonstrated the characteristic growth pattern) enabling differentiation from other possibilities such as fibrodysplasia ossificans progressiva.

Child↗
PubMed1992

Streptococcal myositis.

Streptococcal myositis (SM), is a very serious condition with a high mortality rate. The port of entry of the infection is often unknown. We present here a case report concerning a 68-year-old patient with fulminant SM preceded by symptoms of an upper respiratory tract infection. Haemolytic streptococci of group A were found in the blood, muscle tissue and throat. The patient survived after massive therapeutic interventions including intensive care with intravenous antibiotics, fasciotomy, plasma exchange, controlled respiratory ventilation and exarticulation through the shoulder. The patient's wife fell ill at the same time with a sore throat and the same type of streptococci (T-type 3) was found in both patients.

Aged↗
PubMedDate not supplied

Intracisternal collagen fibrils in proliferative fasciitis and myositis of childhood.

During ultrastructural examination of a difficult to diagnose tumor, short spacing collagen fibrils (periodicity of banding, approximately 43.2 nm) and native collagen fibrils (periodicity of banding, approximately 53 nm) were found in dilated and vacuolated cisternae of rough endoplasmic reticulum and the perinuclear cistern. Original diagnoses from several histopathologists included alveolar soft part sarcoma, malignant fibrous histiocytoma, atypical fibroxanthoma, and myogenic tumor. The finding of intracisternal collagen (which is but a variety of intracellular collagen) led to the conclusion that this was a fibroblastic neoplasm. This, plus a review of the histologic findings, led to the diagnosis of proliferative fasciitis and myositis of childhood.

Adolescent↗