Risk Factors for Severe Outcomes in Patients With Systemic Vasculitis and COVID‐19: A Binational, Registry‐Based Cohort Study

Abstract

Objective COVID‐19 is a novel infectious disease with a broad spectrum of clinical severity. Patients with systemic vasculitis have an increased risk of serious infections and may be at risk of severe outcomes following COVID‐19. We undertook this study to establish the risk factors for severe COVID‐19 outcomes in these patients, including the impact of immunosuppressive therapies. Methods A multicenter cohort was developed through the participation of centers affiliated with national UK and Ireland vasculitis registries. Clinical characteristics and outcomes are described. Logistic regression was used to evaluate associations between potential risk factors and a severe COVID‐19 outcome, defined as a requirement for advanced oxygen therapy, a requirement for invasive ventilation, or death. Results The cohort included 65 patients with systemic vasculitis who developed COVID‐19 (median age 70 years, 49% women), of whom 25 patients (38%) experienced a severe outcome. Most patients (55 of 65 [85%]) had antineutrophil cytoplasmic antibody–associated vasculitis (AAV). Almost all patients required hospitalization (59 of 65 [91%]), 7 patients (11%) were admitted to intensive care, and 18 patients (28%) died. Background glucocorticoid therapy was associated with severe outcomes (adjusted odds ratio [OR] 3.7 [95% confidence interval 1.1–14.9]; P = 0.047), as was comorbid respiratory disease (adjusted OR 7.5 [95% confidence interval 1.9–38.2]; P = 0.006). Vasculitis disease activity and nonglucocorticoid immunosuppressive therapy were not associated with severe outcomes. Conclusion In patients with systemic vasculitis, glucocorticoid use at presentation and comorbid respiratory disease were associated with severe outcomes in COVID‐19. These data can inform clinical decision‐making relating to the risk of severe COVID‐19 in this vulnerable patient group.

Rheumatological complications of Covid 19

“…There is limited knowledge on the outcomes of COVID-19 in patients commenced on Cyclophosphamide and Rituximab for treatment of vasculitis but emerging reports of COVID-19 patients who had been receiving rituximab for their underlying immune-mediated conditions have demonstrated no worse course or outcome compared with those in the general population, with some suggestion that rituximab may affect the cytokine storm seen in COVID-19 and may improve outcomes [ 128 , 129 ]. Data from United Kingdom registry for vasculitis suggests that AAV patients and patients already on corticosteroids prior to developing COVID-19 have worse outcomes [ 130 ].…”

Outcomes of COVID-19 in patients with primary systemic vasculitis or polymyalgia rheumatica from the COVID-19 Global Rheumatology Alliance physician registry: a retrospective cohort study

“…Compared with a recent (2021) study done in the UK and Ireland, which found that 59 (91%) of 65 patients with primary systemic vasculitis were admitted to hospital and 18 (28%) died, our results are reassuring and could reflect an improvement in outcomes over time. 11 , 12 The cause of this change is not known, but it could plausibly be related to more experience with managing COVID-19 or the use of fewer experimental interventions over time. 13 As with the general population, both comorbidities and age were important risk factors for poor outcomes, emphasising the importance of public health measures, risk mitigation, and prioritisation of vaccination in these individuals.…”

Humoral and T-cell responses to SARS-CoV-2 vaccination in patients receiving immunosuppression

“…There is an urgent need to understand the impact of immunosuppressive therapies on the efficacy of vaccines to SARS-CoV-2 1 2. Patients with autoimmune diseases have been considered clinically vulnerable to SARS-CoV-2 infection since the onset of the COVID-19 pandemic,3 and population-based and registry-based studies suggest that they experience significant rates of hospitalisation, severe disease and death during its global spread 4–6…”