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Perifascicular muscle atrophy and complement-mediated microangiopathy, charactreric of dermatomyositis

(A) Cross-section of an H&E-stained muscle biopsy demonstrates the classic perifascicular atrophy (layers of atrophic fibers at the periphery of the fascicle) with necrosis and some inflammatory infiltrates (H&E stain ×100.) (B) Deposition of complement (membranolytic attack complex in green) on the endothelial cell wall of endomysial vessels (stained in red with a lectin Ulex Europaeus) leads to destruction of endothelial cells (confirmed in orange based on the superimposition of red on green). Consequently, in the muscles of patients with dermatomyositis, (C) the density of the endomysial capillaries (in red) is reduced, especially at the periphery of the fascicle, with dilatation of the lumen of the remaining capillaries in an effort to compensate for the ischemic process (x560). (Dalakas MC. Polymyositis, dermatomyositis and inclusion body myositis. In: Kasper DL, Fauci AS, Hauser SL, Longo DL, Jameson JL, Loscalzo J, editors. Harrison’s principles of internal medicine. 19th edition. New York: McGraw-Hill, 2015b:2195-202.)

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