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  • Thyroid ectopy x
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Tiziana de Filippis Laboratory of Endocrine and Metabolic Research, Milan, Italy
Division of Endocrinology and Metabolic Diseases, IRCCS Istituto Auxologico Italiano, Milan, Italy

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Federica Marelli Laboratory of Endocrine and Metabolic Research, Milan, Italy
Division of Endocrinology and Metabolic Diseases, IRCCS Istituto Auxologico Italiano, Milan, Italy

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Maria Cristina Vigone Department of Pediatrics, Vita-Salute University, San Raffaele Scientific Institute, Milan, Italy

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Marianna Di Frenna Department of Pediatrics, Vita-Salute University, San Raffaele Scientific Institute, Milan, Italy

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Giovanna Weber Department of Pediatrics, Vita-Salute University, San Raffaele Scientific Institute, Milan, Italy

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Luca Persani Laboratory of Endocrine and Metabolic Research, Milan, Italy
Division of Endocrinology and Metabolic Diseases, IRCCS Istituto Auxologico Italiano, Milan, Italy
Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy

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congenital or early postnatal onset and identified two novel heterozygous NKX2-1 frameshift mutations that were associated with typical neurological manifestations, absent pulmonary involvement and atypical thyroid phenotypes, such as lingual ectopy or non

Article Type:
Research Article
DOI:
https://doi.org/10.1159/000366274
Volume/Issue:
Volume 3: Issue 4
Free access
Matthew J. Brooks Departments of Cardiology, The Royal Melbourne Hospital, Melbourne, Vic., Australia

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David A. Pattison Departments of Endocrinology, The Royal Melbourne Hospital, Melbourne, Vic., Australia

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Eliza P. Teo Departments of Cardiology, The Royal Melbourne Hospital, Melbourne, Vic., Australia

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Sarah Price Departments of Endocrinology, The Royal Melbourne Hospital, Melbourne, Vic., Australia

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Ronen Gurvitch Departments of Cardiology, The Royal Melbourne Hospital, Melbourne, Vic., Australia

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What Is Known about This Topic • Hyperthyroidism is a recognised cause of coronary artery spasm and routine thyroid function testing should be performed in all patients. • Thyroid dysfunction secondary to amiodarone therapy is common

Article Type:
Case Report
DOI:
https://doi.org/10.1159/000345528
Volume/Issue:
Volume 2: Issue 1
Free access
Cengiz Kara Department of Molecular Medicine, Institute of Graduate Studies, Ondokuz Mayis University, Samsun, Turkey
Department of Pediatric Endocrinology, Faculty of Medicine, Istinye University, Istanbul, Turkey

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Jamala Mammadova Pediatric Endocrinology Unit, Altinbas University Medicalpark Bahçelievler Hospital, Istanbul, Turkey

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Ümmet Abur Department of Molecular Medicine, Institute of Graduate Studies, Ondokuz Mayis University, Samsun, Turkey
Department of Medical Genetics, Faculty of Medicine, Ondokuz Mayis University, Samsun, Turkey

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Cagri Gumuskaptan Department of Molecular Medicine, Institute of Graduate Studies, Ondokuz Mayis University, Samsun, Turkey
Department of Medical Genetics, Faculty of Medicine, Ondokuz Mayis University, Samsun, Turkey

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Elif İzci Güllü Department of Pediatric Endocrinology, Faculty of Medicine, Ondokuz Mayis University, Samsun, Turkey

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Ayhan Dağdemir Department of Molecular Medicine, Institute of Graduate Studies, Ondokuz Mayis University, Samsun, Turkey

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Murat Aydın Department of Pediatric Endocrinology, Faculty of Medicine, Ondokuz Mayis University, Samsun, Turkey

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patients with normal, goitrous or hypoplastic thyroid were included in the study, but those with TD due to ectopy and athyreosis were ruled out. This selection aimed to use financial resources more efficiently by studying CH patients with a more

Article Type:
Research Article
Collections:
Hypothyroidism
DOI:
https://doi.org/10.1530/ETJ-22-0212
Volume/Issue:
Volume 12: Issue 3
Open access
Robert Opitz Institute of Interdisciplinary Research in Molecular Human Biology, Université Libre de Bruxelles, Brussels, Belgium

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Francesco Antonica Institute of Interdisciplinary Research in Molecular Human Biology, Université Libre de Bruxelles, Brussels, Belgium

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Sabine Costagliola Institute of Interdisciplinary Research in Molecular Human Biology, Université Libre de Bruxelles, Brussels, Belgium

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might manifest as either athyreosis, thyroid ectopy, hypoplasia or hemiagenesis [ 3 , 4 ]. All these phenotypes are considered to result from defects in embryonic thyroid development. The molecular mechanisms underlying TD in human newborns, however

Article Type:
Review Article
DOI:
https://doi.org/10.1159/000357079
Volume/Issue:
Volume 2: Issue 4
Free access
Anita Boelen Endocrine Laboratory, Department of Laboratory Medicine, Amsterdam UMC, location University of Amsterdam, Amsterdam, The Netherlands
Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam, The Netherlands
Amsterdam Reproduction & Development Research Institute, Amsterdam, The Netherlands

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Nitash Zwaveling-Soonawala Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam, The Netherlands
Department of Pediatric Endocrinology, Emma Children’s Hospital, Amsterdam UMC, location University of Amsterdam, Amsterdam, The Netherlands

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Annemieke C Heijboer Endocrine Laboratory, Department of Laboratory Medicine, Amsterdam UMC, location University of Amsterdam, Amsterdam, The Netherlands
Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam, The Netherlands
Amsterdam Reproduction & Development Research Institute, Amsterdam, The Netherlands
Endocrine Laboratory, Department of Laboratory Medicine, Amsterdam UMC, location Vrije Universiteit Amsterdam, Amsterdam, The Netherlands

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A S Paul van Trotsenburg Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam, The Netherlands
Department of Pediatric Endocrinology, Emma Children’s Hospital, Amsterdam UMC, location University of Amsterdam, Amsterdam, The Netherlands

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reported incidence of 1 in 3600 live-born children in the Netherlands ( 11 ). Primary CH is mostly (80–85% of the cases) caused by thyroid dysgenesis, a group of entities including absence (thyroid agenesis), misplacement (thyroid ectopy) and hypoplastic

Article Type:
Review Article
Collections:
Hypothyroidism
DOI:
https://doi.org/10.1530/ETJ-23-0041
Volume/Issue:
Volume 12: Issue 4
Open access