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Query: UMLS:C0027121 (myositis)
 4,538 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A double-blind, randomized study was undertaken to evaluate the efficacy and safety of fluvastatin as monotherapy and as combination therapy with niacin in the treatment of hypercholesterolemia refractory to diet. Seventy-four patients with plasma low-density lipoprotein cholesterol (LDL-C) levels > or = 160 mg/dL were treated with fluvastatin, 20 mg/d, or placebo for 6 weeks. Thereafter, immediate-release niacin, at a dosage titrated to a maximum of 3 g/d, was added to both regimens for another 9 weeks. All adverse events were monitored, with particular attention to the evaluation of liver and muscle enzymes. Initial analysis of the data shows that fluvastatin and its combination with niacin was well tolerated and was not associated with any serious adverse events. Small, transient, asymptomatic rises in aspartate aminotransferase (AST) occurred in 28.9% of fluvastatin-niacin treated patients compared to 8.3% in the niacin-placebo control arm (p < 0.05). These were considered clinically insignificant in that no transaminase elevations > 3 times the upper limit of normal occurred. No evidence of myopathy, creatine kinase levels exceeding 10 times the upper limit of normal, myositis, or rhabdomyolysis were demonstrated in this short-term trial. The majority of adverse events resulting in patient withdrawals were ascribed to niacin therapy and included cutaneous vasodilatation, flushing, itching, and rash. These preliminary results suggest that fluvastatin, both alone and combined with niacin, is an effective, safe, and well-tolerated treatment for hypercholesterolemia.
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PMID:Combination therapy with fluvastatin and niacin in hypercholesterolemia: a preliminary report on safety. 819 20

In muscle biopsies of 8 sporadic inclusion-body myositis (S-IBM) and 4 hereditary inclusion-body myopathy (H-IBM) patients, vacuolated muscle fibers contained within their vacuoles strongly immunoreactive inclusions with 2 polyclonal and 1 monoclonal antibodies against prion protein (PrP). By light-microscopy, PrP deposits co-localized with beta-amyloid protein (A beta) and ubiquitin (Ub). By immuno-electronmicroscopy, both PrP and A beta were present on amorphous material and on 6-10 nm amyloid-like fibrils; and PrP and Ub co-localized on cytoplasmic twisted tubulofilaments (TTFs) and on amorphous material. Our study provides the first demonstration of abnormally accumulated PrP in pathological tissue other than brain, and it suggests that PrP may play a role in the pathogenesis of IBM.
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PMID:Prion protein is abnormally accumulated in inclusion-body myositis. 828 Aug 54

We reported a senile male patient with progressive external ophthalmoplegia (PEO) and myositis. The ophthalmoplegia was severe, but other neuromuscular features were nearly normal. Muscle enzymes in serum were moderately elevated. Autoimmune, endocrinological or malignant diseases were not observed during the previous 4 years. Pathology of non-weak limb muscles biopsied twice was consistent with active inflammatory myopathy. The ragged-red or cytochrome c oxidase-negative fibers, which are a hallmark of mitochondrial myopathy with PEO, were not increased in comparison with age-matched control muscles. Analysis of mitochondrial DNA in muscle by the Southern blot method did not reveal any deletions. It was concluded that the inflammatory myopathy, myositis clinically localized at the ocular muscles, is an important and distinct disorder in PEO.
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PMID:Progressive external ophthalmoplegia and myositis. 835 24

Microsporidia are obligate intracellular protozoa that parasitize both vertebrates and invertebrates and are now recognized as important pathogens in individuals infected with human immunodeficiency virus type 1 (HIV-1). We describe the clinical and morphological features of a case of pleistophora (microsporidian) myositis in a patient with AIDS and delineate the stages of the microsporidian life cycle, as visualized by light and electron microscopy. We discuss significant aspects of microsporidian infections in humans and of myopathy attributable to other causes in HIV-1-infected individuals. As far as we know, ours is only the second reported case of microsporidian myositis and the first reported case in a patient with documented HIV-1 infection.
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PMID:Myositis due to Pleistophora (Microsporidia) in a patient with AIDS. 844 94

We report the treatment of four patients with inclusion-body myositis (IBM) and severe slowly progressive weakness using high-dose intravenous immunoglobulin (IVIg). After two monthly infusions, the strength of the proximal and less atrophic muscle groups improved or normalized in three of the four patients. The improvement lasted from 2 to 4 months. Intravenous immunoglobulin is the first treatment modality to improve the strength of some muscles in patients with this disabling inflammatory myopathy. In view of the high cost of IVIg, the unexpected but encouraging results from this pilot study warrant a controlled trial.
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PMID:Treatment of inclusion-body myositis with high-dose intravenous immunoglobulin. 849 40

