Objective To describe the cohort of patients with inflammatory rheumatic diseases (IRD) hospitalized due to SARS-CoV-2 infection in our hospital and to determine the increased risk of severe coronavirus disease regarding no IRD patients. Methods Retrospective single-center observational study of patients with IRD actively monitored in the Department of Rheumatology who were hospitalized due to COVID- 19. Results 41 (1,8%) out of 2,315 patients admitted due to severe SARS-CoV-2 pneumonia suffered from an IRD. The admission Odds ratio (OR) for IRD patients was 1.87 against the general population, and it was higher in patients with Sjögren’s syndrome, vasculitis and systemic lupus erythematosus. Twenty-seven patients were receiving treatment for IRD with corticosteroids, 23 with conventional DMARDs, 12 with biologics (7 rituximab, 4 anti-TNF and 1 abatacept) and 1 with JAK inhibitors. Ten deaths were registered among patients with IRD. A higher hospitalization rate and a higher number of deaths were observed in patients treated with rituximab (OR=12.8) but not in patients treated with anti-TNF (OR=0.9). Conclusion Patients with IRD, especially autoimmune diseases and patients treated with rituximab, may be at higher risk of severe pneumonia due to SARS-Cov 2, compared to the general population. More studies are needed to analyze this association further in order to help managing these patients during the pandemic.

Giant cell arteritis (GCA) is the most common form of vasculitis in individuals older than 50 years in Western countries. To shed light onto the genetic background influencing susceptibility for GCA, we performed a genome-wide association screening in a well-powered study cohort. After imputation, 1,844,133 genetic variants were analyzed in 2,134 case subjects and 9,125 unaffected individuals from ten independent populations of European ancestry. Our data confirmed HLA class II as the strongest associated region (independent signals: rs9268905, p = 1.94 × 10, per-allele OR = 1.79; and rs9275592, p = 1.14 × 10, OR = 2.08). Additionally, PLG and P4HA2 were identified as GCA risk genes at the genome-wide level of significance (rs4252134, p = 1.23 × 10, OR = 1.28; and rs128738, p = 4.60 × 10, OR = 1.32, respectively). Interestingly, we observed that the association peaks overlapped with different regulatory elements related to cell types and tissues involved in the pathophysiology of GCA. PLG and P4HA2 are involved in vascular remodelling and angiogenesis, suggesting a high relevance of these processes for the pathogenic mechanisms underlying this type of vasculitis.

Giant cell arteritis (GCA) and Takayasu’s arteritis (TAK) are major forms of large-vessel vasculitis (LVV) that share clinical features. To evaluate their genetic similarities, we analysed Immunochip genotyping data from 1,434 LVV patients and 3,814 unaffected controls. Genetic pleiotropy was also estimated. The HLA region harboured the main disease-specific associations. GCA was mostly associated with class II genes (HLA-DRB1/HLA-DQA1) whereas TAK was mostly associated with class I genes (HLA-B/MICA). Both the statistical significance and effect size of the HLA signals were considerably reduced in the cross-disease meta-analysis in comparison with the analysis of GCA and TAK separately. Consequently, no significant genetic correlation between these two diseases was observed when HLA variants were tested. Outside the HLA region, only one polymorphism located nearby the IL12B gene surpassed the study-wide significance threshold in the meta-analysis of the discovery datasets (rs755374, P = 7.54E-07; ORGCA = 1.19, ORTAK = 1.50). This marker was confirmed as novel GCA risk factor using four additional cohorts (PGCA = 5.52E-04, ORGCA = 1.16). Taken together, our results provide evidence of strong genetic differences between GCA and TAK in the HLA. Outside this region, common susceptibility factors were suggested, especially within the IL12B locus.