TY - CHAP M1 - Book, Section TI - Immune-Mediated Inflammatory Myopathies A1 - Yazdany, Jinoos A1 - Manno, Rebecca L. A2 - Papadakis, Maxine A. A2 - McPhee, Stephen J. A2 - Rabow, Michael W. A2 - McQuaid, Kenneth R. Y1 - 2022 N1 - T2 - Current Medical Diagnosis & Treatment 2022 AB - KEY CLINICAL UPDATES IN IMMUNE-MEDIATED INFLAMMATORY MYOPATHIESInclusion body myositis, because of its tendency to mimic polymyositis, is a common cause of “treatment-resistant polymyositis.”– In contrast to polymyositis, the typical patient with inclusion body myositis is White, male, and over the age of 50 years.– The onset of inclusion body myositis is more insidious than that of polymyositis or dermatomyositis (eg, occurring over years rather than months), and the distal motor weakness is commonly asymmetric.– Creatine kinase levels are often minimally elevated and are normal in 25%.– Electromyography may show a mixed picture of myopathic and neurogenic abnormalities.– The disease is associated with antibodies to cytoplasmic 5'-nucleotidase 1A (cN1A).– Inclusion body myositis is less likely to respond to therapy.Immune-mediated necrotizing myopathy, although similar to polymyositis, is distinct because of the presence of muscle necrosis.– Autoantibodies aid in diagnosis; anti-SRP antibodies are associated with severe muscle weakness, pain, and cardiac involvement.– Anti-HMGCR antibodies occur in the setting of statin use and are associated with proximal muscle weakness and marked creatine kinase elevations.– Unlike statin-induced myopathy, anti-HMGCR myositis does not resolve when statins are stopped.– Instead, many patients have a severe and unrelenting disease course with persistent weakness. SN - PB - McGraw-Hill Education CY - New York, NY Y2 - 2024/03/29 UR - accessmedicine.mhmedical.com/content.aspx?aid=1184193213 ER -