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Roel Docter
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Georg Hennemann
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Eric P. Krenning
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Robin P. Peeters
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W. Edward Visser
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Eric P. Krenning
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Roel Docter
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Wouter W. de Herder
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Robin P. Peeters
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Wilmar M. Wiersinga
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Tim I.M. Korevaar Department of Internal Medicine and the Rotterdam Thyroid Center, Erasmus University Medical Center, Rotterdam, The Netherlands

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Rima Dhillon-Smith Institute of Metabolism and Systems Research, Tommy’s National Centre for Miscarriage Research and the Birmingham Clinical Trials Unit, the Birmingham Women’s and Children’s NHS Foundation Trust, University of Birmingham, Birmingham, United Kingdom

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Arri Coomarasamy Institute of Metabolism and Systems Research, Tommy’s National Centre for Miscarriage Research and the Birmingham Clinical Trials Unit, the Birmingham Women’s and Children’s NHS Foundation Trust, University of Birmingham, Birmingham, United Kingdom

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

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Alies A. van Mullem Department of Internal Medicine, Erasmus University Medical Centre, Rotterdam, The Netherlands

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Theo J. Visser Department of Internal Medicine, Erasmus University Medical Centre, Rotterdam, The Netherlands

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Robin P. Peeters Department of Internal Medicine, Erasmus University Medical Centre, Rotterdam, The Netherlands

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Thyroid hormone (TH) exerts its biological activity via the TH receptors TRα1 and TRβ1/2, which are encoded by the THRA and THRB genes. The first patients with mutations in THRB were identified decades ago. These patients had a clinical syndrome of resistance to TH associated with high serum TH and nonsuppressed thyroid-stimulating hormone levels. Until recently, no patients with mutations in THRA had been identified. In an attempt to predict the clinical phenotype of such patients, different TRα1 mutant mouse models have been generated. These mice have a variable phenotype depending on the location and severity of the mutation. Recently, the first humans with mutations in THRA were identified. Their phenotype consists of relatively low serum T4 and high serum T3 levels (and thus an elevated T3/T4 ratio), growth retardation, delayed mental and bone development, and constipation. While, in retrospect, certain features present in humans can also be found in mouse models, the first humans carrying a defect in TRα1 were not suspected of having a THRA gene mutation initially. The current review focuses on the clinical consequences of TRα1 mutations.

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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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Caroline M J van Kinschot Department of Internal Medicine, Maasstad Hospital, Rotterdam, The Netherlands
Academic Center for Thyroid Diseases, Department of Internal Medicine, Erasmus Medical Center, Rotterdam, The Netherlands

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Ivona Lončar Academic Center for Thyroid Diseases, Department of Surgical Oncology and Gastrointestinal Surgery, Erasmus MC Cancer Institute, Rotterdam, The Netherlands

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Tessa M van Ginhoven Academic Center for Thyroid Diseases, Department of Surgical Oncology and Gastrointestinal Surgery, Erasmus MC Cancer Institute, Rotterdam, The Netherlands

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W Edward Visser Academic Center for Thyroid Diseases, Department of Internal Medicine, Erasmus Medical Center, Rotterdam, The Netherlands

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Robin P Peeters Academic Center for Thyroid Diseases, Department of Internal Medicine, Erasmus Medical Center, Rotterdam, The Netherlands

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Charlotte van Noord Department of Internal Medicine, Maasstad Hospital, Rotterdam, The Netherlands

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the Thyroid Network Study Group †
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the Thyroid Network Study Group

Objective

Evidence-based treatment guidelines for the management of postthyroidectomy hypocalcemia are absent. The aim of this study was to evaluate a newly developed symptom-based treatment algorithm including a protocolized attempt to phase out supplementation.

Methods

In a prospective multicenter study, patients were treated according to the new algorithm and compared to a historical cohort of patients treated with a biochemically based approach. The primary outcome was the proportion of patients receiving calcium and/or alfacalcidol supplementation. Secondary outcomes were calcium-related complications and predictors for supplementation.

Results

One hundred thirty-four patients were included prospectively, and compared to 392 historical patients. The new algorithm significantly reduced the proportion of patients treated with calcium and/or alfacalcidol during the first postoperative year (odds ratio (OR): 0.36 (95% CI: 0.23–0.54), P < 0.001), and persistently at 12 months follow-up (OR: 0.51 (95% CI: 0.28–0.90), P < 0.05). No severe calcium-related complications occurred, even though calcium-related visits to the emergency department and readmissions increased (OR: 11.5 (95% CI: 4.51–29.3), P <0.001) and (OR: 3.46 (95% CI: 1.58–7.57), P < 0.05), respectively. The proportional change in pre- to postoperative parathyroid hormone (PTH) was an independent predictor for supplementation (OR: 1.04 (95% CI: 1.02–1.07), P < 0.05).

Conclusions

Symptom-based management of postthyroidectomy hypocalcemia and a protocolized attempt to phase out supplementation safely reduced the proportion of patients receiving supplementation, although the number of calcium-related hospital visits increased. For the future, we envision a more individualized treatment approach for patients at risk for delayed symptomatic hypocalcemia, including the proportional change in pre- to post- operative PTH.

