Systemic Lupus Erythematosus Manifestation Following COVID-19

A Case Report

Batool Zamani; Seyed-Masoud Moeini Taba; Mohammad Shayestehpour


J Med Case Reports. 2021;15(29) 

In This Article

Abstract and Introduction


Background: Systemic lupus erythematosus (SLE) is a complex and challenging autoimmune disease. Severe acute respiratory syndrome coronavirus 2 (SARSCoV2) is a novel viral agent that can cause a life-threatening respiratory disorder named coronavirus disease 2019 (COVID19). Association between SARSCoV2 and SLE is not clear. We reported the first case of SLE manifestation following COVID-19.

Case Presentation: A 39-year-old Iranian/Persian man with complaints of fever, scaling on the palms of the hands and feet, lower extremity edema, and ankle swelling was referred to Kashan Rheumatology Clinic in 2020. He was infected with SARS-CoV-2 2 months ago. The patient had proteinuria and was positive for SLE laboratory tests. After one week of treatment with prednisolone (30 mg daily) and hydroxychloroquine, paresthesia, proteinuria, and edema continued. The patient was treated with pulse methylprednisolone (1000 mg for three consecutive days), gabapentin, and vitamin B (300 mg daily), which reduced paresthesia.

Conclusions: This is the first case of SLE manifestation following COVID-19. SARS-CoV-2 may produce autoantibodies or develop the clinical features of subclinical SLE.


Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the breaking of tolerance to nuclear self-antigens and the production of pathogenic autoantibodies. This complex and challenging disease can involve several organs in the body such as skin, eyes, kidney, heart, muscles, and the joints.[1] Previous studies reported that some viruses may be implicated in the etiology of SLE. Epstein–Barr virus (EBV) is as potential causal agent of SLE. In addition, cytomegalovirus, parvovirus B19, and retroviruses can be possible triggers for SLE. Immune reactions against viral antigens may turn against the self-antigens that can lead to autoimmunity (molecular mimicry).[2] There are reports of several cases of SLE that have manifested following acute viral infections (Dengue fever virus).[3]

Severe acute respiratory syndrome coronavirus 2 (SARSCoV2) is a novel viral agent that has caused coronavirus disease 2019 (COVID19). This acute viral infection is frequently associated with respiratory failure, pneumonia, acute respiratory distress syndrome (ARDS), and sepsis.[4] A fulminant increase in the serum pro-inflammatory cytokines including, IL-1, IL-6, IL-12, IFN-γ, TGFβ, and chemokines such as CCL2, CXCL9, CXCL10 was detected in severe cases of COVID19.[5] Although a few case reports have been published on the possible association between coronavirus and autoimmune disorders, the role of this virus in autoimmunity is not clear.[6] To date, several cases have been reported patients with lupus who have been infected with COVID-19,[7] but no data have been published on the onset of clinical manifestations of SLE after getting COVID-19. We reported the first case of SLE manifesting following COVID-19.