Eon Jeong Nam

Kyungpook National University Hospital, Sŏul, Seoul, South Korea

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Publications (22)66.99 Total impact

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    ABSTRACT: Fibromyalgia (FM), characterized by chronic widespread pain, is known to be associated with heightened responses to painful stimuli and atypical resting state functional connectivity among pain-related regions of the brain. Previous studies on FM using resting-state functional magnetic resonance imaging (rs-fMRI) have focused on intrinsic functional connectivity, which maps the spatial distribution of temporal correlations among spontaneous low frequency fluctuation (LFF) in fMRI resting-state data. In the current study, using rs-fMRI data in frequency domain, we investigate the possible alteration of power spectral density (PSD) of low frequency fluctuation in brain regions associated with central pain processing in patients with FM. Resting-state fMRI data were obtained from 19 patients with FM and 20 age-matched healthy female control subjects. For each subject, the PSDs for each brain region identified from functional connectivity maps were computed for the frequency band of 0.01-0.25 Hz. For each group, average PSD was determined for each brain region and a two-sample t-test was performed to determine the difference in power between the two groups. According to the results, patients with FM exhibited significantly increased frequency power in the primary somatosensory cortex (S1), supplementary motor area (SMA), dorsolateral prefrontal cortex (DLPFC), and amygdala. In patients with FM, the increase in PSD did not show an association with depression or anxiety. Therefore, our findings of atypical increased frequency power during resting-state in pain-related brain regions may implicate the enhanced resting-state baseline neural activity in several brain regions associated with pain processing in FM.
    Pain 05/2013; · 5.64 Impact Factor
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    ABSTRACT: OBJECTIVE.: TGFβ-inducible gene-h3 (βig-h3), abundantly expressed in rheumatoid synovium, and matrix metalloproteinases (MMP) play an important role in the pathogenesis of rheumatoid arthritis (RA). The aim of this study was to determine the therapeutic efficacy of βig-h3-derived peptides using MMP-1-dependent target tissue delivery in chronic inflammatory arthritis. METHODS.: The βig-h3 derivative-based peptides, including the 2nd and 4th YH peptides, 4th fas-1 domain, 4th fas-1 truncated for H1 and H2 (dhfas-1), and a MMP1-cleavable composite peptide (MFK24), were cloned. We confirmed the specificity of MFK24 cleavage by immunoblotting after treatment with different proteases. RESULTS.: The 4th YH18 peptide was weakly effective in suppressing arthritis severity in CIA mice. Treatment with higher dose (30mg/kg) of dhfas-1 showed a remarkable efficacy, whereas treatment with lower dose (10mg/kg) revealed only a partial improvement. A composite peptide (MFK24) consisted of dhfas-1 and RGD peptide linked by MMP1 substrate was cleaved by MMP1 specifically. βig-h3-mediated adhesion and migration of NIH3T3 cells were inhibited at low concentration of MFK24. MFK24 suppressed the adhesion of NIH3T3 cells more efficiently compared to either alone or in combination of MFK00 and RGD motif. Therapeutic efficacy of MFK24 in CIA mice was remarkably enhanced with a consistent reduction of expression in inflammatory mediators within joint tissues. CONCLUSION.: A proof of concept design of MMP-cleavable composite peptide, based on βig-h3 derivatives, revealed a marked improvement of therapeutic efficacy for chronic inflammatory arthritis, implicating a new expandable strategy for enhancement of efficacy of two different active molecules in RA. © 2013 American College of Rheumatology.
    Arthritis & Rheumatology 03/2013; · 7.48 Impact Factor
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    ABSTRACT: Chronic widespread pain is a hallmark of fibromyalgia (FM). Previous neuroimaging studies have reported that the pain neuro-matrix in patients with FM showed augmented activation in response to actual pain. However, the effect of observing pain in others among patients with FM remains poorly understood. Both healthy female control subjects (n=24) and female patients with FM (n=23) underwent functional magnetic resonance imaging while observing a series of color pictures depicting others' hands and feet being injured, and a matched set of control pictures that did not show any painful events. Compared with healthy subjects, patients with FM showed a smaller neural response to pain-related versus neutral stimuli in several neural regions, including the thalamus, anterior cingulate cortex, dorsolateral prefrontal cortex, pre- and post-central gyrus, and supplementary motor area. In contrast to augmented pain processing in response to actual experimental pain, patients with FM did not show an enhanced pain response but generally showed lesser activation in cortical regions known to play a role in processing of pain. These hemodynamic alterations observed in patients with FM suggest that patients with chronic pain may empathize less with others in pain, possibly in order to lessen arousal and aversive self-oriented emotions.
