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Little is known about the nature of relationships between sleep disturbance and influencing factors in rheumatoid arthritis. The purpose of this study was to identify factors that influence sleep disturbance and to evaluate mediating effects of depression on sleep disturbance. A nonexperimental, descriptive, correlational study design was adopted. One hundred patients with rheumatoid arthritis were recruited. Inflammatory status and levels of pain, fatigue, functional disability, depression, and sleep disturbance were measured. The factors that directly influenced sleep disturbance were gender, rheumatoid arthritis duration, serum C-reactive protein level, fatigue, and depression. Depression was found to have mediating effects on the relationships between sleep disturbance and arthritis symptoms. Pain, fatigue, and depression were found to have significant direct or indirect impacts on sleep disturbance. Our findings may improve understanding of sleep disturbance and aid the development of effective nursing management strategies for patients with rheumatoid arthritis suffering from sleep disturbance.

BACKGROUND Ankylosing spondylitis (AS) is strongly associated with the human leukocyte antigen (HLA) B27 haplotype. In regions where conventional polymerase chain reaction for HLA typing is available for antigens such as HLA B27 or HLA B51, it is common to perform the HLA B27 test for evaluation of AS. While HLA B27-associated clustered occurrences of AS have been reported in families, we report the first case series of HLA B51-related occurrences of AS in a family. CASE SUMMARY A father and his daughters were diagnosed with AS and did not have the HLA B27 haplotype. Although they were positive for HLA B51, they exhibited no signs of Behçet’s disease (BD). Of the five daughters, one had AS, and three, including the daughter with AS, were positive for HLA B51. The two daughters with the HLA B51 haplotype (excluding the daughter with AS) exhibited bilateral grade 1 sacroiliitis, whereas the daughters without the HLA B51 haplotype did not have sacroiliitis. Thus, this Korean family exhibited a strong association with the HLA B51 haplotype and clinical sacroiliitis, irrespective of the symptoms of BD. CONCLUSION It is advisable to check for HLA B51 positivity in patients with AS/spondyloarthropathy who test negative for HLA B27.

We aimed to investigate how systemic bone metabolism was affected after 1 year of treatment with tumour necrosis factor (TNF) inhibitors in rheumatoid arthritis (RA) patients.A total of 29 seropositive RA patients not treated for osteoporosis were enrolled and TNF inhibitors were administered for a year. Bone mineral density (BMD) at the lumbar spine, femur neck, and total hip was measured at baseline and 12 months after anti-TNF treatment. Blood samples were collected at baseline and 6 and 12 months after anti-TNF treatment and osteoclasts were cultured on bone slices. Weight was the strongest factor influencing systemic bone loss. Patients were categorised into two groups: obese (body mass index (BMI) ≥25 kg/m2) and non-obese (BMI25 kg/m2).All patients showed decreased BMD at all sites. The obese group showed relatively little change in BMD, although the non-obese group showed significant decreases in BMD at all sites after 1 year of treatment with TNF inhibitors. Resorption pits created by osteoclasts decreased at 6 months and increased at 12 months in the non-obese group, while the obese group presented with steadily decreasing sizes of resorption pits at all-time points. Levels of receptor activator of nuclear factor kappa B ligand were significantly decreased at 12 months compared to baseline in the obese group, while they were increased in the non-obese group.One year of treatment with TNF inhibitors failed to halt systemic bone loss in RA patients, but obesity may have protective effects against bone loss.

Background and Objectives Sjögren’s syndrome (SS) is an autoimmune inflammatory disorder of exocrine glands characterized by dry mouth and eye. Recently, ultrasonography has become a valuable tool for the assessment of salivary gland involvement in SS although studies on the usefulness of salivary gland CT is rare. In this regard, we evaluated the diagnostic accuracy of parotid gland CT for SS.Subjects and Method A total of 91 patients with sicca symptoms took a parotid CT, a serology test, an ophthalmologic examination and a minor salivary gland biopsy. At the end, as a standard, we diagnosed the primary SS according to the new 2016 American College of Rheumatology/ European League Against Rheumatism classification criteria. The diagnostic value of parotid CT was compared by the McNemar test.Results Of the total of 91 patients with parotid CT, 37 (40.7%) patients met the SS classification criteria. On the parotid CT, heterogeneity of the parotid gland has the sensitivity of 74.1%, specificity of 70.3%, and accuracy of 71.4%. The abnormal fat tissue deposition showed the sensitivity of 74.1%, specificity of 81.3%, and accuracy of 79.1%. Diffuse calcification was seen in 1/91 SS patients (sensitivity 3.7%, specificity 100%, accuracy 71.4%).Conclusion Parotid CT is helpful for the diagnosis of SS. The presence of heterogeneity and fat tissue deposition are highly sensitive for the accuracy of SS. Diffuse calcification in bilateral parotid glands is highly specific for SS.

As the prevalence of gout and hyperuricemia increases, the comorbidities of gout and hyperuricemia have become a public health burden. In particular, risks of cardiovascular disease (CVD)-related complications are increasing. However, a few guidelines exist for the management of hyperuricemia. This cross-sectional study aimed to investigate the association of serum uric acid with CVD risk in the general population of Korean adults. We examined cross-sectional data from the first and second years of the seventh Korea National Health and Nutrition Examination Survey 2016&ndash, 2017. Among 16,277 participants, 8781 were analyzed. We estimated the CVD risk using a 10-year CVD risk score prediction formula. There was a significant association of serum uric acid with 10-year CVD risk scores after adjusting for physical activity, body mass index, serum creatinine, and alcohol consumption in both sexes (p &lt, 0.001). In the fitted fractional polynomial model, an approximate U-shaped association between serum uric acid levels and 10-year CVD risk scores was found in men. At the serum uric acid level of 6.9 mg/dL, the CVD risk was lowest. An approximate J-shaped association between serum uric acid levels and 10-year CVD risk scores was found in women. Our study showed that hyperuricemia was associated with an increased CVD risk. Hypouricemia was also associated with an increased CVD risk in men. We, therefore, recommend proper management of uric acid levels in the general population to reduce CVD risks.

