Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2011) 26 P631

ECE2011 Poster Presentations Clinical case reports (73 abstracts)

‘Uterine neuroendocrine tumour: an unusual cause of hyponatraemia’ and the role of tolvaptan, a vasopressin V2 receptor antagonist

G Mlawa , S Price , L Fraser , R Green , B Turner & R Guy


Basingstoke Hospital, Basingstoke, UK.


Background: Hyponatraemia is the commonest electrolyte abnormality in clinical practice, and may be a biochemical manifestation of different diseases including malignancy. About 14% of hyponatremia in medical inpatients is due to underlying tumour related conditions.

We present a case of 68 years widow who was referred by her General Practioner with 3 weeks history of nausea, occasional vomiting, confusion, increased urinary frequency, and urinary incontinence but no dysuria. She also complained of chronic constipation, and weight loss. Her past medical history included left knee arthroscopy, cochlea implant and sterilisation in 1976. She was non smoker but her husband was a heavy smoker. On admission she was haemodynamically stable with normal observations. Blood test revealed profound hyponatraemia (Na+118 mmol/l), and serum osmolarity of 247 mOsm/kg, urine osmolarity of 701 mOsm/kg, urinary sodium of 110 mmol/l, random cortisol of 542 nmol/l, in keeping with SIADH. Tumour markers were negative. Chest X-ray was unremarkable but abdominal ultrasound revealed a uterine heterogeneous enhancing mass which was also confirmed on staging CT of chest, abdomen and pelvis. Flexible sigmoidoscopy was normal. Her medications included Paracetamol and Codeine Phosphate. She was started on fluid restriction of 750 ml/24 h. She remained hyponatraemic (116–117 mmol/l) despite this. Oral Demeclocycline 300 mg TDS was added, but she was unable to tolerate it and she was changed to tolvaptan (30 mg od). She was discharged home on tolvaptan (30 mg) and was reviewed by gynaecology team in outpatient clinic; cervical biopsy histology showed a high grade neuroendocrine malignant tumour confirmed by positive immuno labelling for chromogranini, AE1/3 and CAM5.2. She is currently undergoing chemotherapy and still on tolvaptan. Her sodium remains low but at safer levels of 127–130 mmol/l.

Discussion: Hyponatraemia secondary to uterine neuroendocrine tumours is rare and generally associated with chemotherapy treatment rather than being related to the uterine neuroendocrine tumour. Conventional treatment for hyponatraemia due to SIADH was ineffective or not tolerated. Tolvaptan treatment was more successful even though it is mainly used in patient with mild to moderate euvolaemic hyponatraemia. This possibilise hyponatraemia.

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