Your browser doesn't support javascript.
loading
Anti-OJ antibody-positive anti-synthetase syndrome following SARS-CoV-2 infection: a case report and literature review.
Sia, Robin; Massouridis, Benjamin; Kee, Nicholas Ngan; Yong, Bryan; Mclean, Catriona; Campbell, Sian.
Afiliación
  • Sia R; Department of Rheumatology, The Royal Melbourne Hospital, Parkville, Victoria, Australia. robinsiawaijen@gmail.com.
  • Massouridis B; Department of Medicine, The Northern Hospital, Epping, Victoria, Australia.
  • Kee NN; Department of Medicine, The Royal Melbourne Hospital, Parkville, Victoria, Australia.
  • Yong B; Department of Rheumatology, St Vincent's Hospital, Fitzroy, Victoria, Australia.
  • Mclean C; Department of Anatomical Pathology, The Alfred Hospital, Melbourne, Victoria, Australia.
  • Campbell S; Department of Rheumatology, The Royal Melbourne Hospital, Parkville, Victoria, Australia.
BMC Rheumatol ; 8(1): 37, 2024 Aug 29.
Article en En | MEDLINE | ID: mdl-39198878
ABSTRACT

BACKGROUND:

COVID-19 can induce a systemic inflammatory response with variable clinical manifestations. Similar to various viruses, COVID-19 has been implicated in the pathogenesis of autoimmune diseases. This article highlights the potential for infections including the SARS-CoV-2 virus to induce exacerbations of pre-existing autoimmune diseases or even potentially unmask de novo autoimmune diseases in particular anti-synthetase syndrome (ASSD) in predisposed individuals. Although there are other case reports of ASSD following SARS-CoV-2 infection, here we present the first reported case of a gentleman with a newly diagnosed anti-OJ positive anti-synthetase syndrome following SARS-CoV-2 infection. CASE PRESENTATION Described is a case of a 70-year-old man presenting to the emergency department with worsening dyspnea in the context of a recent COVID-19 infection. CT-chest revealed changes suggestive of fibrotic lung disease, consistent with usual interstitial pneumonitis (UIP) pattern. Despite recovery from his COVID-19 illness, the patient subsequently developed proximal myopathy with cervical flexion weakness on further assessment with persistently elevated creatinine kinase (CK). Myositis autoantibodies found a strongly positive anti-OJ autoantibody with MRI-STIR and muscle biopsy performed to further confirm the diagnosis. The patient received pulse methylprednisolone 1 g for 3 days with a long oral prednisolone wean and in view of multiple end-organ manifestations, loading immunoglobulin at 2 g/kg administered over two days was given. In addition, he was then commenced and escalated to a full dose of azathioprine given a normal purine metabolism where he remains in clinical remission to this date. At least 267 cases of rheumatic diseases has been associated with SARS-CoV-2 infection as well as COVID-19 vaccination. A literature search on PubMed was made to determine the amount of case reports describing myositis associated with SARS-CoV-2 infection. We found 3 case reports that fit into our inclusion criteria. Further literature searches on diagnostic approach and treatment of ASSD were done.

CONCLUSION:

Although SARS-CoV-2 infection itself can cause a directly mediated viral myositis, this case report highlights the possibility of developing virus-triggered inflammatory myositis through multiple aforementioned proposed mechanisms. Therefore, further studies are required to explore the relationship and pathophysiology of SARS-CoV-2 infection and the incidence of inflammatory myopathies.
Palabras clave

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: BMC Rheumatol Año: 2024 Tipo del documento: Article País de afiliación: Australia Pais de publicación: Reino Unido

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: BMC Rheumatol Año: 2024 Tipo del documento: Article País de afiliación: Australia Pais de publicación: Reino Unido