Background CT-P10 is a biosimilar of innovator rituximab (RTX), a biological therapy used to treat patients with rheumatoid arthritis (RA) who have responded inadequately to anti-tumor necrosis factor agents. Objective Our objective was to compare the clinical profile of CT-P10 versus RTX in patients with RA who received up to two courses of treatment and were followed for up to 72 weeks. Methods In this multicenter double-blind phase I study, patients were randomized 2:1 to receive CT-P10 1000 mg or RTX 1000 mg at weeks 0 and 2. Based on disease activity, patients could receive a second course of treatment between weeks 24 and 48. Efficacy endpoints, including mean change from baseline in Disease Activity Score using 28 joints (DAS28), safety, immunogenicity, pharmacokinetics, and pharmacodynamics were evaluated. Results In total, 154 patients were randomized to CT-P10 or RTX (n = 103 and 51, respectively); 137 (n = 92 and 45) completed the first course of treatment, of whom 83 (n = 60 and 23) were re-treated. Improvements from baseline in all efficacy endpoints were highly similar between the CT-P10 and RTX groups over both treatment courses. At week 24 after the second course, mean change from week 0 of the first course in DAS28 erythrocyte sedimentation rate was −2.47 and −2.04 for CT-P10 and RTX, respectively, (p = 0.1866) and in DAS28 C-reactive protein was −2.32 and −2.00, respectively (p = 0.3268). The proportion of patients positive for antidrug antibodies at week 24 after the second treatment course was 20.0% and 21.7% in the CT-P10 and RTX groups, respectively. The safety profile of CT-P10 was comparable to that of RTX, and pharmacokinetic and pharmacodynamic properties were similar. Conclusions In patients with RA, efficacy, safety, and other clinical data were comparable between CT-P10 and RTX after up to two courses of treatment over 72 weeks. (ClinicalTrials.gov identifier NCT01534884). Electronic supplementary material The online version of this article (doi:10.1007/s40259-017-0232-7) contains supplementary material, which is available to authorized users.

Background Patients with ankylosing spondylitis (AS) have a higher risk of cardiovascular disease. Atherosclerosis is a main pathological process of cardiovascular disease and calcified plaque is a characteristic feature of atherosclerosis. Inflammation plays a potential role in vascular calcification. There is no previous study revealing the mechanism of vascular calcification in AS. Objectives We investigated the relationship between vascular calcification and inflammation in patients with AS. Methods Sixteen male patients aged over 20 years with AS were enrolled. They fulfilled the modified New York criteria and each of their ankylosing spondylitis disease activity score was more than 2.1. Sex and age matched nine healthy controls were also recruited. Mouse MOVAS (American Type Culture Collection, ATCC®, CRL-2797TM) vascular smooth muscle cells were stabilized in maintenance medium for 24 hours. Then the amount of serum equivalent to 10% of maintenance medium from subjects was added and cells were stimulated for another 72 hours. We exchanged this medium with calcification medium every third day and cells were cultured for another 11 days. After 2 weeks, cells were stained with Alizarin Red S and the optical density (OD) was measured while being compensated by cell viability. For Western blotting, cells were stabilized for 24 hours and stimulated for another 72 hours through the same procedure as that of Alizarin Red S staining. Then we measured the level of protein expression in PPAR-gamma, beta-catenin, TNF-a, interleukin (IL)-23, and MMP7. Results The level of OD of MOVAS cells treated with serum from AS patients (19.503 ± 6.422, mean ± SD) was significantly higher than that from controls (12.724 ± 5.746) (P=0.027, Mann-Whitney test). The level of MMP7 expression of MOVAS cells treated with serum from AS patients (1.921 ± 0.702) was significantly higher than that from controls (0.779 ± 0.191) (P=0.000, Mann-Whitney test). The level of beta-catenin expression of MOVAS cells treated with serum from AS patients (1.292 ± 0.356) was significantly higher than that from controls (0.887 ± 0.310) (P=0.025). There was negative correlation between PPAR-gamma and TNF-a (rho=-0.762, p=0.028, Spearman rank correlation coefficient), and between PPAR-gamma and IL-23 (rho=-0.601, p=0.039); positive correlation between MMP7 and TNF-a (rho=0.833, p=0.010), and between MMP7 and IL-23 (rho=0.797, p=0.002). Conclusion Serum from AS patients showed increased calcification of vascular smooth muscle cells than serum from controls. The level of vascular calcification marker from vascular smooth muscle cells treated with serum from AS patients was significantly higher than that from controls. There were negative relationship between inflammatory markers and inhibitory marker of vascular calcification but positive relationship between inflammatory markers and stimulatory marker of vascular calcification. These findings suggest that vascular calcification by inflammation could be an important cause of cardiovascular disease in AS patients. Acknowledgement This research was supported by Basic Science Research Program through the National Research Foundation of Korea(NRF) funded by the Ministry of Education (NRF-2017R1D1A1B03030825) Disclosure of Interests Seung Yun Lee: None declared, Seong-Ryul Kwon: None declared, Su-Ah Yoon: None declared, Kyong-Hee Jung: None declared, Won Park Consultant for: Celltrion, Inc, Shin-Goo Park: None declared, Mie Jin Lim: None declared

목적: 저자들은 골다공증 치료를 받지 않고 있는 류마티스관절염 환자들에서 골다공증의 위험 요인과 골밀도 검사의 적절한 간격을 알아보고자 하였다. 방법: BMD 측정을 두 번 이상 실시받고, 골다공증을 진단받지 않은 40세 이상의 류마티스 관절염 환자 511명을 후향적으로 조사하였다. 이들을 기저치 BMD가 정상(T-score >-1), 경증 골감소(-1 ≥ T-score > -1.5), 중등도 골감소(-1.5 ≥T-score > -2), 중증 골감소(-2 ≥ T-score > -2.5)의 4군으로 분류하였다. 각 군에서 10%의 환자가 골다공증 또는 골절이 발생되는 기간을 추정하였다. 결과: 총 관찰 기간은 2,214인-년이었고 평균 4.3인-년이었다. 각 군에서 10%의 환자가 골다공증 또는 골절이 발생되는기간은 정상군은 10년 이상, 경증군은 4.3년, 중등도군은 2.5년, 중증군은 1.5년이었다. 결론: 초기 BMD 측정의 T-score가 추후 골다공증이 발생의 가장 강력한 인자였다. 그러므로 류마티스 관절염 환자에서 초기 BMD의 결과에 따른 다음 검사의 적절한 간격 조정이 필요하다.

ObjectiveTo demonstrate pharmacokinetic equivalence of CT-P10 and innovator rituximab (RTX) in patients with rheumatoid arthritis (RA) with inadequate responses or intolerances to antitumour necrosis factor agents.MethodsIn this randomised phase I trial, patients with active RA were randomly assigned (2:1) to receive 1000 mg CT-P10 or RTX at weeks 0 and 2 (alongside continued methotrexate therapy). Primary endpoints were area under the serum concentration–time curve from time zero to last quantifiable concentration (AUC0–last) and maximum serum concentration after second infusion (Cmax). Additional pharmacokinetic parameters, efficacy, pharmacodynamics, immunogenicity and safety were also assessed. Data are reported up to week 24.Results103 patients were assigned to CT-P10 and 51 to RTX. The 90% CIs for the ratio of geometric means (CT-P10/RTX) for both primary endpoints were within the bioequivalence range of 80%–125% (AUC0–last: 97.7% (90% CI 89.2% to 107.0%); Cmax: 97.6% (90% CI 92.0% to 103.5%)). Pharmacodynamics and efficacy were comparable between groups. Antidrug antibodies were detected in 17.6% of patients in each group at week 24. CT-P10 and RTX displayed similar safety profiles.ConclusionsCT-P10 and RTX demonstrated equivalent pharmacokinetics and comparable efficacy, pharmacodynamics, immunogenicity and safety.Trial registration numberNCT01534884.

