Endocrine Abstracts

We report a 33 year old female who presented at 23 weeks gestation with rapid onset polyuria and polydipsia. Fluid input and output was approximately 12 litres per day. She denied any other symptoms. She did not have signs of hypopituitarism, Acromegaly or Cushing’s syndrome. Visual fields were normal to confrontation. Her standard glucose tolerance test, Hba1c, creatinine and calcium were normal. Gestational Diabetes Insipidus was (GDI) suspected. Given her pregnancy, a water deprivation test was not performed. She was able to carry out a short overnight fast from midnight to 6am. Urine output during this period was nearly 2500mls. Fasting urine and serum osmolality were 152mosm/kg (100-900mosm/kg) and 297mosm/kg (285-295mosm/kg) respectively, with a serum sodium of 144mmol/l (133-145 mmol/l). Cortisol measured 1198nmol/l (>400nmol/l), Free T4 13.3pmol/l (12-22pmol/l), TSH 2.0mU/l (0.2-4.0mU/l) and IGF1 17.0nmol/l (14.6-39.9nmol/l). A non-contrast MRI pituitary scan suggested the presence of a 6-8mm microadenoma, which was thought to be insignificant. She was commenced on desmopressin. Symptoms responded well and the rest of her pregnancy was uneventful. She delivered a healthy baby at 39 weeks gestation. Early follow up was arranged with a view to gradually wean off desmopressin. However, we were unable to reduce the dose on several attempts as she reported recurrence of symptoms within hours of missing a dose. She continues to be dependent on desmopressin five years after pregnancy. A repeat MRI pituitary scan with contrast demonstrated a normal pituitary gland. The pituitary bright spot was retained. GDI is normally transient and resolves post partum. A normal MRI pituitary scan here excluded acquired cause of central diabetes insipidus in pregnancy. This suggests that some cases of GDI may persist long term after pregnancy, and it is important to evaluate the situation carefully to avoid abrupt withdrawal of treatment and relapse of symptoms.