The indiscriminate use of zinc oxide nanoparticles (ZnO NPs) in daily life can lead to their release into soil environment. These ZnO NPs can be taken up by crops and translocated to their edible part, potentially causing risks to the ecosystem and human health. In this study, we conducted pot experiments to determine phytotoxicity, bioaccumulation and translocation depending on the size (10 - 30 nm, 80 - 200 nm and 300 nm diameter) and concentration (0, 100, 500 and 1000 mg Zn/kg) of ZnO NPs and Zn ion (Zn2+) in bok choy, a leafy green vegetable crop. After 14 days of exposure, our results showed that large-sized ZnO NPs (i.e., 300 nm) at the highest concentration exhibited greater phytotoxicity, including obstruction of leaf and root weight (42.5 % and 33.8 %, respectively) and reduction of chlorophyll a and b content (50.2 % and 85.2 %, respectively), as well as changes in the activities of oxidative stress responses compared to those of small-sized ZnO NPs, although their translocation ability was relatively lower than that of smaller ones. The translocation factor (TF) values decreased as the size of ZnO NPs increased, with TF values of 0.68 for 10 - 30 nm, 0.55 for 80 - 200 nm, and 0.27 for 300 nm ZnO NPs, all at the highest exposure concentration. Both the results of micro X-ray fluorescence (mu-XRF) spectrometer and bio-transmission electron microscopy (bio-TEM) showed that the Zn elements were mainly localized at the edges of leaves exposed to small-sized ZnO NPs. However, the Zn elements upon exposure to large-sized ZnO NP were primarily observed in the primary veins of leaves in the mu-XRF data, indicating a limitation in their ability to translocate from roots to leaves. This study not only advances our comprehension of the environmental impact of nanotechnology but also holds considerable implications for the future of sustainable agriculture and food safety.

Exposure of the soil environment to metal nanoparticles (MNPs) has been extensive because of their indiscriminate use and the disposal of MNP products in various applications. In MNP-amended soil, various crops can absorb the nanoparticles, and accumulation of the MNPs in farm products has potential risks for bioconcentration in humans and livestock. Here, we evaluated the comparative bioaccumulation, translocation, and phytotoxicity of MNPs (ZnO and CuO NPs) and metal ions (Zn(NO3)2 and Cu(NO3)2) in four different crops, namely lettuce, radish, bok choy, and tomato. We carried out pot experiments to evaluate the phytotoxicity in the crops from the presence of MNPs and metal ions. Phytotoxicity from different treatments differed depending on the plant species, and metal types. In addition, exposure to Zn and Cu showed positive dose-dependent effects on their bioaccumulation in each crop. However, there were no significant differences in metal bioaccumulation depending on whether the crops were exposed to MNPs or metal ions. By calculating the bioconcentration factor (BCF) and translocation factor (TF), we were able to estimate the biological uptake and translocation abilities of MNPs and metal ions for each crop. It was found that lettuce and radish had greater BCFs than bok choy and tomato, while bok choy and tomato had higher TFs. Also, the uptake and translocation of Zn were better than those of Cu. However, the values for BCF and TF for each crop showed no significant differences between MNP and metal ion exposure. A micro X-ray fluorescence (μ-XRF) spectrometer analysis demonstrated that only Zn elements appeared in the primary veins and edges of all leaves and the storage root of radish. Our study aims to estimate bioaccumulation, translocation, and the implied potential risks from MNPs accumulated in different plant species.

