Search

Industrial-scale synthesis of eldecalcitol is described. AA highly diastereoselective epoxidation of p-methoxybenzyl (PMB) protected dienol at room temperature provides the key epoxide intermediate...

IL-17 plays important roles in synovial inflammation and bone destruction in the mouse model of autoimmune arthritis and in rheumatoid arthritis (RA). Cadherin-11 determines the behavior of synovial cells in their proinflammatory and destructive tissue response in inflammatory arthritis, and promotes the invasive behavior of fibroblast-like synoviocytes (FLS). The purpose of this study was to examine the effect of IL-17 on the expression of cadherin-11 in autoimmune experimental arthritis and in RA synovium. The severity of synovial inflammation and bone destruction were examined in IL-17-injected knee joints of mice with collagen-induced arthritis (CIA). Cadherin-11 expression was examined in the synovium of mice with CIA, of IL-1 receptor antagonist (IL-1Ra)-deficient mice and of patients with RA and osteoarthritis (OA). Cadherin-11 expression was also examined in the synovium of IL-17 injected knee joints from CIA mice and in IL-17-stimulated FLS of CIA mice and RA patients. IL-17 aggravated synovial inflammation and bone destruction in CIA. By immunohistochemistry, cadherin-11 expression was increased in the synovium of mice with CIA and IL-1Ra-deficient mice and in patients with RA. Synovial cadherin-11 expression in IL-17-injected knee joints, measured by real-time RT-PCR, Western blot and immunohistochemistry, was increased in CIA. Cadherin-11 expression was significantly increased by IL-17 in cultured FLS of CIA mice and RA patients, and these increases were blocked by NF-κB inhibitors. IL-17 increased the expression of cadherin-11 in vivo and in vitro, which implies that an IL-17-induced increase of cadherin-11 is involved in IL-17-induced aggravation of joint destruction and inflammation.

Background/Aims: To compare the frequency of metabolic syndrome (MetS) and magnitude of insulin resistance, measured by the homeostatic model assessment of insulin resistance (HOMA-IR), between South Korean women with rheumatoid arthritis (RA) and healthy subjects, and to evaluate risk factors for MetS and increased HOMA-IR in patients with RA. Methods: In a cross-sectional setting, 84 female patients with RA and 109 agematched healthy female subjects were consecutively recruited at a universityaffi liated rheumatology center in South Korea. MetS was defined according to the Third Report of the National Cholesterol Education Program`s Adult Treatment Panel (NCEP-ATP III) 2004 criteria. Results: The frequency of MetS did not differ significantly between patients with RA (19%) and healthy subjects (15.6%, p = 0.566), although patients with RA had a higher HOMA-IR compared with healthy subjects (p < 0.001). Patients with RA met the NCEP-ATP III 2004 criteria for high blood pressure more often than healthy subjects (44% vs. 19.3%, p < 0.001), and low high density lipoprotein cholesterol was more prevalent in healthy subjects (33%) than in patients with RA (14.3%, p = 0.004). Although no obvious risk factors for the presence of MetS were identified in patients with RA, higher serum C-reactive protein and disease activity score assessed using the 28-joint count for swelling and tenderness-erythrocyte sedimentation rate significantly contributed to a higher HOMA-IR. Conclusions: Despite their increased insulin resistance, South Korean womenwith RA did not have a significantly higher frequency of MetS compared with that in healthy subjects.

This study was performed to investigate the effects of IL-32 on joint inflammation, bone destruction, and synovial cytokine expressions, and on synovial natural killer (NK) cell expressions in collagen-induced arthritis (CIA). CIA was induced by type II collagen in DBA1 mice, and phosphate-buffered saline (PBS group) or IL-32 (IL-32 group) were injected into both knee joints at day 28 and 32, then mice were killed at day 35. Severity of synovial inflammation and bone destruction was determined by histological scoring method, and synovial cytokine expressions such as IL-1β, TNF-α, IL-17, IL-18, IFN-γ, IL-21, and IL-23 were measured by real-time RT-PCR and western blot. Synovial NK cell expressions were determined by real-time RT-PCR, western blot and immunohistochemistry, and chemokines and chemokine receptors expressions that are associated with NK cell migration were determined by real-time RT-PCR. Scores of synovial inflammation and bone destruction, synovial expressions of IL-1β, TNF-α, IL-18, and IFN-γ were significantly increased in IL-32 group compared with PBS group. Synovial expressions of NK cell, and chemokines (CCL2 and CXCL9) and chemokine receptors (CCR2 and CCR5) that are associated with NK cell migration were significantly increased in IL-32 group compared with PBS group. IL-32 aggravated joint inflammation and bone destruction and increased synovial expressions of inflammatory cytokine and NK cells in CIA. These results suggest that IL-32 play a role in joint inflammation and bone destruction, and IL-32 might be a new target for treatment of rheumatoid arthritis.