Background CT-P10 is a biosimilar candidate of innovator rituximab (RTX) that demonstrated a comparable clinical profile to RTX in a phase I randomized controlled trial (RCT) in rheumatoid arthritis (RA) (ClinicalTrials.gov identifier: NCT01534884). Objective This open-label extension (OLE) study (NCT01873443) compared the efficacy and safety of CT-P10 in patients with RA who received CT-P10 from the outset (i.e., from the start of the RCT and also in the OLE; ‘maintenance group’) with those who received RTX during the RCT and switched to CT-P10 during the OLE (‘switch group’). Methods Patients who completed the RCT were recruited. Based on the Disease Activity Score using 28 joints (DAS28) and predefined safety criteria, patients could receive up to two courses of CT-P10 during the OLE. Efficacy [DAS28 and European League Against Rheumatism (EULAR) response], safety and immunogenicity were assessed. Results Eighty-seven patients were enrolled; 58 and 29 had previously received CT-P10 or RTX, respectively, in the RCT. Of these, 38 (65.5%) and 20 (69.0%) were treated with CT-P10 in the OLE and therefore comprised the maintenance and switch groups, respectively. The mean change in DAS28-erythrocyte sedimentation rate (ESR) from baseline (week 0 of RCT) at week 24 of the first OLE treatment course in the maintenance and switch groups was −2.7 and −2.4, respectively. The proportion of patients with good/moderate EULAR responses was also comparable between groups. Antidrug antibodies were detected in 13.2 and 15.0% of patients in the maintenance and switch groups, respectively, at week 24 of the first OLE course. CT-P10 treatment was well-tolerated when administered for up to 2 years or after switching from RTX. Conclusion In this study population, comparable efficacy and safety profiles were observed in patients who switched from RTX to CT-P10 and those maintained on CT-P10 throughout treatment. Electronic supplementary material The online version of this article (doi:10.1007/s40259-017-0233-6) contains supplementary material, which is available to authorized users.

Objective The full effect of anti-TNF therapy on new bone formation is still in debate in spondylitis fields. We sought to obtain circulating osteoblast-lineage cells in peripheral blood from ankylosing spondylitis (AS) patients and healthy control subjects, and to evaluate the effect of TNF-α on osteoblastogenesis in patients with AS before and after infliximab therapy. Methods Sixteen male patients with AS slated for infliximab therapy and 19 controls were recruited. We cultured osteoblast-lineage cells from peripheral blood and measured the optical density of their alizarin red S staining. We also measured serum P1NP (procollagen type 1 N-terminal propeptide) as an early osteoblast differentiation marker, osteocalcin as a late osteoblast differentiation marker, and inflammatory markers. Results There were significantly more circulating osteoblast-lineage cells in patients than in controls. The number of circulating osteoblast-lineage cells and optical density of Alizarin S staining decreased 14 weeks after infliximab therapy (p=0.028); serum level of P1NP decreased, but that of osteocalcin increased (p=0.002 and 0.007 respectively). Conclusion Our data reveals first, TNF-α stimulates osteoblastogenesis before infliximab therapy in patients with AS; second, infliximab therapy resolves early inflammation, but allows mature osteoblast differentiation in late inflammation. The culture of osteoblast-lineage cells in peripheral blood may be a candidate for a new modality with which study spondylitis and other autoimmune diseases. Funding This study is supported by grant from the National Research Foundation of Korea (NRF-2014R1A1A2058007) to Dr. S-R Kwon

The object of this study was to evaluate the effect of uric acid lowering therapy in reducing the new development of comorbidities and the frequency of acute attacks in gout patients. We retrospectively reviewed patients who were diagnosed to have gout with at least 3 yr of follow up. They were divided into 2 groups; 53 patients with mean serum uric acid level (sUA)

The full effect of anti-TNF therapy on new bone formation is still in debate in spondylitis fields. We sought to obtain circulating osteoblast-lineage cells in peripheral blood from ankylosing spondylitis (AS) patients and healthy control subjects, and to evaluate the effect of before and after anti TNF-α therapy on osteoblastogenesis in patients with AS.Sixteen male patients with AS slated for infliximab therapy and 19 controls were recruited. We cultured osteoblast-lineage cells from peripheral blood and measured the optical density of their Alizarin red S staining. We also measured serum P1NP (procollagen type 1 N-terminal propeptide) as an early osteoblast differentiation marker, osteocalcin as a late osteoblast differentiation marker, and inflammatory markers.There were significantly more circulating osteoblast-lineage cells in patients than in controls. The number of circulating osteoblast-lineage cells and optical density of Alizarin red S staining decreased 14 weeks after infliximab therapy (p=0.028); serum level of P1NP decreased, but that of osteocalcin increased (p=0.002 and 0.007, respectively).Our data reveals that first, the circulating osteoblast-lineage cells are recoverable and increased in AS patients, and also that they decrease after infliximab therapy; second, infliximab therapy resolves early inflammation, but allows mature osteoblast differentiation in late inflammation. The culture of osteoblast-lineage cells in peripheral blood may be a candidate for a new modality with which to study spondylitis and other autoimmune diseases.

Objectives To compare the pharmacokinetics (PK), safety and efficacy of innovator infliximab (INX) and CT-P13, a biosimilar to INX, in patients with active ankylosing spondylitis (AS). Methods Phase 1 randomised, double-blind, multicentre, multinational, parallel-group study. Patients were randomised to receive 5 mg/kg of CT-P13 (n=125) or INX (n=125). Primary endpoints were area under the concentration-time curve (AUC) at steady state and observed maximum steady state serum concentration (C max,ss ) between weeks 22 and 30. Additional PK, efficacy endpoints, including 20% and 40% improvement response according to Assessment in Ankylosing Spondylitis International Working Group criteria (ASAS20 and ASAS40), and safety outcomes were also assessed. Results Geometric mean AUC was 32 765.8 μgh/ml for CT-P13 and 31 359.3 μgh/ml for INX. Geometric mean C max,ss was 147.0 μg/ml for CT-P13 and 144.8 μg/ml for INX. The ratio of geometric means was 104.5% (90% CI 94% to 116%) for AUC and 101.5% (90% CI 95% to 109%) for C max,ss . ASAS20 and ASAS40 responses at week 30 were 70.5% and 51.8% for CT-P13 and 72.4% and 47.4% for INX, respectively. In the CT-P13 and INX groups more than one adverse event occurred in 64.8% and 63.9% of patients, infusion reactions occurred in 3.9% and 4.9%, active tuberculosis occurred in 1.6% and 0.8%, and 27.4% and 22.5% of patients tested positive for anti-drug antibodies, respectively. Conclusions The PK profiles of CT-P13 and INX were equivalent in patients with active AS. CT-P13 was well tolerated, with an efficacy and safety profile comparable to that of INX up to week 30.

