研究者データベース

泉 健太郎(イズミ ケンタロウ)
北海道大学病院 脳・神経・感覚器科
講師

基本情報

所属

  • 北海道大学病院 脳・神経・感覚器科

職名

  • 講師

学位

  • 医学博士(北海道大学)

J-Global ID

研究活動情報

論文

  • BP180と7型コラーゲンを標的抗原とした免疫チェックポイント阻害薬関連表皮下水疱症の1例
    葭本 倫大, 平野 瑶子, 得地 景子, 泉 健太郎, 松本 隆児, 氏家 英之
    日本皮膚科学会雑誌 132 5 1310 - 1310 (公社)日本皮膚科学会 2022年05月
  • Yosuke Mai, Kentaro Izumi, Kaori Sawada, Eijiro Akasaka, Shoko Mai, Daisuke Sawamura, Kazushige Ihara, Shigeyuki Nakaji, Wataru Nishie
    The Journal of investigative dermatology 142 3 Pt B 984 - 987 2022年03月
  • Yoko Hirano, Hiroaki Iwata, Masumi Tsujuwaki, Shoko Mai, Yosuke Mai, Keisuke Imafuku, Kentaro Izumi, Hiroshi Koga, Hideyuki Ujiie
    The Journal of dermatology 49 3 374 - 378 2022年03月 
    Bullous pemphigoid is generally caused by immunoglobulin (Ig)G autoantibodies against hemidesmosomal BP180 and/or BP230. Recently, the concept of IgM pemphigoid has been proposed. A 23-year-old Japanese woman presented with a 4-month history of severely itchy papules showing subepidermal separations with mild neutrophil infiltration. Direct immunofluorescence (DIF) revealed IgM deposits at the dermoepidermal junction, but neither IgG nor IgA deposits. Indirect immunofluorescence on 1 M NaCl-split skin demonstrated deposits on the epidermal side. The optical density (OD) value of a modified IgM enzyme-linked immunosorbent assay for full-length BP180, but not for BP180-NC16A, was increased. The patient was diagnosed with IgM pemphigoid and was treated with diphenyl sulfone at 50 mg/day without recurrence. To confirm the precise autoantigen, we tried to obtain super-resolution imaging. The deposition pattern of IgM autoantibodies seemed to be oriented parallel to that of BP180. The detailed images detect DIF deposits apart from BP180-NC16A staining, but are close to type VII collagen-NC1 staining. This result suggests that the IgM autoantibodies in the patient might target the C-terminus of BP180. IgM pemphigoid is still not a widely accepted concept, and the clinical course remains unknown. We will carefully follow-up the patient. Super-resolution images may help to detect precise autoantigens in autoimmune blistering diseases.
  • Mei Suezawa, Teruki Dainichi, Yo Kaku, Maiko Izumi, Koki Kataoka, Norito Ishii, Hiroshi Koga, Kentaro Izumi, Wataru Nishie
    The Journal of dermatology 48 10 1584 - 1587 2021年10月 
    Dipeptidyl peptidase 4 inhibitors (DPP-4i) are associated with an increased risk of developing bullous pemphigoid (BP) in patients with diabetes. Autoantibodies targeting epitopes on the processed BP180, 120-kDa (LAD-1), and 97-kDa (LABD97) linear immunoglobulin (Ig)A dermatosis antigens are the major autoantibodies in DPP-4i-associated BP. However, no case of mucous membrane pemphigoid (MMP) developing during treatment with DPP-4i has been reported. We report a case of MMP associated with DPP-4i. A man in his late 70s presented with oral mucous membrane erosion and a few blisters on his upper chest and back. He had used linagliptin for diabetes for over 1 year when he presented. The immunological characteristics were similar to DPP4i-associated BP: higher reactivity to LAD-1 and LABD97 than to the full-length BP180. The aphthae achieved remission after oral linagliptin was replaced with sitagliptin. However, 6 months later, the aphthae relapsed and any DPP-4i was discontinued. The aphthae disappeared, and now he is completely free from lesions associated with MMP. This case suggests that the DPP-4i may have shared roles in the production of IgG antibodies to LAD-1 or to LABD97 in the pathogenesis of DPP-4i-associated BP and MMP. Our case highlights the possibility of overlooking the mild MMP in DPP-4i-treated diabetes patients with mucosal lesions.
  • Jumpei Tahara, Sachiko Ono, Takashi Nomura, Yo Kaku, Gyohei Egawa, Teruki Dainichi, Kentaro Izumi, Wataru Nishie, Tetsuya Honda, Kenji Kabashima
    International journal of dermatology 60 9 1159 - 1160 2021年09月
  • Rikuma Kitao, Takeshi Fukumoto, Takashi Hashimoto, Kentaro Izumi, Haruki Jimbo, Chihiro Takemori, Chikako Nishigori
    Journal of Dermatological Science 103 3 190 - 192 2021年08月
  • Takashi Hashimoto, Takahiko Tsunoda, Fumiko Sato, Kentaro Izumi, Wataru Nishie, Norito Ishii, Hua Qian, Xiaoguang Li, Daisuke Tsuruta
    The Australasian journal of dermatology 62 2 e363-e365  2021年05月
  • Inkin Ujiie, Hiroaki Iwata, Norihiro Yoshimoto, Kentaro Izumi, Hiroshi Shimizu, Hideyuki Ujiie
    The Journal of dermatology 48 4 502 - 510 2021年04月 
    Bullous pemphigoid (BP) varies in severity and stratified treatments are needed. However, there are no definitive standards for choosing appropriate treatments. To elucidate the factors involved in choosing treatments and the clinical outcomes of BP, we retrospectively reviewed the clinical records of 78 BP patients at a single center. Of the 78 patients, 49 (62.8%) were treated with oral prednisolone (PSL) and 29 (37.2%) were treated without PSL. The patients with older age, lower Bullous Pemphigoid Disease Area Index (BPDAI), and/or lower anti-BP180NC16a antibody titer at onset tended to be treated without oral PSL. Notably, only 9.1% patients without PSL experienced relapse, whereas 36.7% patients with oral PSL experienced relapse when the PSL was around 0.1 mg/kg. It suggests that the patients with mild disease severity could be well controlled without oral PSL. Receiver-operator curve analysis demonstrated that the cut-off value for the use of oral PSL was 31 for total BPDAI and was 7 for BPDAI skin urticaria/erythema, with a high (>0.9) area under the curve. Notably, none of the patients who were negative for the anti-BP180NC16a antibody at onset experienced relapse even though they were treated without PSL. In conclusion, in BP patients who were negative for anti-BP180NC16a antibody at onset, with a total BPDAI score of less than 31 or with an urticaria/erythema score of less than 7 can be treated without PSL. When the PSL is tapered to around 0.1 mg/kg, we should carefully monitor the patients to detect relapse.
  • N Yoshimoto, S Takashima, T Kawamura, E Inamura, T Sugai, I Ujiie, K Izumi, K Natsuga, W Nishie, H Shimizu, H Ujiie
    Journal of the European Academy of Dermatology and Venereology : JEADV 35 4 e282-e285  2021年04月
  • Kaori Sawada, Tomoyo Sawada, Tadahiro Kobayashi, Akiko Fujiki, Takashi Matsushita, Shigeru Kawara, Kentaro Izumi, Wataru Nishie, Hiroshi Shimizu, Kazuhiko Takehara, Yasuhito Hamaguchi
    Immunological medicine 44 1 1 - 3 2020年07月07日 
    Bullous pemphigoid (BP) is a cutaneous autoimmune blistering disorder. Recently, it has been reported that dipeptidyl peptidase-4 inhibitors (DPP4i) is associated with the development of BP (DPP4i-BP). Patients with DPP4i-BP have autoantibodies (autoAbs) preferentially targeting full-length BP180, but not the BP180NC16a domain. In this report, we described a case of anti-BP230 antibody (Ab)-positive BP receiving DPP4i. A 78-year-old male with a medical history of type 2 diabetes receiving vildagliptin at 100 mg daily for 38 months was referred to our hospital with itching blisters on his body and extremities. Skin biopsy showed subepidermal bulla with eosinophil infiltration. Direct immunofluorescence staining revealed a linear staining pattern with complement C3 and IgG at the subepidermal basement membrane zone. By laboratory testing, autoAbs against BP180NC16a and full-length BP180 were negative by enzyme-linked immunosorbent assay (ELISA); however, anti-BP230 Abs were positive by ELISA (index: 123.91). His HLA genotype was DQB1*04:01 and 05:01. Based on these results, we diagnosed the patient with anti-BP230 Abs-positive BP associated with DPP4i. To the best of our knowledge, this is the first case of DPP4i-BP with only anti-BP230 Abs. Further accumulation of DPP4i-BP cases is needed to clarify the relationship between overall features of DPP4i-BP and anti-BP230 Abs.
