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  2. Hidekata Yasuoka

Hidekata Yasuoka

  (安岡 秀剛)

Profile Information

Affiliation
Fujita Health University
Degree
PhD(Keio University)
J-GLOBAL ID
200901028124352037
researchmap Member ID
1000315081

Research Interests

 4

Research Areas

 2

Research History

 1

Education

 4

Papers

 53
  • Kato M, Kaneko Y, Tanaka Y, Inoo M, Kobayashi-Haraoka H, Amano K, Miyata M, Murakawa Y, Yasuoka H, Hirata S, Nagasawa H, Tanaka E, Miyasaka N, Yamanaka H, Yamamoto K, Yokota I, Atsumi T, Takeuchi T
    Modern rheumatology, 30(3) 1-8, Jun, 2019  Peer-reviewed
    Objectives: To identify predictive factors for remission by tocilizumab monotherapy in rheumatoid arthritis (RA) patients.Methods: This is a post hoc analysis of the SURPRISE study, a 2-year randomized, controlled study comparing the efficacy of tocilizumab with (ADD-ON) and without methotrexate (SWITCH). The primary endpoint was DAS28-ESR remission (<2.6) at week 24. The change in modified total Sharp score from baseline to week 52 (ΔmTSS/year) was also assessed as an endpoint. The effect of clinical parameters at baseline on remission was estimated by logistic regression analysis.Results: In SWITCH (n = 96), CRP, SAA, RF, and DAS28 at baseline showed predictive value for DAS28 remission in unadjusted analysis. Adjusted analysis confirmed SAA and DAS28 as predictive factors, with SAA having the highest value (ROC-AUC = 0.731). Furthermore, structural remission (ΔmTSS/year ≤ 0.5) rate was significantly higher in patients with SAA of < 50.0 μg/mL than other patients. In contrast, in ADD-ON (n = 98), only DAS28 showed predictive value for DAS28 remission. In patients with SAA < 50.0 μg/mL, both DAS28 remission and structural remission rate were comparable between SWITCH and ADD-ON.Conclusion: RA patients with low SAA levels at baseline may benefit similarly from tocilizumab with and without methotrexate.Trial registration number: NCT01120366.
  • Sakata K, Kaneko Y, Yasuoka H, Takeuchi T
    Clinical rheumatology, 39(1) 113-118, Jun, 2019  Peer-reviewed
  • Yasuoka H, Garrett SM, Nguyen XX, Artlett CM, Feghali-Bostwick CA
    American journal of physiology. Lung cellular and molecular physiology, 316(4) L644-L655, Apr, 2019  Peer-reviewed
  • Kondo Y, Suzuki K, Inoue Y, Sakata K, Takahashi C, Takeshita M, Kassai Y, Miyazaki T, Morita R, Niki Y, Kaneko Y, Yasuoka H, Yamaoka K, Yoshimura A, Takeuchi T
    Arthritis research & therapy, 21(1) 14, Jan, 2019  Peer-reviewed
    © 2019 The Author(s). Background: Ultrasonography (US) can directly demonstrate joint inflammation, including grayscale (GS) signs of synovial hypertrophy and power Doppler (PD) techniques to demonstrate increased blood flow and vascularization. Recently, echogenicity, especially hypoechoic synovium, has also been associated with local inflammatory activity. However, only a few studies have demonstrated correlation between histopathologic and immunopathologic evaluation and US findings. The aim of this study was to clarify whether joint US findings including synovial hypertrophy, vascularity, and echogenicity can accurately characterize synovial pathophysiology in patients with active rheumatoid arthritis (RA). Methods: A total of 44 patients with RA were included, both treated (n = 25) and untreated (n = 19) and scheduled for US examination of the knee joint with synovial fluid (SF) aspiration and two treated patients also underwent synovial biopsy. US images were quantitatively analyzed using grayscale assessment of synovial hypertrophy and PD for vascularity and echogenicity. Levels of nine SF cytokines and growth factors were also measured. Results: Both US synovial hypertrophy and PD vascularity significantly correlated with SF inflammatory cytokine levels such as IL-6, IL-8, IL-1β and IL-10 in untreated patients. Angiogenic factors, including vascular endothelial growth factor (VEGF), only correlated with PD vascularity. In the treated patients, the associations between synovial hypertrophy and any cytokines were diminished, although synovial vascularity and echogenicity correlated with IL-6 and VEGF (p < 0.05). Histopathologic analysis revealed that hypoechogenicity of the synovium correlated with marked infiltration of lymphocytes and hypervascularity. Conclusions: We demonstrated the pathophysiological origins of US findings in the joint. The degree of US vascularity of the synovium correlated with local inflammatory cytokine levels and angiogenetic factors in patients with active RA. Synovial echogenicity, and not hypertrophy, correlated with inflammation, especially in treated patients with RA.
  • Tasaki S, Suzuki K, Kassai Y, Takeshita M, Murota A, Kondo Y, Ando T, Nakayama Y, Okuzono Y, Takiguchi M, Kurisu R, Miyazaki T, Yoshimoto K, Yasuoka H, Yamaoka K, Morita R, Yoshimura A, Toyoshiba H, Takeuchi T
    Nature communications, 9(1) 2755, Jul, 2018  Peer-reviewed
    © 2018 The Author(s). Sustained clinical remission (CR) without drug treatment has not been achieved in patients with rheumatoid arthritis (RA). This implies a substantial difference between CR and the healthy state, but it has yet to be quantified. We report a longitudinal monitoring of the drug response at multi-omics levels in the peripheral blood of patients with RA. Our data reveal that drug treatments alter the molecular profile closer to that of HCs at the transcriptome, serum proteome, and immunophenotype level. Patient follow-up suggests that the molecular profile after drug treatments is associated with long-term stable CR. In addition, we identify molecular signatures that are resistant to drug treatments. These signatures are associated with RA independently of known disease severity indexes and are largely explained by the imbalance of neutrophils, monocytes, and lymphocytes. This high-dimensional phenotyping provides a quantitative measure of molecular remission and illustrates a multi-omics approach to understanding drug response.
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Misc.

