SFEEU2024 Society for Endocrinology National Clinical Cases 2024 Poster Presentations (53 abstracts)
1Croydon Hospital, London, United Kingdom; 2Endocrinology SpR, Croydon University Hospital, London, United Kingdom
I present a case of a 32 year old woman who presented in September 2023 with abdominal pain and vomiting. Her blood tests showed; Hb 151 g/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 Hartmanns. Her urine output after admission to ITU was up to 8L 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. She was also noted to have a mildly low Cortisol and therefore underwent a Pituitary MRI to rule out Sheehans Syndrome. The MRI 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. Her Insulin Tolerance test ruled out Cortisol insufficiency and the Water Deprivation test is suggestive of Vasopressin Deficiency / Resistance. Given the good response to low dose oral DDAVP, alongside the loss of posterior pituitary bright up, she is being managed as Cranial Diabetes Insipidus secondary to presumed Lymphocytic Hypophysitis. The fascinating point within this case is 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. Both are under-recognised causes of polyuria. Therefore, this is a woman with Cranial DI which was diagnosed due to an exacerbating secondary Nephrogenic DI.