Background: Long noncoding RNAs (lncRNAs) have recently emerged as important biological regulators and the aberrant expression of lncRNAs has been reported in various diseases including cancer, cardiovascular disease, and diabetes mellitus. However, the role of lncRNAs in the pathogenesis of rheumatoid arthritis (RA) remains unknown. Objectives: Thus, we studied lncRNAs influenced by IL-1, which is one of the key mediators in the pathogenesis of RA, and also investigated whether regulation of NF-κB activation, which is known to be induced by IL-1, could lead to the changes of expression of those lncRNAs. Methods: Fibroblast-like synoviocytes (FLS) were obtained from the knee joints of the patients with RA. The next-generation sequencing (NGS) data were analyzed to identify differentially expressed lncRNAs between unstimulated RA FLS and IL-1-stimulated RA FLS. The expression levels of the top 5 candidates in NGS data were validated by RT-qPCR using extended number of unstimulated RA FLS and IL-1-stimulated RA FLS. IMD-0560, an inhibitor of IκB kinase (IKK) was used for the regulation of NF-κB activation. Activation and inhibition of NF-κB were confirmed by Western blotting. Changed expressions of the lncRNAs were identified by RT-qPCR. Results: NGS analysis revealed up-regulated 30 lncRNAs and down-regulated 15 lncRNAs in IL-1-treated RA FLS compared with unstimulated RA FLS. Top 5 lncRNAs were selected among 30 lncRNAs up-regulated by IL-1 in RA FLS based on fold-change with P-value cutoff. The up-regulated lncRNAs including NR_046035, NR_027783, NR_033422, NR_003133, and NR_049759 were validated by RT-qPCR. IMD-0560 inhibited phosphorylation of IκBα induced by IL-1 in RA FLS. Overexpression of lncRNAs induced by IL-1 was also inhibited by IMD-0560 in RA FLS. Conclusion: Our study revealed that IL-1 increased the expression of NR_046035, NR_027783, NR_033422, NR_003133, and NR_049759 in RA FLS. In addition, the expression of these lncRNAs was regulated by inhibition of NF-κB activation. Thus, our data suggest that the lncRNAs might be involved in the pathogenesis of RA through NF-κB signaling pathway. References: [1]Long noncoding RNAs and human disease. Trends Cell Biol. 2011 Jun;21(6):354-61. [2]A long noncoding RNA mediates both activation and repression of immune response genes. Science. 2013 Aug 16;341(6147):789-92. [3]Long noncoding RNA expression profile in fibroblast-like synoviocytes from patients with rheumatoid arthritis. Arthritis Res Ther. 2016 Oct 6;18(1):227. Disclosure of Interests: None declared

Background High levels of serum immunoglobulin G4 (IgG4) would comprise a useful diagnostic tool in IgG4-related disease, but little information is available about IgG4 in conditions other than IgG4-related disease, including rheumatic diseases. Previous studies indicate that the elevated serum IgG4 in rheumatoid arthritis (RA) is common and disproportional to total IgG. Objectives The aim of study is to evaluate the level of serum IgG4 and IgG4/total IgG ratio in patients with RA. Methods Ninety-six patients with RA and one hundred and thirty-five non-RA controls were enrolled between March 2014 and July 2017. All samples were collected before the treatments. The levels of Serum total IgG and IgG4 were determined by nephelometric assay. The cut-off value of serum IgG4 was 135 mg/dL. Data on clinical variables and disease activity markers, such as numbers of tender and swollen joints, levels of acute phase reactants and disease activity score 28 (DAS28) were recorded in RA patients. We compared the levels of serum IgG4 and the ratio of IgG4/total IgG in rheumatoid arthritis with healthy controls and other rheumatic diseases. This study also investigated the difference the relationship between levels of serum IgG4 and disease activity in RA. Results Among 96 RA patients, the mean of serum IgG4 was 48.0±45.4 mg/dL and 6.3% had elevated serum IgG4. The mean serum IgG4/IgG ratio of RA patients was 3.5%±2.8% (range 0.2%∼16.9%). There was no patient with elevated serum IgG4 in ankylosing spondylitis, systemic lupus erythematosus, Sjogren’s syndrome, and inflammatory myositis. When the patients were divided according to clinical activity, the percentages of the positive serum IgG4 were 25% in active disease group and 4% in low activity group. However, the serum IgG4 levels of the RA patients with active disease activity were not significantly higher than those of the RA patients with low disease activity (58.3±44.3 mg/dL vs. 39.9±30.1 mg/dL). No significant relationship was observed between the ratio of IgG4/total IgG and disease activity. The IgG4 concentrations and total IgG/IgG4 ratios were similar between RA and the other autoimmune diseases (p>0.05). Conclusions Our results showed that elevated serum IgG4 in RA is relatively common. However the presence of the elevated serum IgG4 was not associated with disease activity of RA. Further investigations are needed to explore the clinical significance in a larger study population. References [1] Lin G, et al. Elevation of serum IgG subclass concentration in patients with rheumatoid arthritis. Rheumatol Int2010;30:837–40. [2] Yamamoto M, et al. Value of serum IgG4 in the diagnosis of IgG4-related disease and in differentiation from rheumatic diseases and other diseases. Mod Rheumatol2012;22:419–25. [3] Chen LF, et al. Elevated Serum IgG4 Defines Specific Clinical Phenotype of Rheumatoid Arthritis. Mediators Inflamm2014;2014:635293. Disclosure of Interest None declared