 125
  • Hidekata Yasuoka, Yuka Okazaki, Yutaka Kawakami, Michito Hirakata, Hidetoshi Inoko, Yasuo Ikeda, Masataka Kuwana
    Arthritis and Rheumatism, 50(11) 3658-3662, Nov, 2004  
    Objective. To detect and characterize the autoreactive CD8+ T cells to major histocompatibility complex class 1 chain-related gene A (MICA), a stress-inducible antigen preferentially expressed on the epithelium and endothelium, in patients with Behçet's disease (BD). Methods. A candidate for the antigenic MICA peptide was selected based on its predicted binding affinity for HLA-B51 and proteasomal cleavage sites. Peripheral blood T cells from 14 patients with BD and 15 healthy controls were repeatedly stimulated with the MICA peptide, and the specific T cell response was measured by peptide-induced interferon-γ. Cytotoxic T lymphocyte activity was examined by chromium-51 release from an BLA-151-transfected B cell line in the presence of the MICA peptide. Results. A 9-mer peptide AAAAAIFVI (termed MICA transmembrane [MICA-TM]) was selected as a candidate for the antigenic peptide presented by HLA-B51. A specific T cell response to MICA-TM was detected in 4 patients with BD (29%) but in none of the 15 healthy donors. All 4 responders had HLA-B51 and active disease, and the specific T cell response was lost after the BD-related symptoms disappeared. The MICA-induced T cell response was specifically inhibited by anti-HLA class I antibody or by CD8+ cell depletion. MICA-reactive T cells recognized an HLA-B51-transfected B cell line pulsed with MICA-TM or a B cell line transfected with both HLA-B51 and MICA in the absence of exogenous peptides. Finally, MICA-stimulated T cell lines lysed the HLA-B51-expressing B cell line in the presence of MICA-TM. Conclusion. HLA-B51-restricted cytotoxic T lymphocytes autoreactive to MICA may be involved in the pathogenesis of BD.
  • H Yasuoka, Y Okazaki, Y Kawakami, M Hirakata, H Inoko, Y Ikeda, M Kuwana
    ARTHRITIS AND RHEUMATISM, 50(11) 3658-3662, Nov, 2004  
    Objective. To detect and characterize the autoreactive CD8+ T cells to major histocompatibility complex class I chain-related gene A (MICA), a stress-inducible antigen preferentially expressed on the epithelium and endothelium, in patients with Behcet's disease (BD). Methods. A candidate for the antigenic MICA peptide was selected based on its predicted binding affinity for HLA-B51 and proteasomal cleavage sites. Peripheral blood T cells from 14 patients with BD and 15 healthy controls were repeatedly stimulated with the MICA peptide, and the specific T cell response was measured by peptide-induced interferon-gamma. Cytotoxic T lymphocyte activity was examined by chromium-51 release from an HLA-B51-transfected B cell line in the presence of the MICA peptide. Results. A 9-mer peptide AAAAAIFVI (termed MICA transmembrane [MICA-TM]) was selected as a candidate for the antigenic peptide presented by HLA-B51. A specific T cell response to MICA-TM was detected in 4 patients with BD (29%) but in none of the 15 healthy donors. All 4 responders had HLA-B51 and active disease, and the specific T cell response was lost after the BD-related symptoms disappeared. The MICA-induced T cell response was specifically inhibited by anti-HILA class I antibody or by CD8+ cell depletion. MICA-reactive T cells recognized an HLA-B51-transfected B cell line pulsed with MICA-TM or a B cell line transfected with both HLA-B51 and MICA in the absence of exogenous peptides. Finally, MICA-stimulated T cell lines lysed the HLA-B51-expressing B cell line in the presence of MICA-TM. Conclusion. HLA-B51-restricted cytotoxic T lymphocytes autoreactive to MICA may be involved in the pathogenesis of BD.
