Elia Pancheri1, Massimiliano Lanzafame2, Alberto Zamò3, Andrea Angheben4, Silvia Sartoris5, Antonella Zorzi6, Marzia Boaretti6, Caterina Signoretto6, Valeria Guglielmi1, Sergio Ferrari1, Paola Tonin1, Gaetano Vattemi1. 1. Department of Neurosciences, Biomedicine and Movement Sciences, Section of Clinical Neurology, University of Verona, Verona, Italy. 2. Department of General Medicine, Infectious Diseases and Tropical medicine Section, University of Verona, Verona, Italy. 3. Department of Pathology and Diagnostics, Section of Pathology, University of Verona, Verona, Italy. 4. Centre for Tropical Diseases, Sacro Cuore-Don Calabria Hospital, Negrar, Verona, Italy. 5. Department of Medicine, Immunology Section, University of Verona, Italy. 6. Department of Pathology and Diagnostics, Virology and Microbiology Unit, University of Verona, Italy.
Abstract
BACKGROUND: Several viruses have been described as causes of acquired inflammatory myopathies; however, the mechanisms by which they cause muscle disease are still unclear. The aim of this study was to describe the laboratory features of benign acute myositis in a small case series. METHODS: A detailed pathological and serological analysis was performed in five African migrants who developed an acute viral myositis complicated by rhabdomyolysis. RESULTS: Muscle biopsies clearly documented an inflammatory myopathy with histological features similar to polymyositis including CD8+ T cells surrounding and invading nonnecrotic muscle fibers, CD68+ macrophages and major histocompatibility complex class I antigen upregulation. In addition, positivity for myositis-specific antibodies (MSA), in particular anti-aminoacyl tRNA synthetases, was found in the serum of two patients. CONCLUSIONS: Our study demonstrated that T-cell mediated injury occurs in muscle of patients with acute viral myositis, and that MSA may be present in the serum of these patients.
BACKGROUND: Several viruses have been described as causes of acquired inflammatory myopathies; however, the mechanisms by which they cause muscle disease are still unclear. The aim of this study was to describe the laboratory features of benign acute myositis in a small case series. METHODS: A detailed pathological and serological analysis was performed in five African migrants who developed an acute viral myositis complicated by rhabdomyolysis. RESULTS: Muscle biopsies clearly documented an inflammatory myopathy with histological features similar to polymyositis including CD8+ T cells surrounding and invading nonnecrotic muscle fibers, CD68+ macrophages and major histocompatibility complex class I antigen upregulation. In addition, positivity for myositis-specific antibodies (MSA), in particular anti-aminoacyl tRNA synthetases, was found in the serum of two patients. CONCLUSIONS: Our study demonstrated that T-cell mediated injury occurs in muscle of patients with acute viral myositis, and that MSA may be present in the serum of these patients.