Can the SARS-CoV-2 infection trigger systemic lupus erythematosus? A case-based review

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune and multisystemic chronic inflammatory disease that can affect various organs, including skin, joints, kidneys, lungs and the nervous system. Infectious agents have long been implicated in the pathogenesis of SLE. The new viral infection caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has shown that, in genetically predisposed patients could trigger the presentation or exacerbation of the autoimmune disease. We herein report a case of a 45-year-old man who presented respiratory symptoms, bilateral pleural effusion, ascites, splenomegaly, severe thrombocytopenia and renal failure with proteinuria and hematuria. SARS-CoV-2 PCR confirmed the COVID-19 diagnosis. We diagnosed the patient with SLE based on the clinical manifestations and positive immunological markers (2019 European League Against Rheumatism/American College of Rheumatology, score of 18). Glucocorticoid pulses were administered to the patient, which improved renal function. However, thrombocytopenia was also refractory to IV immunoglobulin and rituximab, so the patient underwent splenectomy. Through a systematic search of the medical literature, we retrieved two cases with newly onset SLE and five cases with previous SLE diagnosis that showed activity of the disease due to SARS-CoV-2 infection. We herein present a systemic review of these cases and discuss the clinical manifestations that could help to the diagnosis of this clinical condition.

COVID-19 and the clinical course of rheumatic manifestations

“…A male patient with lupus presenting with arthritis and thrombocytopenia developed Coombs' positive haemolytic anaemia along with APLA positivity [81]. A review has found two novel cases of lupus, along with flares in ACPA anti-citrullinated peptide antibody, ANA antinuclear antibodies, HLA human leukocyte antigen, IAS intra-articular steroids, NSAID non-steroidal anti-inflammatory drugs, RF rheumatoid factor [71]. A large multi-centric cohort has shown that patients with autoimmune diseases may be at higher risks for developing COVID-19 than the general population [82].…”

Correspondence on ‘Clinical course of coronavirus disease 2019 (COVID-19) in a series of 17 patients with systemic lupus erythematosus under long-term treatment with hydroxychloroquine’

“…1 The new viral infection caused by SARS-CoV-2 seems to lead to the onset or exacerbation of autoimmune diseases in genetically predisposed patients. [2][3][4] SLE is an autoimmune disease prone to flare-ups that are linked to significant morbimortality. Immunosuppressionrelated infections are one of the leading causes of premature death in patients with SLE.…”

“…However, there are currently no data to support a higher infection rate or an increased risk for fatal outcome related to COVID-19 in these patients. [2][3][4][5] One could even speculate the SLE treatment can protect against the serious complications related to COVID-19. 2 In this regard, we read the relevant paper by Mathian et al 1 who evaluated the clinical course of COVID-19 in patients with SLE treated with hydroxychloroquine.…”

Plasmacytoid dendritic cells and type I interferons in flares of systemic lupus erythematosus triggered by COVID-19

“…We recently read with interest the article entitled "Can the SARS-CoV-2 infection trigger systemic lupus erythematosus? A case-based review" by Gracia-Ramos et al [1]. The authors reviewed emerging cases of SARS-CoV-2 infection either flaring-up previously diagnosed-SLE or triggering de novo SLE, and briefly pondered on the underlying mechanistic pathways leading to this association [1].…”

“…A case-based review" by Gracia-Ramos et al [1]. The authors reviewed emerging cases of SARS-CoV-2 infection either flaring-up previously diagnosed-SLE or triggering de novo SLE, and briefly pondered on the underlying mechanistic pathways leading to this association [1]. Here, we would like to highlight the plasmacytoid dendritic cell (pDC) and its major product, type I interferons (IFNs), as a possible link that may explain SLE development or flare-up during the course of SARS-Cov-2 infection.…”