Endocrine Abstracts (2006) 11 P180

Impaired thirst and AVP release due to a reset osmostat in a patient with partial cranial diabetes insipidus (CDI) and subtle pituitary disease

WHMS Chandrasekara, S Khan, SS Lakra, MD Penney & LDKE Premawardhana

Caerphilly Miners’ Hospital, Caerphilly, United Kingdom.

An asymptomatic 66-year-old man was referred for investigation of chronic hypernatraemia. Plasma sodium varied between 146–152 mmol/l and potassium was normal over several years. There was no relevant past, family or drug history. There were no symptoms or signs of hypercotisolism or other endocrinopathy either. Clinical examination was normal.

Initial investigations were as follows – sodium 149 mmol/l, potassium 4.3 mmol/l, urea 7.9 mmol/l, creatinine 117 micromol/l, serum osmolality 317 mmol/kg and urine osmolality 236 mmol/kg. Appropriate screening tests did not reveal hyperaldosteronism, hypercortisolism or major anterior pituitary dysfunction. However, the cortisol response to ACTH was suboptimal (465 nmol/l at 30 minutes). A water deprivation test confirmed partial CDI and low AVP activity to increasing plasma osmolality. A hypertonic saline infusion test (Table 1) revealed an upwardly reset osmostat (increased thresholds for thirst and AVP release). A MRI scan showed a small pituitary gland, partial empty sella and an absent posterior pituitary ‘bright signal.’ Tests to elucidate a cause for his endocrine dysfunction were negative.

Table 1 Hypertonic saline infusion test.
Time (min)Sodium (mmol/l)Serum osmolality (mmol/kg)Plasma AVP (pg/ml)Subjective thirst scale (0–100)

The likely cause of these abnormalities is hypothalamic vascular disease. We have advised a daily fixed fluid intake (with attention to variations in weight and serum sodium) and steroid cover at times of stress. When last reviewed he was still asymptomatic but normonatraemic.

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