OBJECTIVE: We wanted to investigate the incidence of serious infections among the rheumatoid arthritis (RA) patients who were treated with tumor necrosis factor alpha (TNF-alpha) antagonists. METHODS: We enrolled the 175 RA patients who were treated with TNF-alpha antagonists for at least 3 months during February 2003 to July 2008, and these patients were in the SMART-b cohort of Kangnam St. Mary's hospital. Patients were prescribed infliximab, etanercept or adalimumab. The data was retrospectively collected. RESULTS: The incidence of serious infections among the RA patients treated with TNF-alpha was significantly increased according to the survival analysis, as compared with that of those patient treated with conventional DMARDs (p<0.01). The most common serious infection was pneumonia. There was no significant difference in the incidence of serious infections among the three TNF-alpha antagonists used in this study (p=0.96). But the serious infections occurred more often in the patients who received more than 10 mg methotrexate (MTX) per week (p=0.02). CONCLUSION: RA patients treated with TNF-alpha antagonists had a higher incidence of serious infection. Therefore, close monitoring for serious infection is needed for RA patients who are receiving TNF-alpha antagonists.
Antibodies, Monoclonal ; Antibodies, Monoclonal, Humanized ; Antirheumatic Agents ; Arthritis, Rheumatoid ; Cohort Studies ; Humans ; Immunoglobulin G ; Incidence ; Methotrexate ; Pneumonia ; Receptors, Tumor Necrosis Factor ; Retrospective Studies ; Tumor Necrosis Factor-alpha

OBJECTIVE: We wanted to investigate the incidence of serious infections among the rheumatoid arthritis (RA) patients who were treated with tumor necrosis factor alpha (TNF-alpha) antagonists. METHODS: We enrolled the 175 RA patients who were treated with TNF-alpha antagonists for at least 3 months during February 2003 to July 2008, and these patients were in the SMART-b cohort of Kangnam St. Mary's hospital. Patients were prescribed infliximab, etanercept or adalimumab. The data was retrospectively collected. RESULTS: The incidence of serious infections among the RA patients treated with TNF-alpha was significantly increased according to the survival analysis, as compared with that of those patient treated with conventional DMARDs (p<0.01). The most common serious infection was pneumonia. There was no significant difference in the incidence of serious infections among the three TNF-alpha antagonists used in this study (p=0.96). But the serious infections occurred more often in the patients who received more than 10 mg methotrexate (MTX) per week (p=0.02). CONCLUSION: RA patients treated with TNF-alpha antagonists had a higher incidence of serious infection. Therefore, close monitoring for serious infection is needed for RA patients who are receiving TNF-alpha antagonists.
Antibodies, Monoclonal ; Antibodies, Monoclonal, Humanized ; Antirheumatic Agents ; Arthritis, Rheumatoid ; Cohort Studies ; Humans ; Immunoglobulin G ; Incidence ; Methotrexate ; Pneumonia ; Receptors, Tumor Necrosis Factor ; Retrospective Studies ; Tumor Necrosis Factor-alpha

OBJECTIVE: Interleukin-15 (IL-15) recruits and activates synovial T cells, and IL-15 plays an important role in amplifying and perpetuating inflammation in the pathogenesis of rheumatoid arthritis (RA). Stromal cell-derived factor-1 (SDF-1) is a potent chemoattractant for memory T cells in the inflamed RA synovium. This study investigated the effect of IL-15 on SDF-1 production in RA fibroblast-like synoviocytes (FLS). METHODS: The expressions of IL-15 and SDF-1 were determined from the synovium of patients with RA and osteoarthritis (OA) by performing immunohistochemistry. The expressions of SDF-1 was measured from the RA FLS that were cultured with IL-15 and IL-17 by real-time RT-PCR and ELISA. The SDF-1 expression was also measured, via ELISA, from the RA FLS stimulated by IL-15 together with the inhibitors of such intracellular signal molecules as phosphatidylinositol 3-kinase (PI 3-kinase, LY294002), STAT3 (AG490), MAP Kinase (PD98059), NF-kappaB (parthenolide) and activator protein 1 (AP-1, curcumin). RESULTS: IL-15 and SDF-1 were mainly expressed in the RA synovium compared to that of the OA synovium. IL-15 increased the SDF-1 expressions and it, and had an additive effect with IL-17 on the SDF-1 expressions in the cultured RA FLS. The IL-15 induced increase of the SDF-1 expression in the cultured RA FLS was blocked by the inhibitors of PI 3-kinase, NF-kappaB and AP-1. CONCLUSION: The SDF-1 expression was increased in the RA synovium and it was up-regulated by IL-15 in the RA FLS through the PI 3-kinase, NF-kappaB, and AP-1 pathways. These results imply that the IL-15 induced increase of the SDF-1 expressions may be involved in the immunopathogenesis of RA.
Arthritis, Rheumatoid ; Enzyme-Linked Immunosorbent Assay ; Fibroblasts ; Humans ; Immunohistochemistry ; Inflammation ; Interleukin-15 ; Interleukin-17 ; Memory ; NF-kappa B ; Osteoarthritis ; Phosphatidylinositol 3-Kinase ; Phosphatidylinositol 3-Kinases ; Phosphotransferases ; Synovial Membrane ; T-Lymphocytes ; Transcription Factor AP-1