    Neuroscience Research 02/2013; · 2.20 Impact Factor
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    ABSTRACT: The chemokine receptor [C-C chemokine receptor 5 (CCR5)] is expressed on diverse immune effecter cells and has been implicated in the pathogenesis of rheumatoid arthritis (RA). This study sought to determine whether single-nucleotide polymorphisms (SNPs) in the CCR5 gene and their haplotypes were associated with susceptibility to and severity of RA. Three hundred fifty-seven patients with RA and 383 healthy unrelated controls were recruited. Using a pyrosequencing assay, we examined four polymorphisms -1118 CTAT(ins) (/del) (rs10577983), 303 A>G (rs1799987), 927 C>T (rs1800024), and 4838 G>T (rs1800874) of the CCR5 gene, which were distributed over the promoter region as well as the 5' and 3' untranslated regions. No significant difference in the genotype, allele, and haplotype frequencies of the four selected SNPs was observed between RA patients and controls. CCR5 polymorphisms of -1118 CTAT(del) (P = 0.012; corrected P = 0.048) and 303 A>G (P = 0.012; corrected P = 0.048) showed a significant association with radiographic severity in a recessive model, and, as a result of multivariate logistic regression analysis, were found to be an independent predictor of radiographic severity. When we separated the erosion score from the total Sharp score, the statistical significance of CCR5 polymorphisms showed an increase; -1118 CTAT(ins) (/del) (P = 0.007; corrected P = 0.028) and 303 A>G (P = 0.007; corrected P = 0.028). Neither SNPs nor haplotypes of the CCR5 gene showed a significant association with joint space narrowing score. These results indicate that genetic polymorphisms of CCR5 are an independent risk factor for radiographic severity denoted by modified Sharp score, particularly joint erosion in RA.
    Tissue Antigens 08/2012; 80(5):416-23. · 2.93 Impact Factor
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    ABSTRACT: The ethnic heterogeneity and genetic complexity of rheumatoid arthritis (RA) have produced inconsistent results in previous genetic association studies concerning FCRL3. This study sought to delineate the association between the FCRL3 gene polymorphisms and susceptibility to RA and to investigate the effects of the polymorphisms on the progression of joint destruction in RA. RA patients (n = 377) and healthy unrelated controls (n = 298) were recruited. Genotyping of -169 T>C and -110 G>A in the promoter and 1,381 G>A in the intron was accomplished using FRET assays. The distribution of genotypes and haplotypes did not differ between RA patients and controls. When we investigated the role of FCRL3 polymorphisms for the severity of RA, patients with the CC genotype in the -169 T>C polymorphism had a higher modified Sharp score than other genotype groups (p = 0.034) among patients with disease duration ≥10 years. The slope of the regression line for modified Sharp score over disease duration (10.12/year) was significantly steeper in patients with the CC genotype than in the T carriers (5.69/year) at the -169 T>C polymorphism (p = 0.003), indicating the faster progression of radiologic destruction in the CC genotype. In conclusion, polymorphisms of the FCRL3 gene may contribute to the progression of joint destruction rather than susceptibility of RA.
    Human immunology 02/2012; 73(5):537-42. · 2.55 Impact Factor
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    ABSTRACT: Fibromyalgia (FM) is a disorder characterized by chronic widespread pain and frequently associated with other symptoms. Patients with FM commonly report cognitive complaints, including memory problem. The objective of this study was to investigate the differences in neural correlates of working memory between FM patients and healthy subjects, using functional magnetic resonance imaging (MRI). Nineteen FM patients and 22 healthy subjects performed an n-back memory task during MRI scan. Functional MRI data were analyzed using within- and between-group analysis. Both activated and deactivated brain regions during n-back task were evaluated. In addition, to investigate the possible effect of depression and anxiety, group analysis was also performed with depression and anxiety level in terms of Beck depression inventory (BDI) and Beck anxiety inventory (BAI) as a covariate. Between-group analyses, after controlling for depression and anxiety level, revealed that within the working memory network, inferior parietal cortex was strongly associated with the mild (r = 0.309, P = 0.049) and moderate (r = 0.331, P = 0.034) pain ratings. In addition, between-group comparison revealed that within the working memory network, the left DLPFC, right VLPFC, and right inferior parietal cortex were associated with the rating of depression and anxiety? Our results suggest that the working memory deficit found in FM patients may be attributable to differences in neural activation of the frontoparietal memory network and may result from both pain itself and depression and anxiety associated with pain.
