COVID-19 Disease and Dermatomyositis: A Mini-Review

The pandemic of coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 has caused a large number of deaths, and there is still no effective treatment. COVID-19 can induce a systemic inflammatory response, and its clinical manifestations are diverse. Recently, it has been reported that COVID-19 patients may develop myositis and interstitial pulmonary disease similar to dermatomyositis (DM). This condition is similar to the rapidly progressive interstitial lung disease associated with MDA5+ DM that has a poor prognosis and high mortality, and this poses a challenge for an early identification. Suppression of the immune system can protect COVID-19 patients by preventing the production of inflammatory cytokines. This article attempts to explore the possibility of a relationship between COVID-19 and DM in terms of the potential pathogenesis and clinical features and to analyze the therapeutic effect of the immunosuppressive drugs that are commonly used for the treatment of both DM and COVID-19.

Clinical, Radiological And Laboratory Predictors Of Postcovid Interstitial Pulmonary Disease

The Fergana Valley model was used to study the risk of postcovid interstitial lung disease in patients who have had COVID-19 associated pneumonia with 50% or more of the pulmonary parenchyma affected. Predictors of the formation of postcovid pulmonary fibrosis were determined and a risk assessment scale was developed. It was found that the use of ultrasound scanners in the early postcovid period is informative and is not inferior in terms of predicting fibrosis by serial MSCT.

Clinical and tomographic characterization of patients with interstitial lung disease at the Trujillo Regional Teaching Hospital, Peru

Objective To determine the main clinical and tomographic characteristics of patients with diffuse interstitial lung disease at Trujillo Regional Teaching Hospital. Methods Case series. Tomographic examinations and clinical data were obtained from patients with interstitial pulmonary disease who attended the pulmonology service of Trujillo Regional Teaching Hospital. The information collected was recorded and systematized in Excel. For the statistical analysis, SPSS 23.0 program was used. Results Data from 103 patients were obtained, of which 60.2% were female, and 39.8% were male. The average age was 72 years for both groups. Main clinical manifestations were cough (82.5%), dyspnea (76.7%), joint pain (43.7%), weight loss (40.8%), velcro crackles (35%) and digital clubbing (28.2%). Exposure to wood smoke was present in 46.6%, exposure to inorganic dust in 12.6% and fowl ownership in 9.7% of cases. Thirty-one (30.1%) patients presented comorbidities. Among these, rheumatic diseases and arterial hypertension were the most frequent. Non-specific interstitial pneumonia pattern was present in 26.2% of the cases; probable usual interstitial pneumonia in 16.5%; organized type in 12.6%; usual interstitial in 10.7%; acute interstitial in 2.9% and 27.1% had no defined tomographic pattern. Conclusions In the studied population, clinical and tomographic characteristics of interstitial lung parenchymal diseases are variable in magnitude and forms of presentation. Female sex and exposure to fuels were the most frequent associated factors. Connective tissue diseases could also explain study findings.

Methotrexate-induced lung damage in a patient with rheumatoid arthritis

We herein report a case of interstitial lung disease secondary to the use of methotrexate in a patient with rheumatoid arthritis. Differential diagnosis between pneumonitis caused by methotrexate in patients treated with basic methotrexate therapy and interstitial pulmonary disease associated with rheumatoid arthritis is based on the clinical examination and instrumental data. The main condition for favorable clinical outcome in all drug-induced lung disease is drug withdrawal, what was proven in our report.

