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Leonidas Duntas L Duntas, Endocrine Unit, Evgenideion Hospital, Athens , 11528, Greece

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Wilmar M. Wiersinga Department of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

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Leonidas Duntas Endocrine Unit, Evgenidion Hospital, University of Athens Medical School, Athens, Greece

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Valentin Fadeyev Federal Endocrinological Scientific Center, Moscow, Russia

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Birte Nygaard Department of Endocrinology, Herlev Hospital, Herlev, Denmark

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Mark P.J. Vanderpump Department of Endocrinology, Royal Free Hampstead NHS Trust, London, UK

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Background: Data suggest symptoms of hypothyroidism persist in 5–10% of levothyroxine (L-T4)-treated hypothyroid patients with normal serum thyrotrophin (TSH). The use of L-T4 + liothyronine (L-T3) combination therapy in such patients is controversial. The ETA nominated a task force to review the topic and formulate guidelines in this area. Methods: Task force members developed a list of relevant topics. Recommendations on each topic are based on a systematic literature search, discussions within the task force, and comments from the European Thyroid Association (ETA) membership at large. Results: Suggested explanations for persisting symptoms include: awareness of a chronic disease, presence of associated autoimmune diseases, thyroid autoimmunity per se, and inadequacy of L-T4 treatment to restore physiological thyroxine (T4) and triiodothyronine (T3) concentrations in serum and tissues. There is insufficient evidence that L-T4 + L-T3 combination therapy is better than L-T4 monotherapy, and it is recommended that L-T4 monotherapy remains the standard treatment of hypothyroidism. L-T4 + L-T3 combination therapy might be considered as an experimental approach in compliant L-T4-treated hypothyroid patients who have persistent complaints despite serum TSH values within the reference range, provided they have previously received support to deal with the chronic nature of their disease, and associated autoimmune diseases have been excluded. Treatment should only be instituted by accredited internists/endocrinologists, and discontinued if no improvement is experienced after 3 months. It is suggested to start combination therapy in an L-T4/L-T3 dose ratio between 13:1 and 20:1 by weight (L-T4 once daily, and the daily L-T3 dose in two doses). Currently available combined preparations all have an L-T4/L-T3 dose ratio of less than 13:1, and are not recommended. Close monitoring is indicated, aiming not only to normalize serum TSH and free T4 but also normal serum free T4/free T3 ratios. Suggestions are made for further research. Conclusion: L-T4 + L-T3 combination therapy should be considered solely as an experimental treatment modality. The present guidelines are offered to enhance its safety and to counter its indiscriminate use.

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Leonidas H. Duntas Endocrine Unit, Evgenidion Hospital, University of Athens, Athens, Greece

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Georg Brabant Medizinische Klinik I, Universitätsklinikum Schleswig-Holstein, Lübeck, Germany

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Fabio Monzani Department of Clinical and Experimental Medicine, Università di Pisa, Pisa, Italy

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Simon H.S. Pearce Institute of Genetic Medicine, Newcastle University, UK
Royal Victoria Infirmary, Newcastle upon Tyne, UK

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Robin Patrick Peeters Rotterdam Thyroid Center, Department of Internal Medicine, Erasmus Medical Center, Rotterdam, The Netherlands

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Salman Razvi Institute of Genetic Medicine, Newcastle University, UK
Queen Elizabeth Hospital, Gateshead, UK

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Jean-Louis Wemeau Clinique Endocrinologique Marc-Linquette, CHU, Lille, France

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Simon H.S. Pearce Institute of Genetic Medicine, Newcastle University
Royal Victoria Infirmary, Newcastle upon Tyne, UK

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Georg Brabant Medizinische Klinik I, Universitätsklinikum Schleswig-Holstein, Lübeck, Germany

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Leonidas H. Duntas Endocrine Unit, Evgenidion Hospital, University of Athens, Athens, Greece

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Fabio Monzani Department of Clinical and Experimental Medicine, Università di Pisa, Pisa, Italy

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Robin P. Peeters Rotterdam Thyroid Center, Department of Internal Medicine, Erasmus Medical Center, Rotterdam, The Netherlands

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Salman Razvi Institute of Genetic Medicine, Newcastle University
Queen Elizabeth Hospital, Gateshead, UK

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Jean-Louis Wemeau Clinique Endocrinologique Marc Linquette, CHU, Lille, France

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Subclinical hypothyroidism (SCH) should be considered in two categories according to the elevation in serum thyroid-stimulating hormone (TSH) level: mildly increased TSH levels (4.0-10.0 mU/l) and more severely increased TSH value (>10 mU/l). An initially raised serum TSH, with FT<sub>4</sub> within reference range, should be investigated with a repeat measurement of both serum TSH and FT<sub>4</sub>, along with thyroid peroxidase antibodies, preferably after a 2- to 3-month interval. Even in the absence of symptoms, replacement therapy with <smlcap>L</smlcap>-thyroxine is recommended for younger patients (<65-70 years) with serum TSH >10 mU/l. In younger SCH patients (serum TSH <10 mU/l) with symptoms suggestive of hypothyroidism, a trial of <smlcap>L</smlcap>-thyroxine replacement therapy should be considered. For such patients who have been started on <smlcap>L</smlcap>-thyroxine for symptoms attributed to SCH, response to treatment should be reviewed 3 or 4 months after a serum TSH within reference range is reached. If there is no improvement in symptoms, <smlcap>L</smlcap>-thyroxine therapy should generally be stopped. Age-specific local reference ranges for serum TSH should be considered in order to establish a diagnosis of SCH in older people. The oldest old subjects (>80-85 years) with elevated serum TSH ≤10 mU/l should be carefully followed with a wait-and-see strategy, generally avoiding hormonal treatment. If the decision is to treat SCH, then oral <smlcap>L</smlcap>-thyroxine, administered daily, is the treatment of choice. The serum TSH should be re-checked 2 months after starting <smlcap>L</smlcap>-thyroxine therapy, and dosage adjustments made accordingly. The aim for most adults should be to reach a stable serum TSH in the lower half of the reference range (0.4-2.5 mU/l). Once patients with SCH are commenced on <smlcap>L</smlcap>-thyroxine treatment, then serum TSH should be monitored at least annually thereafter.