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Luca Persani L Persani, Medical Biotechnologies and Translational Medicine, University of Milan, Milano, 20149, Italy

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Patrice Rodien P Rodien, EDN, Centre Hospitalier Universitaire d'Angers, Angers, 49933, France

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Carla Moran C Moran, Diabetes & Endocrinology Section, Beacon Hospital, Sandyford, Ireland

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W. Edward Visser W Visser, Department of Internal Medicine and Rotterdam Thyroid Center, Erasmus Medical Center, Rotterdam, Netherlands

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Stefan Groeneweg S Groeneweg, Department of Internal Medicine and Rotterdam Thyroid Center, Erasmus Medical Center, Rotterdam, Netherlands

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

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Samuel Refetoff S Refetoff, Departments of Medicine and Pediatrics, The University of Chicago, Chicago, 60637-1476, United States

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Mark Gurnell M Gurnell, Institute of Metabolic Science, University of Cambridge, Cambridge, United Kingdom of Great Britain and Northern Ireland

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Paolo Beck-Peccoz P Beck-Peccoz, Department of Medical Biotechnology and Translational Medicine, University of Milan, Milano, Italy

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Krishna Chatterjee K Chatterjee, Institute of Metabolic Science, University of Cambridge, Cambridge, CB2 0QQ, United Kingdom of Great Britain and Northern Ireland

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Impaired sensitivity to thyroid hormones encompasses disorders with defective transport of hormones into cells, reduced hormone metabolism and resistance to hormone action. Mediated by heritable single gene defects, these rare conditions exhibit different patterns of discordant thyroid function associated with multisystem phenotypes. In this context, challenges include ruling out other causes of biochemical discordance, making a diagnosis using clinical features together with identification of pathogenic variants in causal genes and managing these rare disorders with a limited evidence base. For each condition, the present guidelines aim to inform clinical practice by summarising key clinical features and useful investigations, criteria for molecular genetic diagnosis and pathways for management and therapy. Specific, key recommendations were developed by combining the best research evidence available with the knowledge and clinical experience of panel members, to achieve a consensus.

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Sander Barnhoorn Department of Molecular Genetics, Erasmus Medical Center, Rotterdam, The Netherlands

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Marcel E Meima Department of Internal Medicine, Academic Center for Thyroid Diseases, Erasmus Medical Center, Rotterdam, The Netherlands

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Robin P Peeters Department of Internal Medicine, Academic Center for Thyroid Diseases, Erasmus Medical Center, Rotterdam, The Netherlands

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Veerle M Darras Laboratory of Comparative Endocrinology, Biology Department, KU Leuven, Leuven, Belgium

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Selmar Leeuwenburgh Department of Internal Medicine, Academic Center for Thyroid Diseases, Erasmus Medical Center, Rotterdam, The Netherlands

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Jan H J Hoeijmakers Department of Molecular Genetics, Erasmus Medical Center, Rotterdam, The Netherlands
Princess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands
Oncode Institute, Utrecht, The Netherlands
Institute for Genome Stability in Ageing and Disease, CECAD Research Centre, Cologne, Germany

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Wilbert P Vermeij Princess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands
Oncode Institute, Utrecht, The Netherlands

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W Edward Visser Department of Internal Medicine, Academic Center for Thyroid Diseases, Erasmus Medical Center, Rotterdam, The Netherlands

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Background

Thyroid hormone signaling is essential for development, metabolism, and response to stress but declines during aging, the cause of which is unknown. DNA damage accumulating with time is a main cause of aging, driving many age-related diseases. Previous studies in normal and premature aging mice, due to defective DNA repair, indicated reduced hepatic thyroid hormone signaling accompanied by decreased type 1 deiodinase (DIO1) and increased DIO3 activities. We investigated whether aging-related changes in deiodinase activity are driven by systemic signals or represent cell- or organ-autonomous changes.

Methods

We quantified liver and plasma thyroid hormone concentrations, deiodinase activities and expression of T3-responsive genes in mice with a global, liver-specific and for comparison brain-specific inactivation of Xpg, one of the endonucleases critically involved in multiple DNA repair pathways.

Results

Both in global and liver-specific Xpg knockout mice, hepatic DIO1 activity was decreased. Interestingly, hepatic DIO3 activity was increased in global, but not in liver-specific Xpg mutants. Selective Xpg deficiency and premature aging in the brain did not affect liver or systemic thyroid signaling. Concomitant with DIO1 inhibition, Xpg −/− and Alb-Xpg mice displayed reduced thyroid hormone-related gene expression changes, correlating with markers of liver damage and cellular senescence.

Conclusions

Our findings suggest that DIO1 activity during aging is predominantly modified in a tissue-autonomous manner driven by organ/cell-intrinsic accumulating DNA damage. The increase in hepatic DIO3 activity during aging largely depends on systemic signals, possibly reflecting the presence of circulating cells rather than activity in hepatocytes.