Carrier woman of Duchenne muscular dystrophy (DMD) can mimic the inflammatory myositis in presenting symptoms. Two diseases should be differentiated by the clinical history, muscle biopsy and genetic study. There are few reports in which both histochemical and genetic study showed the possible link of overlapping inflammatory pathophysiology with dystrophinopathy. We report a 40-yr-old woman who presented with subacute proximal muscle weakness and high serum level of creatine kinase. She had a history of Graves' disease and fluctuation of serum liver aminotransferase without definite cause. MRI, EMG and NCV were compatible with proximal muscle myopathy. Muscle biopsy on vastus lateralis showed suspicious perifascicular atrophy and infiltration of mono-macrophage lineage cells complicating the diagnosis. Dystrophin staining showed heterogeneous diverse findings from normal to interrupted mosaic pattern. Multiple ligation probe amplification and X chromosome inactivation test confirmed DMD gene deletion mutation in exon 44 and highly skewed X inactivation.

Background/Aims: Osteoporotic fractures are an important comorbidity with rheumatoid arthritis (RA). We determined the overall fracture risk as assessed by the World Health Organization (WHO)'s FRAX tool in Korean patients with seropositive RA. Additionally, we compared treatment eligibility according to the criteria of the Korean Health Insurance Review Agency (HIRA), FRAX, and the National Osteoporosis Foundation (NOF). Methods: Postmenopausal women and men ≥ 50 years of age with seropositive RA were recruited from one rheumatism center in Korea. The FRAX score was estimated using the Japanese model. Patients were classified as eligible for treatment using the HIRA, NOF, and FRAX thresholds for intervention. Results: The study of 234 patients included 40 men (17%). The mean age was 60 ± 9 years, and 121 (52%) patients had osteoporosis according to the WHO criteria. The overall median 10-year fracture risk was 13% for major osteoporotic fractures and 3.5% for hip fractures. HIRA guidelines identified 130 patients (56%) eligible for treatment, FRAX included 126 patients (54%), and 151 patients (65%) were included according to NOF guidelines. Older patients with a greater number of risk factors were included by FRAX compared to HIRA. The overall concordance between HIRA and FRAX, expressed as the kappa index, was 0.67, but was as low as 0.44 when limited to patients ≥ 60 years of age. Conclusions: One-half of the patients had osteoporosis requiring treatment. RA patients have a high risk of fracture, and the adoption of a risk-scoring system should be considered. (Korean J Intern Med 2010;25:436446)

Raynaud's phenomenon is characteristic three-phase color change of digits that occurs when hands are exposed to cold and subsequently rewarmed. Raynaud's phenomenon has many possible causes, but evaluation tends to focus on a few notorious etiologies, such as, connective tissue diseases. Thus, having reached a diagnosis, detailed physical exam to rule out other possible causes is often not performed. The authors present a case of mixed connective tissue disease (MCTD) and Takayasu's arteritis overlap in a woman, who showed Raynaud's phenomenon as an initial manifestation. She was first diagnosed as having MCTD, but her treatment did not improve the persistent Raynaud's phenomenon. Several years later, follow-up chest CT showed underlying Takayasu's arteritis and a subsequent physical examination revealed that typical abnormalities consistent with Takayasu's arteritis were present. The authors advocate thorough history taking and complete physical examinations on a routine basis to help unearth other underlying causes.

ObjectivesTo investigate the efficacy and safety of switching from infliximab reference product (RP) to its biosimilar or maintaining biosimilar treatment in patients with ankylosing spondylitis (AS).MethodsThis open-label extension study recruited patients with AS who completed a 54-week, randomised controlled study comparing CT-P13 with RP (PLANETAS). CT-P13 (5 mg/kg) was administered intravenously every 8 weeks from week 62 to week 102. Efficacy end points included the proportion of patients achieving Assessment of SpondyloArthritis international Society (ASAS)20. Antidrug antibodies (ADAs) were measured using an electrochemiluminescent method. Data were analysed for patients treated with CT-P13 in the main PLANETAS study and the extension (maintenance group) and those who were switched to CT-P13 during the extension study (switch group).ResultsOverall, 174 (82.9%) of 210 patients who completed the first 54 weeks of PLANETAS and agreed to participate in the extension were enrolled. Among these, 88 were maintained on CT-P13 and 86 were switched to CT-P13 from RP. In these maintenance and switch groups, respectively, ASAS20 response rates at week 102 were 80.7% and 76.9%. ASAS40 and ASAS partial remission were also similar between groups. ADA positivity rates were comparable (week 102: 23.3% vs 27.4%). Adverse events led to treatment discontinuation during the extension study in 3 (3.3%) and 4 (4.8%) patients, respectively.ConclusionsThis is the first study to show that switching from RP to its biosimilar CT-P13 is possible without negative effects on safety or efficacy in patients with AS. In the maintenance group, CT-P13 was effective and well tolerated over 2 years of treatment.Trial registration numberNCT01571206; Results.

To the Editor, Systemic sclerosis (SSc) is a multisystem autoimmune disease characterized by microvascular disease and fibrosis. Despite advances in its early diagnosis, the mortality rate associat...

Polyarteritis nodosa (PAN) related to hepatitis B is an uncommon vasculitis that is sometimes associated with the rapid progression of distal ischemia. A few recent reports have proposed the use of antiviral therapy. However, there is not yet a consensus for the standard treatment of this disease entity and none of these treatments have been focused on fast symptomatic improvement. We describe here a 39-year-old female patient with PAN related to hepatitis B infection who completely recovered from the acutely progressing ischemic manifestations of her distal extremities with the use of alprostadil infusion (prostaglandin E1). The reactivation of her hepatitis B infection after glucocorticoid and cyclophosphamide therapy was successfully managed by the antiviral lamuvudine therapy. Most importantly, the vasodilator together with the conventional therapy may be desirable in the early stages of the disease before irreversible ischemic tissue damage can occur.

Purpose: This study was conducted to examine the changing patterns of knowledge related to disease, medication adherence, and self-management and to determine if outcomes were more favorable in the experimental group than in the comparison group through 6 months after providing a web-based self-management intervention. Methods: A non-equivalent control group quasi-experimental design was used and 65 patients with gout, 34 in experimental group and 31 in comparison group, were selected from the rheumatic clinics of two university hospitals. Data were collected four times, at baseline, at 1 month, 3 months, and 6 months after the intervention. Results: According to the study results, the changing patterns of knowledge and self-management were more positive in the experimental group than in the control group, whereas difference in the changing pattern of medication adherence between two groups was not significant. Conclusion: The results indicate that the webbased self-management program has significant effect on improving knowledge and self-management for middle aged male patients with gout. However, in order to enhance medication adherence, the web-based intervention might not be sufficient and other strategies need to be added.