  • Seiko Sugiyama, Ryota Tanaka, Hiroaki Hayashi, Kentaro Izumi, Wataru Nishie, Yumi Aoyama
    Acta dermato-venereologica 100 13 adv00178  2020年06月11日
  • Epitope spreading現象によって抗BP180 NC16a抗体が陽転化したdipeptidyl peptidase-IV阻害薬関連水疱性類天疱瘡の3例
    眞井 洋輔, 西江 渉, 泉 健太郎, 葭本 倫大, 森田 裕介, 渡邉 美佳, 豊永 愛恋, 氏家 英之, 岩田 浩明, 藤田 靖幸, 乃村 俊史, 松村 和子, 清水 聡子, 清水 宏
    加齢皮膚医学セミナー 14 2 67 - 67 加齢皮膚医学研究会 2019年12月
  • 鈴木 丈雄, 新熊 悟, 荻根沢 真帆子, 会沢 敦子, 高橋 奈央, 泉 健太郎, 氏家 英之, 西江 渉, 阿部 理一郎
    臨床皮膚科 73 10 813 - 817 (株)医学書院 2019年09月 
    <文献概要>73歳,男性.初診の10年以上前から口腔,鼻腔および咽喉頭粘膜にびらん,潰瘍が出現した.近医耳鼻科でBehcet病を疑われ,プレドニゾロンやコルヒチンの内服などで治療されたが,難治であった.また,初診の3年前から眼球癒着を生じ,眼科で内反症解除術・眼球癒着解除術を施行されたが,術後1ヵ月で再び癒着した.口腔内の難治性潰瘍の精査・加療目的に当科を紹介され受診した.歯肉びらん部の病理組織像では粘膜上皮・固有層間に裂隙を認めた.無疹部であった口唇粘膜の生検組織を用いた蛍光抗体直接法では粘膜上皮直下に線状のIgG沈着を認め,1M食塩水剥離ヒト皮膚を用いた蛍光抗体間接法では患者血清IgGが裂隙の表皮側に沈着した.以上から,抗BP180型粘膜類天疱瘡と考えた.皮膚病変が軽症な粘膜類天疱瘡では,他科で診断が不確定なまま粘膜の難治性潰瘍として長期間治療されることがあるため,他科との密な連携が必要である.
  • Epitope spreading現象によって抗BP180 NC16a抗体が陽転化したdipeptidyl peptidase-IV阻害薬関連水疱性類天疱瘡の3例
    眞井 洋輔, 西江 渉, 泉 健太郎, 葭本 倫大, 森田 裕介, 渡邉 美佳, 豊永 愛恋, 氏家 英之, 岩田 浩明, 藤田 靖幸, 乃村 俊史, 松村 和子, 清水 聡子, 清水 宏
    加齢皮膚医学セミナー 14 1 65 - 65 加齢皮膚医学研究会 2019年06月
  • Kentaro Izumi, Katja Bieber, Ralf J Ludwig
    Frontiers in immunology 10 978 - 978 2019年 
    Autoimmune bullous dermatoses (AIBDs) are a group of rare chronic inflammatory skin diseases, which clinically manifest as blisters and erosions of the skin and/or mucosa. Immunologically, AIBDs are characterized and caused by autoantibodies targeting adhesion molecules in the skin and mucosa. According to the histological location of the blistering, AIBDs are classified into the following two main subtypes: pemphigus (intraepidermal blistering) and pemphigoid (subepidermal blistering). Most AIBDs were potentially life-threatening diseases before the advent of immunosuppressive drugs, especially systemic steroid therapies, which suppress pathogenic immunological activity. Although there have been recent advancements in the understanding of the pathogenesis of AIBDs, glucocorticosteroids and/or adjuvant immunosuppressive drugs are still needed to control disease activity. However, the long-term use of systemic immunosuppression is associated with major adverse events, including death. Based on the growing understanding of AIBD pathogenesis, novel treatment targets have emerged, some of which are currently being evaluated in clinical trials. Within this article, we review the current clinical trials involving pemphigus and pemphigoid and discuss the rationale that lead to these trials. Overall, we aim to foster insights into translational research in AIBDs to improve patient care.
  • Yosuke Mai, Wataru Nishie, Kentaro Izumi, Hiroshi Shimizu
    Frontiers in immunology 10 1224 - 1224 2019年 
    Bullous pemphigoid (BP) is a common autoimmune blistering disease in which autoantibodies target the hemidesmosomal components BP180 and/or BP230 in basal keratinocytes. In BP, 80 to 90% of autoantibodies target the juxtamembranous extracellular non-collagenous 16th A (NC16A) domain of BP180. Recently, the administration of dipeptidyl peptidase-IV inhibitors (DPP4i), which are widely used as antihyperglycemic drugs, has been recognized to be a causative factor for BP. DPP4i-associated BP (DPP4i-BP) autoantibodies tend to target epitopes on non-NC16A regions of BP180, and the pathomechanism for the development of the unique autoantibodies remains unknown. To address the characteristics of DPP4i-BP autoantibodies in detail, we performed epitope analysis of 18 DPP4i-BP autoantibodies targeting the non-NC16A domains of BP180 using various domain-specific as well as plasmin-digested polypeptides derived from recombinant BP180. Firstly, Western blotting showed that only one DPP4i-BP serum reacted with the epitopes on the intracellular domain of BP180, and no sera reacted with the C-terminal domain of the molecule. In addition, only 2 DPP4i-BP sera reacted with BP230 as determined by enzyme-linked immunosorbent assay. Thus, DPP4i-BP autoantibodies were found to mainly target the non-NC16A mid-portion of the extracellular domain of BP. Interestingly, Western blotting using plasmin-digested BP180 as a substrate revealed that all of the DPP4i-BP sera reacted more intensively with the 97-kDa processed extracellular domain of BP180, which is known as the LABD97 autoantigen, than full-length BP180 did. All of the DPP4i-BP autoantibodies targeting the LABD97 autoantigen were IgG1, and IgG4 was observed to react with the molecule in only 7 cases (38.9%). In summary, the present study suggests that IgG1-class autoantibodies targeting epitopes on the processed extracellular domain of BP180, i.e., LABD97, are the major autoantibodies in DPP4i-BP.
  • Kentaro Izumi, Wataru Nishie, Mutsuo Beniko, Hiroshi Shimizu
    Frontiers in immunology 10 1439 - 1439 2019年 
    Background: Anti-hyperglycemic drug dipeptidyl peptidase-IV inhibitors (DPP-4i) have recently been recognized as bullous pemphigoid (BP) inducing drugs. It remains uncertain whether DPP-4i induce BP-IgG autoantibodies before the onset of BP. Objective: To evaluate the effect of DPP-4i in the development of BP-IgG autoantibodies in type 2 diabetes mellitus (T2DM) patients. Methods: A cross-sectional study on 221 DPP-4i (+) and 54 DPP-4i (-) T2DM cases was conducted. BP180 NC16A, BP230, and full-length BP180 ELISAs were used to detect the BP-IgG autoantibodies. We have also statistically analyzed the proportion of age, gender, intake periods of DPP-4i, and hemoglobin A1c level between anti-full-length BP180 IgG-positive and -negative DPP-4i (+) T2DM cases to identify co-founding factors. Results: BP180 NC16A ELISA, BP230 ELISA, and full-length BP180 ELISA were positive in 1.8, 2.2, and 10.9% of DPP-4i (+) T2DM cases, respectively; in contrast, they were positive in 0, 7.4, and 5.6% of DPP-4i (-) T2DM cases, respectively. The odds ratio for the development of BP-IgG autoantibodies detected by full-length BP180 ELISA was 2.070 for DPP-4i (+). There were no significant differences between the genders, intake periods of DPP-4i, nor of hemoglobin A1c levels, the anti-full-length BP180 IgG-positive cases tended to be significantly older than anti-full-length BP180 IgG-negative cases (median 74 vs. 69, p = 0.025) in the DPP-4i (+) T2DM cases. Limitations: We focused the analysis on DPP-4i intake and not on the effects of metformin and other drugs. Conclusion: Exposure to specific DPP-4i may induce the development of anti-full-length BP180 autoantibodies even in T2DM patients without any clinical symptoms of BP. Aging would be a risk factor to develop anti-full-length BP180-IgG autoantibody in DPP-4i (+) T2DM cases.
  • Ken Muramatsu, Hideyuki Ujiie, Ichiro Kobayashi, Wataru Nishie, Kentaro Izumi, Takamasa Ito, Norihiro Yoshimoto, Ken Natsuga, Hiroaki Iwata, Hiroshi Shimizu
    The Journal of allergy and clinical immunology 142 6 1818 - 1830 2018年12月 [査読有り][通常論文]
     
