Endocrine Abstracts

A 36-year-old, previously healthy, man presented with several weeks’ history of gradually worsening headache. He attended A&E after he was woken by sudden worsening of the headache, associated with vomiting and pre-syncopal symptoms. Investigations revealed severe hyponatraemia - serum Na 109 mmol/L. He was also severely hypocortisolaemic – serum cortisol (random) 16 nmol/L, ACTH 19 ng/L. Cranial imaging revealed a 17 mm suprasellar, complex cystic pituitary lesion compressing the optic apparatus; there was no calcification within the mass. He was treated with intravenous saline and glucocorticoids. Serum Na initially improved to 129mmol/L and he felt better. However, after four days, he complained of headache with nausea and his serum sodium declined again. He was clinically euvolaemic and repeat biochemical assessment confirmed a persistent state of antidiuresis despite replacement of glucocorticoids - serum Na 116, urine osmolality 726 mOsm/kg, urine Na 62 mmol/L. He was then treated with fluid restriction, while continuing glucocorticoids, and serum sodium gradually returned to the normal range. He had panhypopituitarism, without polyuria, – serum free T4 6.1 pmol/L (10.5–24.5), TSH 0.68 mU/L, testosterone 0.8 nmol/l (8–29). He commenced appropriate hormone replacement. Serum prolactin was not elevated (101mU/L) and the neurosurgical team planned transsphenoidal debulking; however, repeat pituitary imaging, six weeks later, demonstrated substantial shrinkage of the lesion, now confined to the sella. Six months after presentation, the lesion had regressed further and dynamic endocrine testing, including insulin tolerance test, demonstrated almost complete recovery of pituitary function – he remained partially deficient in growth hormone only. Spontaneous recovery of panhypopituitarism is uncommon in patients with a pituitary mass. This case highlights the complexity of the diagnosis and management of severe, symptomatic hyponatraemia, in patients with a newly discovered sellar lesion.