Background Systemic sclerosis (SSc) is a complex multi-organ autoimmune disease with chronic and heterogeneous clinical manifestations. There is an unmet need for a new biomarker for early diagnosis and classification of SSc. Recent technical advancements have indicated several biomarkers for SSc; among these, platelet factor 4 (PF4), also known as CXCL4, was suggested by a large-cohort proteomic study 1 . PF4 is a chemokine released from activated platelets and is involved in coagulation, inflammation, and angiogenesis, which are influential in SSc pathogenesis. Therefore, PF4 may be an effective biomarker for SSc. Objectives To investigate the efficacy of PF4 as a biomarker for the diagnosis, activity and severity of patients with SSc. Methods Thirty-nine SSc patients (36 female and 3 male; mean age, 58.8±10.42 years; mean disease duration, 7.15±3.92 years; 11 diffuse cutaneous SSc cases and 28 limited cutaneous SSc cases) and 30 healthy controls (HC; 25 female and 5 male; mean age, 46.43±14.43 years) were enrolled. To estimate the circulating PF4 level, levels of platelet poor plasma (PPP) PF4 as well as serum PF4 were measured using an ELISA kit (R&D, Minneapolis, USA). SSc patients were divided into 2 subgroups according to disease activity and based on the presence/absence of interstitial lung disease (ILD), pulmonary hypertension, digital ulcers, and autoantibodies (anti-centromere Ab and anti-Scl70 Ab). Differences between SSc and HC groups were compared by Student9s t -test, and the subgroups were compared using the Mann-Whitney test. Predictive values of serum PF4 and PPP PF4 for SSc diagnosis were evaluated by the area under the receiver operating characteristic curve (AUROC). Results Serum PF4 levels of SSc were lower than those of HC (SSc, 5143.3±1777.5 ng/mL; HC, 5927.4±1348.5 ng/mL; p =0.048) but no significant differences were observed PPP PF4 levels (SSc, 407.2±486.6 ng/mL; HC, 297.3±141.5 ng/mL; p =0.187) between SSc patients and controls. Moreover, no significant differences were observed between active and inactive SSc subgroups and between subgroups with/without ILD, pulmonary hypertension, digital ulcers, and autoantibodies. The AUROC for serum PF4 and PPP PF4 levels was 0.628 (0.497–0.76, cuff of value 3998.5 ng/mL) and 0.491 (0.367–0.65, cuff of value 511.1 ng/mL), respectively. Conclusions In Korean patients with SSc, both serum PF4 and PPP PF4 levels are not efficient biomarkers for SSc diagnosis and do not appear to be associated with clinical activity and severity. References van Roon JA, Tesselaar K, Radstake TR. Proteome-wide analysis and CXCL4 in systemic sclerosis. N Engl J Med. 2014;370(16):1563–4. Disclosure of Interest None declared

Background Systemic sclerosis (SSc) is a complex multi-organ autoimmune disease that is caused by inflammation, vasculopathy and fibrosis. Clinical heterogeneity, unpredictable course, high mortality and resistance to treatment make physicians still frustrated. Recently, there are unmet needs of useful biomarkers for diagnosis, disease activity and severity of SSc. Metabolomics is expected to be a useful tool for the identification of biomarkers and new therapeutic targets. Several researchers have applied metabolomics to autoimmune diseases such as systemic lupus erythematosus, and rheumatoid arthritis. Objectives To identify the biomarker candidates for the diagnosis of SSc using metabolomic analysis. Methods Fifty-five patients (48 females (87%); mean age 59.30 ± 11.44 years; disease duration 6.92 ± 4.36 years; 11 diffuse cutaneous SSc, 44 limited cutaneous SSc) and thirty age, gender matched healthy controls (HCs) were enrolled. Serum samples after 8 h of fasting were stored at -80° and analysed using nuclear magnetic resonance (NMR)-based metabolomics. Results Multivariate analysis showed metabolic differences between SSc and HCs using partial least squares discrimination analysis (PLS-DA: R2Y=0.654, Q2=0.482) and orthogonal partial least squares discrimination analysis (OPLS-DA: R2Y=0.83, Q2=0.674) (Figure 1). We identified nine discriminatory metabolites (p Conclusions There are considerable differences in the serum metabolomic characteristics between SSc and HCs. We expect that metabolomic analysis can be a useful tool for identification of potential diagnostic biomarkers of SSc. Disclosure of Interest None declared

Objective. This study examines the effects of tumor necrosis factor (TNF) blockade on markers of bone metabolism in peripheral blood from active rheumatoid arthritis (RA) patients. Methods. Eighteen patients (16 women, 2 men) aged 50 years (range 37-63 years), with persistently active RA (mean disease duration 7 years) were studied. Most took methotrexate (mean dose 12.5 mg) and all except one received corticosteroid (mean dose 5.7 mg). Four were treated with etanercept, eight received adalimumab and six received infliximab. Before and six months after taking TNF blockers, blood was sampled to obtain peripheral blood mononuclear cells (PBMCs), and serum bone turnover markers and acute phase reactants were measured. PBMCs were seeded and cultured to produce osteoblastic lineage cells and osteoclasts. Results. The formation of calcified nodules by osteoblastic lineage cells from PBMC increased from 205.7±196.3 μmol/well at the baseline to 752.5±671.9 μmol/well after TNF blockade (p＜0.024). The serum levels of bone formation markers, including bone specific alkaline phosphatase and osteocalcin also increased. The number of circulating osteoclasts and area of bone resorption pits made by osteoclasts were reduced after TNF blockade. Conclusion. The activity of circulating osteoblastic lineage cells increased after TNF blockade, whereas peripheral osteoclastogenesis tended to be suppressed. This is the first study of cultured human peripheral osteoblastic lineage cells in RA patients. Given that peripheral bone formation is difficult to study using radiologic methods, culture of these cells may provide a new modality for studying bone metabolism in RA. (J Rheum Dis 2016;23:356-362)

Familial Mediterranean fever (FMF) is an autosomal recessive disease characterized by recurrent episodes of fever accompanied by peritonitis, pleuritis, arthritis, or erysipelas-like erythema. It is known to occur mainly among Mediterranean and Middle Eastern populations such as non-Ashkenazi Jews, Arabs, Turks, and Armenians. FMF is not familiar to clinicians beyond this area and diagnosing FMF can be challenging. We report a 22-yr old boy who presented with fever, arthalgia and abdominal pain. He had a history of recurrent episodes of fever associated with arthalgia which would subside spontaneously or by antipyretics. Autosomal recessive periodic fever syndromes were suspected. Immunoglobulin D (IgD) level in the serum was elevated and DNA analysis showed complex mutations (p.Glu148Gln, p.Pro369Ser, p.Arg408Gln) in the MEFV gene. 3D angio computed tomography showed total thrombosis of splenic vein with partial thrombosis of proximal superior mesenteric vein, main portal vein and intrahepatic both portal vein. This is a case of FMF associated with multiple venous thrombosis and elevated IgD level. When thrombosis is associated with elevated IgD, FMF should be suspected. This is the first adult case reported in Korea.

