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.
Highlights
Systemic lupus erythematosus (SLE) is a multisystemic, chronic and potentially fatal autoimmune disease that causes alterations in various steps of the immune cascade,1 3 Vol.:(0123456789)Rheumatology International (2021) 41:799–809 to 10
Coronavirus disease 19 (COVID-19), a newly emerged respiratory disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has recently become pandemic
The COVID-19 pathophysiology has shown that in genetically predisposed patients, it could lead to the presentation or exacerbations of autoimmune diseases [9]
Summary
Systemic lupus erythematosus (SLE) is a multisystemic, chronic and potentially fatal autoimmune disease that causes alterations in various steps of the immune cascade,. Various pathogens have been implicated in the development of SLE, especially viruses such as human endogenous retroviruses, Epstein-Barr virus, parvovirus B19, cytomegalovirus and human immunodeficiency virus type 1 [6] These agents can contribute to the pathogenesis of the disease by triggering autoimmunity through various mechanisms including structural or functional molecular mimicry, encoding proteins that induce cross-reactive immune responses to self-antigens or modulate antigen processing, activation, or apoptosis of B and T cells, macrophages or dendritic cells [6,7,8]. The patient showed improvement in constitutional and respiratory symptoms His renal function worsened [blood urea nitrogen (BUN) 125.42 mg/dL, urea 281.5 mg/dL] with persistent severe thrombocytopenia (< 10,000/μL) and abnormal liver function tests [serum glutamate-oxalate transaminase (SGOT). We extracted the following data from the selected papers: age, sex, SLE duration, clinical symptomatology, laboratory tests (including immunologic profile), antiviral therapy, SLE therapy, complications and outcome
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