Endocrine Abstracts (2012) 28 P267

Potential pitfalls in the management of thyrotropinoma

Olympia Koulouri1, Narayanan Kandasamy1, Carla Moran1, Alison Melvin2, Neil Donnelly3, Richard Mannion4, John Pickard4, David Halsall5, Krishna Chatterjee1 & Mark Gurnell1

1Institute of Metabolic Science, University of Cambridge & Addenbrooke’s Hospital, Cambridge, United Kingdom; 2Department of Diabetes and Endocrinology, Bedford Hospital NHS Trust, Bedford, United Kingdom; 3Department of ENT, Addenbrooke’s Hospital, Cambridge, United Kingdom; 4Department of Neurosurgery, Addenbrooke’s Hospital, Cambridge, United Kingdom; 5Department of Clinical Biochemistry, Addenbrooke’s Hospital, Cambridge, United Kingdom.

Case Report: A 49-year-old man presented with a two-year history of thyrotoxic symptoms for which he had been investigated on several occasions. He had a past medical history of dilated cardiomyopathy, which had been attributed to excess alcohol consumption, and had also suffered episodes of non-sustained ventricular tachycardia. His family history was strongly positive for autoimmune thyroid disease. Eventually, he was found to have an elevated fT4 (53 pmol/L, RR 12–22) and fT3 (19.8 pmol/L, RR 3.1–6.8) with a non-suppressed ‘inappropriately normal’ TSH (2.9 mU/L, RR 0.25–4). There was no evidence of assay interference. His SHBG was markedly raised at 197 nmol/l (RR 15–55), as was serum alpha-subunit (2.7 IU/L, RR <1.0). TRH testing showed a blunted TSH response: 0min 2.4 mU/L, 20 min 2.7 mU/L, 60 min 2.7 mU/L. Pituitary MRI revealed a calcified macroadenoma (confirmed on CT). Other anterior pituitary function was normal except for significantly elevated total testosterone (48.4 nmol/l, RR 10–30). A diagnosis of TSHoma was made and the patient treated with lanreotide autogel® (resulting in rapid resolution of his hyperthyroxinaemia), followed by transsphenoidal surgery. Histology confirmed a thyrotropinoma. Post-operatively, his TFTs normalized and his cardiac function improved.

Key Learning Points: • Approximately 30% of patients with thyrotropinomas exhibit normal TSH levels. Measurement of TSH alone can therefore result in undue delay or failure to make the diagnosis with adverse clinical sequelae. • Elevated SHBG may result in raised/normal total, but normal/low free testosterone levels (thus masking diagnosis of concomitant hypogonadism), although the possibility of gonadotrophin co-secretion (1.8% of TSHomas) should also be considered. • The finding of calcification within a pituitary adenoma is characteristic and should raise suspicion of a thyrotropinoma. • Somatostatin analogue therapy rapidly normalises TFTs in TSHoma. • Cardiomyopathy may improve/reverse with correction of thyrotoxicosis.

Declaration of interest: There is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported.

Funding: No specific grant from any funding agency in the public, commercial or not-for-profit sector.

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