Background Rheumatoid arthritis (RA) is chronic inflammatory disease characterized by persistent synovitis and structural joint damage with T cell-driven inflammation. Tacrolimus suppress activation of T cells through the inhibition of calcineurin. Objectives We evaluated the efficacy and safety of Tacrobell® (Tacrolimus from Chong Kun Dang Pharma Inc.) in Korean active RA patient who had inadequate response to disease-modifying anti-rheumatic drugs (DMARDs) including Methotrexate (MTX). Methods During the study period from Aug. 2012 to Jun. 2015, in this open labeled, multicenter study, 111 patients were enrolled. Patients were in active disease state with Disease Activity Score28 (DAS28) ≥3.2 despite previously taken at least one conventional DMARD including MTX. Patients had wash out period with DMARDs, except MTX. Patients received Tacrobell® during 24 weeks. The initial dose was 1 mg once daily and was increased to 3mg once daily by 1mg, every 4 weeks. The disease activity was measured by the DAS28-ESR at 4, 8, 16, 24-week after the add on Tacrobell®. Simplified Disease Activity Index (SDAI), Korean Health Assessment Questionnaire (KHAQ)-20, Erythrocyte Sedimentation Rate (ESR), C-Reactive Protein (CRP) and the safety was assessed. Results Data from 97 patients were evaluated in full set analysis. At week-24, EULAR response rate were 83.5% (81 of 97) with improvements from week-16 in 74.2% (72 of 97). Mean DAS28-ESR was continuously decreased of 5.64 at baseline, 4.14 (±1.22, p<0.001) at week-16 and 3.66 (±1.39, p<0.001) at week-24. Efficacy rates according to SDAI were 89.7% (87 of 97) and KHAQ-20 score decreased -2.42 (±4.37, p<0.001) from baseline 7.27 (±4.59) at week-24. Mean ESR was decreased -10.97 (±24.16, p<0.001) at week-16, -14.77 (±24.57, p<0.001) at week-24 from baseline 46.05 (±23.22). Mean CRP was decreased from 2.86 (±7.85, p=0.0578) at baseline to 1.34 (±3.02, p=0.0367) at week-24. The most common adverse events were in gastrointestinal (18 of 108; 16.679%) and respiratory disorder (12 of 108; 16.67%). In serious adverse events (6 of 108, 5.56%), two cases (pneumonia, high glucose level) were related with Tacrobell® and recovered with treatment. At laboratory exam, no abnormal findings with increased BUN or Cr as known common Tacrolimus side effect. Systolic blood pressure increased 2.12 mmHg at week-8. Conclusions This study demonstrated the efficacy of add on Tacrobell® therapy to MTX in patients with active RA. References Tsutomu T., et al (2013) Post-marketing surveillance of the safety and effectiveness of tacrolimus in 3,267 Japanese patients with rheumatoid arthritis Mod Rheumatol.; 24(1):8–16 Takeyuki K., et al (2013) Long-term therapeutic effects and safety of tacrolimus added to methotrexate in patients with rheumatoid arthritis Rheumatol Int.; 33:871–877 Mariko K., et al (2013) Efficacy of adjunct tacrolimus treatment in patients with rheumatoid arthritis with inadequate responses to methotrexate Mod Rheumatol.; 23:788–793 Kawai S., et al. (2011) Efficacy and safety of additional use of tacrolimus in patients with early rheumatoid arthritis with inadequate response to DMARDs-a multicenter, double-blind, parallel-group trial Mod Rheumatol.; 21(5):458–68 Disclosure of Interest None declared

