Background It has been more than a year and a half since the WHO announced a pandemic of a new coronavirus infection caused by SARS-CoV-2. The virus belongs to the respiratory group, but it it can damage various organs and tissues of the body. COVID-19 infection is characterized by pathological activation of immunity, violated synthesis of pro-inflammatory, immunoregulatory, anti-inflammatory cytokines, such as interleukins-1 and -6, tumor necrosis factor α and others. These features contribute to the development of rheumatic diseases and syndromes in people who have had COVID-19. Cellular and humoral immune responses are also of primary importance in the pathogenesis of inflammatory myopathies.

Objectives Description of a case of severe dermatomyositis after COVID-19.

Methods The 34-year-old female patient complained of pain and weakness in the proximal muscles of the upper and lower extremities, difficulty swallowing solid and liquid food, rash on the face, neck, chest and arms. In August 2020 she had a mild case of COVID-19. A month later, flaky erythematous papules like Gottron’s sign appeared on the extensor surfaces of the metacarpophalangeal joints and proximal interphalangeal joints of the hands. Six months later, sore throats, hoarseness of voice, belching of air, choking on solid food and episodes of subfebrility joined. Reflux esophagitis, duodenitis was detected by fibrogastroduodenoscopy. After 9 months, there were muscle pains and muscle weakness, erythema on the face, neck and chest, the patient lost 11 kg. She was hospitalized in the rheumatology department with suspected dermatomyositis.

Results On objective examination: proximal myopathy, erythematous rashes on the face, neck, chest, Gottron’s erythema on the hands. In the analyses: clinical analysis of blood and urine without pathology, ANA 1:1280, creatinkinase 5370 IU/l, with an increase in dynamics up to 9260 IU/l, CRP 0.03 mg /dl, LDH 1023 IU/l, rheumatoid factor and anti-ds DNA were negative. Nasal regurgitation was detected during radiography of the pharynx with contrast. Instrumental examination revealed no signs of a tumor process. Fibrogastroduodenoscopy - superficial reflux-esophagitis, duodenitis, Chest CT - interstitial pneumonitis, abdominal ultrasound without pathology, ECG - sinus rhythm, normal EOS position, accelerated A-V conduction, echocardiography - minor separation of pericardial leaves (up to 5 mm), colonoscopy - dolichosigma.

The patient was diagnosed with idiopathic dermatomyositis of high activity. Because of progressive myopathy and increasing dysphagia, pulse therapy with methylprednisolone500 mg for 3 days and rituximab 1000 mg was performed. She also received metipred 48 mg per day orally, methotrexate 15 mg per week subcutaneously and folic acid 5 mg per week. Against the background of therapy, positive dynamics was noted: swallowing normalized, the severity of myopathy decreased, after 10 days CKdecreased to 2049 IU/l. After 6 months during the control examination: there are no skin rashes, muscle strength is restored, CK 300 IU/l. The dose of methylprednisolone is reduced to 10 mg per day, the patient continues injections of methotrexate 15 mg per week.

Conclusion COVID-19 may be a trigger for the development of inflammatory myopathy. In this clinical case there are features of the course and therapy of inflammatory myopathies in patients after coronavirus infection.

Disclosure of Interests None declared