鈴木 重明 (スズキ シゲアキ)

Suzuki, Shigeaki

写真a

所属(所属キャンパス)

医学部 内科学教室(神経) 内科学(神経) (信濃町)

職名

准教授

メールアドレス

メールアドレス

HP

研究室住所

新宿区信濃町35

研究室電話番号

03-5363-3788

研究室FAX番号

03-3353-1272

外部リンク

総合紹介 【 表示 / 非表示

  • 重症筋無力症の非運動症状

    筋と自己免疫

経歴 【 表示 / 非表示

  • 1993年04月
    -
    1995年04月

    慶應義塾大学内科学教室入局(研修医)

  • 1995年05月
    -
    1996年05月

    川崎市立川崎病院内科

  • 1996年06月
    -
    1997年04月

    慶應義塾大学伊勢慶應病院内科

  • 1997年05月
    -
    2007年03月

    慶應義塾大学医学部内科学(神経,助手)

  • 2003年04月
    -
    2003年09月

    ニューヨーク医科大学留学

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学歴 【 表示 / 非表示

  • 1993年03月

    慶應義塾大学医学部

    大学

学位 【 表示 / 非表示

  • 医学博士, 慶應義塾大学, 2001年10月

 

研究分野 【 表示 / 非表示

  • 神経内科学 (自己免疫)

研究キーワード 【 表示 / 非表示

  • 自己抗体

研究テーマ 【 表示 / 非表示

  • 免疫関連有害事象, 

    2016年01月
    -
    継続中

  • 炎症性筋疾患, 

    2007年04月
    -
    継続中

  • 重症筋無力症, 

    2003年10月
    -
    継続中

 

論文 【 表示 / 非表示

  • Cytometric cell-based assays for anti-striational antibodies in myasthenia gravis with myositis and/or myocarditis

    Kufukihara K., Watanabe Y., Inagaki T., Takamatsu K., Nakane S., Nakahara J., Ando Y., Suzuki S.

    Scientific Reports (Scientific Reports)  9 ( 1 )  2019年12月

     概要を見る

    © 2019, The Author(s). The purposes of the present study were to identify anti-striational antibodies in myasthenia gravis (MG) patients with myositis and/or myocarditis using a combination of cell-based assays and flow cytometry (cytometric cell-based assays) and to describe the main clinical implications. Among 2,609 stored samples collected from all over Japan between 2003 and 2016, we had serum samples from 30 MG patients with myositis and/or myocarditis. Cytometric cell-based assays with titin, ryanodine receptor, and voltage-gated Kv1.4 were performed. Autoantibodies were determined by differences in phycoerythin fluorescence between the 293F cells and titin-transfected cells. MG patients with myositis and/or myocarditis as well as late-onset and thymoma-associated MG had anti-titin, anti-ryanodine receptor, and anti-Kv1.4 antibodies. In contrast, patients with early-onset MG, those with other myopathies and healthy controls did not have anti-titin or anti-Kv1.4 antibodies with some exceptions, but they possessed anti-ryanodine receptor antibodies. Thirty MG patients with myositis and/or myocarditis showed a severe generalized form, and 21 of them had thymoma. Anti-titin and anti-Kv1.4 antibodies were found in 28 (93%) and 15 (50%) patients, respectively, and all patients had at least one of these antibodies. Cytometric cell-based assays thus demonstrated that anti-striational antibodies are biomarkers of MG with myositis and/or myocarditis.

  • Diagnostic potential of sarcoplasmic myxovirus resistance protein A expression in subsets of dermatomyositis

    Uruha A., Allenbach Y., Charuel J., Musset L., Aussy A., Boyer O., Mariampillai K., Landon-Cardinal O., Rasmussen C., Bolko L., Maisonobe T., Leonard-Louis S., Suzuki S., Nishino I., Stenzel W., Benveniste O.