Background Behcet9s disease is a chronic, systemic vasculitis that can involve all sizes of blood vessels. Those complicated symptoms lead to the patient9s impairment of life quality as well as psychological problems. Sleep disturbance is one of the most particular concerns in patients with Behcet9s disease. It has been known that the disease activity of rheumatoid arthritis and ankylosing spondylosis is associated with the sleep quality. However, studies about the sleep quality of patients with Behcet9s disease in Korean population are limited. Objectives The purpose of this study was to find out the effects of sleep quality on Behcet9s disease in Korean population. We also investigated the relationship between depression, quality of life, other clinical findings of Behcet9s. Methods The study was performed by cross-sectional design in two tertiary hospitals. We met one hundred patients with Behcet9s disease, surveyed them face-to-face and conducted the chart review for more clinical informations. Sleep quality was assessed by the Korean version of Pittsburgh sleep quality index (PSQI). Disease activity of Behcet9s disease was evaluated by Behcet9s disease current activity form (BDCAF). Depression was assessed by the Korean version of Beck depression inventory second edition (BDI-2). Quality of life was assessed by the Korean version of the Leeds Behcet9s Disease Quality of Life Measure (BDQoL). Results Among 100 patients, median age was 51 [44.5–56.0] years, median disease duration was 77.5 [24.0–136.0] months and 31% were male. Those who met the diagnostic critera of fibromyalgia were 28 patients. The frequency of poor sleep quality (PSQI >5) was 67%. Patients with poor sleep quality tend to have higher BDI2, BDCAF and pain VAS score (P<0.001, P=0.028, and P=0.011). Female rate was significantly higher, and BDQoL was lower in poor sleeper group (P=0.004 and P<0.001). Among 7 PSQI components, daytime dysfunction was higher in patients with high disease activity (P=0.03). Total PSQI score were strongly correlated with BDCAF score, BDI-2 score, BDQoL score, and pain VAS score (P=0.02, P<0.001, P<0.001, and P<0.001, respectively). Conclusions The low quality of sleep is associated with disease activity, depression and quality of life in Korean patients with Behcet9s disease. We expect better disease control will improve the sleep quality. References Tascilar NF, Tekin NS, Ankarali H, Sezer T, Atik L, Emre U, Duysak S, Cinar F. J Sleep Res 2012;21:281–8. Melikoglu MA, Melikoglu M. Rheumatol Int 2010;30:941–6. Disclosure of Interest None declared

Background: Chemotherapy-induced neuropathic pain is difficult to treat. Pentoxifylline inhibits the production of inflammatory cytokines including tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β). Objective: The aims of our study were to investigate the analgesic and preventive effects of pentoxifylline on paclitaxel-induced neuropathic pain in rats and to identify its mechanisms of action. Study Design: Controlled animal study. Methods: Neuropathic pain was induced with intraperitoneally injected paclitaxel on 4 alternate days in male Sprague-Dawley rats. Pentoxifylline was administered systemically as a single injection and a continuous infusion before or after the injection of paclitaxel. The mechanical threshold for allodynia was measured by using von Frey filaments. Protein levels and localization of inflammatory cytokines were performed by using Western blotting and immunohistochemistry, respectively. Results: After the rats developed neuropathic pain behavior, a single intraperitoneal injection and continuous infusion of pentoxifylline ameliorated paclitaxel-induced mechanical allodynia. In addition, systemic infusion of pentoxifylline in the early phase of the development of pain behavior delayed the onset of paclitaxel-induced pain behavior. Paclitaxel increased the levels of the catalytic subunit α of protein kinase A, phosphorylated nuclear factor κB, TNF-α, and IL-1β in the lumbar dorsal root ganglia. Pentoxifylline decreased the paclitaxel-induced TNF-α and IL1β levels. In addition, IL-1β was expressed in neurons and satellite cells in the lumbar dorsal root ganglia after paclitaxel. Limitations: Although this study was performed in the animal model by well-designed manner, clinical study will be needed to confirm the analgesic effect of pentoxifylline. Conclusion: Pentoxifylline alleviated chemotherapy-induced neuropathic pain in rats by reducing the levels of inflammatory cytokines in dorsal root ganglia and may be effective chemotherapyinduced neuropathic pain in patients. Key words: Chemotherapy, chronic pain, inflammatory cytokines, neuropathic pain, paclitaxel, pain behavior, pain treatment, pentoxifylline, phosphodiesterase inhibitor