  • T Satoh, JP Pandey, Y Okazaki, H Yasuoka, Y Kawakami, Y Ikeda, M Kuwana
    BRITISH JOURNAL OF HAEMATOLOGY, 124(6) 796-801, Mar, 2004  
    Single nucleotide polymorphisms (SNPs) of inflammatory cytokine genes were examined in 84 adult Japanese patients with chronic immune thrombocytopenic purpura (ITP) and 56 race-matched healthy controls. The SNPs examined were within the genes encoding tumour necrosis factor (TNF)-alpha (-238 G/A and -308 G/A), TNF-beta (+252 G/A), and interleukin (IL)-1beta (-511 C/T and +3953 T/C). Of these SNPs, the frequency of the TNF-beta (+252) G/G phenotype was significantly higher in ITP patients than in healthy controls (21% vs. 7%, P = 0.04, odds ratio = 3.6, 95% confidence interval 1.1-11.1), while no significant association was detected for the other SNPs. The distribution of the TNF-beta (+252) phenotype was not associated with human leucocyte antigen class II alleles or the therapeutic response in ITP patients. The frequency of circulating anti-glycoprotein IIb/IIIa antibody-producing B cells was significantly higher in ITP patients with the TNF-beta (+252) G/G phenotype than in those with the G/A or A/A phenotype (11.9 +/- 4.9 vs. 6.8 +/- 4.9 and 3.7 +/- 2.8 per 10(5) peripheral blood mononuclear cells; P = 0.02 and P &lt; 0.001, respectively). These findings suggest that the SNP located at TNF-beta (+252) contributes to susceptibility to chronic ITP by controlling the autoreactive B-cell responses to platelet membrane glycoproteins.
  • 第48回日本リウマチ学会総会, 2004  
  • 第48回日本リウマチ学会総会, 2004  
  • 第48回 日本リウマチ学会総会, 2004  
  • Annual Scientific Meeting of American College of Rheumatology, 2004  
  • Annual Scientific Meeting of American College of Rheumatology, 2004  
  • 加藤 雅志, 佐藤 慎二, 鈴木 美佐子, 岡 浩子, 金子 裕子, 安岡 秀剛, 野島 崇樹, 諏訪 昭, 平形 道人, 池田 康夫
    日本臨床免疫学会会誌, 27(5) 345-349, 2004  
  • 第19回日本臨床リウマチ学会総会, 2004  
  • 第101回日本内科学会総会, 2004  
  • Annual Scientific Meeting of American College of Rheumatology, 2004  
  • 安岡 秀剛, 桑名 正隆
    臨床免疫, 42(2) 214-217, 2004  
  • Arthritis & Rheumatism, 50(11) 3658-3662, 2004  
  • Annual Scientific Meeting of American College of Rheumatology, 2004  
  • Annual Scientific Meeting of American College of Rheumatology, 2004  
  • Annual Scientific Meeting of American College of Rheumatology, 2004  
  • 42(2) 214-217, 2004  
  • H Yasuoka, H Ihn, TA Medsger, M Hirakata, Y Kawakami, Y Ikeda, M Kuwana
    JOURNAL OF IMMUNOLOGY, 171(12) 6883-6890, Dec, 2003  
    Nearly all autoantibody specificities in sera from patients with systemic sclerosis (SSc) target proteins distributed ubiquitously, and Abs against proteins whose expression is restricted to the affected sites have not been identified. In this study we describe SSc-specific autoantibody to a novel testicular Ag, termed protein highly expressed in testis (PHET), which is ectopically over-expressed in SSc dermal fibroblasts. A partial cDNA encoding PHET was isolated by immunoscreening of a HepG2 cDNA library with an SSc serum. PHET appeared to be a member of the UniGene cluster Hs.129872, but had a unique exon composition and a characteristic mRNA expression profile restricted to the testis. Serum Abs to a recombinant PHET fragment were detected in nine (8.4%) of 107 SSc patients, but in none of 50 systemic lupus erythematosus patients or 77 healthy controls. In SSc patients, the presence of anti-PHET