    BACKGROUND: Regulatory T (Treg) cells play a crucial role in peripheral immune tolerance in multiple organs, including the skin. Thus far, the effect of peripheral immune tolerance failure on autoantibody-related autoimmune reactions to the skin is unclear. OBJECTIVE: We sought to elucidate the target autoantigens in the skin under the condition of Treg cell dysfunction caused by forkhead box P3 (Foxp3) gene mutations in scurfy mice and patients with immunodysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) syndrome. METHODS: Sera and skin from scurfy mice and sera from patients with IPEX syndrome were analyzed to detect target autoantigens by using immunofluorescence studies, ELISAs, and immunoblotting. The pathogenicity of scurfy IgG was examined by using a passive transfer experiment. CD4+ T cells from scurfy mice were transferred to immunodeficient mice to examine their pathogenicity. Signal transducer and activator of transcription 6 (Stat6)-/- scurfy mice were analyzed to further clarify the molecular pathway of autoantibody production. Follicular helper T-cell counts are measured in Stat6-/- scurfy mice and scurfy mice. RESULTS: Scurfy mice spontaneously generated IgG autoantibodies to the dermal-epidermal junction, which had been class-switched from IgM within 12 days after birth. The target autoantigens were murine BP230 and type XVII collagen (COL17). The scurfy polyclonal autoantibodies did not induce skin fragility in neonatal mice. Autoantibody production was induced by CD4+ T cells from scurfy mice and was ameliorated by Stat6 gene knockout in association with a decrease of follicular helper T cells. We also identified autoantibodies to COL17 and BP230 in patients with IPEX syndrome and found an association between production of autoantibodies to COL17 and an eczematous skin phenotype. CONCLUSIONS: Dysregulation of Treg cells generates autoantibodies to COL17 and BP230 in vivo.
  • Tuusa J, Lindgren O, Tertsunen HM, Nishie W, Kokkonen N, Huilaja L, Izumi K, Herukka SK, Miettunen J, Shimizu H, Remes AM, Tasanen K
    The Journal of investigative dermatology 139 2 293 - 299 2018年10月 [査読有り][通常論文]
     
    Neurologic patients have an increased risk for bullous pemphigoid (BP), in which autoantibodies target BP180, a cutaneous basement membrane protein also expressed in the brain. Here we show that 53.6% of sera from patients with multiple sclerosis (MS) (n = 56) had IgG reactivity against full-length BP180 in immunoblotting, while in BP180 non-collagenous 16A ELISA (n = 143), only 7.7% of MS samples studied were positive. Epitope mapping with 13 fusion proteins covering the entire BP180 polypeptide revealed that in MS and Alzheimer's disease (AD) patients, IgG autoantibodies target regions located in the intracellular and mid-extracellular parts of BP180, but not the well-known BP epitopes located in the non-collagenous 16A domain and the distal part of extracellular domain. In indirect immunofluorescence analysis, 8.1% of MS sera recognized the cutaneous basement membrane and in full-length BP180 ELISA analysis, 7.5% MS and AD sera were positive, indicating that these autoantibodies rarely recognize BP180 in its native conformation. Thus, in MS and AD patients, BP180 autoantibodies have a different epitope profile than in patients with BP, and seldom bind to native BP180. This explains the inability of these autoantibodies to cause skin symptoms. Our results suggest that the autoantibodies against BP180 alone are not sufficient to induce BP in MS and AD patients.
  • Schauer F, Kern JS, Virtic O, Technau-Hafsi K, Meiss F, Thoma K, Athanasiou I, Sitaru C, Di Zenzo G, Izumi K, Nishie W, Shimizu H, Bruckner-Tuderman L, Kiritsi D
    The British journal of dermatology 2018年09月 [査読有り][通常論文]
  • Mai Y, Nishie W, Izumi K, Yoshimoto N, Morita Y, Watanabe M, Toyonaga E, Ujiie H, Iwata H, Fujita Y, Nomura T, Sato-Matsumura KC, Shimizu S, Shimizu H
    The British journal of dermatology 179 3 790 - 791 2018年09月 [査読有り][通常論文]
  • Takama H, Yoshida M, Izumi K, Yanagishita T, Muto J, Ohshima Y, Nishie W, Shimizu H, Akiyama M, Watanabe D
    Acta dermato-venereologica 98 10 983 - 984 2018年08月 [査読有り][通常論文]
  • Yuta Kage, Yukie Yamaguchi, Takahisa Uchida, Kentaro Izumi, Wataru Nishie, Hiroshi Shimizu, Norito Ishii, Takashi Hashimoto, Michiko Aihara
    The Journal of dermatology 45 7 e205-e206 - e206 2018年07月 [査読有り][通常論文]
  • Kawaguchi Y, Shimauchi R, Nishibori N, Kawashima K, Oshitani S, Fujiya A, Shibata T, Ohashi N, Izumi K, Nishie W, Shimizu H, Arima H, Sobajima H
    Journal of diabetes investigation 10 2 392 - 398 2018年06月 [査読有り][通常論文]
     