Angioimmunoblastic T cell lymphoma (AITL) is a rare non-Hodgkin lymphoma that presents with pro- found immune dysfunction and immunodeficiency. The clinical and laboratory findings associated with AITL are similar to those of rheumatic disease, and AITL has been reported to be concurrent in patients with several rheumatic diseases. We present one case of AITL occurring in a patient with ankylosing spondylitis (AS) after treatment with etanercept. Constitutional symptoms and aggravation of peripheral arthritis in elderly AS patients may be due not only to flare-ups of AS but also to other complicating diseases, such as lymphoma. Although the occurrence of lymphoma in AS patients treated with etanercept has only rarely been reported, clinicians should keep in mind that instances of aggravation of peripheral arthritis in elderly AS patients occurring after immunosuppressant treatment may be due to other complicating systemic diseases such as AITL, rather than the rheumatic disease itself. Further study is needed in order to investigate whether or not using a TNF-a blocker such as etanercept increases the risk of lymphoma, especially for cases associated with Epstein- Barr virus.

Behcet's disease (BD) is a form of systemic vasculitis with the classic triad of recurrent oral and genital ulcers along with uveitis. In BD, muscular involvement is very rare. We report a case of muscular involvement in BD with characteristic findings using ultrasonography, computed tomography, and magnetic resonance imaging.

(1) To compare the serum levels of Dickkopf-1 (DKK-1) and bone biomarkers in patients with ankylosing spondylitis (AS) and healthy controls. (2) To examine the effects of anti-tumor necrosis factor-α (TNF-α) therapy for 3 months on bone biomarkers in patients with AS. We measured the levels of DKK-1, osteocalcin, osteoprotegerin, and C-terminal telopeptide of type I collagen (CTX-1) in patients with AS and in healthy controls at baseline and 3 months after initiating anti-TNF-α therapy in AS patients. Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) scores were also measured before and after anti-TNF-α therapy in AS patients. Serum levels of DKK-1 were significantly lower in the AS patients than in the controls (P < 0.0001). Osteocalcin and osteoprotegerin levels were significantly higher in the AS patients than in the controls (P < 0.0001). Serum levels of DKK-1 were not changed after the 3-month anti-TNF-α therapy. Osteocalcin level increased (P < 0.0001), osteoprotegerin level and BASDAI scores decreased (P = 0.025 and P < 0.0001, respectively) significantly after the 3-months anti-TNF-α therapy. Serum DKK-1 level was lower in patients with AS than in healthy controls and did not change after 3 months of anti-TNF-α therapy in the AS patients despite the marked improvement in BASDAI scores. These findings suggest the low serum DKK-1 level is related to the pathogenesis of new bone formation in AS, which is resistant to TNF-α blocking therapy.

We investigated acute effects of intermittent large dose bisphosphonate therapy in osteoporotic patients. Peripheral blood mononuclear cells were incubated with alendronate (100 microM) for 18 hr, in vitro and cytokine expressions were measured by real-time RT-PCR. Pamidronate 30 mg was administered on 26 osteoporotic patients; and acute phase reactants, inflammatory cytokines and bone biomarkers were measured. The in vitro study showed significant increase in mRNA expression of IL-6, TNF-alpha and IFN-gamma. A notable rise in serum C-reactive protein (CRP) was observed over 3 days after pamidronate infusion (P=0.026). Serum levels of TNF-alpha, IL-6 and IFN-gamma were also significantly increased (P=0.009, 0.014, 0.035, respectively) and the increase in IL-6 levels were strongly correlated with CRP levels (P=0.04). Serum calcium and c-telopeptide levels rapidly decreased after the treatment (P=0.02

Objective.We introduce the use of 99mTc-hydroxymethylene diphosphonate (HDP) digital blood flow scintigraphy to diagnose Raynaud’s phenomenon (RP).Methods.Fifty-seven patients with RP and 60 healthy controls were recruited. One hand was chilled by immersion into water at 4°C, and then an intravenous bolus of 740 MBq of 99mTc-HDP was injected. The radioactivity from the second to the fifth fingers of both hands was recorded. Acquisition was performed at a rate of one frame per 2 seconds until 155 frames. We calculated 4 ratios by comparing the activity curves of the chilled hand with those of the ambient hand.Results.The chilled to ambient hand ratio of the initial slope was significantly lower in the patients with RP (0.28 ± 0.18) than in the controls (0.78 ± 0.20) (p < 0.001). The chilled to ambient hand ratio of the first peak height, 30-second area under the curve, and blood pool uptake were also lower in the patients with RP than in controls (p < 0.001 for each). The initial slope ratio of 0.51, used as a cutoff value, showed a sensitivity of 91.2% and specificity of 93.3%. The loss of the initial spike curve, the presence of a slowly progressing radioactivity curve, and the inhomogeneous radioactivity uptake in the blood pool image in either hand were characteristic findings of the patients with RP (p < 0.001).Conclusion.99mTc-HDP digital blood flow scintigraphy after one-hand chilling is a noninvasive, accurate, and quantitative method to evaluate RP.

Background Many authors tried to elucidate the relationship among the inflammation, osteoblast activity or new bone formation, and adipogenesis in patients with ankylosing spondylitis (AS). But the results were disappointing. Objectives We investigated the relationship among the inflammation, osteoblast activity or new bone formation, and adipogenesis in patients with AS by novel cell culture technique of osteoblast in peripheral blood and other methods. Methods Male sixteen individuals with AS were enrolled. They met modified New York criteria and were candidates for infliximab therapy. Sex and age matched nineteen controls were also recruited. Peripheral blood mononuclear cells were collected and cultured in growth medium. Once cell multi-layering has been observed (about 7 days), cells were transferred to differentiation medium and cultured for 3 weeks. Cells were then fixed and stained with alizarin S stain to detect any calcified nodules. The optical density (OD) of alizarin S was measured for quantitative analysis. We evaluated the numbers, the differences and relationship of 1) the numbers of circulating osteoblast precursors in peripheral blood, 2) the OD of alizarin S red staining of circulating osteoblast precursors, 3) P1NP (total procollagen type 1 N-terminal propeptide), c-terminal telopeptide (CTX), osteocalcin, triglyceride, low density lipoprotein cholesterol (LDL), apolipoprotein A-1, apolipoprotein B, lipoportein (a) with enzyme linked immunosorbent assay (ELISA), 4) erythrocyte sedimentation rate (ESR), c-reactive protein (CRP), Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) before and after 14 week infliximab therapy, 5) bone densitometry (BMD) before infliximab therapy in patients with AS. Results The number of osteoblast precursor cells and optic density of alizarin S were decreased after infliximab therapy (p=0.028 for optic density of alizarin S). The serum level of P1NP was decreased after infliximab therapy (p=0.002). The serum level of triglyceride was tend to increased, but that of lipoprotein (a) was decreased (p=0.07, p=0.007 separately). There were positive correlation between the BASDAI and the serum level of triglyceride (r =0.666, p=0.005), ESR and lipoprotein (a) (r =0.594, p=0.015), CRP and CTX (r =0.648, p=0.012), CRP and P1NP (r =0.631, p=0.016); negative correlation between BASDAI and femur total T score of BMD (r = -0.79, p=0.006) before infliximab therapy. They showed positive correlation between the difference of the serum level of LDL and that of osteocalcin (r =0.566, p=0.022), Alizarin S OD and apoprotein B (r =0.943, p=0.005), Alizarin S OD and osteocalcin (r =0.829, p=0.042); negative correlation between the difference of the serum level of LDL and ESR (r = -0.614, p=0.011) before and after infliximab therapy. Conclusions The circulating osteoblasts in peripheral blood and the serum level of P1NP were decreased significantly after 14 weeks of infliximab therapy. This result could be indirect evidence that infliximab therapy appeared to diminish osteoblast activity or new bone formation in patients with AS. There were strong relationship among inflammation, osteoblast activity, and adipogenesis before and after infliximab therapy in patients with AS. Disclosure of Interest S.-R. Kwon Grant/research support from: From Celltrion, Korea, Republic of, W. park: None declared, M.-J. Son: None declared, M.-J. Lim: None declared, K.-H. Jung: None declared