Polymyositis/dermatomyositis are rare autoimmune diseases. Classification is usually performed according to the criteria of Bohan and Peter. The occurrence of myositis-specific autoantibodies has recently been described in inflammatory myopathies. Approximately half of the patients can now be classified by these specific autoantibodies. Several of these autoantibodies (anti-aminoacyl-tRNA synthetases, anti-SRP, anti-Mi2) are strongly associated with the clinical presentation. We may expect that in the future different subsets of these diseases will be increasingly identified by serum antibodies. We report on a patient with myopathy, pulmonary fibrosis and polysynovitis, a typical clinical presentation of the anti-Jo1 syndrome (anti-synthetase syndrome).
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PMID:[Myositis, polysynovitis and pulmonary fibrosis: anti-Jo-1 syndrome]. 857 93

This review emphasizes new advances in seeking the pathogenic mechanisms of sporadic inclusion-body myositis and hereditary inclusion-body myopathy syndromes. Clinical and pathologic similarities and differences between sporadic and hereditary forms are described. Hypotheses are presented regarding the possible causes and consequences of abnormally accumulated intramyofiber beta-amyloid precursor protein (beta APP) (including beta-amyloid protein and C- and N-terminal epitopes), hyperphosphorylated tau, alpha 1-antichymotrypsin, apolipoprotein E, prion protein, ubiquitin, nicotinic acetylcholine receptor and its 43-kD associated protein, fibroblast growth factor, and transforming growth factor-beta. Also increased are beta APP mRNA and prion protein mRNA. Striking similarities between the pathology of muscle specimens from sporadic inclusion-body myositis and samples from the brains of patients with Alzheimer's disease in regard to Congo red positivity and accumulations of several proteins are discussed. Because most of the proteins that pathologically accumulate throughout the abnormal muscle fibers also accumulate focally at normal human neuromuscular junctions, the possible "junctionalization" of nonjunctional nuclei as a pathogenic mechanism in the muscle fiber is discussed.
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PMID:New advances in the understanding of sporadic inclusion-body myositis and hereditary inclusion-body myopathies. 857 68

Intravenous immunoglobulin (IVIg) is a new modality used to help treat conditions associated with immune dysregulation. The inflammatory myopathies are a group of complex diseases including dermatomyositis, polymyositis, and inclusion-body myositis. Overall evaluation of IVIg in myopathy has been hampered by difficulty in accurately diagnosing and assessing disease activity. The lack of large, well controlled, double-blind trials has precluded clear evaluation of the effectiveness of IVIg in these diseases. However, from the data presented in published reports, it appears that IVIg may be useful in the treatment of inflammatory myopathies, particularly dermatomyositis.
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PMID:Treatment of inflammatory myopathy with intravenous gamma globulin. 857 71

In recent years, several new autoantibody tests have been developed and are being used in the field of rheumatology, including the antineutrophil cytoplasmic antibody (ANCA) and myositis-specific antibodies such as anti-Jo1. Positive test results for ANCAs reveal one of two basic staining patterns: cytoplasmic (c-ANCA) or perinuclear (p-ANCA). The Jo1 antibody test is often helpful at the time of diagnosis of a new case of idiopathic inflammatory myopathy. Herein this article reviews the clinical utility of the new tests in conjunction with the established autoantibody tests including antinuclear antibodies and extractable nuclear antibodies. Both the antinuclear antibody and extractable nuclear antibody tests are helpful in diagnosing connective tissue diseases. Before the results of any of these tests can be interpreted, the physician must consider the sensitivity, specificity, and negative and positive predictive values. Positive results must be analyzed in the clinical context and in relationship to other autoantibody test results.
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PMID:Use and interpretation of rheumatologic tests: a guide for clinicians. 863 64

Giant cell myocarditis is a rare idiopathic inflammatory heart disease characterized histologically by multinucleated giant cells, and clinically by rapid progressive heart failure, arrhythmias, or sudden death, often within hours to days of initial symptoms. There are two previously reported cases of giant cell myocarditis with idiopathic orbital myositis. We report a similar case in a patient who also had vitiligo, a diagnostic endomyocardial biopsy, and survival because of a cardiac transplant. Giant cell myocarditis should be monitored for in the course of inflammatory orbital myopathy because of its life-threatening fulminant course.
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PMID:Orbital myositis, vitiligo, and giant cell myocarditis. 869 13


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