    AIMS/INTRODUCTION: Bullous pemphigoid (BP) might be drug-induced. The present study evaluated the relationship between BP and dipeptidyl peptidase-4 inhibitors (DPP4Is). MATERIALS AND METHODS: We recruited patients diagnosed with BP at Ogaki Municipal Hospital from 1 December 2009 through 31 December 2017. We retrospectively collected data from medical records and divided patients into two groups based on whether they received DPP4Is. Additionally, we determined the incidence of BP in patients who were first prescribed DPP4Is at our hospital during the study period. RESULTS: Of 168 patients diagnosed with BP, 133 (79.1%) were positive for anti-BP180NC16a antibody. A total of 32 (19.0%) patients had been prescribed a DPP4I, 21 of whom (65.6%) were positive for anti-BP180NC16a antibody; this rate was lower than that in patients not receiving a DPP4I (82.3%; P = 0.0360). A total of 16 patients with type 2 diabetes mellitus had not been prescribed a DPP4I; only one (6.3%) was positive for anti-BP180NC16a antibody (P = 0.0339). During the study period, 9,304 patients were prescribed DPP4Is, eight of whom developed BP; six (75.0%) had non-inflammatory BP, and five of the six (83.3%) were negative for anti-BP180NC16a antibody. CONCLUSIONS: The positive rate of anti-BP180NC16a antibody was lower in BP patients with DPP4I than without DPP4I, regardless of type 2 diabetes mellitus. The antibody titer was low in both the overall and type 2 diabetes mellitus populations. The prevalence of BP in 9,304 patients receiving DPP4Is was 0.0859%, which is higher than that in the general population. As DPP4Is are common diabetes treatments, we must be aware of the risk of BP.
  • Hideyuki Ujiie, Ken Muramatsu, Taisei Mushiroda, Takeshi Ozeki, Hideaki Miyoshi, Hiroaki Iwata, Akinobu Nakamura, Hiroshi Nomoto, Kyu Yong Cho, Norihiro Sato, Machiko Nishimura, Takamasa Ito, Kentaro Izumi, Wataru Nishie, Hiroshi Shimizu
    The Journal of investigative dermatology 138 5 1201 - 1204 2018年05月 [査読有り][通常論文]
  • Nobuki Maki, Wataru Nishie, Maya Takazawa, Maki Kakurai, Tomoko Yamada, Naoka Umemoto, Masaaki Kawase, Kentaro Izumi, Hiroshi Shimizu, Toshio Demitsu
    Journal of Dermatology 45 5 600 - 602 2018年05月01日 [査読有り][通常論文]
     
    Bullous pemphigoid (BP) is a common autoimmune blistering disorder with unknown etiology. Recently, increasing numbers of BP cases which developed under the medication with dipeptidyl peptidase-4 inhibitors (DPP4i), widely used antihyperglycemic drugs, have been reported in published works. Here, we report a case of DPP4i (teneligliptin)-associated BP that developed in a 70-year-old Japanese man. Interestingly, the patient had acquired reactive perforating collagenosis (ARPC), which is also known to be associated with the onset of BP. In the present case, clinical, histopathological and immunological findings suggested that DPP4i rather than ARPC was associated with the onset of BP.
  • 落葉状天疱瘡合併の悪性黒色腫に免疫チェックポイント阻害薬を投与した1例
    前田 拓哉, 柳 輝希, 今福 恵輔, 北村 真也, 秦 洋郎, 泉 健太郎, 氏家 英之, 岩田 浩明, 清水 宏
    日本皮膚科学会雑誌 128 5 1232 - 1232 (公社)日本皮膚科学会 2018年05月
  • Yosuke Mai, Wataru Nishie, Kazumasa Sato, Moeko Hotta, Kentaro Izumi, Kei Ito, Kazuyoshi Hosokawa, Hiroshi Shimizu
    Frontiers in Immunology 9 542 - 542 2018年04月12日 [査読有り][通常論文]
     
    Bullous pemphigoid (BP) is a common autoimmune blistering disease in which autoantibodies mainly target the hemidesmosomal component BP180 (also known as type XVII collagen) in basal keratinocytes. Various triggering factors are known to induce BP onset, including radiotherapy, burns, ultraviolet exposure, surgery, and the use of dipeptidyl peptidase-IV inhibitors (DPP4i), which are widely used antihyperglycemic drugs. Here, we present a case of BP triggered by a thermal burn under medication with DPP4i. A 60-year-old man with type II diabetes had been treated with the DPP4i linagliptin for 1 year. After the right forearm experienced a thermal burn, blisters developed around the burned area and gradually spread over the whole body with the production of autoantibodies targeting the non-NC16A domain of BP180. The diagnosis of BP was confirmed by immunohistopathological examination. Upon withdrawal of linagliptin and treatment with topical steroid and minocycline, complete remission was achieved after 4 months. Previously, 13 cases of BP that developed after thermal burns have been reported, and our case shared some of the clinical features of these thermal burn-induced BP cases. Interestingly, the present case also showed the typical clinical, histopathological, and immunological features of the non-inflammatory type of DPP4i-associated BP (DPP4i-BP). Although the pathogenesis of BP remains uncertain, the present case suggests that DPP4i may trigger the onset of BP similarly to a thermal burn. In addition, the clinical and histopathological features of DPP4i-BP may be distinct from other types of BP.
  • Kazumasa Oya, Masanao Fujii, Shijima Taguchi, Wataru Nishie, Kentaro Izumi, Hiroshi Shimizu
    European Journal of Dermatology 28 2 250 - 251 2018年03月01日 [査読有り][通常論文]
  • 落葉状天疱瘡合併悪性黒色腫に免疫チェックポイント阻害薬を投与した1例
    前田 拓哉, 柳 輝希, 今福 恵輔, 北村 真也, 秦 洋郎, 泉 健太郎, 氏家 英之, 岩田 浩明, 清水 宏
    日本皮膚科学会雑誌 128 1 61 - 61 (公社)日本皮膚科学会 2018年01月
  • Linagliptin treatment associated-bullous pemphigoid presenting severe mucosal erosions
    Mukaijo J, Kanaoka M, Kawano K, Matsukura S, Hibiya T, Miyake A, Izumi K, Nishie W, Shimizu H, Aihara M
    Journal of Cutaneous Immunology and Allergy 1 2 77 - 78 2018年 [査読有り][通常論文]
  • Allergic contact dermatitis caused by 2-hydroxyethyl acrylate in a moisturizing face pack in a handmade acrylic accessory enthusiast.
    Mukaijo J, Kanaoka M, Kawano K, Matsukura S, Hibiya T, Miyake A, Izumi K, Nishie W, Shimizu H, Aihara M
    Contact Dermatitis 79 6 383 - 385 2018年 [査読有り][通常論文]
  • Keisuke Imafuku, Hiroaki Iwata, Mayumi Kamaguchi, Kentaro Izumi, Ken Natsuga, Hideyuki Ujiie, Wataru Nishie, Hiroshi Shimizu
    Experimental Dermatology 26 12 1171 - 1174 2017年12月01日 [査読有り][通常論文]
     
