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Objective: To compare the clinical effectiveness of two treatment strategies for active rheumatoid arthritis (RA) refractory to conventional synthetic disease-modifying anti-rheumatic drugs (csDMARDs): starting TNF inhibitors (TNFIs) or changing csDMARDs., Methods: We used two nationwide Korean RA registries for patient selection. TNFI users were selected from the BIOPSY, which is an inception cohort of RA patients starting biologic DMARDs. As a control group, we selected RA patients with moderate or high disease activity from the KORONA database whose treatment was changed to other csDMARDs. After comparing baseline characteristics between the two groups in either unmatched or propensity score matched cohorts, we compared potential differences in the 1-year remission rate as a primary outcome and changes in HAQ-DI and EQ-5D scores as secondary outcomes., Results: A total of 356 TNFI starters and 586 csDMARD changers were identified from each registry as unmatched cohorts, and 294 patients were included in the propensity score matched cohort. In the intention-to-treat analysis, TNFI starters had higher 1-year remission rates than csDMARD changers in both unmatched (19.1 vs. 18.4%, p < 0.01) and matched cohorts (19.7 vs. 15.0%, p < 0.01). In per protocol analysis, TNFI starters had much higher remission rates in unmatched (37.2 vs. 28.0%, p = 0.04) and matched cohorts (35.4 vs. 19.1%, p = 0.04). However, in matched cohorts, no significant differences were observed between two groups in HAQ-DI and EQ-5D scores., Conclusions: We compared the clinical effectiveness of the two treatment strategies for active RA refractory to csDMARDs. TNFI starters showed higher 1-year remission rates than csDMARD changers.

The purpose of this study was to identify the characteristic magnetic resonance imaging (MRI) findings in neuropsychiatric systemic lupus erythematosus (NPSLE) and to investigate the association between MRI findings and neuropsychiatric manifestations in SLE. Brain MRIs with a diagnosis of SLE from 2002 to 2013 from three tertiary university hospitals were screened. All clinical manifestations evaluated by brain MRI were retrospectively reviewed. If the clinical manifestations were compatible with the 1999 NPSLE American College of Rheumatology (ACR) nomenclature and case definitions, the brain MRIs were assessed for the presence of white matter hyperintensities, gray matter hyperintensities, parenchymal defects, atrophy, enhancement, and abnormalities in diffusion-weighted images (DWI). The number, size, and location of each lesion were evaluated. The neuropsychiatric manifestation of each brain MRI was classified according to the 1999 ACR NPSLE case definitions. The associations between MRI findings and NPSLE manifestations were examined. In total, 219 brain MRIs with a diagnosis of SLE were screened, and 133 brain MRIs met the inclusion criteria for NPSLE. The most common MRI abnormality was white matter hyperintensities, which were observed in 76 MRIs (57.1 %). Gray matter hyperintensities were observed in 41 MRIs (30.8 %). Parenchymal defects were found in 31 MRIs (23.3 %), and atrophy was detected in 20 MRIs (15.0 %). Patients who had seizures were more associated with gray matter hyperintensities than patients with other neuropsychiatric manifestations. Patients with cerebrovascular disease were more associated with gray matter hyperintensity, parenchymal defects, and abnormal DWI than patients with other neuropsychiatric manifestations. In addition to white matter hyperintensities, which were previously known as SLE findings, we also noted the presence of gray matter hyperintensities, parenchymal defects, and abnormal DWI in a substantial portion of SLE patients, particularly in those with cerebrovascular disease or seizures.

This retrospective study of 432 patients was conducted between 2000 and 2009 to compare immunosuppressive therapy responses in uveitis accompanied or unaccompanied by rheumatic diseases. We divided patients into two groups: uveitis related or unrelated to rheumatic diseases. The clinical improvement after treatment was measured at the end of the observation period. Of the 432 patients with uveitis, 33 (7.6%) patients suffered from associated rheumatic diseases and 399 (92.4%) patients did not. The groups showed similar clinical features, but the mean age at onset of uveitis was lower in the rheumatic disease group (44.06 ± 2.13 years vs. 48.23 ± 0.81 years). The rheumatic diseases included spondyloarthropathy (31%), Behcet's disease (27%), rheumatoid arthritis (18%), systemic lupus erythematosus (15%), Sjogren's syndrome (6%), and mixed connective tissue disease (3%). Erythrocyte sedimentation rate and C-reactive protein level were increased in uveitis associated with rheumatic diseases, whereas ocular complications were not. The response to immunosuppressive therapy was significantly increased in cases of uveitis associated with rheumatic diseases (P < 0.05). Therefore, during early treatment, uveitis accompanied by rheumatic diseases showed better response to immunosuppressive therapy and less frequent complications.

Kaposi sarcoma (KS) is a vascular neoplasm mainly affecting the skin of the limbs that has previously been associated with rheumatoid arthritis (RA). When compared with the RA patients treated with corticosteroids and immunosuppressive drugs, the reported number of KS in RA patients was very rare. Although the exact mechanisms of developing KS in RA patients are unclear, some drugs which include corticosteroid have been suggested as an etiological factor in previous case reports of RA and KS. We report, here in, another case of KS associated with the initiation of leflunomide in a patient with RA.

This study designed to assess the relationship between tumor necrosis factor (TNF)-α promoter polymorphisms and disease susceptibility to human leukocyte antigen (HLA)-B27-positive ankylosing spondylitis (AS). One hundred and nineteen HLA-B27(+) AS patients, 95 HLA-B27(+) healthy controls, and 135 random healthy controls were enrolled in this study. Six single nucleotide polymorphisms (SNPs) of the TNF-α promoter at positions -1031T/C, -863C/A, -857C/T, -646G/A, -308G/A, and -238G/A were analyzed. Differences between groups were evaluated using the chi-square test or Fisher's exact test. Haplotypes from each SNP were constructed, and differences in haplotypic frequencies between groups were evaluated. There were significant differences in the allelic and genotypic frequencies of 1031T/C, -863C/A, and -857C/T TNF-α promoters polymorphisms between HLA-B27(+) AS patients and random controls, but not between patients with AS and HLA-B27(+) healthy individuals. TNF-α polymorphisms did not influence the extra-spinal clinical features in patients with AS. The haplotypic sequence -1031T/-863C/-857C/-308G increased the risk of susceptibility to AS compared to random controls (P (corr) < 0.001, OR = 2.756, 95% CI = 1.894-4.010), whereas the sequence -1031C/-863A/-857C/-308G appeared to be associated with decreased susceptibility to AS compared to random controls (P (corr) = 0.006, OR = 0.396, 95% CI = 0.231-0.679). This study indicates that TNF-α promoter polymorphism between controls and AS patients with HLA-B27(+) genetic background is not associated with susceptibility to AS. However, TNF-α polymorphism, irrespective of HLA-B27, increases risk of susceptibility to AS in general population.