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. 2021 Mar 1;71(3):689–695. doi: 10.1007/s12020-020-02603-y

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Pathophysiology and clinical characteristics of MCT8 deficiency. Tissues that rely on MCT8 for thyroid hormone transport are relatively hypothyroid, whereas tissues that are independent of MCT8 are in a thyrotoxic state, caused by the increased serum T3 concentrations. TH thyroid hormone, PACs premature atrial complexes, SHBG sex hormone binding globulin, CK creatine kinase, BMI body mass index