The COVID-19 pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), remains a serious health crisis (1, 2). COVID-19 infections vary from asymptomatic or mild through to severe disease, with lethal complications such as progressive pneumonia, acute respiratory distress syndrome, and BACKGROUND. Limited information is available on the impact of immunosuppressants on COVID-19 vaccination in patients with immune-mediated inflammatory diseases (IMID).METHODS. This observational cohort study examined the immunogenicity of SARS-CoV-2 mRNA vaccines in adult patients with inflammatory bowel disease, rheumatoid arthritis, ankylosing spondylitis, or psoriatic disease, with or without maintenance immunosuppressive therapies. Ab and T cell responses to SARS-CoV-2, including neutralization against SARS-CoV-2 variants, were determined before and after 1 and 2 vaccine doses. RESULTS.We prospectively followed 150 subjects, 26 healthy controls, 9 patients with IMID on no treatment, 44 on anti-TNF, 16 on anti-TNF with methotrexate/azathioprine (MTX/AZA), 10 on anti-IL-23, 28 on anti-IL-12/23, 9 on anti-IL-17, and 8 on MTX/AZA. Ab and T cell responses to SARS-CoV-2 were detected in all participants, increasing from dose 1 to dose 2 and declining 3 months later, with greater attrition in patients with IMID compared with healthy controls. Ab levels and neutralization efficacy against variants of concern were substantially lower in anti-TNF-treated patients than in healthy controls and were undetectable against Omicron by 3 months after dose 2. CONCLUSIONS.Our findings support the need for a third dose of the mRNA vaccine and for continued monitoring of immunity in these patient groups.FUNDING. Funded by a donation from Juan and Stefania Speck and by Canadian Institutes of Health (CIHR)/COVID-Immunity Task Force (CITF) grants VR-1 172711 and VS1-175545 (to THW and ACG), CIHR FDN-143250 (to THW), GA2-177716 (to VC, ACG, and THW), and GA1-177703 (to ACG) and the CIHR rapid response network to SARS-CoV-2 variants, CoVaRR-Net (to ACG).

The main objective of this study was to evaluate the clinical differences and the pattern and extent of organ damage in late-onset systemic lupus erythematosus (SLE). A nested case-control study was performed from patients with SLE followed in the Rheumatology Unit of the State University of Campinas between 1974 and 2005. Patients who developed SLE after the age of 49 were considered late-onset SLE. SLE patients with age <49 years, matched for sex, ethnicity, disease duration and organ damage at study entry were randomly chosen to compose the control group. Baseline and cumulative clinical manifestations, laboratory data, SLE disease activity index (SLEDAI), Systemic Lupus International Collaborating Clinics/American College of Rheumatology-damage index (SDI) and mortality were compared between groups. At diagnosis and follow-up, late-onset group had lower SLEDAI scores when compared with younger age onset. Clinically, they presented less frequently arthritis (P = 0.0002) and malar rash (P = 0.02) and more frequently Raynaud's phenomenon (P = 0.002) and arterial hypertension (P = 0.02) when compared with young onset at diagnosis. Late-onset SLE received lower total corticosteroid dose (P < 0.001) and less frequently cyclophosphamide (P = 0.01). During the study period, late-onset SLE had always lower SLEDAI scores (P = 0.001). At study endpoint, late-onset SLE patients had significantly higher SDI scores (P = 0.001) and a higher mortality rate when compared with younger onset group (P < 0.01). In conclusion, late-onset SLE is milder on presentation and during course of disease, but patients have more organ damage and a higher rate of mortality than young onset SLE. Patients with late onset should be followed with close monitoring and early identification of complications is mandatory in this subgroup of patients with SLE.

PsA patients suffer from more severe subclinical atherosclerosis compared with patients with PsC. This difference is independent of traditional cardiovascular risk factors and correlates with PsA disease duration, more severe skin disease and increased inflammatory markers.

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