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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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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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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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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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Zhongli Chen Department of Internal Medicine, Academic Centre for Thyroid Diseases, Erasmus University Medical Center Rotterdam, The Netherlands

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

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Wesley Flach Department of Internal Medicine, Academic Centre for Thyroid Diseases, Erasmus University Medical Center Rotterdam, The Netherlands

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Linda J de Rooij Department of Internal Medicine, Academic Centre for Thyroid Diseases, Erasmus University Medical Center Rotterdam, The Netherlands

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Sena Yildiz Department of Internal Medicine, Academic Centre for Thyroid Diseases, Erasmus University Medical Center Rotterdam, The Netherlands

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Alexander Teumer Institute for Community Medicine, University Medicine Greifswald, Greifswald, Germany
DZHK (German Center for Cardiovascular Research), Partner Site Greifswald, Greifswald, Germany
Department of Psychiatry and Psychotherapy, University Medicine Greifswald, Greifswald, Germany

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Matthias Nauck DZHK (German Center for Cardiovascular Research), Partner Site Greifswald, Greifswald, Germany
Institute of Clinical Chemistry and Laboratory Medicine, University Medicine Greifswald, Germany

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Rosalie B T M Sterenborg Department of Internal Medicine, Academic Centre for Thyroid Diseases, Erasmus University Medical Center Rotterdam, The Netherlands
Department of Epidemiology, Erasmus Medical Center, Rotterdam, The Netherlands
Department of Internal Medicine, Radboud University Medical Center, Nijmegen, The Netherlands

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Joost H W Rutten Department of Internal Medicine, Radboud University Medical Center, Nijmegen, The Netherlands

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Marco Medici Department of Internal Medicine, Academic Centre for Thyroid Diseases, Erasmus University Medical Center Rotterdam, The Netherlands
Department of Epidemiology, Erasmus Medical Center, Rotterdam, The Netherlands
Department of Internal Medicine, Radboud University Medical Center, Nijmegen, The Netherlands

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

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

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Objective

Thyroid hormone (TH) transport represents a critical first step in governing intracellular TH regulation. It is still unknown whether the full repertoire of TH transporters has been identified. Members of the solute carrier (SLC) 22 family have substrates in common with the known TH transporters of the organic anion-transporting peptide family. Therefore, we screened the SLC22 family for TH transporters

Methods

Uptake of 1 nM of iodothyronines or sulfated iodothyronines in COS1 cells expressing SLC22 proteins was performed.

Results

We first tested 25 mouse (m) SLC22 proteins for TH uptake and found that the majority of the organic anion transporter (OAT) clade were capable of 3,3’,5-triiodothyronine and/or thyroxine (T4) transport. Based on phylogenetic tree analysis of the mouse and human (h) SLC22 family, we selected eight hSLC22s that grouped with the newly identified mouse TH transporters. Of these, four tested positive for uptake of one or more substrates, particularly hSLC22A11 showed robust (3-fold over control) uptake of T4. Uptake of sulfated iodothyronines was strongly (up to 17-fold) induced by some SLC22s, most notably SLC22A8, hSLC22A9, mSLC22A27 and mSLC22A29. Finally, the zebrafish orthologues of SLC22A6/8 drOatx and drSlc22a6l also transported almost all (sulfated) iodothyronines tested. The OAT inhibitors lesinurad and probenecid inhibited most SLC22 proteins.

Conclusions

Our results demonstrated that members of the OAT clade of the SLC22 family constitute a novel, evolutionary conserved group of transporters for (sulfated) iodothyronines. Future studies should reveal the relevance of these transporters in TH homeostasis and physiology.

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