Background
Inflammatory myopathy is generally categorized into generalized inflammatory myopathies (gIM), which affect muscles throughout the body, and focal inflammatory myopathies (fIM), which are localized to specific muscles or muscle groups. This report details a case of immune-mediated polymyositis in a dog, successfully diagnosed using MRI and IHC and managed with immunosuppressive therapy. Case presentation: A 5-year-old castrated male Poodle was admitted to our hospital presenting with lethargy and exercise intolerance. Biochemical analysis revealed significantly elevated serum levels of aspartate aminotransferase (AST) and creatine kinase (CK). Physical examination showed muscle atrophy in the hind legs, but further orthopedic and neurological examinations identified no additional abnormalities. MRI demonstrated hyperintense and heterogeneous signal changes across the muscles, including contrast enhancement, suggesting inflammatory myopathy. This diagnosis was confirmed through histopathological examination, which revealed inflammatory lesions with fibrous tissue proliferation within the muscle tissue. To investigate the presence and type of inflammatory cells and vascular changes, aiding in the differential diagnosis of inflammatory myopathies, immunohistochemistry (IHC) was performed, revealing positive findings for CD8+, CD4+, and VEGF in the evaluated tissue, leading to a diagnosis of polymyositis. Conclusions: The dog was diagnosed with immune-mediated polymyositis and treatment was initiated with prednisolone at 1 mg/kg twice daily and azathioprine at 2 mg/kg once daily. Following the administration of these immunosuppressive agents, CK levels returned to normal, and the dog's exercise intolerance and lethargy resolved. The thickness of the hind legs also increased progressively. The dog has maintained an improved condition under continued immunosuppressive therapy for four months. This case highlights the critical role of MRI and immunohistochemistry in diagnosing immune-mediated polymyositis, demonstrating their alternative capability in cases where conventional electromyography (EMG) is not feasible in this context.
Conclusions
The dog was diagnosed with immune-mediated polymyositis and treatment was initiated with prednisolone at 1 mg/kg twice daily and azathioprine at 2 mg/kg once daily. Following the administration of these immunosuppressive agents, CK levels returned to normal, and the dog's exercise intolerance and lethargy resolved. The thickness of the hind legs also increased progressively. The dog has maintained an improved condition under continued immunosuppressive therapy for four months. This case highlights the critical role of MRI and immunohistochemistry in diagnosing immune-mediated polymyositis, demonstrating their alternative capability in cases where conventional electromyography (EMG) is not feasible in this context.