New-onset dermatomyositis following COVID-19: A case report

Abstract

Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Most of the infected individuals have recovered without complications, but a few patients develop multiple organ involvements. Previous reports suggest an association between COVID-19 and various inflammatory myopathies, in addition to autoimmune diseases. COVID-19 has been known to exacerbate preexisting autoimmune diseases and trigger various autoantibodies and autoimmune disease occurrence. Here we report a case of complicated COVID-19 with anti-synthetase autoantibodies (ASSs) presenting with skin rash, muscle weakness, and interstitial lung disease (ILD) and subsequently diagnosed with dermatomyositis (DM). A 47-year-old Japanese male patient without any previous history of illness, including autoimmune diseases, presented with a high fever, sore throat, and cough. Oropharyngeal swab for SARS-Cov-2 polymerase chain reaction tested positive. He was isolated at home and did not require hospitalization. However, his respiratory symptoms continued, and he was treated with prednisolone (20 mg/day) for 14 days due to the newly developing interstitial shadows over the lower lobes of both lungs. These pulmonary manifestations remitted within a week. He presented with face edema and myalgia 4 weeks later when he was off corticosteroids. Subsequently, he presented with face erythema, V-neck skin rash, low-grade fever, and exertional dyspnea. High-resolution computed tomography of the chest showed ILD. Biochemical analysis revealed creatine kinase and aldolase elevations, in addition to transaminases. Anti-aminoacyl tRNA synthetase (ARS) was detected using an enzyme-linked immunosorbent assay (170.9 U/mL) (MESACUP™ (Medical & Biological Laboratories, Japan), and the tRNA component was identified as anti-PL-7 and anti-Ro-52 antibodies using an immunoblot assay [EUROLINE Myositis Antigens Profile 3 (IgG), Euroimmun, Lübeck,Germany]. The patient was diagnosed with DM, especially anti- synthase antibody syndrome based on the presence of myositis-specific antibodies, clinical features, and pathological findings. The present case suggests that COVID-19 may have contributed to the production of anti-synthetase antibodies (ASAs) and the development of de novo DM. Our case highlights the importance of the assessment of patients who present with inflammatory myopathy post-COVID-19 and appropriate diagnostic work-up, including ASAs, against the clinical features that mimic DM after post-COVID-19.

Keywords: COVID-19; anti-aminoacyl tRNA synthetase (ARS) antibodies; anti-synthetase antibodies; autoimmune diseases; dermatomyositis.

Figure 1

Skin findings on admission. Physical examination revealed skin manifestation of dermatomyositis. (A) Mechanic’s hand, (B) V-neck sign on the chest, and (C) whiplash-like erythema on the back.

Figure 2

Clinical imagings. (A) Chest non-contrast CT findings. Chest non-contrast CT revealed bilateral ground-glass opacity. (B) MRI findings of bilateral lower limbs. MRI shows high signals on STIR in the bilateral vastus lateralis, suggesting muscular inflammation. MRI, magnetic resonance imaging; STIR, short T1 inversion recovery. (C-E) The slide showed (C) inflammatory cell infiltration around the myofiber bundles, (D) perivascular inflammatory cell infiltration, and (E) CD8-positive lymphocytes infiltration in atrophy of the myofibers. CT, computed tomography; HE, hematoxylin-eosin; MRI, magnetic resonance imagin; STIR, short T1 inversion recovery; CD, cluster of differentiation.

Figure 3

Clinical course. AST, aspartate aminotransferase; CK, creaine kinase; COVID-19, coronavirus disease 2019; CRP, C-reactive protein; CT, cycle threshold; IVIG, intravenous immunoglobulin; PCR, polymerase chain reaction; PSL, prednisolone; TAC, tacrolimus.