    PLoS ONE 01/2012; 7(6):e37808. · 3.73 Impact Factor
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    ABSTRACT: Aseptic endocarditis is an uncommon complication of Behçet's disease (BD). We describe a rare case of a 39-year-old female who had BD with aseptic endocarditis of the tricuspid valve (TV) presenting as tricuspid stenosis. She was diagnosed with BD four years ago. The mucocutaneous lesions were well-controlled with colchicine and short courses of corticosteroids. She remained free of signs and symptoms of BD for one year without any medication. Three months before admission, she gradually developed dyspnea on exertion and peripheral edema. Echocardiography revealed dilated right atrium and markedly thickened TV with severe stenosis. TV replacement was performed. Pathologic examination of the valve showed fibrinoid necrotic material and inflammatory cell infiltration. Blood cultures and cultures of the excised valve were negative for microorganisms.
    Korean Circulation Journal 07/2011; 41(7):399-401.
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    ABSTRACT: The objective of this study is to investigate the association between the -283C/T polymorphism at the promotor of DNMT3B gene and susceptibility to rheumatoid arthritis (RA) and to evaluate the effect of the polymorphism on clinical features such as progression of joint destruction in RA. A total of 309 patients with RA were compared with 297 control subjects. Genotyping of the -283C/T polymorphism was performed by real-time sequencing using Pyrosequencer. The genotype frequencies of the polymorphism at position -283 were not significantly different between patients with RA and controls. There were significantly positive correlations between the modified Sharp score and the disease duration for carriers of each genotype (y = 9.546x + 19.998, p < 0.001, for T allele carriers, y = 6.185x + 34.424, p < 0.001 for CC homozygotes). The slope of regression line of the T allele carriers was significantly steeper than that of the CC homozygotes (p = 0.014). In conclusion, our results suggest that the -283C/T polymorphism of the DNMT3B gene is a genetic marker related to the joint destruction of RA.
    Rheumatology International 09/2009; 30(10):1299-303. · 2.21 Impact Factor
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    ABSTRACT: We investigated potential associations between rheumatoid arthritis (RA) and interferon regulatory factor 5 (IRF5) polymorphisms in a metaanalysis. This metaanalysis included 5 case-control studies, which provided a total of 6582 RA cases and 5375 controls. Odds ratios (OR) were employed to evaluate the risk of RA according to the 4 single-nucleotide polymorphisms (SNP) in IRF5 (rs729302, rs2004640, rs752637, and rs2280714) and data were analyzed in respect to association between alleles. Among 4 candidate SNP, rs729302, rs2004640, and rs2280714 were statistically significant; both allele C of rs729302 and allele G of rs2004640 within the promoter region of IRF5 were associated with a protective effect [random-effects (RE) OR 0.889, 95% confidence interval (CI) 0.803-0.977, p=0.015 for rs729302; and RE OR 0.905, 95% CI 0.848-0.965, p=0.002 for rs2004640]. Similar results were also obtained in T allele of rs2280714 in the 3'-untranslated region (RE OR 0.927, 95% CI 0.866-0.992, p=0.029). There was no evidence of publication bias from funnel-plot asymmetry and Egger's regression test. Our metaanalysis supported the evidence of the significant role of IRF5 polymorphisms in RA.
