In December 2019, numerous coronavirus disease 2019 (COVID-19) cases were reported in Wuhan, China, which has since spread throughout the world. However, its impact on rheumatoid arthritis (RA) patients is unknown. Herein, we report a case of COVID-19 pneumonia in a 61-year-old female RA patient who was receiving conventional disease-modifying antirheumatic drugs (cDMARDs). The patient presented with a 4-day history of myalgia and febrile sensation. COVID-19 was confirmed by real-time polymerase chain reaction (PCR). Chest X-ray showed increased opacity on the right lower lung area, and C-reactive protein level was slightly elevated. The patient was treated with antiviral agents (lopinavir/ritonavir), and treatment with cDMARDs was discontinued except hydroxychloroquine. Her symptoms and laboratory results gradually improved. Three weeks later, real-time PCR for COVID-19 showed negative conversion, and the patient was discharged without any complications.

Kim Y, et al. J Korean Med Sci. 2020 Oct;35(48):e423. https://doi.org/10.3346/jkms.2020.35.e423

Connective tissue disease-associated interstitial lung disease (CTD-ILD) represents a significant cause of morbidity and mortality. It is characterized by the progressive convergence of chronic inflammation, immune dysregulation, and fibrotic remodeling in the lung parenchyma. While often conceptualized through a model of idiopathic pulmonary fibrosis (IPF), CTD-ILD is fundamentally an immune-driven pathology with distinct inflammatory mechanisms in which adaptive immunity plays a profound role. This narrative review explores the “inflammation–immunity–fibrosis continuum” in CTD-ILD, elaborating the intricate cellular and molecular pathways that distinguish it from IPF. We highlight the central role of persistent T-cell responses and B-cell dysregulation, which often occur within organized tertiary lymphoid structures in the lung. This review examines how these immune processes are propagated by multiple cytokine pathways, including the TGF-β/SMAD, JAK/STAT, and phosphodiesterase-4 signaling pathways, which serve as crucial links between inflammation and fibrosis. This distinct immune mechanism in CTD-ILD explains why immunomodulatory agents are a cornerstone of CTD-ILD treatment, in contrast to their limited efficacy in IPF, and emphasizes the current paradigm of combining immunosuppression with antifibrotic drugs to target the dual drivers of the disease.