    Neuropathology and Applied Neurobiology (Neuropathology and Applied Neurobiology)  45 ( 5 ) 513 - 522 2019年08月

    ISSN  03051846

     概要を見る

    © 2018 British Neuropathological Society Aims: To elucidate the diagnostic value of sarcoplasmic expression of myxovirus resistance protein A (MxA) for dermatomyositis (DM) specifically analysing different DM subforms, and to test the superiority of MxA to other markers. Methods: Immunohistochemistry for MxA and retinoic acid-inducible gene I (RIG-I) was performed on skeletal muscle samples and compared with the item presence of perifascicular atrophy (PFA) in 57 DM patients with anti-Mi-2 (n = 6), -transcription intermediary factor 1 gamma (n = 10), -nuclear matrix protein 2 (n = 13), -melanoma differentiation-associated gene 5 (MDA5) (n = 10) or -small ubiquitin-like modifier activating enzyme (n = 1) autoantibodies and with no detectable autoantibody (n = 17). Among the patients, nine suffered from cancer and 22 were juvenile-onset type. Disease controls included antisynthetase syndrome (ASS)-associated myositis (n = 30), immune-mediated necrotizing myopathy (n = 9) and inclusion body myositis (n = 5). Results: Sarcoplasmic MxA expression featured 77% sensitivity and 100% specificity for overall DM patients, while RIG-I staining and PFA reached respectively 14% and 59% sensitivity and 100% and 86% specificity. In any subset of DM, sarcoplasmic MxA expression showed higher sensitivity than RIG-I and PFA. Some anti-MDA5 antibody-positive DM samples distinctively showed a scattered staining pattern of MxA. No ASS samples had sarcoplasmic MxA expression even though six patients had DM skin rash. Conclusions: Sarcoplasmic MxA expression is more sensitive than PFA and RIG-I expression for a pathological diagnosis of DM, regardless of the autoantibody-related subgroup. In light of its high sensitivity and specificity, it may be considered a pathological hallmark of DM per se. Also, lack of MxA expression in ASS supports the idea that ASS is a distinct entity from DM.

  • A case of anti-titin antibody positive nivolumab-related necrotizing myopathy with myasthenia gravis

    Isami A., Uchiyama A., Shimaoka Y., Suzuki S., Kawachi I., Fujita N.

    Rinsho shinkeigaku = Clinical neurology (Rinsho shinkeigaku = Clinical neurology)  59 ( 7 ) 431 - 435 2019年07月

     概要を見る

    A 53-year-old man suffering from squamous cell lung cancer presented with bilateral ptosis and bulbar palsy a month after initial treatment with the immune checkpoint inhibitor nivolumab. The symptoms showed worsening from midday, suggesting myasthenia gravis (MG), although anti-AChR antibody was negative. Although no muscle weakness was detected, the CK level was elevated to 5,255 IU/l, and MRI of the thigh revealed inflammation of the bilateral rectus femoris muscle. A muscle biopsy showed signs of necrotizing myopathy with expression of sarcolemmal HLA class I and accumulation of macrophages, CD4, CD8, and CD20-positive lymphocytes. Positivity for anti-titin antibody, one of the anti-striated muscle antibodies, was evident. The patient was diagnosed as having nivolumab-related necrotizing myopathy with myasthenia gravis, an immune-related adverse event (irAE). Treatment with prednisolone rapidly ameliorated the symptoms, and the serum CK level normalized. There have been several reports of nivolumab-related myositis with MG. On the basis of the muscle pathology and antibody data, we were able to clarify that necrotizing myopathy was related to the pathogenesis of this case.

  • Concurrent positive anti-3-hydroxy-3-methylglutaryl-coenzyme a reductase antibody with reducing body myopathy: Possible double trouble

    Tanboon J., Sanmaneechai O., Charuvanij S., Sangruchi T., Galindo-Feria A., Lundberg I., Ohnuki Y., Shiina T., Suzuki S., Nishino I.

