Endocrine Abstracts

An 84-year-old lady presented with a month’s history of polyuria and polydipsia. She reported waking up seven times during the night to pass urine and constantly feeling thirsty. Her measured 24-hour urine output was 4.9 L. She was otherwise doing well with a past medical history of hypertension, hyperlipidaemia, gastro-oesophageal reflux disease and prolonged hospital admission 20 years ago for Guillain Barré syndrome. Her drug history included Lisinopril, Atorvastatin, Amitriptyline and Omeprazole. She did not smoke or drink alcohol. Physical examination was normal, including a neurological assessment. Investigations showed a serum osmolality of 303 mOsm/kg, an inappropriately low urine osmolality of 95 mOsm/kg and a serum sodium of 144 mmol/l within normal range. Her copeptin level was low at 1.7 pmol/l. Her thyroid function tests, cortisol and HbA1c levels were normal. Her eGFR was adequate at 80 mL/min/1.73 m2, with normal potassium and calcium levels. She was diagnosed with arginine vasopressin (AVP) deficiency and started on oral desmopressin. She achieved good symptom control with oral desmopressin 300 mg daily. An MRI pituitary scan showed a normal posterior pituitary bright spot, pituitary stalk and infundibulum. A central, discrete, small hypo-enhancing lesion in the pituitary was detected, with mild deviation of the stalk to the left. The anterior pituitary hormone profile was normal. She then became increasingly unwell and presented to the emergency department 3 weeks later with acute confusion, vomiting and febrile at 38⁰C. Her sodium level was within normal range at 144 mmol/l with improved serum and urine osmolality of 300 mOsm/kg and 559 mOsm/kg respectively. She was transferred to the high dependency unit. Desmopressin was converted to subcutaneous administration. The differential diagnoses included infectious encephalitis, metabolic or autoimmune encephalopathy, central venous thrombosis, lymphoma or malignancy. All investigations including CT chest, abdomen and pelvis, autoimmune screen, lactate dehydrogenase (LDH), angiotensin converting enzyme (ACE) and blood film were normal. Clinical improvement was noted with aciclovir and a drop in white cell count was noted on CSF results. She was therefore treated empirically for viral encephalitis for 2 weeks. An MRI head scan showed extensive deep white matter ischaemic changes. This case highlights the workup and management of AVP deficiency, complicated by probable viral encephalitis. The diagnosis is likely idiopathic AVP deficiency but a vascular impairment of the inferior hypophyseal artery system is possible in view of extensive ischaemic changes in the brain. IgG4 related hypophysitis is a rare but remains a possible diagnosis. IgG4 level and pituitary MDT outcome is pending.