OBJECTIVE: Interleukin-15 (IL-15) recruits and activates synovial T cells, and IL-15 plays an important role in amplifying and perpetuating inflammation in the pathogenesis of rheumatoid arthritis (RA). Stromal cell-derived factor-1 (SDF-1) is a potent chemoattractant for memory T cells in the inflamed RA synovium. This study investigated the effect of IL-15 on SDF-1 production in RA fibroblast-like synoviocytes (FLS). METHODS: The expressions of IL-15 and SDF-1 were determined from the synovium of patients with RA and osteoarthritis (OA) by performing immunohistochemistry. The expressions of SDF-1 was measured from the RA FLS that were cultured with IL-15 and IL-17 by real-time RT-PCR and ELISA. The SDF-1 expression was also measured, via ELISA, from the RA FLS stimulated by IL-15 together with the inhibitors of such intracellular signal molecules as phosphatidylinositol 3-kinase (PI 3-kinase, LY294002), STAT3 (AG490), MAP Kinase (PD98059), NF-kappaB (parthenolide) and activator protein 1 (AP-1, curcumin). RESULTS: IL-15 and SDF-1 were mainly expressed in the RA synovium compared to that of the OA synovium. IL-15 increased the SDF-1 expressions and it, and had an additive effect with IL-17 on the SDF-1 expressions in the cultured RA FLS. The IL-15 induced increase of the SDF-1 expression in the cultured RA FLS was blocked by the inhibitors of PI 3-kinase, NF-kappaB and AP-1. CONCLUSION: The SDF-1 expression was increased in the RA synovium and it was up-regulated by IL-15 in the RA FLS through the PI 3-kinase, NF-kappaB, and AP-1 pathways. These results imply that the IL-15 induced increase of the SDF-1 expressions may be involved in the immunopathogenesis of RA.
Arthritis, Rheumatoid ; Enzyme-Linked Immunosorbent Assay ; Fibroblasts ; Humans ; Immunohistochemistry ; Inflammation ; Interleukin-15 ; Interleukin-17 ; Memory ; NF-kappa B ; Osteoarthritis ; Phosphatidylinositol 3-Kinase ; Phosphatidylinositol 3-Kinases ; Phosphotransferases ; Synovial Membrane ; T-Lymphocytes ; Transcription Factor AP-1

MicroRNAs (miRNAs) are small, single-stranded, non-coding RNA molecules of 20~22 nucleotides, which are involved in many biologic functions such as development, cell proliferation, differentiation, and apoptosis. In addition to these biologic functions, recent reports have demonstrated that miRNAs play important roles in the development of the immune system and the regulation of immune responses. Dysregulation of miRNAs might be involved in the pathogenesis of autoimmune diseases such as rheumatoid arthritis (RA). Recent studies have shown that miR-146a, miR-155, and miR-203 are overexpressed in RA and that miR-124a is under expressed in RA. miR-146 downregulates the expression of IL-1 receptor associated kinase 1 and TNF receptor-associated factor 6 involved in IL-1beta signaling, and miR-155 suppresses the expression of matrix metalloproteinases 1 and 3, suggesting that these miRNAs act as negative feedback regulators of inflammation and tissue damage in RA. In this report, we review the current knowledge about miRNAs and summarize the involvement of miRNAs in RA.
Apoptosis ; Arthritis, Rheumatoid ; Autoimmune Diseases ; Cell Proliferation ; Immune System ; Inflammation ; Interleukin-1 ; Matrix Metalloproteinases ; MicroRNAs ; Nucleotides ; Phosphotransferases ; RNA, Untranslated ; TNF Receptor-Associated Factor 6

MicroRNAs (miRNAs) are small, single-stranded, non-coding RNA molecules of 20~22 nucleotides, which are involved in many biologic functions such as development, cell proliferation, differentiation, and apoptosis. In addition to these biologic functions, recent reports have demonstrated that miRNAs play important roles in the development of the immune system and the regulation of immune responses. Dysregulation of miRNAs might be involved in the pathogenesis of autoimmune diseases such as rheumatoid arthritis (RA). Recent studies have shown that miR-146a, miR-155, and miR-203 are overexpressed in RA and that miR-124a is under expressed in RA. miR-146 downregulates the expression of IL-1 receptor associated kinase 1 and TNF receptor-associated factor 6 involved in IL-1beta signaling, and miR-155 suppresses the expression of matrix metalloproteinases 1 and 3, suggesting that these miRNAs act as negative feedback regulators of inflammation and tissue damage in RA. In this report, we review the current knowledge about miRNAs and summarize the involvement of miRNAs in RA.
Apoptosis ; Arthritis, Rheumatoid ; Autoimmune Diseases ; Cell Proliferation ; Immune System ; Inflammation ; Interleukin-1 ; Matrix Metalloproteinases ; MicroRNAs ; Nucleotides ; Phosphotransferases ; RNA, Untranslated ; TNF Receptor-Associated Factor 6

No abstract available.
Gout ; Light

No abstract available.
Gout ; Light

No abstract available.
Hip ; Hip Joint ; Osteoma, Osteoid

No abstract available.
Amyloidosis