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Hui Yi Ng Department of Clinical Medicine, Level 4, Macquarie University, 2 Technology Place, Macquarie University, New South Wales, Australia

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Divya Namboodiri Department of Clinical Medicine, Level 4, Macquarie University, 2 Technology Place, Macquarie University, New South Wales, Australia

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Diana Learoyd University of Sydney, Faculty of Medicine and Health, Northern Clinical School, Reserve Road St Leonards, New South Wales, Australia

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Andrew Davidson Department of Neurosurgery, Level 2, Macquarie University, 2 Technology Place Macquarie University, New South Wales, Australia

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Bernard Champion Department of Clinical Medicine, Level 4, Macquarie University, 2 Technology Place, Macquarie University, New South Wales, Australia

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Veronica Preda Department of Clinical Medicine, Level 4, Macquarie University, 2 Technology Place, Macquarie University, New South Wales, Australia

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Summary

Co-secreting thyrotropin/growth hormone (GH) pituitary adenomas are rare; their clinical presentation and long-term management are challenging. There is also a paucity of long-term data. Due to the cell of origin, these can behave as aggressive tumours. We report a case of a pituitary plurihormonal pit-1-derived macroadenoma, with overt clinical hyperthyroidism and minimal GH excess symptoms. The diagnosis was confirmed by pathology showing elevated thyroid and GH axes with failure of physiological GH suppression, elevated pituitary glycoprotein hormone alpha subunit (αGSU) and macroadenoma on imaging. Pre-operatively the patient was rendered euthyroid with carbimazole and underwent successful transphenoidal adenomectomy (TSA) with surgical cure. Histopathology displayed an elevated Ki-67 of 5.2%, necessitating long-term follow-up.

Learning points:

  • Thyrotropinomas are rare and likely under-diagnosed due to under-recognition of secondary hyperthyroidism.

  • Thyrotropinomas and other plurihormonal pit-1-derived adenomas are more aggressive adenomas according to WHO guidelines.

  • Co-secretion occurs in 30% of thyrotropinomas, requiring diligent investigation and long-term follow-up of complications.

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Maria Cabrer Endocrine Unit, Hospital Comarcal d’Inca, Inca, Spain

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Guillermo Serra Endocrine Unit, Hospital Universitari Son Espases, Palma, Spain

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María Soledad Gogorza Endocrine Unit, Hospital Universitari Son Espases, Palma, Spain

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Vicente Pereg Endocrine Unit, Hospital Universitari Son Espases, Palma, Spain

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Summary

Chromosome 22q11.2 deletion syndrome (22q11.2DS) is a genetic syndrome that may present with hypocalcemia due to primary hypoparathyroidism (PH) at any age. We report a new diagnosis of 22q11.2DS in a 57-year-old man who presented with symptomatic hypocalcemia. It is important to consider genetic causes of hypocalcemia due to PH regardless of age.

Learning points:

  • It is important to discard genetic cause of primary hypoparathyroidism in a patient without autoimmune disease or prior neck surgery.

  • A new diagnosis of a hereditary disease has familial implications and needs genetic counselling.

  • It is also important to discard other syndrome’s comorbidities.

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I R Wallace Regional Centre for Endocrinology and Diabetes, Royal Victoria Hospital, Grosvenor Road, Belfast, BT12 6BA, UK

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E Healy Department of Neuropathology, Royal Victoria Hospital, Grosvenor Road, Belfast, BT12 6BA, UK

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R S Cooke Department of Neurosurgery, Royal Victoria Hospital, Grosvenor Road, Belfast, BT12 6BA, UK

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P K Ellis Department of Radiology, Royal Victoria Hospital, Grosvenor Road, Belfast, BT12 6BA, UK

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R Harper Department of Endocrinology and Diabetes, Ulster Hospital, Dundonald, BT16 1RH, UK

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S J Hunter Regional Centre for Endocrinology and Diabetes, Royal Victoria Hospital, Grosvenor Road, Belfast, BT12 6BA, UK

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Summary

TSH-secreting pituitary adenomas are rare and the optimal investigation and management is uncertain. We describe a case of a 43 year-old woman with a TSH-secreting pituitary adenoma, highlighting diagnostic testing and our use, pre-operatively of somatostatin analogue therapy, which induced biochemical euthyroidism and a reduction in tumour size.

Learning points

  • The differential diagnosis of the syndrome of inappropriate TSH secretion is non-thyroidal illness, medications, assay interference due to heterophilic antibodies, thyroid hormone resistance and TSH-secreting pituitary adenoma.

  • TRH stimulation test and triiodothyronine suppression test assist in differentiating thyroid hormone resistance and TSH-secreting pituitary adenoma.

  • Somatostatin analogue therapy can induce biochemical euthyroidism and reduce tumour size.

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