Endocrine Abstracts

The anti-natriuretic properties of growth hormone (GH) are well established. GH deficiency (GHD) results in salt and water depletion and studies confirm that replacement leads to sodium and vasopressin-mediated water retention, in patients with intact posterior pituitary function.

We report the case of a 20-year-old male patient with septo-optic dysplasia, fixed cranial diabetes insipidus (DI) and an abnormal thirst threshold. He first presented after birth with developmental delay and subsequently developed DI aged 12 years along with hypothyroidism. His fluid balance and sodium levels remained stable for many years on a fixed dose of DDAVP and supervised fluid intake of 2.5 litres.

Aged 18, with symptomatology in keeping with cortisol deficiency and on the basis of a poor cortisol rise on glucagon testing, he was found to be ACTH deficient. On hydrocortisone replacement therapy he rapidly became hypernatraemic indicating that a relative deficiency of cortisol had been masking the severity of his DI.

A new sodium homeostasis was established with 3 litres fluid intake and he remained stable for the following 6 months. However, increasing central adiposity and decreasing levels of alertness led to a diagnosis of severe GH deficiency, and GH replacement was commenced. There was an immediate reduction in visceral adiposity and increase in levels of activity. However, severe hypernatraemia developed (peak 161 mmol/l). Hence in the presence of a fixed fluid and DDAVP intake, the powerful anti-natriuretic effects of GH were clearly demonstrated.

Most GHD patients have intact posterior pituitary function. This case report demonstrates the complex interaction between anterior pituitary hormone replacement and salt and water homeostasis. In particular it highlights the powerful anti-natriuretic properties of GH, which have been clearly demonstrated in this patients’ case, where in the presence of other fixed parameters, the potent effects of physiological doses of GH have been seen.