Exploring Autoimmune Consequences of COVID-19 Infection

Le résumé fourni par la source

Abstract Introduction: Post-COVID autoimmune diseases are on the rise, with COVID-19 triggering autoantibody production in genetically predisposed individuals. While autoimmune vasculitis, myositis, and ILD have been more commonly observed, reports of post-COVID autoimmunity manifesting as Anti-synthetase syndrome are less frequent. We present four cases of new-onset autoimmune myositis and/or interstitial lung disease following COVID-19 infection. Case 1: 32-year-old male with a recent COVID-19 infection presented with worsening dyspnea, cough, night sweats, and weight loss. Physical exam revealed dry crackles and hyperkeratosis of the fingers. Labs were positive for PL-12 and anti-SS-A antibodies, elevated aldolase, and rheumatoid factor. CT imaging showed diffuse ground-glass opacities (GGO) and subpleural septal thickening. Lung biopsy revealed nonspecific interstitial pneumonia-organizing pneumonia. The patient was diagnosed with anti-synthetase syndrome and started on prednisone and azathioprine. Case 2: 44-year-old male with COVID-19 five months prior presented with exertional dyspnea. Labs showed elevated C3, and positive DS-DNA and PL-12 antibodies. CT showed mixed fibrotic and inflammatory infiltrates in the mid and lower lung zones. Cryobiopsy indicated cryptogenic organizing pneumonia. The patient was diagnosed with amyopathic dermatomyositis and treated with CellCept, prednisone, and nintedanib. Case 3: 69-year-old female, with a history of tobacco use, presented with worsening dyspnea and cough 6 months post-COVID. Labs showed anti-SAE1 antibodies. CT revealed traction bronchiectasis and honeycombing, with lower-lobe predominance. PFTs showed mild restriction. She was started on prednisone, with plans for antifibrotic therapy if lung function declined. Case 4: A 65-year-old female with new-onset gait imbalance and muscle weakness after COVID-19 infection had elevated CPK and aldolase, with positive ANA, anti-Jo1, and anti-SSA antibodies. CT showed bronchovascular and subpleural GGO. Muscle biopsy showed type II fiber atrophy. She was diagnosed with antisynthetase syndrome and started on prednisone and CellCept. Discussion: Emerging evidence suggests COVID-19 triggers the release of autoantibodies in genetically susceptible individuals, including antinuclear antibodies (ANA), anti-Ro/SSA, rheumatoid factor (RF), and antibodies against IFN. Studies show a higher prevalence of myositis-associated antibodies in COVID-19 patients. Molecular mimicry, where SARS-CoV-2 proteins resemble self-antigens, is believed to drive post-COVID autoimmunity. Research has identified immunogenic epitopes linked to autoimmune dermatomyositis. The virus can also cause cytokine storms through excessive immune activation. Additionally, SARS-CoV-2 uses ACE2 receptors, found on alveolar epithelial and skeletal muscle cells, potentially explaining the pulmonary involvement and myositis observed in COVID-19 cases. Early recognition of the link between SARS-CoV-2 and autoimmune myositis/ILD can lead to timely immunosuppressive therapy and improved outcomes.

Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.