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New-onset dermatomyositis following COVID-19: A case report. Frontiers in immunology 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 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. 10.3389/fimmu.2022.1002329
[When COVID-19 encounters interstitial lung disease: challenges and management]. Ren Y H,Wang S Y,Liu M,Guo Y M,Dai H P Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases In December 2019, a new type of coronavirus pneumonia (COVID-19) emerged in Wuhan, Hubei, and spread rapidly to China. The lung injury and repair caused by COVID-19 has many similarities with the onset and progression of interstitial lung disease (ILD) . Therefore, it is difficult to distinguish between COVID-19 and some types of new-onset ILD or other causes leading to acute exacerbation of ILD. Clinicians need to comprehensively analyze the epidemic history, disease onset characteristics, clinical manifestations, image characteristics, serological andpathogenic microorganism test results to confirm diagnosis. Because of this, the article will discuss the issues related to the differential diagnosis and management of COVID-19 and ILD, and try to provide reasonable suggestions. 10.3760/cma.j.cn112147-20200315-00339
Pulmonary fibrosis and COVID-19. The American journal of the medical sciences The COVID-19 pandemic has caused the death of millions and many more have been infected worldwide. The causative virus, SARS-CoV-2, affects the lung where it elicits an aggressive inflammatory response leading to respiratory failure in severe cases. This infection has been linked to pulmonary fibrosis, a process characterized by fibroproliferation and the exaggerated deposition of collagen and other extracellular matrices. These events damage the lung architecture, especially its gas-exchanging units, leading to hypoxemic respiratory failure. The mechanisms by which the virus affects the lung remain incompletely understood, but it is postulated that after entering the airways, the virus binds to Angiotensin Converting Enzyme (ACE) receptors on the surface of epithelial cells, not only stimulating oxidative stress and inflammation, but also promoting the expression of soluble pro-fibrotic factors responsible for the accumulation of fibroblasts, their activation into myofibroblasts, and their unregulated expression of extracellular matrices. These events may trigger the rapid progression or exacerbation of underlying interstitial lung disorders or promote fibrosis in a previously healthy lung. Although the natural progression of such conditions cannot always be predicted, fibrosis may progress even after the virus has been eliminated or, in cases where it does not progress, may become irreversible, leading to long-standing symptoms like shortness of breath and exercise intolerance resulting from loss of lung function. Although COVID-19 related pulmonary fibrosis is not common, preventive measures like vaccination are encouraged, as they are expected to reduce infection or its severity, thereby decreasing the possibility of life-changing respiratory conditions such as pulmonary fibrosis. 10.1016/j.amjms.2023.07.006
COVID-19 and acute exacerbation of interstitial lung disease. Kondoh Yasuhiro,Kataoka Kensuke,Ando Masaru,Awaya Yukikazu,Ichikado Kazuya,Kataoka Mikio,Komase Yuko,Mineshita Masamichi,Ohno Yasushi,Okamoto Hiroaki,Ooki Takashi,Tasaka Yuri,Tomioka Hiromi,Suda Takafumi Respiratory investigation We conducted a study to examine the effect of COVID-19 on the acute exacerbation of interstitial lung disease (AE-ILD) early in the COVID-19 epidemic (January 1-April 30, 2020). An online questionnaire survey was conducted, which was completed by 134 hospitals. During this period, 854 patients with AE-ILD (including 12 cases of COVID-AE-idiopathic pulmonary fibrosis were hospitalized at 128 hospitals. In comparison, the total number of AE-ILD hospitalizations during the same period in 2019 was 894. The number of hospitalizations increased at 17 hospitals, decreased at 27, and remained the same at 88 hospitals in 2020 compared to the same period in 2019. In 2020, COVID-19-related acute exacerbations had a significantly worse prognosis than non-COVID-19-related acute exacerbations in both 30-day and 90-day mortality. Because the prognosis of AE-ILD associated with COVID-19 is extremely poor, prevention of COVID-19 is especially important for patients with ILD. 10.1016/j.resinv.2021.06.007