Objective The aim was to evaluate the most relevant cell populations involved in vascular homeostasis as potential biomarkers of SLE-related cardiovascular disease (CVD). Methods Low-density granulocytes (LDGs), monocyte subsets, endothelial progenitor cells, angiogenic T (Tang) cells, CD4+CD28null and Th1/Th17 lymphocytes and serum cytokine levels were quantified in 109 SLE patients and 33 controls in relationship to the presence of subclinical carotid atheromatosis or cardiovascular disease. A second cohort including 31 recent-onset SLE patients was also included. Results Raised monocyte and LDG counts, particularly those LDGs negative for CD16/CD14 expression (nLDGs), in addition to the ratios of monocytes and nLDGs to high-density lipoprotein-cholesterol (HDLc) molecules (MHR and nLHR, respectively), were present in SLE patients with traditional risk factors or subclinical atheromatosis but not in those who were CV-free, thus revealing their value in the identification of patients at risk of CVD, even at the onset of disease. Accordingly, nLDGs were correlated positively with carotid intima–media thickness (cIMT) and with inflammatory markers (CRP and IL-6). A bias towards more differentiated monocyte subsets, related to increased IFN-α and IL-17 serum levels, was also observed in patients. Intermediate monocytes were especially expanded, but independently of their involvement in CVD. Finally, CD4+CD28null, Th17 and Th1 lymphocytes were increased, with CD4+CD28null and Th17 cells being associated with cIMT, whereas endothelial progenitor and Tang cell levels were reduced in all SLE patients. Conclusion The present study highlights the potential use of MHR and nLHR as valuable biomarkers of CVD risk in SLE patients, even at diagnosis. The increased amounts of nLDGs, monocytes, Th17 and senescent-CD28null subsets, coupled with reduced pro-angiogenic endothelial progenitor cells and Tang cells, could underlie the development of atheromatosis in SLE.

Treatment for antineutrophil cytoplasmic antibody (ANCA)associated vasculitis usually raises questions about the risk of infections. Particular attention has been given to the impact of drugs such as cyclophosphamide and B-cell depletory therapies on the severity of COVID-19. Monti et al 1 suggest that receiving biological disease-modifying antirheumatic drugs may not increase risk of COVID-19. Furthermore, Guilpain et al 2 reported a woman treated with rituximab and low-dose prednisone due to granulomatosis with polyangeitis proteinase 3-antineutrophil cytoplasmic antibody (PR3-ANCA) vasculitis, who developed pneumonia associated with COVID-19 with a milder evolution than expected in other series. Here, we present a 64-year-old woman diagnosed of myeloperoxidase-ANCA microscopic polyangiitis in 2014, with secondary hypertrophic pachymeningitis, sinusitis and constitutional syndrome. Her main comorbidities were hypercholesterolaemia and areata alopecia. On 25 November 2019, vasculitis relapsed and was treated with two infusions of 1000 mg rituximab given 2 weeks apart, in addition to three bolus of 125 mg methilprednisolone. The patient improved and received maintenance treatment with 7.5 mg/day prednisone and a doublestrenght tablet of trimethropim-sulfamethoxazole 3 days a week. While on holidays at her daughter's house in The Netherlands, on 7 March 2020 her husband developed fever >38°C, odynophagia, discomfort and dyspnoea. He was finally admitted to a hospital and diagnosed with COVID-19 infection by reverse transcription PCR (RT-PCR) on a nasopharyngeal swab. At the same time, she presented feverish, asthenia, myalgia, lack of appetite, headache, anosmia and dysgeusia, and was treated with paracetamol at home, improving after 2 weeks. One month later, after returning home in Spain, she came to our clinic for evaluation due to her exposure to COVID-19. Blood test results showed positive immunochromatographicspecific IgG antibodies assay for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). IgM antibodies and nasopharyngeal swab (RT-PCR) were both negative. Cytometric studies revealed 10 B lineage cells. Serum immunoglobulin showed moderately decreased IgM (0.23 g/L), and normal IgG and IgA concentrations. A test for ANCAs was positive, with a perinuclear staining pattern, and an ELISA confirmed the presence of myeloperoxidase ANCA at a titre of 5.3 U/mL (reference range <1). Patients with compromised immune systems represent a susceptible population in which infections may have devastating consequences. The impact of rituximab treatment on SARS-CoV-2 infection remains to be clarified. As hyperinflammation underlies the mechanism of severe COVID-19, the immunocompromised situation may prevent them from virus-induced cytokine storm syndrome. 3 Transcriptome data including RNA-seq and GeneChip human genome arrays show that glucocorticoids and some disease modifying anti-rheumatic drugs (DMARDs) (tocilizumab, methotrexate, hydroxychloroquine, tofacitinib, azathioprine and so on) could suppress the c...

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