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Ilaria Muller Thyroid Research Group, Division of Infection and Immunity, Cardiff University, Cardiff, United Kingdom

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Carla Moran Wellcome Trust-MRC Institute of Metabolic Science, University of Cambridge, Cambridge, United Kingdom

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Beatriz Lecumberri Department of Endocrinology and Nutrition, La Paz University Hospital, IdiPAZ, Autonomous University of Madrid, Madrid, Spain

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Brigitte Decallonne Department of Endocrinology, University Hospitals Leuven, Leuven, Belgium

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Neil Robertson Division of Psychological Medicine and Clinical Neurosciences, Cardiff University, Cardiff, United Kingdom

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Joanne Jones Department of Clinical Neurosciences, University of Cambridge, Cambridge, United Kingdom

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Colin M. Dayan Thyroid Research Group, Division of Infection and Immunity, Cardiff University, Cardiff, United Kingdom

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Thyroid dysfunction (TD) frequently occurs as an autoimmune complication of immune reconstitution therapy (IRT), especially in individuals with multiple sclerosis treated with alemtuzumab, a pan-lymphocyte depleting drug with subsequent recovery of immune cell numbers. Less frequently, TD is triggered by highly active antiretroviral therapy (HAART) in patients infected with human immunodeficiency virus (HIV), or patients undergoing bone-marrow/hematopoietic-stem-cell transplantation (BMT/HSCT). In both alemtuzumab-induced TD and HIV/HAART patients, the commonest disorder is Graves’ disease (GD), followed by hypothyroidism and thyroiditis; Graves’ orbitopathy is observed in some GD patients. On the contrary, GD is rare post-BMT/HSCT, where hypothyroidism predominates probably as a consequence of the associated radiation damage. In alemtuzumab-induced TD, the autoantibodies against the thyrotropin receptor (TRAb) play a major role, and 2 main aspects distinguish this condition from the spontaneous form: (1) up to 20% of GD cases exhibit a fluctuating course, with alternating phases of hyper- and hypothyroidism, due to the coexistence of TRAb with stimulating and blocking function; (2) TRAb are also positive in about 70% of hypothyroid patients, with blocking TRAb responsible for nearly half of the cases. The present guidelines will provide up-to-date recommendations and suggestions dedicated to all phases of IRT-induced TD: (1) screening before IRT (recommendations 1–3); (2) monitoring during/after IRT (recommendations 4–7); (3) management of TD post-IRT (recommendations 8–17). The clinical management of IRT-induced TD, and in particular GD, can be challenging. In these guidelines, we propose a summary algorithm which has particular utility for nonspecialist physicians and which is tailored toward management of alemtuzumab-induced TD. However, we recommend prompt referral to specialist endocrinology services following diagnosis of any IRT-induced TD diagnosis, and in particular for pregnant women and those considering pregnancy.

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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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