    Type XVII collagen (COL17) and the non-collagenous 16A (NC16A) domain is regarded as the major pathogenic domains for bullous pemphigoid (BP). Some patients with BP have autoantibodies against parts of COL17 outside the NC16A domain (hereinafter the non-NC16A domain) and show less inflammatory manifestations. There were no significant differences in titres and IgG subclasses between NC16A-BP and non-NC16A-BP as determined by indirect immunofluorescent microscopy. The neutrophil activation capacities determined by ROS release did not differ between NC16A-BP and non-NC16A-BP. However, NC16A-BP IgG depleted COL17 in a dose-dependent manner. Treatment with NC16A-BP IgG, but not with non-NC16A-BP IgG, significantly decreased the adhesion strength. We speculate that the differences in clinical severity between NC16A-BP and non-NC16A-BP relate to the degree of COL17 depletion.
  • Takuya Maeda, Teruki Yanagi, Keisuke Imafuku, Shinya Kitamura, Hiroo Hata, Kentaro Izumi, Hideyuki Ujiie, Hiroaki Iwata, Hiroshi Shimizu
    INTERNATIONAL JOURNAL OF DERMATOLOGY 56 12 1477 - 1479 2017年12月 [査読有り][通常論文]
  • Ellen Toyonaga, Wataru Nishie, Kentaro Izumi, Ken Natsuga, Hideyuki Ujiie, Hiroaki Iwata, Jun Yamagami, Yoshiaki Hirako, Daisuke Sawamura, Wataru Fujimoto, Hiroshi Shimizu
    JOURNAL OF INVESTIGATIVE DERMATOLOGY 137 12 2552 - 2559 2017年12月 [査読有り][通常論文]
     
    Transmembrane collagen XVII (COL17) is a hemidesmosomal component of basal keratinocytes that can be targeted by autoantibodies in autoimmune blistering disorders, including linear IgA dermatosis (LAD). COL17 can be physiologically cleaved within the juxtamembranous extracellular NC16A domain, and LAD autoantibodies preferentially react with the processed ectodomains, indicating that the processing induces neoepitopes. However, the details of how neoepitopes develop have not been elucidated. In this study, we show that C-terminal processing of COL17 also plays a role in inducing neoepitopes for LAD autoantibodies. First, the mAb hC17-ect15 targeting the 15th collagenous domain of COL17 was produced, which showed characteristics similar to LAD autoantibodies. The mAbs preferentially reacted with C-terminally deleted (up to 682 amino acids) recombinant COL17, suggesting that C-terminal processing shows neoepitopes on the 15th collagenous domain. The LAD autoantibodies also react with C-terminal deleted COL17. Therefore, neoepitopes for LAD autoantibodies also develop after C-terminal processing. Finally, the passive transfer of the mAb hC17-ect15 into human COL17-expressing transgenic mice failed to induce blistering disease, suggesting that neoepitope-targeting antibodies are not always pathogenic. In summary, this study shows that C-terminal processing induces dynamic structural changes and neoepitopes for LAD autoantibodies on COL17.
  • Keiko Shiba-Tokuchi, Reine Moriuchi, Yusuke Morita, Yuka Takashima, Takahisa Shirato, Yuta Koike, Kentaro Izumi, Wataru Nishie, Satoko Shimizu
    JOURNAL OF DERMATOLOGY 44 12 e365 - e366 2017年12月 [査読有り][通常論文]
  • Moeko Hotta, Teruki Yanagi, Tatsuro Sugai, Shinichi Nakazato, Kentaro Izumi, Hiroo Hata, Kohei Okada, Hideki Goto, Yoshihiro Matsuno, Hiroshi Shimizu
    JOURNAL OF DERMATOLOGY 44 12 e359 - e360 2017年12月 [査読有り][通常論文]
  • Ken Natsuga, Wataru Nishie, Machiko Nishimura, Satoru Shinkuma, Mika Watanabe, Kentaro Izumi, Hideki Nakamura, Yoshiaki Hirako, Hiroshi Shimizu
    HUMAN MUTATION 38 12 1666 - 1670 2017年12月 [査読有り][通常論文]
     
    Plectin is a linker protein that interacts with intermediate filaments and 4 integrin in hemidesmosomes of the epidermal basement membrane zone (BMZ). Type XVII collagen (COL17) has been suggested as another candidate plectin binding partner in hemidesmosomes. Here, we demonstrate that plectin-COL17 binding helps to maintain epidermal BMZ organization. We identified an epidermolysis bullosa (EB) simplex patient as having markedly diminished expression of plectin and COL17 in skin. The patient is compound heterozygous for sequence variants in the plectin gene (PLEC); one is a truncation and the other is a small in-frame deletion sequence variant. The in-frame deletion is located in the putative COL17-binding domain of plectin and abolishes the plectin-COL17 interaction in vitro. These results imply that disrupted interaction between plectin and COL17 is involved in the development of EB. Our study suggests that protein-protein binding defects may underlie EB in patients with unidentified disease-causing sequence variants.
  • Norihiro Yoshimoto, Teruki Yanagi, Wakana Matsumura, Inkin Ujiie, Kentaro Izumi, Satomi Ando, Wataru Nishie, Kyoko Fujii, Hiroshi Nishihara, Hiroshi Shimizu
    INTERNATIONAL JOURNAL OF DERMATOLOGY 56 12 1459 - 1461 2017年12月 [査読有り][通常論文]
  • Hideyuki Kosumi, Teruki Yanagi, Kentaro Izumi, Takamasa Ito, Hiroshi Shimizu
    CONTACT DERMATITIS 77 6 419 - + 2017年12月 [査読有り][通常論文]
  • Hideyuki Kosumi, Kentaro Izumi, Ken Natsuga, Yasuyuki Yamaguchi, Akira Itami, Hiroshi Shimizu
    Acta Dermato-Venereologica 97 10 1245 - 1246 2017年11月01日 [査読有り][通常論文]
  • Kentaro Izumi, Wataru Nishie, Yosuke Mai, Hideyuki Ujiie, Hiroaki Iwata, Ken Natsuga, Hiroshi Shimizu
    JOURNAL OF DERMATOLOGICAL SCIENCE 88 2 247 - 248 2017年11月 [査読有り][通常論文]
  • Kazumasa Oya, Masanao Fujii, Shijima Taguchi, Wataru Nishie, Kentaro Izumi, Hiroshi Shimizu
    JOURNAL OF DERMATOLOGY 44 10 E238 - E239 2017年10月 [査読有り][通常論文]
  • Hideyuki Kosumi, Takamasa Ito, Yasuyuki Fujita, Kentaro Izumi, Yuka Maya, Teruki Yanagi, Ken Natsuga, Hideyuki Ujiie, Satoru Shinkuma, Toshifumi Nomura, Naoya Sadanobu, Hiroshi Shimizu
    JOURNAL OF PEDIATRICS 188 305 - + 2017年09月 [査読有り][通常論文]
  • Kamaguchi M, Iwata H, Ujiie H, Izumi K, Natsuga K, Nishie W, Asaka T, Kitagawa Y, Shimizu H
    The British journal of dermatology 178 2 e119 - e121 2017年09月 [査読有り][通常論文]
  • 抗BP230抗体と全長BP180タンパクを用いたELISAが陽性であった水疱性類天疱瘡の1例
    小越 達也, 金岡 美和, 向所 純子, 河野 克之, 山口 由衣, 相原 道子, 松倉 節子, 小森 絢子, 泉 健太郎, 西江 渉
    日本皮膚科学会雑誌 127 6 1376 - 1376 (公社)日本皮膚科学会 2017年05月
  • Hiroaki Iwata, Mayumi Kamaguchi, Hideyuki Ujiie, Machiko Nishimura, Kentaro Izumi, Ken Natsuga, Satoru Shinkuma, Wataru Nishie, Hiroshi Shimizu
    LABORATORY INVESTIGATION 96 12 1301 - 1310 2016年12月 [査読有り][通常論文]
     