Background: Although polymorphisms of the catechol-O-methyl transferase (COMT) gene have been implicated in altered pain sensitivity, results concerning the association between COMT gene polymorphisms and fibromyalgia (FM) are equivocal. We assessed the associations between COMT single-nucleotide polymorphisms (SNP) and FM risk and symptom severity.Methods: In total, 409 FM patients and 423 controls were enrolled. Alleles and genotypes at five positions [rs6269 (A>G), rs4633 (C>T), rs4818 (C>G), rs4680 (C>G) and rs165599 (A>G)] in the COMT gene were genotyped from peripheral blood DNA.Results: Alleles and genotypes of the rs4818 COMT gene polymorphism were significantly associated with increased susceptibility to FM. The rs4818 GG genotype was more strongly associated with FM compared to the CC genotype (OR = 1.680, 95% CI: 1.057, 2.672, p = 0.027). Although allele and genotype frequencies did not differ among groups, the rs4633 CT genotype was not associated with the presence of FM following adjustment for age and sex (OR = 0.745; 95% CI: 0.558, 0.995; p = 0.046). However, no association was observed between clinical measures and individual COMT SNPs. In haplotype analysis, there was a significant association between ACG haplotype and FM susceptibility sex (OR = 2.960, 95% CI: 1.447, 6.056, p = 0.003) and the number of tender points (p = 0.046).Conclusions: This large-scale study suggests that polymorphisms of the COMT gene may be associated with FM risk and pain sensitivity in Korean FM patients. However, our results differed to those of previous studies, suggesting ethnic variation in COMT gene polymorphisms in FM.What does this study add: By contrast to Caucasian and Latin-American populations, the COMT gene polymorphisms are associated with FM risk and pain sensitivity in Korean FM patients, suggesting ethnic variation in COMT gene polymorphisms.

Background Interleukin-21 (IL-21) has various effects on a number of immune cells including B cells, T cells, natural killer (NK) and NKT cells. One of the essential roles of IL-21 is to contribute to autoantibody production as a result of promoting hyperactivity of B cells. Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by pathogenic autoantibody production and systemic organ damage. A few studies have been conducted for investigating the contribution of IL-21 to the pathogenesis of murine SLE. However, only limited studies have been performed concerning the role of IL-21 in human SLE and the results are still controversial. Objectives The aim of this study was to evaluate whether IL-21 participates in the pathogenesis of human SLE. Methods Serum IL-21 levels were measured in SLE, osteoarthritis (OA) patients and healthy controls (HC). Serum IL-21 levels were analyzed for revealing the correlation with laboratory data or a disease activity index for SLE. Kidney tissues from patients with lupus nephritis and controls were used for evaluating the expression of IL-21 and IL-21R. Normal portions of human kidneys removed for renal carcinoma were used as normal controls. Results Serum levels of IL-21 were increased in the patients with SLE as compared to the patients with OA or HC. Serum IL-21 levels of the patients with SLE were positively correlated with serum levels of IgG, the titers of anti–double-stranded DNA antibodies and the scores of SLE Disease Activity Index. SLE patients with low C4 concentrations had higher serum IL-21 levels than those with normal C4 concentrations. The expression of IL-21 was higher in renal tubular epithelial cells of the patients with lupus nephritis than in those of controls. Conclusions This study reveals the association between IL-21 and disease activity in the patients with SLE. We also first demonstrate IL-21 expression in renal tissue of the patients with lupus nephritis. These findings suggest that IL-21 is critically implicated in the pathogenesis of SLE. References Ettinger R, Kuchen S, Lipsky PE: Interleukin 21 as a target of intervention in autoimmune disease. Annals of the rheumatic diseases 2008, 67 Suppl 3:iii83–86. Herber D, Brown TP, Liang S, Young DA, Collins M, Dunussi-Joannopoulos K: IL-21 has a pathogenic role in a lupus-prone mouse model and its blockade with IL-21R.Fc reduces disease progression. Journal of immunology 2007, 178(6):3822–3830. Disclosure of Interest None declared