    Neuromuscular Disorders (Neuromuscular Disorders)  29 ( 7 ) 543 - 548 2019年07月

    ISSN  09608966

     概要を見る

    © 2019 Elsevier B.V. Anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase myopathy is less common in children but has been associated with more favorable prognosis than adult patients after immunotherapies. We report anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase antibody positivity in a 6-year-old boy with progressive muscle weakness, scoliosis, spinal rigidity, multiple joint contractures, mild left ventricular hypertrophy, and elevated serum creatine kinase. In contrast to most of previously reported pediatric anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase myopathy, he showed little response to immunotherapies. Muscle biopsy contained changes suggestive of myofiber necrosis and regeneration and reducing bodies. The diagnosis of reducing body myopathy was later confirmed by reported c.368A>G (p.His123Arg) mutation in the FHL1 gene. Although the level of association between these two conditions is still inconclusive, this is the first report of concurrent positive anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase antibody with reducing body myopathy emphasizing the possibility of co-occurrence of immune mediated necrotizing myopathy and muscular dystrophy and importance of comprehensive diagnostic investigations in unusual cases.

  • Inflammatory myopathy associated with PD-1 inhibitors

    Seki M., Uruha A., Ohnuki Y., Kamada S., Noda T., Onda A., Ohira M., Isami A., Hiramatsu S., Hibino M., Nakane S., Noda S., Yutani S., Hanazono A., Yaguchi H., Takao M., Shiina T., Katsuno M., Nakahara J., Matsubara S., Nishino I., Suzuki S.

    Journal of Autoimmunity (Journal of Autoimmunity)  100   105 - 113 2019年06月

    ISSN  08968411

     概要を見る

    © 2019 Elsevier Ltd Objective: To characterize the inflammatory myopathy associated with programmed cell death 1 inhibitors (PD-1 myopathy). Methods: We studied 19 Japanese patients with PD-1 myopathy (13 men and 6 women, mean age 70 years), who were referred to Keio University. As control groups, we used 68 patients with anti-signal recognition particle antibodies, 51 patients with anti-aminoacyl transfer RNA synthetase antibodies and 460 healthy subjects. Results: In regard to muscle-disease severity, 10 patients showed a mild form of disease and 9 patients showed a severe form. Non-small cell lung cancer was the most common underlying cancer. PD-1 inhibitor consisted of 11 nivolumab and 8 pembrolizumab. PD-1 myopathy occurred 29 days on average after the first administration of PD-1 inhibitor. The initial manifestation of muscle weakness was ptosis in 10 patients, 15 patients had ptosis, 13 diplopia, 8 facial muscle weakness, 10 bulbar symptoms, 13 limb weakness, 14 neck weakness, 4 cardiac involvement, 6 respiratory involvement and 16 myalgia. Ocular, facial, cardiac and respiratory involvement and myalgia were more frequently observed than controls. Serum creatine kinase was increased to 5247 IU/L on average. Autoantibodies related to inflammatory myopathy were negative, while anti-striational antibodies were found in 13 (68%)patients. HLA-C*12:02 alleles were more frequently detected than healthy controls. Muscle pathology was characterized by multifocal necrotic myofibers with endomysial inflammation and expression of MHC class I. Immunosuppressive therapy with corticosteroids was generally effective for muscle weakness. Conclusions: Based on our clinical, histological and immunological findings, PD-1 myopathy is a discrete subset of inflammatory myopathy.