Background Digital ulcer (DU) is a significant cause of pain, functional disability and quality-of-life impairment in patients with systemic sclerosis (SSc). DU can occur even in patients with very early/early SSc (called the “window of opportunity” of SSc). Therefore, the identification of risk factors of DU can improve the SSc outcome. Several large cohort studies have reported risk factors of DU in SSc [1]. However, the risk factors of DU in patients with SSc have not been described in Korea yet. Objectives To determine the prevalence and risk factors of DU in Korean patients with SSc. Methods Ninety consecutive SSc patients with at least 6 months of follow-up were enrolled from January 2014 to December 2014 in tertiary hospital rheumatism center. Demographic data, clinical characteristics, internal organ involvements, comorbidities, laboratory findings, and disease-specific factors were obtained through medical records and patients interviews, retrospectively. Results Thirty-seven patients (41%) had a history or present digital ulceration and 43% of them had recurrent DU. Patients with DU were thin, had higher modified Rodnan skin score (mRSS), showed frequent pigmentation, microsomia, finger flexion contracture, acroosteolysis and calcinosis. They had anti-Scl 70 antibody, advanced nailfold capillary changes (active and late pattern) and interstitial lung disease more frequently than in patients without DU (Table 1.). In a multiple logistic regression analysis, mRSS (OR =1.178, 95% C.I. =1.06-1.31, p-value =0.002) was the sole risk factor of DU. A nailfold capillary microscopic finding was the only risk factor of recurrence of DU (p-value =0.025). Conclusions In Korean SSc patients, Rodnan skin score is a risk factor of DU and advanced nailfold capillary change is a risk factor for recurrent DU. We need more attention to treat those SSc patients with high mRSS and advanced nailfold capillary change. References Silva I, Almeida J, Vasconcelos C. A PRISMA-driven systematic review for predictive risk factors of digital ulcers in systemic sclerosis patients. Autoimmun Rev. 2015;14(2):140-152 Disclosure of Interest None declared

SAPHO syndrome, characterized by synovitis, acne, pustulosis, hyperostosis, and osteitis is rare compared to other spondyloarthropathies. It is also difficult to diagnose, and treatment methods have not yet been fully identified. Approximately 72% of patients are diagnosed with at least one other disease before a final diagnosis of SAPHO syndrome. In addition, SAPHO syndrome is subject to a delayed diagnosis period of 4.5 to 9.1 years. Medications such as non-steroidal anti-inflammatory drugs, disease-modifying anti-rheumatic drugs, and tumor necrosis factor inhibitors are used in treatment of SAPHO syndrome. Bisphosphonate is also used for refractory SAPHO syndrome; however, most reports on this relate to intravenous injection of medication. The authors experienced and subsequently reported on a case involving a patient with SAPHO syndrome accompanied by fracture and infection of the left second finger who was treated with the oral biphosphonate, alendronate. (J Rheum Dis 2015;22:313-316)

Eosinophilic granulomatosis with polyangiitis (EGPA), previously called Churg-Strauss syndrome, is an anti-neutrophil cytoplasmic antibody associated vasculitis, accompanied by asthma, hypereosinophilia, nonfixed pulmonary infiltrates, and sinusitis. Peripheral neuropathy is common in patients with EGPA; however, a few cases of EGPA with central nervous system (CNS) involvement have been reported. A 45-year-old female referred for right side weakness and posterior neck pain was diagnosed as EGPA with subarachnoid hemorrhage and mononeuritis multiplex. She was effectively treated with a high dose glucocorticoid, cyclophosphamide, and intravenous immunoglobulin. EGPA with CNS involvement is uncommon and causes significant morbidity and mortality. Therefore more rapid and accurate diagnostic evaluation may be required. EGPA should be considered in patients with neurological symptoms and hypereosinophilia. (J Rheum Dis 2015;22:190-194)

We wanted to see whether the active inflammation in Behcet's disease (BD) can cause a thrombotic disorder by decreasing the protein S (PS) activity, and we evaluated the relationship between the decreased PS activity and the disease activity of BD. We included 122 patients with BD whose PS activity levels were measured. In 51 patients, the PS activity was measured again when there were changes in the number of items of "The Behcet's Disease Current Activity Form (BDCAF)". The thrombosis rate was 2.5% (3/122), and the PS activity was low in all three of the patients with thrombosis. The incidence of low PS activity in the total 122 BD patients was 27% (33/122). The incidence of the low PS activity in the active BD patients was 33.7% (31/92), and this was significantly more frequent than in the inactive BD patients, (6.7%, 2/30) (chi(2)-test, P value = 0.0038). The decrease of PS activity had good correlation with the increase of the number of BDCAF items (r = -0.351, P value = 0.012). The PS activity decrease is related to the BD activity. The low PS activity can be the risk factor for thrombotic disorder and also the activity marker for BD and other inflammatory diseases.

