P067 Covid- 19 infection as a trigger for immune inflammatory myositis

Abstract

Abstract Background/Aims Increasing experience in managing patients with COVID-19 infection has demonstrated the development of autoimmune phenomena following infection. We describe a patient with preceding COVID-19 infection who presented with inflammatory immune myositis, positive myositis antibodies and a normal creatine kinase. Methods N/A Results A 61-year-old Caucasian female presented feeling generally unwell and with weakness. She had COVID-19 infection 4 months prior, which necessitated admission to the Intensive Care Unit (ITU), treatment with dexamethasone and oxygen and subsequent discharge with home continuous positive airway pressure (CPAP). Other co-morbidities included atrial fibrillation, chronic kidney disease stage three, hypertension, obesity, recent pulmonary embolism, obstructive sleep apnoea, chronic lymphoedema and hypercholesterolaemia on atorvastatin. Her mobility had been gradually reducing over the previous months to now requiring a wheelchair. Neurological examination demonstrated bilateral proximal lower limb weakness, power 3/5 and an unsafe swallow, for which a naso-gastric tube was inserted. A non-specific erythematous pruritic rash was noted on the arms. Full body Computerised tomography (CT) and Magnetic Resonance Imaging (MRI) of the brain and spine were unremarkable. Creatinine kinase (CK) was within normal limits at 81, and C-reactive protein (CRP) was mildly raised at 36. C3 was low at 0.67 and C4 low at 0.03. Cryoglobulins were not detected. She was positive for antinuclear antibody (ANA) (1:320 titre), Ro-52, PM-Scl75, and anti-La. Anti-dsDNA was negative. Electromyography could not be performed due to the presence of chronic lymphoedema. MRI showed symmetrical STIR hyperintense signal changes in the quadriceps muscles bilaterally. A muscle biopsy showed a small focus of mild lymphocyte infiltration in the endomysial connective tissue, mild increase in acid phosphatase expression in many fibres in dotlike pattern, overexpression of HLA-ABC with deposits of complement found in in endomysial capillaries, consistent with a diagnosis of inflammatory myopathy. Following commenced of 60 mg prednisolone daily, there was a marked improvement in swallowing and the NG tube was removed. A positron emission tomography (PET) scan showed non-specific marrow, splenic and adrenal hyperplasia. The patient was then started on mycophenolate mofetil (MMF), but was switched to azathioprine due to side effects. On review following discharge, the patient continues to require a wheelchair to mobilise, but there has been improvement in her swallow and she reports feeling better within herself. Conclusion Inflammatory myositis is a rare sequela of COVID-19 infection. The development of myositis-specific antibodies post infection has previously been described. This case highlights the significant dysphagia and debility despite a normal CK and the need for a high index of suspicion. Possible triggers of an inflammatory response predisposing to autoimmune phenomena include molecular mimicry, bystander activation, exposure of previously hidden epitopes to activated T cells, activation of Toll-like receptors and activation of the complement system. Disclosure G. Bartminski: None. A. Vijayan: None. K. Beharry: None. D. De Lord: None.