Endocrine Abstracts

I present a case of a 32 year old Vietnamese woman who presented on 3rd September 2023 with abdominal pain and vomiting. Her blood tests showed; Hb 151g/l, WCC 18.3, Na 130 mmol/l, K 1.8 mmol/l, Ur 4.7 mmol/l, Creatinine 91 umol/l, Corrected Calcium 2.93 mmol/l, Phosphate 0.54 mmol/l, Lipase 191 unilts/l. Venous Blood Gases showed pH 7.25, Bicarbonate 15.6, Lactate 1.9, pCO2 4.5, Glucose 7.0 mmol/l. She had a background of treated TB aged 25, recent diagnosis of H. Pylori gastritis, and gave birth in September 2022. Her son was born with congenital complete heart block and she had positive Anti-Ro and Anti-La antibodies. She was managed in the ITU and received concentrated potassium infusions and Hartmann’s. Her urine output after admission to ITU was up to 8 L per day with doses of 0.5 -1 mg parenteral DDAVP intermittently. The DDAVP was not effective at reducing her urine output initially. Her Sodium climbed to 161 mmol/l after 48 hours and her calcium and potassium normalised within 24 hours. They suspected Sheehan’s syndrome. She had a Cortisol checked at 0600 on 7th September which was 251 nmol/l and then started Glucocorticoid replacement. She started regular 100 mg twice daily oral DDAVP on 9th September, and she remained on 10/5/5 mg oral hydrocortisone. She was discharged on 12th September on 100 mg DDAVP at night and replacement doses of Hydrocortisone. At this point her Urine Output was about 2 L per day. She had an MRI Pituitary on 8th September which showed a potentially thickened pituitary stalk and a loss of posterior pituitary bright-up. She returned for an Insulin Tolerance Test on 24th October. The Nadir glucose was 1.4 mmol/l. The peak Cortisol was 476 nmol/l, and GH was 4.03 mg/l. Hydrocortisone was stopped. She then had a Water Deprivation Test 5th December. At the start of the test the Serum Osmolality 291 mmol/kg, with a Urine Osmolality of 140 mmol/kg. At 8 hours the Serum Osmolality was 298 mmol/kg with a Urine Osmolality of 228 mmol/kg. Upon clinical review she notices an ongoing good response to low-dose DDAVP and she is being managed as Cranial Diabetes Insipidus secondary to presumed Lymphocytic Hypophysitis. We suspect that her lack of improvement initially, despite Desmopressin, is due to nephrogenic DI secondary to hypokalaemia and gradient washout secondary to a history of polyuria.