Objective: Systemic sclerosis (SSc) and rheumatoid arthritis (RA) are autoimmune diseases that have similar clinical and immunologic characteristics. To date, several shared SSc–RA genetic loci have been identified independently. The aim of the current study was to systematically search for new common SSc–RA loci through an interdisease meta–genome‐wide association (meta‐GWAS) strategy.Methods: The study was designed as a meta‐analysis combining GWAS data sets of patients with SSc and patients with RA, using a strategy that allowed identification of loci with both same‐direction and opposite‐direction allelic effects. The top single‐nucleotide polymorphisms were followed up in independent SSc and RA case–control cohorts. This allowed an increase in the sample size to a total of 8,830 patients with SSc, 16,870 patients with RA, and 43,393 healthy controls.Results: This cross‐disease meta‐analysis of the GWAS data sets identified several loci with nominal association signals (P < 5 × 10⁻⁶) that also showed evidence of association in the disease‐specific GWAS scans. These loci included several genomic regions not previously reported as shared loci, as well as several risk factors that were previously found to be associated with both diseases. Follow‐up analyses of the putatively new SSc–RA loci identified IRF4 as a shared risk factor for these 2 diseases (P_combined = 3.29 × 10⁻¹²). Analysis of the biologic relevance of the known SSc–RA shared loci identified the type I interferon and interleukin‐12 signaling pathways as the main common etiologic factors.Conclusion: This study identified a novel shared locus, IRF4, for the risk of SSc and RA, and highlighted the usefulness of a cross‐disease GWAS meta‐analysis strategy in the identification of common risk loci.

Background.: The epidemiological and clinical characteristics of solid organ transplant (SOT) patients during the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) epidemic remains unclear. We conducted a matched retrospective cohort study to compare clinical outcomes among SOT recipients with the general population and to assess immunosuppression management. Methods.: Adult SOT recipients with laboratory polymerase chain reaction–confirmed SARS-CoV-2 infection admitted to a tertiary-care hospital in Barcelona, Spain, from March 11 to April 25, 2020, were matched to controls (1:4) on the basis of sex, age, and age-adjusted Charlson’s Index. Patients were followed for up to 28 days from admission or until censored. Primary endpoint was mortality at 28 days. Secondary endpoints included admission to the intensive care unit and secondary complications. Drug–drug interactions (DDI) between immunosuppressants and coronavirus disease 2019 (COVID-19) management medication were collected. Results.: Forty-six transplant recipients and 166 control patients were included. Mean (SD) age of transplant recipients and controls was 62.7 (12.6) and 66.0 (12.7) years, 33 (71.7%) and 122 (73.5%) were male, and median (interquartile range) Charlson’s Index was 5 (3–7) and 4 (2–7), respectively. Mortality was 37.0% in SOT recipients and 22.9% in controls (P = 0.51). Thirty-three (71.7%) patients underwent transitory discontinuation of immunosuppressants due to potential or confirmed DDI. Conclusions.: In conclusion, hospitalized SOT recipients with COVID-19 had a trend toward higher mortality compared with controls, although it was not statistically significant, and a notable propensity for DDI.

To determine whether lung involvement is related to microvascular perturbations, nailfold videocapillaroscopy (NVC) was performed in patients with systemic sclerosis (SSc). A cross-sectional study was consecutively accomplished in 152 SSc patients. NVC, a pulmonary function test and echocardiography were undergone within a 3-month period. Finally, 134 patients with at least eight NVC (200× magnification) images were selected for quantitative and qualitative examinations. Patients with interstitial lung disease presented lower median capillary density (4.86/mm vs 5.88/mm, p = 0.005) and higher median of neoangiogenesis (0.56/mm vs 0.31/mm, p = 0.005). A higher quantity of neoangiogenesis capillaries was found in patients with pulmonary arterial hypertension (0.70/mm vs 0.33/mm, p = 0.008). Multivariate linear regression analysis established a correlation between neoangiogenesis and decreased forced vital capacity (FVC) (p < 0.001): for each capillary with neoangiogenesis visualized on average per 1 mm, FVC was 7.3% reduced. In qualitative NVC, a late pattern as defined by Cutolo was also associated with lower FVC (p = 0.018). The number of giant capillaries was associated with reduced diffusion capacity of the lung for carbon monoxide (DLCO) (p = 0.016); for each giant capillary per 1 mm, DLCO was 11.8% diminished. A good correlation was observed between distinctive quantitative and qualitative NVC features with lung functional parameters such as FVC and DLCO. It is suggested that vasculopathy could play a role in SSc lung involvement.