To the Editor: Various musculoskeletal manifestations can develop in a patient receiving chemotherapy for malignancy1,2,3,4,5,6. We previously examined the occurrence and prognosis of chemotherapy-related arthropathy (CRA) in 18 patients with a variety of cancers with favorable responses after a mean of 3 months’ treatment with nonsteroidal antiinflammatory drugs (NSAID) and disease-modifying antirheumatic drugs (DMARD)7. However, that study was limited by the small number of enrolled patients and its retrospective design. Therefore, on the basis of our previous report, a multicenter randomized open-label pilot study was designed to evaluate whether adding hydroxychloroquine (HCQ) to NSAID modifies disease activity in CRA. Our study was conducted in accord with the ethical principles of the Declaration of Helsinki and was approved by the institutional review boards of the hospitals involved. We obtained written informed consent from all participants. We registered our trial in the database of the Clinical Research Information Service (http://ncrc.cdc.go.kr/cris: KCT0000160) as a randomized clinical trial (RCT). The open-labeled RCT was carried out at 7 tertiary hospitals from April 2007 to June … Address correspondence to Dr. C-H. Suh, Department of Rheumatology and BK21 Division of Cell Transformation and Restoration, Ajou University School of Medicine, San 5, Wonchon-dong, Yeongtong-gu, Suwon, South Korea 443-721. E-mail: chsuh{at}ajou.ac.kr

Background/Aims Our aim was to assess whether short-term treatment with soluble tumor necrosis factor (TNF) receptor affects circulating markers of bone metabolism in rheumatoid arthritis (RA) patients. Methods Thirty-three active RA patients, treated with oral disease-modifying antirheumatic drugs (DMARDs) and glucocorticoids for > 6 months, were administered etanercept for 12 weeks. Serum levels of bone metabolism markers were compared among patients treated with DMARDs at baseline and after etanercept treatment, normal controls and naive RA patients not previously treated with DMARDs (both age- and gender-matched). Results Bone-specific alkaline phosphatase (BSALP) and serum c-telopeptide (CTX)-1 levels were lower in RA patients treated with DMARDs than in DMARD-naive RA patients. After 12 weeks of etanercept treatment, serum CTX-1 and sclerostin levels increased. In patients whose DAS28 improved, the sclerostin level increased from 1.67 ± 2.12 pg/mL at baseline to 2.51 ± 3.03 pg/mL, which was statistically significant (p = 0.021). Increases in sclerostin levels after etanercept treatment were positively correlated with those of serum CTX-1 (r = 0.775), as were those of BSALP (r = 0.755). Conclusions RA patients treated with DMARDs showed depressed bone metabolism compared to naive RA patients. Increases in serum CTX-1 and sclerostin levels after short-term etanercept treatment suggest reconstitution of bone metabolism homeostasis.

Although it is difficult to reach a diagnosis in patients who complain of pain or sensitivity to cold in their hands, Raynaud's phenomenon is most often suspected in such cases. Symptoms of Raynaud’s phenomenon include pallor, cyanosis, and redness following cold exposure. Glomus tumors can also increase patients’ sensitivity to cold. In this case, our patient complained of symptoms indicative of Raynaud’s phenomenon. Although treatment of Raynaud’s phenomenon improved the symptoms, pain persisted in the fourth finger of the left hand. We diagnosed the patient with a glomus tumor and, after surgical treatment, the patient’s symptoms improved. Here, we have also reviewed and discussed a number of reports of glomus tumors associated with Raynaud’s disease. Diagnosing a glomus tumor in the hand may take some time, and the diagnosis could be further delayed if accompanied by Raynaud’s phenomenon. Although glomus tumors are rare, we suggest that clinical awareness is important for early diagnosis and treatment. (Korean J Med 2014;87:765-770)

Background Interleukin-6 (IL-6), a proinflammatory cytokine, is thought to play a major pathological role in rheumatoid arthritis (RA). Tocilizumab is humanized anti IL-6 receptor monoclonal antibody which has been shown to improve signs and symptoms of RA. Objectives To investigate the efficacy and safety of tocilizumab in a Korean population. Methods This clinical trial was a 24-week phase III, randomized, double-blind, placebo-controlled, multicenter trial with two treatments arms and conducted from October, 2009 to October, 2010. The eligible patients had moderate to severe active RA, inadequately responding to MTX (or DMARDs). Tocilizumab at a dose of 8mg/kg or placebo were administered in a blinded manner, intravenously every 4 weeks, with stable dose of methotrexate (MTX) or other DMARDs. Results Total of 80 patients completed 24 week’s treatment with 40 patients in each treatment arm. At week 24, proportions of ACR 20, ACR 50, DAS28 remission and EULAR response were significantly higher in Tocilizumab group than in placebo group ( p p =0.0002, p =0.0002 and p p =0.0002, p =0.0055, respectively). Adverse drug reactions were more frequent in Tocilizumab group than in placebo group as follows; increased SGPT (21%), granulocytopenia (17%), leukocytopenia (15%), hypercholesterolemia (13%), pharyngitis (13%), and increased SGOT (10%). There were more incidences of serious adverse drug reactions in Tocilizumab group than in placebo group, but it was not significant ( p =0.0548). Conclusions In Korean population, administration of tocilizumab 8 mg/kg in combination with MTX (with or without other DMARDs) reduced RA activity significantly. Most of RA activity parameters including ACR 20, ACR 50, DAS 28 remission and EULAR response were achieved more frequently in Tocilizumab group than in placebo group. Tocilizumab was generally well tolerated since no safety issue was observed during the study. This study was financially supported by JW Pharmaceutical Co. (KFDA clinical trial-146). References Maini RN, et al. Arthritis Rheum. 2006;54(9):2817-29. Jones G, et al. Ann Rheum Dis. 2010;69(1):88-96. Disclosure of Interest None Declared

Background The thermography measures blood flow indirectly by measuring skin surface temperature [[1][1]]. The characteristic of Raynaud phenomenon is cold-induced vasoconstriction in distal extremities which in turn, lowers skin temperature. Objectives The aim of this study was to determine whether the infrared thermography on hands and feet is useful for diagnosis of Raynaud’s phenomenon (RP). Methods Fifty-seven patients with RP (primary RP, n=33; secondary RP, n=24) and 120 healthy volunteers were recruited. After acclimation to room temperature for 30 minutes, patients were evaluated by thermal imaging of the palmar aspects of hands and dorsal aspects of feet. Temperature drop from palm (center) to each finger and from foot dorsum (center) to each toe were compared between RP patients and controls. Results Temperature drop from palm to fingers and from foot dorsum to toes differed significantly between RP patients and controls. Area under the curve analysis showed that the temperature difference drop in 1st (big) toe (cutoff value: 3.11°C) best differentiated RP patients from controls (sensitivity : 72% -74%, specificity : 65 - 67%, [Fig. 1][2]). ![Figure][3] Conclusions Thermographic assessment of the skin temperature drop from the foot dorsum to 1st toe is useful for diagnosing RP. It was previously reported that about 90% of patients presented with features of RP of the feet [[2][4]]. Thus it clearly indicates that infrared thermography of the feet as the initial workup of Raynaud phenomenon could provide reliable data for diagnosis. In particular, the 1st toe provided the best thermographic parameter for diagnosis of RP among toes. The 1st toe is larger in size and has more obvious boundaries in imaging, which allows confident location for regions of interest to be drawn. 1. Jones BF. A reappraisal of the use of infrared thermal image analysis in medicine. IEEE Transactions Med Imaging 1998;17:1019–27. 2. La Montagna G et al. Foot involvement in systemic sclerosis: a longitudinal study of 100 patients. Semin Arthritis Rheum. 2002;31:248-55. Disclosure of Interest None Declared [1]: #p-7 [2]: #F1 [3]: pending:yes [4]: #p-8