Disease relevance of Myositis

• We conclude that long-term therapy with zidovudine can cause a toxic mitochondrial myopathy, which coexists with a T-cell-mediated inflammatory myopathy that is restricted to MHC-I antigen, and is indistinguishable from the myopathy associated with primary HIV infection or polymyositis in HIV-seronegative patients [1].
• The occurrence of renal failure and myositis in the spectrum of phenytoin hypersensitivity reactions is discussed, and the importance of a morbilliform rash in a patient receiving phenytoin is emphasized [2].
• The sera of six patients with autoimmune disease, predominantly myositis with pulmonary fibrosis, contain antibodies of the PL-12 specificity [3].
• Increased expression of HLA ABC class I antigens by muscle fibres in Duchenne muscular dystrophy, inflammatory myopathy, and other neuromuscular disorders [4].
• Causes of the eosinophilia-myalgia syndrome other than L-tryptophan include parasitic myositis (that is, trichinosis), acute tropical myositis, sarcoidosis, granulomatous myositis, polymyositis, collagen vascular diseases, neoplastic myositis, and eosinophilic myositis [5].

Psychiatry related information on Myositis

• Does overexpression of betaAPP in aging muscle have a pathogenic role and a relevance to Alzheimer's disease? Clues from inclusion body myositis, cultured human muscle, and transgenic mice [6].
• Ids II-28, V-88 and I-402 were elevated in serum from patients with Sjögren's syndrome and II-28 Id in serum from patients with myositis and RA [7].

High impact information on Myositis

• Pravastatin-associated inflammatory myopathy [8].
• Myositis autoantibody inhibits histidyl-tRNA synthetase: a model for autoimmunity [9].
• Furthermore, increased autoantigen expression correlates with differentiation state, such that myositis autoantigen expression is increased in cells that have features of regenerating muscle cells [10].
• Enhanced autoantigen expression in regenerating muscle cells in idiopathic inflammatory myopathy [10].
• In 62% (21/34) of the cases sera from patients with myositis and in 58% (30/52) of the cases sera from patients with SLE reacted with the 20S proteasome [11].

Chemical compound and disease context of Myositis

• Myositis with tretinoin [12].
• Myositis in association with carbimazole therapy [13].
• Male sex, lower creatine kinase levels, slower rate of progression, and peripheral neuropathy were also more common in inclusion body myositis and unresponsive polymyositis than in responsive polymyositis and dermatomyositis patients [14].
• Comparison of weakness progression in inclusion body myositis during treatment with methotrexate or placebo [15].
• Oral administration of N-monomethyl-L-arginine, an inhibitor of nitric oxide synthase (NOS), reduced urinary nitrate excretion and also the severity of myositis [16].

Biological context of Myositis

• Conditional up-regulation of MHC class I in skeletal muscle leads to self-sustaining autoimmune myositis and myositis-specific autoantibodies [17].
• We demonstrate that HLA-G, a nonclassical major histocompatibility complex class I antigen, is expressed in muscle fibers in various inflammatory myopathies [18].
• Muscle fibers in inflammatory myopathies and cultured myoblasts express the nonclassical major histocompatibility antigen HLA-G [18].
• CONCLUSION: Fas/FasL is involved in muscle cell apoptosis in at least 2 of the inflammatory myopathies, PM and DM [19].
• Induction of cell adhesion molecules on muscle cells by IFN gamma may be an important mechanism for the localization of T cells in the affected muscles of patients with autoimmune myositis [20].

Anatomical context of Myositis

• Of 36 patients with other inflammatory myopathies, 1 patient had faint MxA staining of myofibers and 3 of capillaries [21].
• In all control and inclusion body myositis or myopathy biopsy specimens, ApoE immunoreactivity was strong at the postsynaptic domain of neuromuscular junctions; nonjunctional regions of normal fibers were negative for ApoE [22].
• Serial urinary creatine excretion and serum enzyme studies were of value in differenting steroid myopathy from a flare of myositis in patients with connective tissue disease [23].
• We describe the unreported pattern of inflammatory myopathy with abundant macrophages (IMAM) as a main differential diagnosis of postimmunization aluminum hydroxide-induced macrophagic myofasciitis (MMF) [24].
• Intervertebral disk calcification and spine fusion were observed in patients with Klippel-Feil syndrome, myositis ossificans progressive, juvenile rheumatoid arthritis, ankylosing spondylitis, and surgical spine fusion [25].

Gene context of Myositis

• CONCLUSION: PMS1 autoantibodies are myositis specific [26].
• Expression of the costimulatory molecule BB-1, the ligands CTLA-4 and CD28, and their mRNA in inflammatory myopathies [27].
• IL-1ra levels were particularly elevated in patients with active myositis and decreased in response to treatment [28].
• We found in 21 cases of autoimmune myositis various amounts of inflammatory cells expressing interleukin (IL)-1 alpha and -beta, IL-2, IL-4, tumor necrosis factor (TNF) -alpha and -beta, and interferon (IFN)-gamma and its receptor [29].
• MCP-1 mRNA was detected in scattered macrophages in each inflammatory myopathy [30].

Analytical, diagnostic and therapeutic context of Myositis

• Six myositis and two control sera had apparent specific antibody detectable only by ELISA [31].
• All but one immunodiffusion negative myositis sera (a high binder by ELISA) inhibited less than 50% of the average with normal serum [31].
• Radioimmunoprecipitation assays were performed with sera from 91 patients with various inflammatory muscle diseases and from 254 control patients with other rheumatic diseases [32].
• Drug therapy of the idiopathic inflammatory myopathies: predictors of response to prednisone, azathioprine, and methotrexate and a comparison of their efficacy [33].
• Muscle biopsy confirmed the presence of inflammatory myopathy; deposits of immunoglobulin G (IgG), immunoglobulin M (IgM) or third component of complement (C3) were not detected by immunofluorescence [34].

References