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This case-control study aimed to analyze the clinical features and determine the expression of type I interferon-induced genes in systemic lupus erythematosus (SLE) patients harboring the CD11b rs1143679 single-nucleotide polymorphism (SNP) and elucidate whether it is involved in the relapses of SLE. One hundred twenty-five relatively inactive SLE patients with SLEDAI scores < 6, including 102 CD11b rs1143679 G allele patients as controls and 23 rs1143679 A allele carriers as cases, were enrolled from the SLE patient specimen bank in the Department of Rheumatology and Immunology. The sample set was retrospectively analyzed for differences in clinical features, and quantitative PCR and Western blot analyses were performed to evaluate the relative expression of type I interferon (IFN)-inducible genes. The 24-h urinary protein levels in the case group were significantly elevated, and serum C3 levels were significantly reduced compared with those in the control group (P = 0.019 and P = 0.021, respectively). The relative mRNA levels of IFN-inducible genes IFIT1, IFIT4, and ISG15 in the case group were higher than that in the control group (P = 0.0257, 0.0344, and 0.0311, respectively) and matched with the Western blot results. The relative expression of type I IFN-inducible genes in inactive SLE patients harboring the CD11b rs1143679 polymorphism was higher than that in other lupus patients. These findings suggest that the rs1143679 SNP can precipitate relapses in inactive SLE patients. • The rs1143679 GA genotype was associated with SLE clinical features. • The rs1143679 GA genotype showed higher interferon-inducible gene expression relative to the GG genotype.

To investigate the association of serum interleukin-11 (IL-11) with disease activity and occurrence of interstitial lung disease (ILD) in patients with rheumatoid arthritis (RA).One hundred and six RA patients were included, including 31 with ILD. All patients were divided into two groups according to the 28-joint Disease Activity Score (DAS28), active-disease group (DAS283.2) and target-achieved group (DAS28≤3.2). Serum IL-11 was detected by ELISA. Serum autoantibodies [anticitrullinated protein antibody (ACPA) and rheumatoid factor (RF)], inflammatory markers [C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR)], and complete blood count were measured with routine methods.Serum IL-11 was upregulated in RA patients compared with healthy controls (HC), and increased more significantly in patients with ILD (RA-ILD) than patients without ILD (RA-nonILD). In both RA-ILD and RA-nonILD patients, serum level of IL-11 was higher in the active-disease group than that in the target-achieved group. Pearson correlation analysis confirmed that IL-11 was positively correlated with DAS28. No significant correlation was found between serum level of IL-11 and ACPA or RF. IL-11 was positively correlated with ESR and CRP levels and PLT count in RA patients.IL-11 was found to be involved in the development of arthritis and ILD in RA patients, and might constitute a potential target for the treatment of RA-ILD.

To retrospectively analyze the efficacy and safety of febuxostat on gout patients with low serum uric acid level. A study was conducted in Nanjing First Hospital from October 2015 to September 2016. Thirty nine acute gouty arthritis patients from the emergency and outpatient department were included. Patients met the 2015 Gout Classification Criteria revised by American College of Rheumatology/European League Against Rheumatism (ACR/EULAR) and had urate deposition around the joints detected by dual-energy computerized tomography (DECT). Patients whose serum uric acid (SUA) were between 5.0 and 7.0 mg/dl (300–420 μmol/l) received febuxostat treatment to maintain the SUA level between 3.0 and 5.0 mg/dl for 1 year. Efficacy and safety of febuxostat were observed during the process. Three of 39 subjects were excluded because of adverse events (AEs) after receiving an initial febuxostat treatment for 2 months. Thirty six subjects were enrolled. The mean SUA level was reduced significantly from 6.51 ± 0.28 mg/dl at baseline to 4.24 ± 0.38 mg/dl and SUA of all subjects decreased by 34.8% compared with baseline. After 1-year treatment, the volume of tophus was reduced approximately 62.8%. Serum creatinine decreased stepwise in 8 gout patients with chronic kidney diseases from 162.5 ± 9.2 μmol/l to 131.4 ± 11.0 μmol/l. Two months after initiation of treatment, the number of gout flares began to markedly decrease and almost did not occur after 1 year. After the 1-year treatment of febuxostat, the average SUA level declined significantly, and the renal function improved gradually. There was nearly complete abolition of gout flares by the end of the study. Tophi resolved markedly compared with baseline as assessed by DECT. Furthermore, only a few people experienced adverse events. Febuxostat has a notable effect for gout patients in the lower SUA level range.