Abs was associated with diffuse cutaneous SSc and lung involvement (p = 0.02 and 0.01, respectively). PCR-based quantitative analysis of PHET mRNA expression in cultured dermal fibroblasts showed increased expression of PHET mRNA in SSc fibroblasts compared with control fibroblasts. PHET-reactive Abs purified from SSc sera stained the cytoplasm of SSc dermal fibroblasts, and the staining intensity tended to be more prominent on SSc compared with control fibroblasts. These findings suggest that the autoantibody response to PHET can be induced by ectopic overexpression of PHET in dermal fibroblasts in SSc patients.
  • H Yasuoka, H Ihn, TA Medsger, M Hirakata, Y Kawakami, Y Ikeda, M Kuwana
    JOURNAL OF IMMUNOLOGY, 171(12) 6883-6890, Dec, 2003  
    Nearly all autoantibody specificities in sera from patients with systemic sclerosis (SSc) target proteins distributed ubiquitously, and Abs against proteins whose expression is restricted to the affected sites have not been identified. In this study we describe SSc-specific autoantibody to a novel testicular Ag, termed protein highly expressed in testis (PHET), which is ectopically over-expressed in SSc dermal fibroblasts. A partial cDNA encoding PHET was isolated by immunoscreening of a HepG2 cDNA library with an SSc serum. PHET appeared to be a member of the UniGene cluster Hs.129872, but had a unique exon composition and a characteristic mRNA expression profile restricted to the testis. Serum Abs to a recombinant PHET fragment were detected in nine (8.4%) of 107 SSc patients, but in none of 50 systemic lupus erythematosus patients or 77 healthy controls. In SSc patients, the presence of anti-PHET Abs was associated with diffuse cutaneous SSc and lung involvement (p = 0.02 and 0.01, respectively). PCR-based quantitative analysis of PHET mRNA expression in cultured dermal fibroblasts showed increased expression of PHET mRNA in SSc fibroblasts compared with control fibroblasts. PHET-reactive Abs purified from SSc sera stained the cytoplasm of SSc dermal fibroblasts, and the staining intensity tended to be more prominent on SSc compared with control fibroblasts. These findings suggest that the autoantibody response to PHET can be induced by ectopic overexpression of PHET in dermal fibroblasts in SSc patients.
  • 第31回日本臨床免疫学会, 2003  
  • 第47回日本リウマチ学会総会, 2003  
  • Annual Scientific Meeting of American College of Rheumatology, 2003  
  • 2003  
  • 39(4) 475-478, 2003  
  • 第30回日本臨床免疫学会, 2002  
  • International Symposium on Sjogren's Syndrome, 2002  
  • 第30回日本臨床免疫学会総会, 2002  
  • 第498回日本内科学会関東地方会, 2002  
  • 第43回関東リウマチ研究会, 2002  
  • 第5回強皮症研究会, 2002  
  • 第14回日本神経免疫学会学術集会, 2002  
  • 第12回日本神経免疫学会, 2002  
  • 第46回日本リウマチ学会総会, 2002  
  • 第46回日本リウマチ学会総会, 2002  
  • 第46回日本リウマチ学会総会, 2002  
  • 第46回日本リウマチ学会総会, 2002  
  • 第46回日本リウマチ学会総会，学術集会, 2002  
  • 第46回日本リウマチ学会総会, 2002  
  • A. Furuta, T. Fujii, H. Yasuoka, R. Takada, M. Hirakata, T. Mimori
    Modern Rheumatology, 12(2) 178-181, 2002  
    A 26-year-old Japanese woman with systemic lupus erythematosus (SLE) developed severe hypertension and an increased active renin concentration (ARC), ischemic colitis, and splenic infarction. She had antiphospholipid antibodies (APA), multiple intrarenal microaneurysms, and multiple stenoses of the mesenteric arteries. Combination therapy with antihypertensive agents, aspirin, warfarin, and corticosteroids (30mg daily) controlled her abdominal symptoms and hypertension. Multiple intrarenal microaneurysms in SLE with APA may be the cause of severe hypertension and elevated serum ARC.