    The Journal of Rheumatology 03/2009; 36(4):693-7. · 3.26 Impact Factor
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    ABSTRACT: To determine the efficacy and safety of the combination of leflunomide and methotrexate for the treatment of patients with active rheumatoid arthritis (RA) in an open, non-comparative, multicentre trial. Seventy-four patients with active RA were enrolled to receive concomitantly leflunomide (no loading dose, 10 mg/day) and methotrexate (starting at 7.5 mg/week and titrating up to 15 mg/week) for 20 weeks. The primary end-point was a 20% improvement in the American College of Rheumatology (ACR) criteria at 20 weeks. Safety measures included evaluation of adverse events at each visit and laboratory data, including haematology and liver function tests. Intention-to-treat analyses were conducted. Sixty-five patients completed 20 weeks of treatment, and 71.6% were responders based on the ACR20 criteria. After 20 weeks, the mean changes were -16.3 for tender joint count, -12.0 for swollen joint count, -44.0 for physician global assessment, -34.3 for patient global assessment, -22.7 for erythrocyte sedimentation rate, and -0.65 for the Health Assessment Questionnaire score. Adverse events occurred in 40.5% of the patients, and were considered serious in four patients who discontinued therapy. Abnormal liver function was noted for 16 patients (21.6%). Two of these patients were withdrawn from the study; after discontinuing the medication, their liver function recovered fully. THE combination of leflunomide and methotrexate was effective and well tolerated in the treatment of active RA patients. This combination may be a useful option as an initial treatment for active RA before starting biological agents.
    Scandinavian journal of rheumatology 01/2009; 38(1):11-4. · 2.51 Impact Factor
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    ABSTRACT: Polymyositis-like syndrome characterized by proximal muscle weakness and elevation of muscle enzymes may be a presenting manifestation of hypothyroidism. Camptocormia, which can be caused by myopathy of the paraspinal muscles, is an involuntary truncal flexion of the thoracolumbar spine while standing or walking. Among various neuromuscular disorders, hypothyroidism has not been reported in the literature as a cause of camptocormia. This is the first report of polymyositis-like syndrome with camptocormia caused by hypothyroidism.
    Rheumatology International 09/2008; 29(3):339-42. · 2.21 Impact Factor
  • The Journal of the Korean Rheumatism Association 01/2008; 15(3).
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    ABSTRACT: Combined tramadol/acetaminophen is used to treat pain related to osteoarthritis. However, adverse events (AEs) leading to discontinuation can occur. Dose titration may decrease the risk for AEs. The aim of this study was to assess the effect of tramadol/acetaminophen titration on the development of AEs leading to treatment discontinuation in patients with knee osteoarthritis. This 2-week, multicenter, randomized, double-blind, double-dummy, add-on study was conducted at 12 tertiary referral university hospitals in the Republic of Korea. Patients aged 35 to 75 years with knee osteoarthritis receiving a stable dose of NSAIDs and with a daily mean pain-intensity score of > or = 4 on a numeric rating scale (NRS) (0 = no pain to 10 = worst pain) during the 48 hours prior to enrollment were eligible. Patients were randomly assigned to receive 1 tablet of tramadol/acetaminophen 37.5/325 mg QD and 1 placebo BID for 3 days, followed by 1 active tablet BID and 1 placebo QD for 4 days, followed by 1 active tablet TID for 7 days (titration group) or 1 tablet of combined tramadol 37.5 mg/acetaminophen 325 mg TID for 14 days (nontitration group). The primary outcome measure was the rate of treatment discontinuation due to AEs. Secondary outcome measures were time to discontinuation due to AEs, prevalences and characteristics of AEs, decrease from baseline in pain intensity as measured on the NRS, and change in the Korean version of the Western Ontario and McMaster Universities (K-WOMAC) index score (scale: 0 = best to 100 = worst). A total of 250 patients were enrolled (92.0% female; mean [SD] age, 60.2 [7.8] years; mean [SD] weight, 60.0 [9.2] kg [range, 37.5-90.7 kg]; all Korean). The discontinuation rate was significantly lower in the titration group than in the nontitration group (10.5% vs 26.2%; P < 0.001). The Kaplan-Meier survival curve showed that the rates of discontinuation due to AEs were similar in the 2 groups up to day 2, but thereafter the discontinuation rate was significantly lower in the titration group. The most common AEs were nausea (12.1% and 24.6% in the titration and nontitration groups, respectively; P = 0.008), vomiting (4.0% and 17.2%; P < 0.001), and dizziness (9.7% and 22.1%; P = 0.005). No serious AEs were reported in either group. Tramadol/acetaminophen use was associated with a similar decrease from baseline in pain in both the titration and nontitration groups (mean [SD] Delta: NRS, -1.60 [1.62] vs -1.68 [1.58]; total K-WOMAC, -12.86 [13.73] vs -12.52 [16.58]). In this population of Korean patients with knee osteoarthritis pain managed with a stable dose of NSAIDs, titration of tramadol/acetaminophen over 12 days was associated with improved tolerability and a significantly lower discontinuation rate compared with nontitration. Both regimens significantly reduced from baseline associated with osteoarthritis.
