A 31-year-old woman presented with oligomenorrhoea and a raised prolactin. Pituitary scan revealed a 1.8 cm pituitary mass with compression of the optic chiasm. TSH was normal at 3.66 mIU/l with a raised FT4 of 25.8 pmol/l. The rest of pituitary function was normal. Visual fields demonstrated a bitemporal upper quadrantanopia. A diagnosis of TSH-secreting pituitary adenoma was suspected because of the high normal TSH in the presence of a high FT4. She underwent transsphenoidal surgery which resulted in good decompression of the visual pathway. Histology showed a non-functioning pituitary adenoma with negative staining for all pituitary hormones including TSH. Post-op pituitary function was normal including FT4 of 16.4 pmol/l and TSH of 0.77 mIU/l and pituitary scan showed a small residual tumour. Soon after surgery the patient defaulted from follow up. She was re-referred after three years with headache, visual disturbance, and weight loss. FT4 was elevated at 30.3 pmol/l and TSH was 2.6 mIU/l. Repeat MRI showed an increase in the size of the pituitary tumour. Visual fields and alpha subunit were normal. There had been a gradual rise in FT4 and TSH since surgery and given the increase in tumour size along with biochemical changes suggesting a TSHoma, it was decided to give the patient a trial of somatostatin analogue therapy. Response to therapy was excellent with FT4 and TSH reducing to 12.4 pmol/l and 0.7 mIU/l and significant tumour shrinkage confirming a diagnosis of TSHoma.
TSHomas are rare pituitary tumours characterized by high levels of circulating free thyroid hormones in the presence of non-suppressed TSH. Surgery is the usual first line of therapy. In this case the histology failed to confirm the diagnosis. Subsequent clinical course and positive biochemical and radiological response to somatostatin analogue therapy was suggestive of a TSHoma.