  • FURUYA Yoshiaki, SUZUKI Misako, ABE Hiroko, KANEKO Yuko, YASUOKA Hidekata, NOJIMA Takaki, SATO Shinji, SUWA Akira, HIRAKATA Michito, IKEDA Yasuo
    Nihon Naika Gakkai Kaishi, 91(12) 3510-3512, 2002  
  • International Symposium on Sjogren's Syndrome, 2002  
  • A. Furuta, T. Fujii, H. Yasuoka, R. Takada, M. Hirakata, T. Mimori
    Modern Rheumatology, 12(2) 178-181, 2002  
    A 26-year-old Japanese woman with systemic lupus erythematosus (SLE) developed severe hypertension and an increased active renin concentration (ARC), ischemic colitis, and splenic infarction. She had antiphospholipid antibodies (APA), multiple intrarenal microaneurysms, and multiple stenoses of the mesenteric arteries. Combination therapy with antihypertensive agents, aspirin, warfarin, and corticosteroids (30mg daily) controlled her abdominal symptoms and hypertension. Multiple intrarenal microaneurysms in SLE with APA may be the cause of severe hypertension and elevated serum ARC.
  • T Fujii, T Nojima, H Yasuoka, S Satoh, K Nakamura, M Kuwana, A Suwa, M Hirakata, T Mimori
    RHEUMATOLOGY, 40(12) 1398-1404, Dec, 2001  
    Objective. To determine cytokines and MHC class II alleles in Japanese patients with adult Still's disease (ASD) and clarify the association between those profiles and chronic articular disease. Methods. Of 35 patients with ASD (13 men, 22 women, mean age at onset 34.0 yr), 17 (49%) had chronic arthritis (&gt;6 months, chronic articular ASD) and 18 (51%) lacked chronic arthritis (systemic ASD). Cytokines and cytokine receptors in sera were measured by ELISA. Correlations of each cytokine with disease activity or C-reactive protein (CRP) were determined. MHC class II alleles were examined by polymerase chain reaction methods. Results. In chronic articular ASD, female gender was more frequent and liver dysfunction and myalgia were rarer than in systemic ASD. In active disease, the white blood cell count was lower, but total IgG was greater in patients with chronic articular ASD than in those with systemic ASD. Tumour necrosis factor (TNF) alpha, soluble TNF receptor 2 and interleukin (IL)-18 were increased in both types of ASD, even in remission. Soluble IL-2 receptors, IL-4 and IL-18 levels were correlated with disease activity or CRP value only in chronic articular ASD. Interferon gamma and IL-8 remained increased only in chronic articular ASD, even when disease activity, including IL-6 and CRP, was low. DRB1*1501 (DR2) and DRB1*1201 (DR5) alleles were more frequent in chronic articular than in systemic ASD, whereas DQB1*0602 (DQ1) was frequently observed in both types of ASD. Conclusion. The present study suggests that ASD with chronic articular disease has distinct clinical, cytokine and immunogenetic profiles.
  • T Fujii, T Nojima, H Yasuoka, S Satoh, K Nakamura, M Kuwana, A Suwa, M Hirakata, T Mimori
    RHEUMATOLOGY, 40(12) 1398-1404, Dec, 2001  
    Objective. To determine cytokines and MHC class II alleles in Japanese patients with adult Still's disease (ASD) and clarify the association between those profiles and chronic articular disease. Methods. Of 35 patients with ASD (13 men, 22 women, mean age at onset 34.0 yr), 17 (49%) had chronic arthritis (&gt;6 months, chronic articular ASD) and 18 (51%) lacked chronic arthritis (systemic ASD). Cytokines and cytokine receptors in sera were measured by ELISA. Correlations of each cytokine with disease activity or C-reactive protein (CRP) were determined. MHC class II alleles were examined