Incidence of Autoimmune Rheumatic Diseases Following COVID-19 Infection

Mandana  Khodashahi; Maryam  Sahebari; Zahra  Rezaieyazdi; Mohammad  Basil Al-Obaidi; Masoumeh  Salari; Rozita  Khodashahi; Zahra  Mirfeizi; Hassan  Mehrad Majd; Muhammed  Joghatayi

doi:10.18502/jimc.v9i2.21177

Mandana Khodashahi Rheumatic Diseases Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
Maryam Sahebari Rheumatic Diseases Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
Zahra Rezaieyazdi Rheumatic Diseases Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
Mohammad Basil Al-Obaidi Rheumatic Diseases Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
Masoumeh Salari Rheumatic Diseases Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
Rozita Khodashahi Transplant Research Center, Clinical Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran
Zahra Mirfeizi Rheumatic Diseases Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
Hassan Mehrad Majd Clinical Research Development Unit, Faculty of Medicine, Ghaem Hospital, Mashhad University of Medical Sciences, Mashhad, Iran
Muhammed Joghatayi Rheumatic Diseases Research Center, Mashhad University of Medical Sciences, Mashhad, Iran

DOI: https://doi.org/10.18502/jimc.v9i2.21177

Keywords: Autoimmune diseases, COVID-19, Humans, Hypothyroidism, Rheumatic diseases, Thyroxine

Abstract

Background: The relationship between COVID-19 and autoimmune rheumatic diseases remains complex, with growing evidence suggesting that severe COVID-19 may trigger or exacerbate autoimmune rheumatic diseases. This study aimed to assess the prevalence of AIRDs following COVID-19 infection and identify factors associated with their onset.

Methods: A total of 183 patients diagnosed with Autoimmune Rheumatic Diseases (AIRDs) within 30 days post-COVID-19 were evaluated. Data were collected on demographics, comorbidities, disease severity, and inflammatory markers. Cox and logistic regression analyses were conducted to assess risk factors associated with AIRD development.

Results: The findings indicate a notable link between severe COVID-19 and the onset of AIRDs, with higher inflammatory markers significantly associated with increased risk. Interestingly, hypothyroidism appeared to have a protective effect, potentially due to the immunomodulatory effects of treatments like levothyroxine. These findings align with some literature suggesting an immune dysregulation following COVID-19. Despite the insights, the cross-sectional design of the study limits the ability to establish causality.

Conclusion: This study underscores the significant role of severe COVID-19 and elevated inflammatory markers in the development of AIRDs. The protective effect of hypothyroidism could open avenues for future therapeutic considerations. Further, longitudinal studies are essential to better understand the mechanisms driving these associations and explore interventions aimed at reducing AIRD risk in post-COVID-19 patients.