    Macropinocytosis is an endocytic pathway that is involved in the nonselective fluid uptake of extracellular fluid. Bullous pemphigoid (BP) is an autoimmune subepidermal blistering disease associated with autoantibodies to type XVII collagen (COL17), which is a component of hemidesmosome. When keratinocytes are treated with BP-IgG, COL17 internalizes into cells by way of the macropinocytosis. We investigated the mechanism of COL17 macropinocytosis using DJM-1 cells, a cutaneous squamous cell carcinoma cell line. First, non-hemidesmosomal COL17 was preferentially depleted by stimulation with the BP-IgG in the DJM-1 cells. To investigate the signaling involved in COL17-macropinocytosis, the inhibition of small GTPase family members Rac1 and Cdc42 was found to strongly repress COL17 internalization; in addition, the Rho inhibitor also partially blocked that internalization, suggesting these small GTPases are involved in signaling to mediate COL17-macropinocytosis. Western blotting using Phostag-SDS-PAGE demonstrated high levels of COL17 phosphorylation in DJM-1 cells under steady-state condition. Treatment with BP-IgG increased the intracellular calcium level within a minute, and induced the overabundant phosphorylation of COL17. The overabundant phosphorylation of COL17 was suppressed by a protein kinase C (PKC) inhibitor. In addition, PKC inhibitor repressed COL17 endocytosis using cell culture and organ culture systems. Finally, the depletion of COL17 was not observed in the HEK293 cells transfected COL17 without intracellular domain. These results suggest that COL17 internalization induced by BP-IgG may be mediated by a PKC pathway. In summary, BP-IgG initially binds to COL17 distributed on the plasma membrane, and COL17 may be internalized by means of a macropinocytic pathway related to the phosphorylation of the intracellular domain by PKC.
  • Kentaro Izumi, Wataru Nishie, Yosuke Mai, Mayumi Wada, Ken Natsuga, Hideyuki Ujiie, Hiroaki Iwata, Jun Yamagami, Hiroshi Shimizu
    JOURNAL OF INVESTIGATIVE DERMATOLOGY 136 11 2201 - 2210 2016年11月 [査読有り][通常論文]
     
    Bullous pemphigoid (BP) is a major autoimmune blistering skin disorder, in which a majority of the autoantibodies (autoAbs) target the juxtamembranous extracellular noncollagenous 16A domain (NC16A) domain of hemidesmosomal collagen XVII. BP-autoAbs may target regions of collagen XVII other than the NC16A domain; however, correlations between epitopes of BP-autoAbs and clinical features have not been fully elucidated. To address correlations between the clinical features and specific epitopes of BP-autoAbs, we evaluated the epitope profiles of BP-autoAbs in 121 patients. A total of 87 patients showed a typical inflammatory phenotype with erythema and autoAbs targeting the anti-NC16A domain, whereas 14 patients showed a distinct noninflammatory phenotype, in which autoAbs specifically targeted the midportion of collagen XVII, but not NC16A. Interestingly, this group clinically showed significantly reduced erythema associated with scant lesional infiltration of eosinophils. Surprisingly, 7 of the 14 cases (50.0%) received dipeptidyl peptidase-IV inhibitors for the treatment of diabetes. Dipeptidyl peptidase-IV inhibitors were used in 3 of 76 (3.9%) typical cases of BP with autoAbs targeting NC16A; thus, dipeptidyl peptidase-IV inhibitors are thought to be involved in the development of atypical noninflammatory BP. This study shows that the autoAb profile differentiates between inflammatory and noninflammatory BP, and that noninflammatory BP may be associated with dipeptidyl peptidase-IV inhibitors.
  • Ellen Toyonaga, Hiroaki Iwata, Moeko Hotta, Norihiro Yoshimoto, Kentaro Izumi, Hiroshi Shimizu
    AMERICAN JOURNAL OF MEDICINE 129 11 1163 - 1165 2016年11月 [査読有り][通常論文]
  • Mayumi Wada, Wataru Nishie, Hideyuki Ujiie, Kentaro Izumi, Hiroaki Iwata, Ken Natsuga, Hideki Nakamura, Yoshimasa Kitagawa, Hiroshi Shimizu
    JOURNAL OF INVESTIGATIVE DERMATOLOGY 136 5 938 - 946 2016年05月 [査読有り][通常論文]
     
    In bullous pemphigoid, the common autoimmune blistering disorder, IgG autoantibodies target various epitopes on hemidesmosomal transmembrane collagen XVII (COL17)/BP180. Antibodies (Abs) targeting the extracellular noncollagenous 16th A domain of COL17 may be pathogenic; however, the pathogenic roles of Abs targeting non-noncollagenous 16th A regions are poorly understood. In this study using a pathogenic and a nonpathogenic monoclonal antibody (mAb) targeting the noncollagenous 16th A domain (mAb TS39-3) and the C-terminus domain (mAb C17-C1), respectively, we show that endocytosis of immune complexes after binding of Abs to cell surface COL17 is a key phenomenon that induces skin fragility. Passive transfer of IgG1 mouse mAb TS39-3 but not mAb C17-C1 induces dermal-epidermal separation in neonatal human COL17-expressing transgenic mice. Interestingly, mAb C17-C1 strongly binds with the dermal-epidermal junction of the recipient mice skin, suggesting that binding of Abs with COL17 is insufficient to induce skin fragility. In cultured normal human epidermal keratinocytes treated with these mAbs, mAb TS39-3 but not mAb C17-C1 internalizes immune complexes after binding with cell surface COL17 via macropinocytosis, resulting in reduced COL17 expression. This study shows that pathogenicity of Abs targeting COL17 is epitope dependent, which is associated with macropinocytosis-mediated endocytosis of immune complexes and finally results in the depletion of COL17 expression in basal keratinocytes.
  • Wataru Nishie, Ken Natsuga, Hiroaki Iwata, Kentaro Izumi, Hideyuki Ujiie, Ellen Toyonaga, Hiroo Hata, Hideki Nakamura, Hiroshi Shimizu
    AMERICAN JOURNAL OF PATHOLOGY 185 5 1361 - 1371 2015年05月 [査読有り][通常論文]
     
