Abstract

Introduction: Polymyositis is an immune-mediated syndrome secondary to defect in cellular immunity, frequently associated with other autoimmune diseases, maybe idiopathic, or known etiology which have the most frequent cancer or infection. In the case of viral infections, an agent can cause an injury uprightly muscle tissue, also damaging the vascular endothelium to release cytokines, which leads to a defect in expression of major histocompatibility complex and the susceptibility of muscle to destruction. In the clinical case which is described below, as an etiological factor for polymyositis arises an acute Epstein–Barr virus. Case report: Man, 45 years old, leucodermic firefighter with a history of chronic sinusitis and a former smoker. Without chronic medication. Appealed to the U.S. by frame with a month of evolution of generalized and progressive myalgia, generalized decrease in muscle strength with predominantly distal, anorexia, night sweats and weight loss quantified in about 10 kg. No fever or other symptoms. On admission he had noted the general decline in muscle mass, flaccid tetraparesia 3/3 predominantly distal — grade 3 in lower limbs, sensitively maintained. AST 708 UI/L, ALT 577 UI/L, LDH 4015 UI/L, and rhabdomyolysis with CK 25,129 UI/L. Serial serology for EBV was indicative of recent infection, TC-chest revealed consolidated nonspecific changes and pathological results of muscle biopsy revealed an extensive area of necrosis with inflammatory infiltrate with eosinophils and B lymphocytes. Described neurogenic EMG signs of active denervation in distal muscles of the lower limbs. The study to autoimmunity, Ac. Anti-SRP positive and initially positive ANA,with subsequent negative. Microbiological, serological to zoonoses, thyroid function and neoplasm were negative. For worsening muscle atrophy, the patient developed a restrictive ventilatory framework, diffusion of CO2 decreased and elevated markers of myocardial necrosis (without electrocardiographic or ecocardiographic changes) was transferred to Unit of Intensive Therapy and was subjected to non-invasive ventilation and initiated therapy 3 mg/kg/day with methylprednisolone. Despite on the poor prognosis associated with anti-SPR, the patient had a good clinical outcome in physical rehabilitation program, with the interference myopathy secondary to corticosteroids; did complete weaning of corticosteroids. Complaints about pain remained reasonably controlled with pregabalin. She was discharged with diagnosis of polymyositis with Ac anti-SRP secondary to EBV infection, followed in Outpatient Internal Medicine and Autoimmune Diseases.

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