by polymerase chain reaction methods. Results. In chronic articular ASD, female gender was more frequent and liver dysfunction and myalgia were rarer than in systemic ASD. In active disease, the white blood cell count was lower, but total IgG was greater in patients with chronic articular ASD than in those with systemic ASD. Tumour necrosis factor (TNF) alpha, soluble TNF receptor 2 and interleukin (IL)-18 were increased in both types of ASD, even in remission. Soluble IL-2 receptors, IL-4 and IL-18 levels were correlated with disease activity or CRP value only in chronic articular ASD. Interferon gamma and IL-8 remained increased only in chronic articular ASD, even when disease activity, including IL-6 and CRP, was low. DRB1*1501 (DR2) and DRB1*1201 (DR5) alleles were more frequent in chronic articular than in systemic ASD, whereas DQB1*0602 (DQ1) was frequently observed in both types of ASD. Conclusion. The present study suggests that ASD with chronic articular disease has distinct clinical, cytokine and immunogenetic profiles.
  • S. Suzuki, M. Kuwana, H. Yasuoka, K. Tanaka, Y. Fukuuchi, Y. Kawakami
    Journal of the Neurological Sciences, 189(1-2) 59-64, Aug 15, 2001  
    The aim of this study was to elucidate the roles of human leukocyte antigen (HLA) class II genes in disease susceptibility in Japanese adult patients with myasthenia gravis (MG). A number of studies have shown that MG is correlated with DR3 in Caucasians. In Japanese, infantile MG is associated with DR9, but the HLA class II alleles associated with adult MG remains unclear. HLA-DRB1 and DQB1 alleles were determined by genotyping in 75 Japanese adult patients with MG and in 115 race-matched healthy adults. No statistically significant difference was observed in the overall prevalences of DRB1 and DQB1 alleles between MG patients and healthy controls, even when the patients and controls were stratified on the basis of their gender. MG patients with DQB1*0604 were younger and those with DQB1*0402 were older at disease onset than those without (P=0.03 and 0.008, respectively). Concomitant autoimmune thyroid disease was associated with DRB1*0803 (P=0.0009, corrected P=0.04). In addition, anti-acetylcholine receptor antibody levels were significantly higher in patients with DQB1*0604 than in those without (P=0.045). These findings indicate that immunogenetic backgrounds in Japanese adult MG patients are heterogeneous and are apparently different from those in Caucasian patients. Copyright © 2001 Elsevier Science B.V.
  • S. Suzuki, M. Kuwana, H. Yasuoka, K. Tanaka, Y. Fukuuchi, Y. Kawakami
    Journal of the Neurological Sciences, 189(1-2) 59-64, Aug 15, 2001  
    The aim of this study was to elucidate the roles of human leukocyte antigen (HLA) class II genes in disease susceptibility in Japanese adult patients with myasthenia gravis (MG). A number of studies have shown that MG is correlated with DR3 in Caucasians. In Japanese, infantile MG is associated with DR9, but the HLA class II alleles associated with adult MG remains unclear. HLA-DRB1 and DQB1 alleles were determined by genotyping in 75 Japanese adult patients with MG and in 115 race-matched healthy adults. No statistically significant difference was observed in the overall prevalences of DRB1 and DQB1 alleles between MG patients and healthy controls, even when the patients and controls were stratified on the basis of their gender. MG patients with DQB1*0604 were younger and those with DQB1*0402 were older at disease onset than those without (P=0.03 and 0.008, respectively). Concomitant autoimmune thyroid disease was associated with DRB1*0803 (P=0.0009, corrected P=0.04). In addition, anti-acetylcholine receptor antibody levels were significantly higher in patients with DQB1*0604 than in those without (P=0.045). These findings indicate that immunogenetic backgrounds in Japanese adult MG patients are heterogeneous and are apparently different from those in Caucasian patients. Copyright © 2001 Elsevier Science B.V.
