SFEBES2013 Poster Presentations Clinical practice/governance and case reports (79 abstracts)
1Sheffield Teaching Hospitals NHS Trust, Sheffield, UK; 2University of Sheffield, Sheffield, UK.
We report two cases of hypernatraemia with reset osmostat and pituitary dysfunction.
A 35-year-old male was referred with Graves thyrotoxicosis associated with hypokalaemic periodic paralysis and an incidental serum sodium 154 mmol/l. He complained of polyuria and nocturia but denied excessive thirst and was otherwise well. Height was 193 cm with BMI 29.5. He had gynaecomastia and sparse body hair. He had a small 6 ml right testicle (originally undescended) and 15 ml left testicle. A very high arched, possibly cleft palate was noted suggesting a midline defect. Serum osmolality was 314 mOsm/kg with urine osmolality 1025mOsm/kg. Testosterone was 5.0 nmol/l, LH 5.6 IU/l and FSH 5.0 IU/l. Prolactin, IGF-1, synacthen test, renin and aldosterone were normal. Pituitary MRI was normal. Urine osmolality dropped in response to a water load although he remained hypernatraemic with hyperosmolar plasma. There was direct evidence of osmoregulatory control over AVP levels consistent with hypernatraemia and reset osmostat.
An 18-year-old male was admitted following an incidental serum sodium 163 mmol/l whilst being investigated for joints pain. He denied excessive thirst or polyuria. Examination showed BMI 40.4, short stature (154 cm), small hands, size 5 feet and gynaecomastia. Testicular volumes were 15ml. Serum osmolality was 330 mOsm/kg, urine osmolality 731 mOsm/kg and urine sodium 172 mmol/l. Initial hospital treatment with 5% Glucose reduced his sodium to 155 mmol/l, urine osmolality to 296 mOsm/kg and urine output increased. Prolactin was 2000 mIU/l, LH 6.3 IU/l, FSH 1.0 IU/l and testosterone 5.7 nmol/l. IGF1 was low with peak GH 4.5 μg/l on ITT. TSH, FT4 and synacthen test were normal. Pituitary MRI was normal. He has been started on dopamine agonist therapy.
Essential hypernatraemia is rare and usually secondary to traumatic brain injury or surgery. In our cases, there was no such history, and both patients had partial hypopituitarism. The likely cause in both was congenital and in one case, there was evidence of a congenital midline defect.