ABSTRACT
Background: Novel Coronavirus pneumonia 2019 (COVID-19) is a systemic infectious disease with prominent involvement of the respiratory tract, due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)[1]. Systemic lupus erythematosus is charcterized by an aberrant immune response with the presence of circulating autoantibodies, lymphopenia, and proinfammatory[2]. They are immune-compromised and vulnerable to infections with immune-suppressants treatment. However, data regarding the impact of COVID-19 pandemic in patients with SLE and drug use were relatively scarce. Objectives: The prevalence of COVID-19 in SLE patients was estimated by means of meta-analysis, and the effect of the use of anti-rheumatic drugs on the clinical outcome of SLE patients with COVID-19 was investigated. Methods: Cross-sectional investigations and case series on SLE and COVID-19 published by CBM, CNKI, China Science and Technology Journal Database, Wan Fang Data, PubMed, Embase, Web of Science, Cochrane Library and Medline from its establishment to November 10, 2021 were searched. Random effects model was used to pool data. Heterogeneity and risk of bias was examined with I-squared index (I2) statistic. Inconsistency was evaluated by using the I2. Egger tests were used for the evaluation of potential publication bias (STATA v.12.0). Results: A total of 14 studies comprising 5365 patients were identifed (Table 1). Overall prevalence of COVID-19 in SLE patients was 1.5% (95%CI: 1.2%-1.8%). Eight of the studies included patients who used hydroxychloroquine as part of their treatment regimen, with 29.8% (95%CI: 25.8%-33.8%) hospitalization rates and 14.6% (95%CI: 11.5%-17.8%) adverse outcome rates. Among patients treated with hydroxychloroquine throughout the course of disease, the prevalence was 0.7% (95%CI: 0.4%-1.0%, Figure 1). Conclusion: Patients with SLE had a higher risk of COVID-19. Hydroxychloro-quine might beneft to reduce the overall hospitalization rate and prevalence rate of COVID-19, and alleviate infammatory damage in the chronic stage of viral infection by inhibiting over activation of the immune system.