Background Interleukin-17A (IL-17A) plays a critical role in the pathogenesis of rheumatoid arthritis (RA), which is characterized by exaggerated synovial proliferation. Autophagy is required to prevent accumulation of cellular damage and to ensure cellular homeostasis. Dysregulated autophagy has been reported to be involved in the pathogenesis of several diseases such as cancer and infections. Here, we hypothesized that IL-17A, a key cytokine in the development of RA, might have an impact on autophagic flux and that aberrant autophagy might be involved in expansion of synovial fibroblasts in the patients with RA, which is stimulated by pro-inflammatory cytokines. Objectives The aims of this study were (1) to evaluate whether IL-17A influences on autophagic flux in the synovium of the patients with RA and (2) to investigate whether the modulation of autophagy can regulate migration and proliferation of fibroblast-like synoviocytes (FLS) from the patients with RA (RA-FLS) under inflammatory milieu. Methods Synovial tissue was obtained from the patients with RA or osteoarthritis (OA) during total knee replacement surgery. FLS was cultured with IL-17A, autophagy inducer or inhibitor. The expression of marker proteins for autophagic flux (LC3B, Beclin1, Atg5, p62) and the formation of autophagolysosome (LAMP1) were analyzed by western blot. A migration scratch assay was used to assess FLS migration in response to stimulation with IL-17A. Proliferation of FLS was determined by the viable cell count using trypan blue. Bafilomycin was used for inhibiting autophagic flux. Results The expression of autophagy markers (LC3B, Beclin1, Atg5) was increased in the synovium of the patients with RA than in that of the patients with OA. Autophagy was also enhanced in RA-FLS compared with OA-FLS. IL-17A upregulated the expression of LC3B, Atg5, Beclin1, LAMP1 in RA-FLS. In particular, IL-17A-induced accumulation of p62 was prominent in RA-FLS. Migration and proliferation of FLS stimulated by IL-17A was suppressed by the inhibition of autophagy. Conclusions This study reveals that IL-17A stimulates autophagic flux and that intervention of autophagy can control IL-17A-induced migration and proliferation of FLS. Our results also provide additional evidence for a significant role of autophagy in the pathogenesis of RA. Thus, we suggest that autophagy might be a potential therapeutic target for the management of RA. References Lin NY, Beyer C, Giessl A, et al. Autophagy regulates TNFα-mediated joint destruction in experimental arthritis. Ann Rheum Dis. 2013 May;72(5):761–8. Connor AM, Mahomed N, Gandhi R, et al. TNFα modulates protein degradation pathways in rheumatoid arthritis synovial fibroblasts. Arthritis Res Ther. 2012 Mar 14;14(2):R62. Disclosure of Interest None declared

Background Headaches is common in patients with systemic lupus erythematosus (SLE) [1]. However, the lack of specific clinical distinctions for headache in SLE has made it difficult to elucidate its pathophysiology. Chronic daily headache (CDH) is a category of headache disorders that occurs more than 15 days per month and is associated with a profound decline in the quality of life [2]. Objectives The aim of this study is to investigate the clinical characteristics of CDH in patients with SLE and their association with disease severity and the quality of life. Methods A total of 40 consecutive patients with SLE participated in the survey. We investigated headache characteristics, visual analogue scale (VAS) for pain, and six-question headache impact test (HIT-6) to evaluate the impact of headache on the quality of life. The patients underwent required blood tests for assessment of disease activity using the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI). Results Six patients (15%) met the criteria for CDH. The total score of HIT-6 is significantly higher in SLE patients with CDH than in those patients who suffered from headache without CDH (P=0.027). SLE patients with CDH in particular had a higher prevalence of “wish could lie down” than those who suffered from headache without CDH (P=0.017). The multivariate regression analysis indicates that the headache days per month was a predictor for headache-related disabilities. Conclusions As far as we know, this is the first study of its kind to evaluate the correlation of CDH and the quality of life in Korean patients with SLE. CDH may deteriorate the quality of life in patients with SLE. References Cuadrado MJ, Sanna G. Headache and systemic lupus erythematosus. Lupus 2003;12:943–6. Pascual J, Colas R, Castillo J. Epidemiology of chronic daily headache. Curr Pain Headache Rep 2001;5:529–36. Disclosure of Interest None declared

