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Endocrine Abstracts (2014) 34 P70 | DOI: 10.1530/endoabs.34.P70

Heart of England NHS Foundation Trust, Birmingham, UK.


A 21-year-old lady referred for an endocrine review from labour ward HDU after developing polyurea and polydipsia following a difficult labour which was complicated by severe post-partum haemorrhage.

She was passing about 500 ml of urine per hour and drinking around ten jugs of water a day. Her bedside observations were stable and her capillary blood glucose level was 4.7 mmol/l. She was referred to ITU where she had a stat dose of IV-desmopressin. Further history revealed 2 weeks history of polyurea and polydipsia prior to labour.

Laboratory investigations showed a plasma glucose of 4.9 mmol/l. Her urea and creatinine were normal and her eGFR was >90 ml/min. Her sodium level was high at 146 mmol/l. Her serum osmolality was 296 mosm (275–295) and her urine osmolality was 78 mosm (300–1 000). Her urinary sodium excretion was 24 mmol.

Further tests revealed normal TSH of 2.63 mIU/l and a normal cortisol of 557 nmol/l. Her prolactin level was 2 630 IU/l and she continued to lactate normally. Her pituitary MRI scan was unremarkable, so diagnosis of Sheehan’s syndrome was excluded.

She was started on oral desmopressin for suspected diabetes insipidus and she responded well; with urine output going down to 2 420 ml. Unfortunately, she did not stay in hospital to have her fluid deprivation test done.

This was an unusual case of gestational diabetes insipidus which is frequently under-diagnosed because polyurea is often considered normal during pregnancy. It is thought to be due to excessive placental vasopressinase in the 3rd trimester which breaks down ADH. It is very important to diagnose and treat gestational diabetes insipidus early because it can lead to significant morbidity and mortality (rapid onset hypernatraemia leading to central pontine demyelination and baby’s death).

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