    Pemphigoid is a common autoimmune blistering disorder in which autoantibodies target transmembrane collagen XVII (COL17), a component of hemidesmosomes in basal keratinocytes. The ectodomain of COL17 can be cleaved from the cell surface within the juxtamembranous extracellular NC16A domain, and, interestingly, certain autoantibodies of pemphigoid patients preferentially react with the shed ectodomain. These findings suggest that COL17 ectodomain shedding generates neoepitopes on the shed form; however, the regulatory mechanism of the shedding in in vivo skin and the pathogenicity of the neoepitope-targeting antibodies still are uncertain. To address these issues, we produced rabbit antibodies specifically reacting with N-terminal cleavage sites of the shed COL17 ectodomain. The antibodies showed that certain amounts of the human COL17 ectodomain are cleaved physiologically at Gln(525) in in vivo skin. In contrast, migrating human keratinocytes cleave COL17 at Leu(524) but not at Gln(525). The passive transfer of antibodies reacting with an N-terminal cleavage site of the mouse COL17 ectodomain into neonatal wild-type mice failed to induce blister formation, even though the antibodies bound to the dermal-epidermal junctions, indicating that cleavage site-specific antibodies have reduced or absent pathogenicity for blister formation. This study shows the ectodomain shedding of COL17 to be a physiological event in in vivo human skin that probably generates nonpathologic epitopes on the cleavage sites.
  • Horie K, Izumi K, Nishie W, Nomura T, Nomura Y, Arita K, Shimizu H
    The Journal of dermatology 42 1 101 - 102 2015年01月 [査読有り][通常論文]
  • Hideyuki Ujiie, Tetsumasa Sasaoka, Kentaro Izumi, Wataru Nishie, Satoru Shinkuma, Ken Natsuga, Hideki Nakamura, Akihiko Shibaki, Hiroshi Shimizu
    JOURNAL OF IMMUNOLOGY 193 9 4415 - 4428 2014年11月 [査読有り][通常論文]
     
    Complement activation and subsequent recruitment of inflammatory cells at the dermal/epidermal junction are thought to be essential for blister formation in bullous pemphigoid (BP), an autoimmune blistering disease induced by autoantibodies against type XVII collagen (COL17); however, this theory does not fully explain the pathological features of BP. Recently, the involvement of complement-independent pathways has been proposed. To directly address the question of the necessity of the complement activation in blister formation, we generated C3-deficient COL17-humanized mice. First, we show that passive transfer of autoantibodies from BP patients induced blister formation in neonatal C3-deficient COL17-humanized mice without complement activation. By using newly generated human and murine mAbs against the pathogenic noncollagenous 16A domain of COL17 with high (human IgG1, murine IgG2), low (murine IgG1), or no (human IgG4) complement activation abilities, we demonstrate that the deposition of Abs, and not complements, is relevant to the induction of blister formation in neonatal and adult mice. Notably, passive transfer of BP autoantibodies reduced the amount of COL17 in lesional mice skin, as observed in cultured normal human keratinocytes treated with the same Abs. Moreover, the COL17 depletion was associated with a ubiquitin/proteasome pathway. In conclusion, the COL17 depletion induced by BP autoantibodies, and not complement activation, is essential for the blister formation under our experimental system.
  • ヒト17型コラーゲン全長リコンビナントタンパクを用いた新規ELISAの確立
    泉 健太郎, 西江 渉, 氏家 英之, 清水 宏
    日本皮膚科学会雑誌 124 10 1928 - 1929 (公社)日本皮膚科学会 2014年09月
  • Kentaro Izumi, Ken Arita, Keita Horie, Daichi Hoshina, Hiroshi Shimizu
    ACTA DERMATO-VENEREOLOGICA 94 2 225 - 226 2014年 [査読有り][通常論文]
  • Kentaro Izumi, Teruki Yanagi, Masashi Akiyama, Reine Moriuchi, Ken Arita, Hiroshi Shimizu, Masashi Akiyama
    INTERNATIONAL JOURNAL OF DERMATOLOGY 52 10 1274 - 1275 2013年10月 [査読有り][通常論文]
  • 堀江 啓太, 秦 洋郎, 馬場 慶子, 泉 健太郎, 本間 英里奈, 氏家 英之, 青柳 哲, 細川 正夫, 清水 宏
    臨床皮膚科 67 3 249 - 253 (株)医学書院 2013年03月 
    70歳,男性.初診の約2週間前から右鎖骨上窩の皮下腫瘤を自覚していた.近医で施行された穿刺吸引細胞診で悪性黒色腫のリンパ節転移と診断され,全身精査・加療目的に当科紹介受診となった.初診時,原発を疑わせる皮疹はなく,PET/CTでも右鎖骨上窩の皮下腫瘤のみにしかFDGの集積を認めなかった.上部消化管内視鏡検査を施行したところ,食道内に20×15mmの隆起性黒色病変があり,生検にて食道原発の悪性黒色腫と診断した.食道亜全摘,噴門側胃切除,3領域リンパ節郭清施行し,食道原発悪性黒色腫Stage IIと診断し,術後DAV-フェロン療法5コースを追加した.食道原発悪性黒色腫は非常に稀で,通常のより予後不良である.頸部あるいは鎖骨上窩リンパ節の転移性病変を見た際には,原発となりうる咽頭,喉頭,および消化管の内視鏡検査などによる直視下での病変検索を怠ってはいけないことを留意すべきであると考えた.(著者抄録)
  • Wakana Omiya, Hideyuki Ujiie, Masashi Akiyama, Kentaro Izumi, Akio Shigematsu, Masahiro Onozawa, Hiroshi Shimizu
    EUROPEAN JOURNAL OF DERMATOLOGY 22 5 711 - 712 2012年09月 [査読有り][通常論文]
  • 皮膚結節性アミロイドーシスの2例
    泉 健太郎, 猪熊 大輔, 笠井 麻希, 藤田 靖幸, 氏家 英之, 山中 快子, 伊藤 圭, 清水 宏
    日本皮膚科学会雑誌 122 1 51 - 51 (公社)日本皮膚科学会 2012年01月
  • Rinko Osawa, Masashi Akiyama, Kentaro Izumi, Hideyuki Ujiie, Kaori Sakai, Ikue Nemoto-Hasebe, Teruki Yanagi, Hiroko Koizumi, Hiroshi Shimizu
    JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY 64 5 991 - 993 2011年05月 [査読有り][通常論文]
  • 飯谷麻里, 小玉和郎, 泉健太郎, 藤田靖幸, 阿部由紀子, 阿部理一郎, 清水宏
    日本皮膚病理組織学会会誌 26 2 37  2011年03月20日 [査読無し][通常論文]
  • Satoru Aoyagi, Hiroo Hata, Kentaro Izumi, Maria Maroto Iitani, Hiroshi Shimizu
    ACTA DERMATO-VENEREOLOGICA 90 4 440 - 441 2010年 [査読有り][通常論文]
  • Aoyagi S, Izumi K, Hata H, Kawasaki H, Shimizu H
    Clinical and experimental dermatology 34 e744 - 7 8 2009年12月 [査読有り][通常論文]

