Thyrotropin-secreting pituitary adenomas (TSHomas) are a rare entity, representing approximately 0.5-2% of all pituitary tumours, with an estimated prevalence of around one case per million.1 They are characterised by autonomous secretion of thyroid-stimulating hormone (TSH), leading to the hallmark finding of elevated free thyroid hormone levels and an inappropriately non-suppressed TSH. Diagnosis requires dynamic testing along with exclusion of interference from laboratory assays or medications.2
The case is a 50-year-old male with a background of obesity and osteoarthritis, on no regular medications, who presented to a local hospital in December 2019. He complained of abdominal distension, palpitations, dyspnoea, weight loss of 15kg, increased shoe size, skin tags, and poor libido. He was found to have atrial fibrillation, mild acral features, and clinical features of biventricular heart failure. Initial testing revealed a free thyroxine of 44pmol/L (RR 7.0-17.0pmol/L), a free triiodothyronine of 6.6pmol/L (RR 3.5-6.0pmol/L) and TSH of 6.0mU/L (RR 0.3-4.5mU/L) and an elevated IGF-1 level of 86nmol/L (RR 8.8-29nmol/L). Echocardiogram revealed an ejection fraction of 10-15%. Thyroid interference studies, TRH stimulation test, growth hormone suppression test and magnetic resonance imaging was undertaken to confirm the diagnosis of a TSH/GH co-secreting pituitary macroadenoma. Octreotide long-acting release (LAR) was commenced in May 2020 to achieve a euthyroid state prior to transsphenoidal surgical resection; surgery ultimately was significantly delayed due to the coronavirus pandemic. After two months, he had achieved euthyroidism and IGF-1 was reduced to 39nmol/L, later becoming normalised after 6 months. He underwent surgery in June 2021 with histopathology confirming a plurihormonal Pit-1 lineage adenoma with positive staining for TSH and growth hormone.
A recent review of published TSHoma cases demonstrated approximately 40% of patients had pluri-hormonal tumours, with co-secretion of growth hormone being most common.3 Therapeutic response to somatostatin analogues is dependent on the relative pattern of somatostatin receptor expression.4