Genetic variants of small airways and interstitial pulmonary disease in children

Genetic variants of small airways and interstitial pulmonary disease have not been comprehensively studied. This cluster of respiratory disorders usually manifests from early infancy (‘lung disease in utero’). In this study, 24 variants linked to these entities are described. The variants involved two genes associated with surfactant metabolism dysfunction (ABCA3 and CSF2RB), two with pulmonary fibrosis (MUC5B and SFTP), one with bronchiectasis (SCNN1B), and one with alpha-1-antitrypsin deficiency (SERPINA1). A nonsense variant, MUC5B:c.16861G > T, p.Glu5621*, was found in homozygous state in two siblings with severe respiratory disease from birth. One of the siblings also had heterozygous SFTPA1:c.675C > G, p.Asn225Lys, which resulted in a more severe respiratory disease. The sibling with only the homozygous MUC5B variant had lung biopsy, which showed alveolar simplification, interstitial fibrosis, intra-alveolar lipid-laden macrophages, and foci of foreign body giant cell reaction in distal airspaces. Two missense variants, MUC5B:c.14936 T > C, p.Ile4979Thr (rs201287218) and MUC5B:c.16738G > A, p.Gly5580Arg (rs776709402), were also found in compound heterozygous state in two siblings with severe respiratory disease from birth. Overall, the results emphasize the need for genetic studies for patients with complex respiratory problems. Identifying pathogenic variants, such as those presented here, assists in effective family counseling aimed at genetic prevention. In addition, results of genetic studies improve the clinical care and provide opportunities for participating in clinical trials, such as those involving molecularly-targeted therapies.

Pulmonary complications due to COVID-19 – a literature review

Introduction: irst cases of a disease called coronavirus disease 2019 (COVID-19), caused by a novel virus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) of the coronavirus family, were detected in December 2019. The disease is manifested by a variety of symptoms and can run a different course: from oligosymptomatic or asymptomatic to the development of acute respiratory failure and even death. Aim: The aim of this paper is to provide critical analysis of the potential pulmonary complications after COVID-19 infection. Material and methods: We have provided the systematic literature review based on which we have discussed the pathophysiology of COVID-19, its outcomes, risk factors and pulmonary complications. Results and discussion: The organs that are most often affected by a SARS-CoV-2 infection are the lungs. An infection with this virus can lead to a severe respiratory tract illness, both in the acute phase and as a complication after a relatively mild case. There are numerous observations of patients convalescing from COVID-19 who suffer from the interstitial pulmonary disease with fibrosis. There are also reported cases of spontaneous pneumothorax after COVID-19. Conclusions: It should be borne in mind that other late complications may appear with time.

Scutellarein inhibits BLM-mediated pulmonary fibrosis by affecting fibroblast differentiation, proliferation, and apoptosis

Introduction: Idiopathic pulmonary fibrosis (IPF) is a progressive and irreversible interstitial pulmonary disease that has a poor prognosis. Scutellarein, which is extracted from the traditional Chinese medicine Erigeron breviscapus, is used to treat a variety of diseases; however, the use of scutellarein for the treatment of pulmonary fibrosis and the related mechanisms of action have not been fully explored. Methods: This study was conducted using a well-established mouse model of pulmonary fibrosis induced by bleomycin (BLM). The antifibrotic effects of scutellarein on histopathologic manifestations and fibrotic marker expression levels were examined. The effects of scutellarein on fibroblast differentiation, proliferation, and apoptosis and on related signaling pathways were next investigated to demonstrate the underlying mechanisms. Results: In the present study, we found that scutellarein alleviated BLM-induced pulmonary fibrosis, as indicated by histopathologic manifestations and the expression levels of fibrotic markers. Further data demonstrated that the ability of fibroblasts to differentiate into myofibroblasts was attenuated in scutellarein-treated mice model. In addition, we obtained in vitro evidence that scutellarein inhibited fibroblast-to-myofibroblast differentiation by repressing TGF-β/Smad signaling, inhibited cellular proliferation by repressing PI3K/Akt signaling, and increased apoptosis of fibroblasts by affecting Bax/Bcl2 signaling. Discussion: In general, scutellarein might exert therapeutic effects on pulmonary fibrosis by altering the differentiation, proliferation, and apoptosis of fibroblasts. Although scutellarein has been demonstrated to be safe in mice, further studies are required to investigate the efficacy of scutellarein in patients with IPF.