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Endocrine Abstracts (2025) 113 WC3.3 | DOI: 10.1530/endoabs.113.WC3.3

1Sheffield Teaching Hospitals NHS Trust, Sheffield, United Kingdom; 2Doncaster and Bassetlaw Teaching Hospitals NHS Trust, Doncaster, United Kingdom


Introduction: Central hyperthyroidism, characterized by elevated thyroid hormones (FT3 and FT4) and inappropriately normal or elevated TSH, presents a diagnostic challenge. The two primary differential diagnoses are TSH-secreting pituitary adenomas (TSHomas) and resistance to thyroid hormone (RTH). While both conditions can cause similar biochemical abnormalities, they have distinct underlying mechanisms. Differentiating between these conditions requires dynamic testing, imaging, and, in the case of RTH, genetic testing.

Case Report: A 43-year-old male presented with elevated TSH (6.28 mU/l), FT4 (31.7 pmol/l), and FT3 (8.3 pmol/l), consistent with central hyperthyroidism. These findings had remained consistent since 2012, with an FT4 of 29.3 pmol/l. The patient reported no symptoms of hyperthyroidism, including no tremors, palpitations, or significant weight changes. He did mention experiencing headaches twice a week but denied visual disturbances, galactorrhea, or changes in libido. On clinical examination, his heart rate was normal (75 BPM), and his BMI was 29.1. The patient’s medical history included atrial fibrillation and asthma, for which he takes Bisoprolol, Atorvastatin, and Ezetimibe. Laboratory tests excluded Dysalbuminemic Hyperthyroxinemia, and thyroid antibodies were negative. Pituitary MRI revealed a 5 mm microadenoma on the right side, with no abnormalities in the pituitary stalk, optic chiasm, or cavernous sinuses. These findings raised suspicion for TSHoma. However, further investigation was needed to clarify the diagnosis. The patient was referred to the pituitary multidisciplinary team (MDT) for further evaluation, which included a complex pituitary scan and TRH stimulation test. Genetic testing was also recommended to rule out RTH, a condition in which tissues, including the pituitary, are resistant to thyroid hormone feedback.

Conclusion: This case presents a diagnostic challenge of elevated TSH with high FT3 and FT4, where the differential diagnosis includes TSHoma and RTH. The TRH stimulation test is crucial in differentiating these conditions, with TSHoma typically showing a blunted or absent TSH response, while RTH may show exaggerated or normal TSH response despite elevated thyroid hormones. Pituitary MRI remains essential for diagnosing TSHoma, while genetic testing is the definitive tool for diagnosing RTH. While the diagnosis is still pending, this case highlights the importance of a thorough diagnostic approach, including dynamic testing, imaging, and genetic analysis to guide appropriate management.

Volume 113

Society for Endocrinology Clinical Update 2025

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