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タイトル: A unique profile of insulin antibody titer in islet‐transplanted patients
著者: Keidai, Yamato
Fujikura, Junji  kyouindb  KAKEN_id  orcid https://orcid.org/0000-0002-9668-8174 (unconfirmed)
Nakamura, Toshihiro
Anazawa, Takayuki  kyouindb  KAKEN_id  orcid https://orcid.org/0000-0002-7625-5750 (unconfirmed)
Ito, Ryo
Ogura, Masahito
Hatano, Etsuro
Inagaki, Nobuya
著者名の別形: 境内, 大和
藤倉, 純二
中村, 聡宏
穴澤, 貴行
伊藤, 遼
小倉, 雅仁
波多野, 悦朗
稲垣, 暢也
キーワード: Immunosuppression therapy
Insulin antibodies
Islet transplantation
発行日: Nov-2022
出版者: Wiley
Asian Association for the Study of Diabetes (AASD)
誌名: Journal of Diabetes Investigation
巻: 13
号: 11
開始ページ: 1939
終了ページ: 1942
抄録: Insulin antibodies (IAs) can cause glycemic variability. Islet transplantation (ITx) is a treatment for insulin-deficient diabetes that aims to establish on-target glycemic control in the absence of hypoglycemia. To date, there has not been a detailed case study of the association between ITx and IA levels. In this study, we identified a unique profile of IA titers, which differed from glutamic acid decarboxylase antibody titers, in four ITx patients. IA levels decreased with intensified immunosuppressive therapy, whereas glutamic acid decarboxylase antibodies increased transiently after ITx. These data suggest the possibility that IAs, unlike other islet autoantibodies, were eliminated due to immunosuppression after transplantation therapy. The disappearance of IAs, as well as the restoration of regulated insulin secretion after ITx, might have a positive effect on glycemic control in recipients with diabetes. Furthermore, this unique feature is suggestive of immunological pathogenesis and has implications for the treatment of IA-causing disease conditions.
著作権等: © 2022 The Authors. Journal of Diabetes Investigation published by Asian Association for the Study of Diabetes (AASD) and John Wiley & Sons Australia, Ltd.
This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
URI: http://hdl.handle.net/2433/283288
DOI(出版社版): 10.1111/jdi.13878
PubMed ID: 35735779
出現コレクション:学術雑誌掲載論文等

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