Dermatomyositis following COVID-19 infection

INTRODUCTION: Viruses have been shown to reveal autoimmune diseases like type1 diabetes and systemic connectivities like dermatomyositis (DM). Coronavirus disease 2019 (COVID-19) is best known for its respiratory symptoms but multiple systems could be affected in acute or post COVID-19 infection period. Clinical dermatomyositis following COVID-19 infection was exceptionally reported. OBSERVATION: We report a case of a 61-year- woman with no medical history observed in March 2021 with bilateral edema. Doppler ultrasound demonstrated a superficial venous thrombosis of saphenous veins. The patient had a suspicious epidemiological history, and her chest CT scans showed lung damage similar to that caused by COVID-19. PCR test for Coronavirus confirmed the infection. She was treated by curative anticoagulation, steroids and oxygen therapy. Two months after her leaving, she was presented in internal medicine's department with pulmonary embolism despite good anti coagulation. Her PCR test for Coronavirus was negative. At her admission, she was complained of asthenia weight loss and pain in scapular and pelvic muscles. Physical examination revealed erythematous patches with edema in periorbital areas. Chest auscultation found bilateral basal lung crepitation. Bilateral proximal muscle weakness in upper and lower extremities was objectified. Oral examination found ulcerations in the lower gingiva. We found signs of arthritis in wrists and proximal interphalangeal joints. Biological tests showed anemia (hemoglobin =8.6 g/dl), accelerated erythrocyte sedimentation rate (65 mm H1) ; high C-reactive protein(119 mg/l)d biological myolysis and cytolydid (Creatinin kinase = 1052 U/l, LDH = 478 AST/ALT 238 U/l/119 U/l). Infectious investigations including HCV, HBV and HIV serology were negative. Thyroid function test was in normal range. Neoplastic research was negative. Immunologic analysis revealed positive antinuclear antibodies (ANA) with anti JO1 antibodies. Anti cardiolipin antibodies and kit-myositis were negatives. Electromyographic findings revealed inflammatory myositis. The patient was treated by high doses of steroids then progressively decreased. Good progress was noticed. CONCLUSION: Dermatomyositis is an inflammatory myopathy relatively rare. An elevation of its incidence was noticed during the pandemic period coinciding of corona virus [1]. Viral infections could induce autoimmunity and may be the eliciting event in the pathogenesis of myositis [2]. In our case, dermatomyositis is hypothetically linked to viral trigger on the background of genetic predisposition. The spectrum of complications following COVID-19 is broad but incidence is too rare including Idiopathic thrombocytopenic purpura, Guillain-Barré syndrome and autoimmune haemolytic anaemia recorded in 1, 5 and 7 patients respectively, 4–13 days following onset of COVID-19 symptoms. We assume that true dermatomyositis, triggered by COVID-19 may occur and the immunopathogenicity is via type 1 IFN pathway. Tanboon et al. commented that 58-year-old COVID-19 patient reported to have myositis may actually have dermatomyositis.