    Clinical Therapeutics 07/2007; 29(7):1381-9. · 2.23 Impact Factor
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    ABSTRACT: To study the expression of LIGHT (tumor necrosis factor superfamily 14) and herpesvirus entry mediator (HVEM; tumor necrosis factor receptor superfamily 14) in rheumatoid arthritis (RA) and to determine the regulatory role of LIGHT on the effector functions of fibroblast-like synoviocytes (FLS). The expression of LIGHT and HVEM was assessed by immunohistochemical staining of synovial tissue and by flow cytometric analysis of mononuclear cells. The presence of HVEM and lymphotoxin beta receptor was measured by reverse transcriptase-polymerase chain reaction and by flow cytometry. The regulation of effector molecules, including matrix metalloproteinases (MMPs) and adhesion molecules, was evaluated. The adhesiveness of FLS was determined by adhesion assay. HVEM was detected in most cell types within rheumatoid synovial tissue, while only a few cells were positive for LIGHT. In RA patients, LIGHT expression was significantly up-regulated only in CD20+ B cells and monocytes, whereas the mean fluorescence intensity of HVEM was down-regulated in mononuclear cells. The stimulation of FLS with LIGHT resulted in the production of MMPs and the expression of adhesion molecules, which were efficiently inhibited by dexamethasone. LIGHT-mediated up-regulation of MMPs and intercellular adhesion molecule 1 was blocked by inhibitors of NF-kappaB and JNK, whereas up-regulation of vascular cell adhesion molecule 1 was blocked by inhibitors of phosphatidylinositol 3-kinase, as well as NF-kappaB. These data suggest that binding of LIGHT with its receptors may play a role in the progression of inflammation within rheumatoid synovium, especially by mediating the interactions between infiltrating inflammatory cells and stromal cells. These findings thus emphasize the relevance of LIGHT as a potential therapeutic target in RA.
    Arthritis & Rheumatology 05/2007; 56(4):1106-17. · 7.48 Impact Factor
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    The Journal of the Korean Rheumatism Association 01/2007; 14(4).
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    ABSTRACT: To delineate the expression of transforming growth factor beta-inducible gene h3 (betaIG-H3) in rheumatoid synovitis and to determine the regulatory role of betaIG-H3 in the adhesion and migration of fibroblast-like synoviocytes (FLS). Synovial tissue was obtained from patients with rheumatoid arthritis (RA) during joint replacement surgery, and FLS were isolated using enzymatic treatment. Immunohistochemical staining was performed to show the expression of betaIG-H3 within rheumatoid synovium. Synthesis of betaIG-H3 from FLS was determined by semiquantitative reverse transcription-polymerase chain reaction, Western blot analysis, and enzyme-linked immunosorbent assay. Cell adhesion and migration assays were performed using the YH18 peptide in the fourth fas-1 domain of betaIG-H3 and function-blocking antibodies to integrins. Expression of betaIG-H3 was up-regulated in RA synovial tissue compared with synovial tissue from patients with osteoarthritis. FLS isolated from RA synovial tissue constitutively produced betaIG-H3, which was up-regulated by transforming growth factor beta1, interleukin-1beta, and tumor necrosis factor alpha. Although FLS expressed a variety of integrins, betaIG-H3 mediated adhesion and migration of FLS through interaction with alpha v beta3 integrin. Cytokines failed to affect the betaIG-H3-mediated adhesion. However, migration of FLS guided by betaIG-H3 was enhanced by interferon-gamma and platelet-derived growth factor type BB. The YH18 peptide in the fourth fas-1 domain of betaIG-H3 inhibited adhesion and migration in a dose-dependent manner. The results suggest that betaIG-H3, which is abundantly expressed in RA synovial tissue, plays a regulatory role in chronic destructive inflammation through the modulation of the adhesion and migration of FLS. This finding indicates the relevance of betaIG-H3 and alpha v beta3 integrin-interacting motifs as potential therapeutic targets in this disease.