その他活動・業績

  • M. Zheng, H. Ujiie, K. Muramatsu, K. C. Sato-Matsumura, T. Maeda, I. Ujiie, H. Iwata, K. Izumi, W. Nishie, H. Shimizu British Journal of Dermatology 178 (6) 1449 -1450 2018年06月
  • 奥平 あずさ, 松岡 摩耶, 松浦 哲彦, 門野 岳史, 川上 民裕, 相馬 良直, 泉 健太郎, 西江 渉, 清水 宏 皮膚科の臨床 60 (5) 593 -594,607-610 2018年05月 [査読無し][通常論文]
  • H. Kosumi, T. Yanagi, K. Izumi, T. Ito, H. Shimizu Journal of the European Academy of Dermatology and Venereology 32 (4) e126 -e127 2018年04月01日 [査読無し][通常論文]
  • N. Yoshimoto, H. Ujiie, Y. Hirata, K. Izumi, W. Nishie, H. Shimizu Journal of the European Academy of Dermatology and Venereology 31 (4) e187 -e189 2017年04月01日 [査読無し][通常論文]
  • Y. Yamaguchi, S. Nakazato, K. Izumi, M. Ieko, T. Nomura, H. Shimizu JOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY AND VENEREOLOGY 31 (1) E45 -E46 2017年01月 [査読無し][通常論文]
  • K. Natsuga, W. Nishie, M. Nishimura, S. Shinkuma, M. Watanabe, K. Izumi, H. Nakamura, Y. Hirako, H. Shimizu JOURNAL OF INVESTIGATIVE DERMATOLOGY 136 (9) S186 -S186 2016年09月 [査読無し][通常論文]
  • H. Iwata, H. Ujiie, K. Izumi, K. Natsuga, S. Shinkuma, W. Nishie, H. Shimizu JOURNAL OF INVESTIGATIVE DERMATOLOGY 136 (9) S172 -S172 2016年09月 [査読無し][通常論文]
  • H. Iwata, K. Imafuku, K. Izumi, M. Wada, K. Natsuga, H. Ujiie, W. Nishie, H. Shimizu JOURNAL OF INVESTIGATIVE DERMATOLOGY 135 S4 -S4 2015年09月 [査読無し][通常論文]
  • 椎谷 千尋, 夏賀 健, 泉 健太郎 臨床皮膚科 = Japanese journal of clinical dermatology 69 (10) 731 -734 2015年09月 [査読無し][通常論文]
  • Piezogenic pedal papulesの3例
    椎谷 千尋, 夏賀 健, 泉 健太郎, 青柳 哲, 清水 宏 日本皮膚科学会雑誌 125 (6) 1281 -1281 2015年05月 [査読無し][通常論文]
  • 抗NC16A抗体を有さない軽症の水疱性類天疱瘡の1例
    今福 恵輔, 岩田 浩明, 泉 健太郎, 夏賀 健, 氏家 英之, 西江 渉, 清水 宏 日本皮膚科学会雑誌 125 (4) 915 -915 2015年04月 [査読無し][通常論文]
  • 水疱性類天疱瘡自己抗原である17型コラーゲンの異なるエピトープに対する抗体の病原性解析
    和田 麻友美, 西江 渉, 氏家 英之, 泉 健太郎, 岩田 浩明, 夏賀 健, 清水 宏, 北川 善政 北海道歯学雑誌 35 (2) 188 -188 2015年03月 [査読無し][通常論文]
  • Piezogenic pedal papulesの3例
    椎谷 千尋, 夏賀 健, 泉 健太郎, 青柳 哲, 清水 宏 日本皮膚科学会雑誌 124 (11) 2134 -2134 2014年10月 [査読無し][通常論文]
  • W. Nishie, W. Mayumi, K. Natsuga, K. Izumi, H. Shimizu JOURNAL OF INVESTIGATIVE DERMATOLOGY 134 S13 -S13 2014年09月 [査読無し][通常論文]
  • W. Nishie, H. Ujiie, K. Izumi, H. Shimizu JOURNAL OF INVESTIGATIVE DERMATOLOGY 133 S20 -S20 2013年05月 [査読無し][通常論文]
  • 中村 裕之, 泉 健太郎, 八百坂 遵 Skin Cancer 27 (1) 56 -59 2012年 [査読無し][通常論文]
     
    症例1:82歳,女性。初診の2年前から痛痒い感覚が持続していた。初診時肛門左側に40×25 mm大のやや紅い黒色調局面が存在した。症例2:63歳,女性。項部の基底細胞癌加療後,肛囲の皮疹について診察依頼があった。発症時期は不明だが,2,3ヵ月前から排便時出血を認めるようになった。肛門左側に10×8 mm大の蝋様光沢を有する黒色局面が存在した。いずれの症例も病理組織学的に基底細胞癌と診断し,単純切除・縫縮を行った。肛囲は基底細胞癌発生部位としては比較的稀なのでその特徴について文献的考察を行った。
  • 泉健太郎, 阿部理一郎, 方波見謙一, 守内玲寧, 浜坂明日香, 阿部由紀子, 清水宏, 川村邦子 日本皮膚科学会雑誌 121 (14) 3363 2011年12月20日 [査読無し][通常論文]
  • 泉 健太郎, 有田 賢, 長谷部 育恵 臨床皮膚科 64 (7) 477 -480 2010年06月 [査読無し][通常論文]
  • 青柳 哲, 秦 洋郎, 泉 健太郎, 清水 宏 Skin cancer : official organ of the Japanese Society for Skin Cancer = 皮膚悪性腫瘍研究会機関誌 24 (2) 234 -238 2009年10月10日 [査読無し][通常論文]
     
    鼻部の基底細胞癌に対して,Mohs micrographic surgeryの手法を術中迅速病理診断に取り入れ,その際,二枚のメス刃を平行に固定したdouble-bladed scalpelを使用し,確実かつ効率的に治療し得た症例を経験した。59歳男性。約5年前に出現した左鼻翼から鼻尖部にかけての3cm大の境界不明瞭な萎縮性陥凹を伴う病変に対して,術中に凍結切片にて病理組織学的な腫瘍の浸潤範囲を確認しつつ切除を行った。計2回の追加切除にて組織学的な陰性を確認し,耳介軟骨移植と皮弁による即時再建を行った。<br> 本邦でも,従来の迅速病理診断にMohs micrographic surgeryの手法を加えることが,腫瘍の境界が不明瞭な症例に対しての確実性が高い治療法のひとつになると考えられた。その際,double-bladed scalpelを用いることは,手技自体も簡便となる工夫と考えられた。
  • 西 正吾, 木下 裕介, 泉 健太郎, 深堀 晋, 増田 智広, 浅野目 晃 脳卒中の外科 37 (6) 453 -460 2009年 [査読無し][通常論文]
     
    For the supra-aortic atherosclerotic stenoses, neurovascular and neuro-interventional approaches have been performed. Interventional approaches have risk of thrombo-embolic events, while vascular approaches have surgical stress. We developed and applied a method for cerebral protection for stenting of supra-aortic stenoses and introduce our method in this article. <br> We performed stenting in 20 supra-aortic stenoses from April 2006 to March 2008. Our cerebral protection method, a modified application of the “Mouse Trap” (“Mouse in a Trap”) method usually used for CAS patients, was applied for 5 patients (1 CCA origin stenosis, 1 brachio-cephalic artery stenosis, 1 SA stenosis, 1 VA V3-V4 stenosis, 1 ICA petrous segment stenosis). The stenotic lesion was dilated and stented, while the lesion was endovascularily trapped with the occlusion balloon and so on.<br> After each manipulation (predilation, stenting, post-dilation), the blood with the clots and debris was aspirated, filtrated, and returned to the body via the vein. We modified the method for supra-aortic stenotic lesions according to their anatomical location, but maintained the principle of the “Mouse Trap” method.<br> In all 5 cases, the protection procedure was done without worsening of clinical findings. However, high intensity areas on DWI were subclinically found in 2 patients.<br> Although this study covered only a small number of cases, non-CAS supra-aortic atherosclerotic stenoses cases were safely stented under a modified “Mouse Trap” cerebral protection system.<br>

教育活動情報

主要な担当授業

  • 基本医学研究
    開講年度 : 2021年
    課程区分 : 修士課程
    開講学部 : 医学院
    キーワード : 皮膚、遺伝子治療、遺伝子診断、水疱症、遺伝性皮膚疾患、がんプロフェッショナル
  • 皮膚科学
    開講年度 : 2021年
    課程区分 : 学士課程
    開講学部 : 医学部
    キーワード : 皮膚科 皮膚疾患


Copyright © MEDIA FUSION Co.,Ltd. All rights reserved.