  • S. Suzuki, M. Kuwana, H. Yasuoka, K. Tanaka, Y. Fukuuchi, Y. Kawakami
    Journal of the Neurological Sciences, 189(1-2) 59-64, Aug 15, 2001  
    The aim of this study was to elucidate the roles of human leukocyte antigen (HLA) class II genes in disease susceptibility in Japanese adult patients with myasthenia gravis (MG). A number of studies have shown that MG is correlated with DR3 in Caucasians. In Japanese, infantile MG is associated with DR9, but the HLA class II alleles associated with adult MG remains unclear. HLA-DRB1 and DQB1 alleles were determined by genotyping in 75 Japanese adult patients with MG and in 115 race-matched healthy adults. No statistically significant difference was observed in the overall prevalences of DRB1 and DQB1 alleles between MG patients and healthy controls, even when the patients and controls were stratified on the basis of their gender. MG patients with DQB1*0604 were younger and those with DQB1*0402 were older at disease onset than those without (P=0.03 and 0.008, respectively). Concomitant autoimmune thyroid disease was associated with DRB1*0803 (P=0.0009, corrected P=0.04). In addition, anti-acetylcholine receptor antibody levels were significantly higher in patients with DQB1*0604 than in those without (P=0.045). These findings indicate that immunogenetic backgrounds in Japanese adult MG patients are heterogeneous and are apparently different from those in Caucasian patients. Copyright © 2001 Elsevier Science B.V.
  • S Suzuki, M Kuwana, H Yasuoka, K Tanaka, Y Fukuuchi, Y Kawakami
    JOURNAL OF THE NEUROLOGICAL SCIENCES, 189(1-2) 59-64, Aug, 2001  
    The aim of this study was to elucidate the roles of human leukocyte antigen (HLA) class II genes in disease susceptibility in Japanese adult patients with myasthenia gravis (MG). A number of studies have shown that MG is correlated with DR3 in Caucasians. In Japanese, infantile MG is associated with DR9, but the HLA class II alleles associated with adult MG remains unclear. HLA-DRB1 and DQB1 alleles were determined by genotyping in 75 Japanese adult patients with MG and in 115 race-matched healthy adults. No statistically significant difference was observed in the overall prevalences of DRB1 and DQB1 alleles between MG patients and healthy controls, even when the patients and controls were stratified on the basis of their gender. MG patients with DQB1*0604 were younger and those with DQB1*0402 were older at disease onset than those without (P = 0.03 and 0.008, respectively). Concomitant autoimmune thyroid disease was associated with DRB1*0803 ( P = 0.0009, corrected P = 0.04). In addition, anti-acetylcholine receptor antibody levels were significantly higher in patients with DQB1*0604 than in those without ( P = 0.045). These findings indicate that immunogenetic backgrounds in Japanese adult MG patients are heterogeneous and are apparently different from those in Caucasian patients. (C) 2001 Elsevier Science B.V. All rights reserved.
  • 第45回日本リウマチ学会総会, 2001  

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