A Case of Lymphocytic Hypophysitis Presenting in Hyponatraemic Crisis
Miss Fiona Davidson, Dr Matt Oldfield, Dr Geetha Natarajan.
Case Report: A 37 year old woman presented to A&E with a 3 day history of vomiting. A course of fluoxetine had been prescribed by her GP 5 days prior to presentation. On examination she was found to be drowsy and confused. She was peripherally cold but blood pressure and heart rate were both normal. There was no evidence of pigmentation or myxoedema, no peripheral visual disturbance nor galactorrhoea. She was polyuric and polydipsic. She reported feeling lethargic and depressed since the birth of her 2nd child 3 years previously. Delivery had been uneventful with the exception of a severe headache. She had elected not to breastfeed. She had been oligomenorrhoeic since delivery.
Admission bloods revealed a profound hyponatraemia with sodium 101 mmol/L (NR 133 145) and hypocalcaemia, albumin adjusted calcium 1.84 mmol/L (NR 2.20 2.60) a slightly low magnesium of 0.65 mmol/L (NR 0.70 1.0 mmol/L) and phosphate of 0.5 mmol/L (NR 0.8 1.5). CRP, renal function and liver function tests were normal.
Further investigations revealed secondary hypothyroidism with TSH 1.59 mIU/L (NR 0.27 4.20) FT4 2.9 pmol/L (12.0 22.0) and a low IGF-1; cortisol, prolactin and gonadotrophins were in the normal range. Urine sodium (18 mmol/L) and osmolality (260 mOsm/kg) were inappropriate in the context of hyponatraemia. The normal cortisol (616 nmol/L) was felt to be inadequate in the context of acute illness and IV hydrocortisone was initiated prior to commencing thyroxine replacement.
MRI pituitary revealed a small involuted gland. An MRI scan from 3 years previously showed a slightly enlarged gland. In the absence of any history of significant blood loss or radiological evidence of sarcoid or adenoma, a presumptive diagnosis of lymphocytic hypophysitis with subsequent atrophy was made.
Discussion: This is a complex case that highlights the difficulties in providing a definitive diagnosis of lymphocytic hypophysitis in the post-inflammatory phase when biopsy is no longer appropriate. It also reminds us of the importance of clinical context in the interpretation of cortisol. This case was unusual in that hypoadrenalism is most usually associated with hypercalcaemia. There have been a handful of case reports of hypoadrenalism associated with hypocalcaemia but the mechanism is unknown. In all reported cases, as happened in this case, the calcium normalized with hydrocortisone replacement alone.