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      Administration of thiamazole for Graves’ disease might trigger the onset of type 1 diabetes

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          Abstract

          Thiamazole might trigger the onset of type 1 diabetes.

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          Allele specificity of structural requirement for peptides bound to HLA- DRB1*0405 and -DRB1*0406 complexes: implication for the HLA-associated susceptibility to methimazole-induced insulin autoimmune syndrome

          Self-peptides bound to HLA-DR4 (DRA-DRB1*0405 complex) were eluted from the purified DR4 complex, fractionated on reverse-phase HPLC, and subjected to NH2-terminal sequencing. Seven independent sequences were obtained, and all putative peptides synthesized bound to DRB1*0405 as well as DRB1*0406 complex, which differ only at DR beta residues 37, 57, 74, and 86. Binding assay using analogue peptides of a DR4 binder GSTVFDNLPNPE revealed that FxxLxN is an important anchor motif necessary for binding (where x is any amino acid), which was common to DRB1*0405 and 0406. Determination of the binding affinity of 60 synthetic AAFAALANAA-based analogue peptides showed that substituting F to W or C; L to F, W, or Y; and N to Q or S on AAFAALANAA changed the affinity substantially between DRB1*0405 and DRB1*0406. It is noteworthy that all patients with methimazole-induced insulin autoimmune syndrome are positive for DRB1*0406 and negative for DRB1*0405. Interestingly, the quantitative structural motif identified in this study predicted that 8TSICSLYQLE17 of human insulin alpha chain may bind specifically to DRB1*0406 using its 10IxxLxQ15 motif. Indeed, DRB1*0406 complex bound 8TSICSLYQLE17 with a high affinity, and in striking contrast, DRB1*0405 complex did not. Furthermore, a short-term T cell line specific to human insulin established from a DRB1*0406- bearing individual did show reactivity with a peptide fragment containing the 10IxxLxQ15 motif. Although this fragment probably exists at a very low level under normal physiological conditions due to the disulfide bond between flanking cysteine residues (6Cys-11Cys), a reducing compound such as methimazole may cleave the disulfide bond in vivo and allow DR alpha-DRB1*0406 complex on antigen-presenting cells to bind much of the linear fragment of insulin alpha chain, which may lead to the activation of self-insulin-specific T-helper cells.
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            Simultaneous occurrence of type 1 diabetes mellitus and Graves' disease: a report of two cases and a review of the literature.

            Two unrelated Japanese women, 41 and 27 years of age, were admitted with histories of thirst, weight loss and palpitations of a few weeks' duration. Both were diagnosed to have diabetic ketosis or ketoacidosis with acute-onset type 1 diabetes (T1D) and Graves' disease (GD) (autoimmune polyglandular syndrome type 3 variant; APS3v), and were treated with intensive insulin therapy and anti-thyroid drugs. Human leukocyte antigen examinations showed that both cases had the HLA-A2, A24, B54, and DRB1*04:05-DQA1*03:03-DQB1*04:01 haplotype, which made them susceptible not only to APS3v, but also to both acute-onset T1D and GD. The genetic background of patients strongly contributes to the simultaneous occurrence of T1D and GD.
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              Author and article information

              Contributors
              asmd@saitama-med.ac.jp
              Journal
              J Diabetes Investig
              J Diabetes Investig
              10.1111/(ISSN)2040-1124
              JDI
              Journal of Diabetes Investigation
              John Wiley and Sons Inc. (Hoboken )
              2040-1116
              2040-1124
              14 June 2018
              September 2018
              : 9
              : 5 ( doiID: 10.1111/jdi.2018.9.issue-5 )
              : 1228-1229
              Affiliations
              [ 1 ] Department of Endocrinology and Diabetes Biomedical Research Center Saitama Medical University Moroyama Saitama Japan
              [ 2 ] Division of RI Laboratory Biomedical Research Center Saitama Medical University Moroyama Saitama Japan
              Author notes
              [*] [* ] Corresponding author. Akira Shimada

              Tel.: +81‐49‐276‐1204

              Fax: +81‐49‐294‐9752

              E‐mail address: asmd@ 123456saitama-med.ac.jp

              Author information
              http://orcid.org/0000-0002-3954-4983
              Article
              JDI12784
              10.1111/jdi.12784
              6123042
              29900683
              1c0759a0-9750-426f-a914-c1313fa715fe
              © 2018 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 http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

              History
              : 25 September 2017
              : 10 November 2017
              : 27 November 2017
              Page count
              Figures: 1, Tables: 0, Pages: 2, Words: 984
              Categories
              Letter to the Editor
              Letters to the Editor
              Custom metadata
              2.0
              jdi12784
              September 2018
              Converter:WILEY_ML3GV2_TO_NLMPMC version:version=5.4.7.1 mode:remove_FC converted:04.09.2018

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