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edematous changes on MRI scans would be helpful, suggesting a dystrophy as opposed to PM EMG can be useful, as the presence of diffuse myotonic discharges should lead to the consideration of proximal myotonic myopathy a condition that we have frequently seen misdiagnosed as PM Importantly, the diagnosis of PM requires a muscle biopsy It is essential to look for histopathological features that would suggest IBM: rimmed vacuoles, eosinophilic inclusions, ragged red bers, cytochrome oxidase negative bers, amyloid deposits, and inclusions on EM However, the absence of these ndings does not exclude the diagnosis of IBM Muscle biopsy is essential to look for features that might suggest a dystrophy, metabolic myopathy such as acid maltase de ciency, or necrotizing myopathy
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rophy of type 2 muscle bers and perimysial brosis However, 5 17% of patients with scleroderma have myositis which can occur in either of its two major forms progressive systemic sclerosis or CREST (Calcinosis, Raynaud s phenomena, Esophageal dysmotility, Sclerodactyly, Telangiectasia) syndrome21,83 86 Patients with scleroderma-myositis have increased serum CK levels and irritable and myopathic EMGs Detailed descriptions of the immunohistopathology on muscle biopsies are lacking, and therefore it is dif cult to ascertain if these can have features of DM or PM Most patients with CREST syndrome have anticentromere antibodies, while anti-Scl-70 antibodies are common in patients with progressive systemic sclerosis Some patients with scleroderma myositis have anti-PMScl (also called anti-PM-1) antibodies37,87
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Most patients with PM improve with immunosuppressive therapies but usually require life-long treatment20,42,66 Some retrospective studies suggest that PM does not respond to immunosuppressive agents as well as DM However, interpretation of the results of these retrospective series is dif cult, as the diagnosis of PM was usually made on the basis of Bohan and Peter criteria rather than on more current criteria based on strict clinical and histological criteria
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Sj gren syndrome is characterized by dryness of the o eyes and mouth (sicca syndrome) and other mucosal membranes Muscle pain and weakness are common in Sj gren syndrome, but true myositis is rare Muso cle weakness is usually due to disuse atrophy secondary to arthritis and pain Nonetheless, myositis can occur with Sj gren syndrome21,88 90 About 90% of pao tients have ANAs directed against ribonucleoproteins, speci cally SS-A (Ro) and less commonly SS-B (La) antibodies
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The term overlap syndrome is applied when DM or PM is associated with other well-de ned connective tissue diseases (CTDs) such as scleroderma, mixed connective tissue disease (MCTD), Sj gren syndrome, systemic o lupus erythematosus (SLE), or rheumatoid arthritis1,3 In our experience53,83,64 and others,16 the muscle biopsies in patients with overlap syndrome resemble DM, a necrotizing myopathy, or are associated with nonspeci c (eg, perivascular and perimysial) in ammatory cell in ltrates as opposed to PM (at least if de ned by CD8+ cells invading non-necrotic muscle bers) The prognoses are related in part to the underlying CTD Retrospective series of patients that suggest that myositis associated with overlap syndromes is more responsive to immunosuppressive treatment than isolated DM and PM, but again prospective studies are lacking20,35,42,66
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SLE is an autoimmune disorder affecting multiple organ systems As with other CTDs, weakness is not unusual in SLE but is most often the result of disuse atrophy Nevertheless, myositis can occur with SLE21,53,91,92 Most patients with SLE have positive ANA titers that are directed against native DNA (highly speci c for SLE) and ribonuclear proteins (RNPs) The anti-RNP antibodies are present in less than half of patients with SLE and include anti-SS-A and anti-SS-B (also present in Sj gren s o syndrome), anti-U1 RNP (also present in mixed connective tissue disease), and anti-Sm (speci c for SLE) Of note, gene expression studies in peripheral blood of patients with SLE demonstrated an upregulation of type 1 interferon-inducible genes, similar to what is seen in gene expression studies of muscle biopsies in DM53 In this regard, MxA is highly expressed in both SLE blood and DM muscle Both disorders are also associated with tubular reticular inclusions in endothelial cells on EM Thus, DM and SLE likely share a similar pathogenic basis with abnormalities involving the innate immune system
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