HYPONATREMIA AND TSHoma

THE ODD COUPLE

Abstract

INTRODUCTION/BACKGROUND
We present a case of syndrome of inappropriate antidiuresis (SIAD) as a rare presentation of TSH-secreting pituitary macroadenoma.

CASE
A 57-year-old postmenopausal female with no prior medical illness presented with recurrent admissions for symptomatic hyponatremia associated with abdominal pain and vomiting. She denied symptoms of hypothyroidism or hyperthyroidism. There was no history of medication intake. Family history was unremarkable. She was clinically euvolemic, and never exhibited clinical signs of hypo- or hyperthyroidism. There was no goitre. Serial investigations showed hyponatremia (nadir of 114 mmol/L) and hypoosmolality (nadir of 257 mmol/kg), with elevated urine sodium (90-153 mmol/L) and urine osmolality (360-600 mmol/kg). Copeptin was elevated at 55.7 pmol/L (normal range: <13.1). Further investigations showed a persistently discordant thyroid function test (TFT), with elevated free-T4 (range: 24.3-34.3 pmol/L) and non-suppressed thyroid stimulating hormone (TSH) (range: 1.19-4.07 mIU/L), similar across different laboratory platforms. Serum alpha-subunit of TSH was 0.6 IU/L, with TSH molar ratio of 3.1. Morning cortisol level was normal (598 nmol/L). Other pituitary hormones were appropriate for age and postmenopausal status. Whole body CT-scan was negative for malignancy, but incidentally showed a sellar mass. MRI confirmed a sellar mass measuring 1.1 x 2.1 x 2.1 cm, with suprasellar and cavernous extension, and chiasmal compression, with no features of apoplexy. Posterior pituitary T1 bright spot was present and displaced posteriorly. Her hyponatremia improved with fluid restriction and rescue doses of tolvaptan. The sellar tumour was resected trans-sphenoidally. Histopathological examination confirmed a diagnosis of pituitary adenoma, which stained negative for ACTH, GH and PRL. TSH-staining was unavailable. Postoperatively, her TFT and sodium levels normalized.

CONCLUSION
Hyponatremia is a rare presentation for pituitary adenomas, especially in the absence of hypocortisolism or hypothyroidism. SIAD has been reported in nonfunctioning pituitary adenomas, pituitary apoplexy and central hypothyroidism and hypocortisolism. This is postulated to be due to exaggerated arginine-vasopressin (AVP) secretion due to local mass effect.