Background Research on the safety and effects of febuxostat in stage 4 or 5 CKD patients is very limited. There are some studies where research on hyperuricemia patients with gout history has been conducted [1, 2], but there is little data on cases of application to patients actually in order to treat gout. Objectives This study aims to examine the clinical effects of febuxostat in cases of allopurinol-refractory hyperuricemia during treatment of gout in dialysis patients or stage 4 CKD patients. Methods Patients selected had been administered febuxostat for six months or longer because of allopurinol-refractory hyperuricemia during treatment of gout from May 2012 to February 2014. The patients met the American College of Rheumatology criteria for acute gout. The age, gender, duration of gout, cause of CKD, serum uric acid (SUA), estimated glomerular filtration rate (eGFR), creatinine, and doses of febuxostat were investigated in patients whose eGFR had been less than 45 mL/min per 1.73 m2 among the patients before the initiation of febuxostat administration Results A total of 25 patients were enrolled. The number of stage 3b (30 ≤ eGFR <45) CKD patients, stage 4 (15 ≤ eGFR <30) patients, and stage 5 (eGFR <15) patients was 13, 6, and 6, respectively, and all six patients at stage 5 CKD were undergoing hemodialysis or peritoneal dialysis. During the six-month observation period, gout recurred in none of the patients. The six stage 5 patients9 SUA decreased from 7.2±0.7 mg/dL at baseline to 4.9±2.2 mg/dL (p<0.05), the stage 4 CKD patients9 SUA reduced from 8.9±2.8 mg/dL at baseline to 6.7±4.4 mg/dL (p<0.05), and the stage 3b CKD patients9 SUA dropped from 8.8±1.9 mg/dL to 5.6±2.1 mg/dL (p<0.05) six months after the administration of febuxostat. In addition, the eGFR did not statistically change in the CKD stage 3b and 4 patients. Conclusions In gout treatment of dialysis patients or CKD stage 4 patients with allopurinol-refractory hyperuricemia, febuxostat inhibited gout recurrence and effectively decreased SUA during a period of six months. References Horikoshi, et al. Clin Exp Nephrol. 2013:17;149-50. Shibagaki, et al. Hypertens Res. 2014:37;919-25. Disclosure of Interest None declared

Background Research on the safety and effects of febuxostat in stage 4 or 5 CKD patients is very limited. There are some studies where research on hyperuricemia patients with gout history has been conducted [1, 2], but there is little data on cases of application to patients actually in order to treat gout. Objectives This study aims to examine the clinical effects of febuxostat in cases of allopurinol-refractory hyperuricemia during treatment of gout in dialysis patients or stage 4 CKD patients. Methods Patients selected had been administered febuxostat for six months or longer because of allopurinol-refractory hyperuricemia during treatment of gout from May 2012 to February 2014. The patients met the American College of Rheumatology criteria for acute gout. The age, gender, duration of gout, cause of CKD, serum uric acid (SUA), estimated glomerular filtration rate (eGFR), creatinine, and doses of febuxostat were investigated in patients whose eGFR had been less than 45 mL/min per 1.73 m 2 among the patients before the initiation of febuxostat administration Results A total of 25 patients were enrolled. The number of stage 3b (30 ≤ eGFR Conclusions In gout treatment of dialysis patients or CKD stage 4 patients with allopurinol-refractory hyperuricemia, febuxostat inhibited gout recurrence and effectively decreased SUA during a period of six months. References Horikoshi, et al. Clin Exp Nephrol. 2013:17;149-50. Shibagaki, et al. Hypertens Res. 2014:37;919-25. Disclosure of Interest None declared

Background Systemic erythematosus lupus (SLE) is an autoimmune disease with multi-organ involvement and diverse autoantibodies are associated with SLE [1]. Recently, many reports have suggested that anti-C reactive protein (CRP) antibody is more prevalent in patients with SLE, and the level of anti-CRP antibody increases when the disease flares up [2]. Objectives This study was performed to investigate the relationship between anti-CRP antibody and the disease activity markers in Korean patients with SLE. Methods 29 patients with SLE and 30 healthy people were enrolled between April 2014 and November 2014. The presence of anti-CRP antibody was analyzed by enzyme-linked immunosorbent assay (ELISA). Data on clinical variables and disease activity markers, such as complement, anti-dsDNA antibody, and systemic lupus erythematosus disease activity index (SLEDAI) were recorded. Results The level of serum anti-CRP antibody in SLE patients was significantly higher than that of healthy controls (p=0.035). However, anti-CRP antibody levels were not positively correlated with the complement levels, the SLEDAI score, and anti-dsDNA antibody levels. And also there was no significant difference in the level of anti-CRP antibody between the patient group with lupus nephritis and the patient group without lupus nephritis. Conclusions This study shows the presence of serum anti-CRP antibody in Korean SLE patients. But there was no significant relationship between anti-CRP antibody and disease activity, lupus nephritis. These findings are not consistent with previous study that anti-CRP antibody is a useful marker to evaluate the disease activity. References Shere Y, et al. Semin Arthritis Rheum 2004;34:501-37. Sjöwall C, et al. Arthritis Res Ther 2004;6:R87-R94. Disclosure of Interest None declared

