RESUMO
OBJECTIVE: There is a limited understanding of racial disparities in adverse pregnancy outcomes (APO) among women with rheumatic diseases. The aim of our study was to conduct a systematic literature review to evaluate the impact of race on APO in women with rheumatic diseases. METHODS: Databases were searched to find reports of APO stratified by race among women with rheumatic diseases. The initial searches were conducted in July 2020 and updated in March 2021. Of the final included articles, the full text was reviewed, and data was extracted from each study using a standard data abstraction form. RESULTS: Ten studies with a total of 39,720 patients met our eligibility criteria. There was a greater propensity for APO in racial minorities with rheumatic diseases compared to their White counterparts. Among women with systemic lupus erythematosus (SLE), Black women had the highest odds of APOs, particularly those with a concomitant diagnosis of antiphospholipid syndrome. Pooled meta-analysis could not be done due to multiple factors, including heterogeneity between studies. CONCLUSION: Racial minorities with rheumatic diseases are more prone to APO compared to their White counterparts. One limitation is the lack of standardized criteria for APO, which prohibited direct comparison between studies. There is also a paucity of data looking at APOs among women with rheumatic diseases other than SLE. Further research is needed to explore the drivers of these racial disparities to guide targeted solutions for those in the greatest need.
Assuntos
Síndrome Antifosfolipídica , Lúpus Eritematoso Sistêmico , Doenças Reumáticas , Gravidez , Humanos , Feminino , Resultado da Gravidez , Lúpus Eritematoso Sistêmico/complicações , Síndrome Antifosfolipídica/complicações , Doenças Reumáticas/complicaçõesRESUMO
In the midst of the COVID-19 pandemic, further understanding of its complications points towards dysregulated immune response as a major component. Systemic lupus erythematosus (SLE) is also a disease of immune dysregulation leading to multisystem compromise. We present a case of new-onset SLE concomitantly with COVID-19 and development of antiphospholipid antibodies. An 18-year-old female that presented with hemodynamic collapse and respiratory failure, progressed to cardiac arrest, and had a pericardial tamponade drained. She then progressed to severe acute respiratory distress syndrome, severe ventricular dysfunction, and worsening renal function with proteinuria and hematuria. Further studies showed bilateral pleural effusions, positive antinuclear and antidouble-stranded DNA antibodies, lupus anticoagulant, and anticardiolipin B. C3 and C4 levels were low. SARS-Cov-2 PCR was positive after 2 negative tests. She also developed multiple deep venous thrombosis, in the setting of positive antiphospholipid antibodies and lupus anticoagulant. In terms of pathophysiology, COVID-19 is believed to cause a dysregulated cytokine response which could potentially be exacerbated by the shift in Th1 to Th2 response seen in SLE. Also, it is well documented that viral infections are an environmental factor that contributes to the development of autoimmunity; however, COVID-19 is a new entity, and it is not known if it could trigger autoimmune conditions. Additionally, it is possible that SARS-CoV-2, as it happens with other viruses, might lead to the formation of antiphospholipid antibodies, potentially contributing to the increased rates of thrombosis seen in COVID-19.