HUMORAL and CELLULAR SARS-COV-2 VACCINE RESPONSES in PATIENTS with GIANT CELL ARTERITIS and POLYMYALGIA RHEUMATICA

ABSTRACT

Background: Giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) are overlapping autoinfammatory diseases affecting people over 50 years. The diseases are treated with immunosuppressive drugs such as prednisolone, metho-trexate, lefunomide and tocilizumab. Even though GCA and PMR patients have a substantially higher risk for infections, little is known about humoral and cellular immune responses after vaccination in these patients. Objectives: In this study we assessed the immunogenicity and safety of SARS-CoV-2 vaccinations in these diseases. Methods: Patients (n=45 GCA, n=33 PMR) visited the outpatient clinic twice pre-vaccination and 4 weeks post-vaccination (BNT162b2 or ChAdOx1 vaccine). Patients with previous SARS-CoV-2 infection were excluded. In both pre-and post-vaccination samples, anti-Spike antibody concentrations were assessed and compared to age-, sex-and vaccine-matched control groups (n=98). In addition, the frequency of SARS-CoV-2 Spike-specifc T-cells was assessed by IFN-γ ELIspot assay, and side-effects and disease activity were recorded. Results: The GCA/PMR patients, as a group, did not have reduced antibody concentrations compared to controls. However, linear regression analysis revealed a signifcant association of methotrexate and >10mg/day prednisolone use with lower antibody concentrations in GCA/PMR patients. Evidence of cellular immunity, as assessed by ELIspot assay, was found in 67% of GCA/PMR patients, and was correlated with humoral immunity (Figure 1). Patients using >10mg/day prednisolone had reduced cellular immunity. Importantly, vaccination did not lead to signifcant side-effects or changes in disease activity. Conclusion: SARS-CoV-2 vaccination was safe for GCA/PMR patients and immunogenicity was comparable to other older individuals. However, patients using methotrexate and particularly >10mg/day prednisolone did show lower vaccine responses, which corroborates fndings in other autoinfammatory patient populations. These patients may therefore be at higher risk of (potentially even severe) breakthrough SARS-CoV-2 infection.