    Arthritis & Rheumatology 10/2006; 54(9):2734-44. · 7.48 Impact Factor
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    ABSTRACT: Vascular endothelial growth factor (VEGF) is important for angiogenesis and inflammation, both of which are codependent and contribute to the pathophysiology of Behcet disease (BD). The increased expressions of VEGF have been observed in the active stage and in the ocular inflammation of BD. Polymorphisms of the VEGF gene have been associated with chronic inflammatory disease including rheumatoid arthritis. We sought to investigate whether polymorphisms on the regulatory region of the VEGF gene are associated with susceptibility of Korean patients with BD. One hundred one native Korean patients with BD and 138 healthy unrelated controls were recruited. Genotype and allele frequencies of the four selected polymorphisms (-2578, -1154, -634, and 936) were not different between the BD group and controls. Among the BD patients, the frequency of the -634 CC genotype decreased in patients with uveitis (2.6% vs. 20.6%, adjusted OR = 0.100, 95% CI 0.011-0.875, p = 0.037), although it became insignificant after correction for multiple comparisons. These results indicate that the VEGF gene polymorphisms are not associated with BD in the Korean population, but they may be involved in the development of the ocular inflammation of BD.
    Human Immunology 11/2005; 66(10):1068-73. · 2.30 Impact Factor
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    ABSTRACT: To investigate the role of polymorphisms of the vascular endothelial growth factor (VEGF) gene in susceptibility to ankylosing spondylitis (AS), and their relationship to clinical features and radiographic severity. This study included 157 patients with AS and 140 healthy unrelated controls. Polymorphisms of the VEGF gene were analysed by the polymerase chain reaction (PCR)-restriction fragment length polymorphism assay and amplification refractory mutation system-PCR. Haplotypes were reconstructed using the Bayesian algorithm. Radiographic severity was assessed by the Bath Ankylosing Spondylitis Radiological Index (BASRI). The genotype frequencies of the polymorphisms were in Hardy-Weinberg equilibrium. The distributions of genotypes and alleles did not differ between AS patients and controls. Among the six haplotypes reconstructed based on the tight linkage disequilibrium at positions -2578, -1154 and -634 (pairwise linkage disequilibrium coefficient, r = 0.361-0.706), no haplotype was associated with susceptibility to AS. Clinical features were analysed for the four haplotypes (CGC, CGG, AAG, AGG) which were prevalent. In carriers of the AGG haplotype, the frequency of cervical spine involvement was significantly higher (P = 0.002, P(corr) = 0.036) and that of patients showing a BASRI score >6 was also higher (P = 0.025, P(corr) = 0.45). This study demonstrates that polymorphisms of the VEGF gene may contribute to disease severity in AS.
    Rheumatology 11/2005; 44(10):1299-302. · 4.21 Impact Factor
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    ABSTRACT: A rare manifestation of systemic lupus erythematosus (SLE) is cerebral venous sinus thrombosis (CVST), in which early diagnosis and aggressive therapy are of prime importance for favorable outcome. The pathogenesis of CVST is largely unknown, but it is thought to be caused by cerebral vasculitis, antiphospholipid antibodies or other conditions associated with enhanced coagulability. We describe two cases of SLE with CVST which were not associated with antiphospholipid antibodies. Both cases were treated with immunosuppressants (intravenous methylprednisolone and cyclophosphamide pulse therapy) and anticoagulant drugs (heparin and subsequent maintenance therapy with warfarin). There was a marked improvement of neurologic symptoms with the disappearance of thrombus in a follow-up MRI. The possibility of CVST should be considered in any patients with SLE who show neuropsychiatric manifestations.
    Journal of Korean Medical Science 07/2001; 16(3):351-4. · 1.25 Impact Factor
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    ABSTRACT: Myelodysplastic syndromes (MDS) are a group of refractory anemias resulting from a clonal stem cell disorder often associated with cytogenetic abnormalities. There is increasing recognition of immunological abnormalities in patients with MDS, including defective B- and T-cell function, hyper- or hypogammaglobulinemia and monoclonal gammopathy. MDS have been associated with Sjögren's syndrome, polymyalgia rheumatica, relapsing polychondritis and systemic lupus erythematosus. Although there may be various rheumatologic features, including acute arthritis in MDS, chronic inflammatory arthritis is uncommonly combined. There have been a few reports that described cases of rheumatoid arthritis (RA) concurrent with MDS, but advanced rheumatoid arthritis with typical joint deformities has rarely been reported. We report a case of rheumatoid arthritis with atlantoaxial subluxation combined with refractory anemia in a 31-year-old woman.
    Journal of Korean Medical Science 07/1999; 14(3):319-22. · 1.25 Impact Factor