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Rodrigo Moreno-Reyes R Moreno-Reyes, Department of Nuclear Medicine, Université Libre de Bruxelles, Bruxelles, 1050, Belgium

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Ulla Feldt-Rasmussen U Feldt-Rasmussen, Department of Endocrinology and Metabolism, University of Copenhagen, Kobenhavn, 1165, Denmark

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Agnieszka Piekiełko-Witkowska A Piekiełko-Witkowska, Department of Biochemistry and Molecular Biology, Centre of Postgraduate Medical Education, Warsaw, 01-813, Poland

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Adriana Gaspar da Rocha A Gaspar da Rocha, Public Health Unit, University of Porto Institute of Molecular Pathology and Immunology, Porto, 4200-465, Portugal

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Corin Badiu C Badiu, National Institute of Endocrinology "C Davila" University of Medicine and Pharmacy, Bucharest, Romania

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Josef Koehrle J Koehrle, Institut für Experimentelle Endokrinologie, Berlin, Germany

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Leonidas Duntas L Duntas, Metabolism and Diabetes National Kapodistrian University of Athens, Athens, Greece

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Abstract

In 2022, the European Chemicals Agency (ECHA) made a statement concluding that iodine is an endocrine disruptor (ED). "We stress the fact that the ECHA opinion ECHA/BPC/357/2022 is based on their misguidedly zooming in on exclusively the biocidal products (e.g., hand disinfectants, disinfection of animals’ teats/udder, embalming fluids before cremation, etc.) that contain molecular iodine (I2), entirely neglecting [see the 2013 ECHA Regulation (EU) n°528/2012 describing iodine as being of “great importance for human health”. Clearly, the current sweeping and erroneous classification of “iodine” as an endocrine disruptor is ill-advised. We moreover call upon the scientific and medical community at large to use the accurate scientific nomenclature, i.e., iodide or iodate instead of “iodine” when referring to iodized salts and food prepared there with. Drugs, diagnostic agents, and synthetic chemicals containing the element iodine in the form of covalent bonds must be correctly labelled ‘’iodinated’’, if possible, using each time their distinctive and accurate chemical or pharmacological name.

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Rodrigo Moreno-Reyes Department of Nuclear Medicine, Hospital Erasme, Université Libre de Bruxelles, Brussels, Belgium

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Ulla Feldt-Rasmussen Department of Endocrinology and Metabolism, University Hospital Rigshospitalet, and Faculty of Ηealth and Clinical Sciences, University of Copenhagen, Copenhagen, Denmark

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Agnieszka Piekiełko-Witkowska Centre of Postgraduate Medical Education, Centre of Translational Research, Department of Biochemistry and Molecular Biology, Warsaw, Poland: Basic Lead of the European Society of Endocrinology Focus Area on Thyroid

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Adriana Gaspar da Rocha Public Health Unit, ULS Baixo Mondego, Figueira da Foz, Portugal Institute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), Porto, Portugal Health Investigation and Innovation Institute (i3S), University of Porto, Porto, Portugal

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Corin Badiu National Institute of Endocrinology "C. Davila" University of Medicine and Pharmacy, Bucharest, Romania

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Josef Köhrle Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institut für Experimentelle Endokrinologie, Berlin, Germany: Co-Lead of the European Society of Endocrinology Focus Area on Environmental Endocrinology

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Leonidas Duntas Evgenideion Hospital, Unit of Endocrinology, Metabolism and Diabetes, National Kapodistrian University of Athens, Athens, Greece

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Graphical abstract

Abstract

In 2022, the European Chemicals Agency (ECHA) made a statement concluding that iodine is an endocrine disruptor (ED). We stress the fact that the ECHA opinion ECHA/BPC/357/2022 is based on their misguidedly zooming in on exclusively the biocidal products (e.g. hand disinfectants, disinfection of animals’ teats/udder, embalming fluids before cremation) that contain molecular iodine (I2), entirely neglecting the 2013 ECHA Regulation (EU) no. 528/2012 describing iodine as being of ‘great importance for human health’. Clearly, the current sweeping and erroneous classification of ‘iodine’ as an endocrine disruptor is ill-advised. We moreover call upon the scientific and medical community at large to use the accurate scientific nomenclature, i.e. iodide or iodate instead of ‘iodine’ when referring to iodized salts and food prepared there with. Drugs, diagnostic agents, and synthetic chemicals containing the element iodine in the form of covalent bonds must be correctly labeled ‘iodinated’, if possible, using each time their distinctive and accurate chemical or pharmacological name.

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