pISSN: 2093-940X, eISSN: 2233-4718 Copyright c 2014 by The Korean College of Rheumatology This is a Free Access article, which permits unrestricted non-commerical use, distribution, and reproduction in any medium, provided the original work is properly cited. A Case of Tjalma Syndrome Coincidentally Accompanied by an Ovarian Teratoma Successfully Treated with Intravenous Immunoglobulin-G Adjunctive Therapy

Treatments for patient with ankylosing spondylitis (AS) include non-steroidal anti-inflammatory drugs (NSAIDs), disease-modifying antirheumatic drugs (DMARDs) and anti-tumor necrosis factor-alpha (TNFα) agents. However, owing to the well-known nephrotoxicity of NSAIDs and some DMARDs, the use of these drugs is limited in AS patients with renal insufficiency. As the pharmacokinetics and metabolism of anti-TNFα agents in patients of end stage renal disease, especially those receiving peritoneal dialysis (PD), have not been investigated well, little is known about treating them with anti-TNFα agents. We described the safety and efficacy of etanercept, a soluble fusion protein comprising the TNF receptor 2 in linkage with the Fc portion of immunoglobulin G, in a 40-year-old male AS patient receiving PD.

Castleman’s disease is a rare atypical lymphoproliferative disorder. Although HHV-8 has been reported to be a cause of Castleman’s disease, the etiology and pathogenesis of the disease remains mostly unknown. We experienced a 51year-old female patient who was concurrently diagnosed with Castleman’s disease and systemic lupus erythematosus. Castleman’s disease has been rarely reported in patients with systemic lupus erythematosus. Thus, we report the case and briefly discuss relevant articles.

Objective. A higher prevalence of metabolic syndrome (MetS) has been described in various rheumatic diseases such as rheumatoid arthritis and systemic lupus erythematosus, but no direct studies have investigated the prevalence of MetS in systemic sclerosis (SSc) patients compared with the general population. We compared the frequency of MetS and insulin resistance, as measured by Homeostatic assessment model-insulin resistance (HOMAIR) between female SSc patients and healthy subjects. Methods. In a cross-sectional setting, 35 female SSc patients and 84 age and sex-matched healthy subjects were consecutively recruited at a single center of a tertiary hospital between 2009 and 2010. MetS was defined according to the National Cholesterol Education Program’s Adult Treatment Panel (NCEP-ATP III) 2004 criteria, using the Asian criteria for central obesity. Results. The frequency of MetS was not significantly higher in SSc patients (20.0%) than in healthy subjects (14.3%, p=0.425), but SSc patients had an increased insulin resistance measured by HOMA-IR (p=0.001). Significantly more patients with SSc had increased triglyceride concentrations (p=0.004) and fewer SSc patients tended to meet the waist circumference criterion (p=0.051) according to the individual MetS features. Additionally, there were no significant differences in age, high-sensitivity C-reactive protein, body mass index, HOMA-IR, disease duration, cumulative glucocorticoids dose, modified Rodnan skin score or the proportion of limited SSc cases according to the absence or presence of MetS in SSc patients. Conclusion. Unlike other rheumatic diseases, our preliminary report did not show a significant difference in the prevalence of MetS between female SSc patients and healthy subjects.

Soon Myung Jung 1 , Jin Taek Yoo 1 , Young Hwan Kim 1 , Yu Na Seo 2 , Na Young Lee 3 , Seong Geun Lee 4 , Seong Hu Park, Young Eun Park, Seung Hoon Baek, Geun Tae Kim, Sung-Il Kim, Joung Wook Lee Departments of Internal Medicine, Radiology and Pediatrics, Busan St. Mary’s Medical Center, Department of Internal Medicine, Pusan National University School of Medicine, Kosin University College of Medicine, Busan, Korea

Rheumatoid arthritis is associated with an increased risk of hematological malignancy as a result of the RA itself or its treatment. We report here on an unusual case of a 55-year-old female with long-standing rheumatoid ar- thritis and who was treated with low dose methotrexate and hydrochloroquine. She was diagnosed with chronic myelogenous leukemia that manifested with severe throm- bocytosis and basophilia, and this was treated with im- atinib mesylate. After 6 months, she achieved a complete cytogenetic response of the CML and a complete reso- lution of all the RA symptoms without DMARDs.