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Elske T. Massolt Division of Endocrinology, Erasmus MC, Rotterdam, The Netherlands
Rotterdam Thyroid Center, Department of Internal Medicine, Erasmus MC, Rotterdam, The Netherlands

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Mahdi  Salih Division of Endocrinology, Erasmus MC, Rotterdam, The Netherlands

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Carolien M. Beukhof Division of Endocrinology, Erasmus MC, Rotterdam, The Netherlands
Rotterdam Thyroid Center, Department of Internal Medicine, Erasmus MC, Rotterdam, The Netherlands

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Boen L.R. Kam Department of Nuclear Medicine, Erasmus MC, Rotterdam, The Netherlands

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J.W. Burger Division of Surgical Oncology, Department of Surgery, Erasmus MC, Rotterdam, The Netherlands

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W. Edward Visser Division of Endocrinology, Erasmus MC, Rotterdam, The Netherlands
Rotterdam Thyroid Center, Department of Internal Medicine, Erasmus MC, Rotterdam, The Netherlands

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Ewout J. Hoorn Department of Nephrology and Transplantation, Erasmus MC, Rotterdam, The Netherlands

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Robin P. Peeters Division of Endocrinology, Erasmus MC, Rotterdam, The Netherlands
Rotterdam Thyroid Center, Department of Internal Medicine, Erasmus MC, Rotterdam, The Netherlands

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Background: Hypothyroidism has been associated with impaired urinary concentrating ability. However, previous reports on thyroid hormone and urinary concentrating ability in humans only studied a limited number of patients with autoimmune thyroid disease or used healthy controls instead of paired analysis within the same patients. Objective: To study the urinary concentrating ability in athyreotic patients with differentiated thyroid cancer on and off levothyroxine treatment as they are exposed to different thyroid states as part of their treatment in the absence of an autoimmune disease. Design and Methods: We studied 9 patients (mean age of 42.7 years) during severe hypothyroid state (withdrawal of levothyroxine before radioactive iodine therapy) and TSH-suppressed state (on levothyroxine therapy). At these two points, serum and urine samples were collected after 14 h of overnight fasting without any food or drink. Results: Serum and urine osmolality were not significantly different between on and off levothyroxine treatment. Serum creatinine levels were significantly higher in patients off versus on levothyroxine treatment (87.0 vs. 71.0 µmol/L, respectively; p = 0.044) and, correspondingly, the estimated glomerular filtration rate was significantly lower (89.6 vs. 93.1 mL/min, respectively; p = 0.038). Conclusion: Short-term, severe hypothyroidism has no effect on urinary concentrating ability. Our study confirms the well-known effects of thyroid hormone on serum creatinine concentrations.

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Henry Völzke Institute for Community Medicine, University Medicine Greifswald, Greifswald, Germany

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Iris Erlund Department of Public Health Solutions, National Institute for Health and Welfare (THL), Helsinki, Finland

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Alicja Hubalewska-Dydejczyk Department of Endocrinology, Jagiellonian University Medical College, Krakow, Poland

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Till Ittermann Institute for Community Medicine, University Medicine Greifswald, Greifswald, Germany

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

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Margaret Rayman University of Surrey, Surrey, United Kingdom

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Monika Buchberger Department of Public Health and Health Technology Assessment, UMIT, University for Health Science, Medical Informatics and Technology, Hall, Austria

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Uwe Siebert Department of Public Health and Health Technology Assessment, UMIT, University for Health Science, Medical Informatics and Technology, Hall, Austria

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Betina H. Thuesen Research Centre for Prevention and Health, Glostrup, Denmark

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Michael B. Zimmermann Swiss Federal Institute of Technology, Zürich Department of Health Sciences and Technology, Zürich, Switzerland

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Stefan Grünert Biolution GmbH, Vienna, Austria

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John H. Lazarus Institute of Molecular Medicine, Cardiff University, Cardiff, United Kingdom

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Background: Iodine deficiency disorders (IDD) represent a global health threat to individuals and societies. IDD prevention programmes have been introduced in many parts of the world. However, challenges remain, particularly in Europe due to fragmentation and diversity of approaches that are not harmonized. Objectives: This review is dedicated to the public-health impact of IDD prevention programmes. It sums up experiences collected by the EUthyroid consortium so far and provides information on stakeholders that should be involved in actions directed to improve the impact of IDD prevention. Methods: A joint European database for combining registry-based outcome and monitoring data as well as tools for harmonizing study methods were established. Methods for analyzing thyroglobulin from a dried blood spot are available for assessing the iodine status in the general population and at-risk groups. Mother-child cohorts are used for in-depth analysis of the potential impact of mild-to-moderate iodine deficiency on the neurocognitive development of the offspring. A decision-analytic model has been developed to evaluate the long-term effectiveness and cost effectiveness of IDD prevention programmes. Results: EUthyroid has produced tools and infrastructure to improve the quality of IDD monitoring and follows a dissemination strategy targeting policymakers and the general public. There are tight connections to major stakeholders in the field of IDD monitoring and prevention. Conclusions: EUthyroid has taken steps towards achieving a euthyroid Europe. Our challenge is to inspire a greater sense of urgency in both policymakers and the wider public to address this remediable deficit caused by IDD.

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