Paracentesis is a diagnostic, therapeutic procedure performed in patients with ascites. It is generally thought to be a safe procedure and transfusion of platelet concentrate or fresh frozen plasma is not recommended before the procedure, because the incidence of clinically significant bleeding is very low. We report a case of lateral abdominal wall hematoma due to the injury of the deep circumflex iliac artery after paracentesis in patient with alcoholic liver cirrhosis who was treated with transcatheter arterial embolization.

GOALS:We intended to analyze the relationship between specific human leukocyte antigen (HLA)-DRB1 alleles and development of hepatocellular carcinoma (HCC) in chronic hepatitis B (CHB) patients. STUDY:A database of 468 consecutive CHB patients who received lamivudine for more than 12 months between July 1996 and February 2011 was retrospectively analyzed. Sera and buffy coats samples were obtained between April 2008 and April 2010. Six-digit HLA-DRB1 genotyping was performed with sequence-based typing. Serum α fetoprotein levels and ultrasonography or computed tomography image studies were assessed every 3 to 6 months for surveillance of HCC. RESULTS:At baseline, median age was 43 years (range, 16 to 71) [male: 359 (76.7%); HBeAg positivity: 385 (82.3%)]. Among the 27 HLA-DRB1 alleles identified, HLA-DRB1*090102, *080302, and *070101 were the most frequent (>10%). HCC was diagnosed in 36 (7.7%) patients during the median follow-up of 69 months. The frequency of the HLA-DRB1*140101 allele was 9.0% and significantly higher in patients of the HCC group than those of the non-HCC group (19.4 vs. 8.1%, P=0.014). The 2-year, 4-year, and 6-year cumulative rates of HCC development were markedly higher in patients with HLA-DRB1*140101 than those without HLA-DRB1*140101 (2.4, 8.2, and 25.1% vs. 1.9, 4.7, and 7.4%, respectively, P=0.011). No other HLA-DRB1 alleles were associated with HCC development. Baseline clinical characteristics did not differ between patients with and without HLA-DRB1*140101. CONCLUSIONS:The HLA-DRB1*140101 allele may be potentially associated with increased risk of HCC development in CHB patients, irrespective of the replicative activity of hepatitis B virus and antiviral responsiveness.

A 31-year-old man was admitted to our hospital due to hydrocephalus with neurosarcoidosis. Ventriculo-peritoneal shunting was performed in the right lateral ventricle with intravenous methylprednisolone. Subsequently, after 4 months, additional ventriculo-peritoneal shunting in the left lateral ventricle was performed due to the enlarged left lateral ventricle and slit-like right lateral ventricle. After 6 months, he was re-admitted due to upward gaze palsy, and magnetic resonance image showed an isolated fourth ventricle with both the inlet and outlet of fourth ventricle obstructed by recurrent neurosarcoidosis. Owing to the difficulty of using an endoscope, we performed neuronavigator-guided ventriculo-peritoneal shunting via the left lateral transcerebellar approach for the treatment of the isolated fourth ventricle with intravenous methyl prednisolone. The patient was discharged with improved neurological status.

Acute spontaneous subdural hematoma (SDH) of arterial origin is very rare. We report a case of acute spontaneous SDH that showed contrast media extravasation from cortical artery on angiograms. A 58-year-old male patient developed sudden onset headache and right hemiparesis. Brain CT scan demonstrated acute SDH at left convexity. The patient was drowsy mentality on admission. He had no history of head trauma. Cerebral angiography was performed and revealed a localized extravasation of the contrast media from distal cortical MCA branch. After angiography, the patient deteriorated to comatose mentality. Decompressive craniectomy for removal of SDH was performed. We verified the arterial origin of the bleeding and coagulated the bleeding focus. The histological diagnosis was aneurysmal artery. He recovered after surgery with mild disability. In a case of acute spontaneous SDH, the possibility of a cortical artery origin should be considered.