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KOARA(リポジトリ)収録論文等 【 表示 / 非表示

総説・解説等 【 表示 / 非表示

研究発表 【 表示 / 非表示

  • 脳虚血・再灌流時のサイクリックAMP応答因子結合蛋白(CREB)リン酸化と細胞保護

    田中耕太郎,鈴木重明,傳法倫久,小堺有史

    第80回日本生理学会大会, 2003年03月, その他

  • オリゴデンドロサイトおよびその前駆細胞の脳虚血反応

    田中耕太郎,永田栄一郎,鈴木重明,傳法倫久,小堺有史

    第14回日本脳循環代謝学会総会, 2002年11月, その他

  • 実験的脳虚血後のIL-6 cytokine family共有受容体GP130の細胞局在

    鈴木重明,田中耕太郎,野川茂,傳法倫久,小堺有史,福内靖男

    第14回日本脳循環代謝学会総会, 2002年11月, 口頭(一般)

  • Activation and proleferation of oligodendrocyte progenitor cells after brain ischemia

    Tanaka Kotaro, Nogawa Shigeru, Ito Daisuke, Suzuki Shigeaki, Dembo Tomohisa, Kosakai Arifumi, Fukuuchi Yasuo

    Joint international symposium on molecular mechanism and epochal therapeutics dor ischemic stroke and dementia, 2002年10月, その他

  • COX-2 expression in brains of patients with familial Alzheimer's disease

    Nogawa Shigeru, Takao Motoki, Suzuki Shigeaki, Tanaka Kortaro, Koto Atsuo, Fukuuchi Yasuo, Hayakawa Isao

    International Symposium on Molecular Mechanism and Epochal Therapeutics for Ischemic Stroke Dementia, 2002年10月, ポスター(一般)

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競争的資金等の研究課題 【 表示 / 非表示

  • 壊死性ミオパチーに関連する自己抗体の病態機序の解明と臨床応用に向けて

    2017年04月
    -
    2020年03月

    文部科学省・日本学術振興会, 科学研究費助成事業, 鈴木 重明, 基盤研究(C), 補助金,  代表

  • 自己抗体を介する炎症性筋疾患の臨床像・筋病理の解析と病態機序の解明

    2014年04月
    -
    2017年03月

    文部科学省・日本学術振興会, 科学研究費助成事業, 鈴木 重明, 基盤研究(C), 補助金,  代表

     研究概要を見る

    免疫介在性壊死性ミオパチー (immune-mediated necrotizing myopathy, IMNM)に関連し抗signal recognition particle (SRP)抗体と抗3-hydroxy-3-methylglutary-coenzyme A reductase (HMGCR) 抗体の意義を明らかにした.IMNM患者において抗SRP抗体が39%,抗HMGCR抗体が25%で検出され,抗SRP抗体は抗HMGCR抗体と比べ,重症例が多かった.HLA-DRB1遺伝子解析からDRB1*08:03と抗SRP抗体,DRB1*11:01と抗HMGCR抗体の関連を証明した.

  • 横紋筋細胞を用いた免疫沈降法による自己抗体検索の臨床応用に向けて

    2011年04月
    -
    2014年03月

    文部科学省, 科学研究費(基盤研究C), 鈴木重明, 補助金,  代表

  • 慢性期脳虚血の病態におけるStat3リン酸化の意義

    2008年04月
    -
    2011年03月

    文部科学省, 科学研究費(基盤研究C), 補助金,  代表

  • 重症筋無力症患者における電位依存性Kチャネル(Kv1.4)に対する自己抗体の意義

    2006年04月
    -
    2008年03月

    文部科学省, 科学研究費(若手研究B), 鈴木重明, 補助金,  代表

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知的財産権等 【 表示 / 非表示

  • Cytometric cell-based assayによる抗横紋筋抗体の測定

    特願:   2018年02月 

    特許, 共同, 国内出願

受賞 【 表示 / 非表示

  • 2015年度日本神経治療学会活動賞

    2016年11月

  • 日本神経免疫学会創世賞

    2014年09月

  • 日本内科学会奨励賞

    2009年04月

  • 慶應医学三四会奨励賞

    2006年11月

 

担当授業科目 【 表示 / 非表示

  • 内科学(神経)講義

    2019年度

  • 内科学講義

    2019年度

  • 免疫学

    2019年度

担当経験のある授業科目 【 表示 / 非表示

  • 神経疾患各論(多発性硬化症・免疫介在性脳炎)

    慶應義塾, 2015年度