Endocrine Abstracts

Arginine vasopressin deficiency (AVP-D) is a rare condition that can happen following brain surgery or trauma, as well as conditions affecting the hypothalamus and pituitary gland. Here we describe a case of 76-year old man who had AVP-D secondary to large suprasellar mass of unknown aetiology. He presented with generalised malaise, weight loss, polyuria and polydipsia. Past medical histories include type two diabetes mellitus with Hba1c 52 mmol/mol, Graves’ thyrotoxicosis on carbimazole, asthma and hypertension. Random capillary blood glucose monitoring was satisfactory. Blood results showed acute kidney injury with hypernatraemia. The initial fluid balance monitoring, although performed poorly, as well as paired serum and urine investigations on admission did not meet the diagnostic criteria of AVP-D. He was therefore treated for acute kidney injury. Following some improvement in kidney function with intravenous fluids and with malignancy concern, CT head scan was performed which showed suspicious 1.9 cm suprasellar pituitary lesion. CT thorax, abdomen and pelvis did not show any malignancies. Subsequent MRI pituitary showed an enhancing multi-lobulated suprasellar mass lesion, with the main bulk situated in the hypothalamic region and encasing the third ventricle, associated with mass-effect and adjacent vasogenic oedema. He was therefore started on dexamethasone treatment. Subsequent strict documented urine output exceed 5 l/daily with significant nocturia. Repeat paired serum and urine investigations revealed AVP-D and pituitary profile showed panhypopituitarism. ESR was found incidentally raised. Desmopressin therapy was commenced and gradually improved his urine output and electrolytes. He was referred to neurosurgical multi-disciplinary team, with plans to investigate the suprasellar mass, including serum and CSF tumour markers as well as the potential need for biopsy. A repeat MRI Head was done a week apart after and this time it showed significant size reduction of the lesion. This was accompanied by some improvement in the ESR. As there was no evidence of mass effect now, and to avoid ‘masking’ the diagnosis on subsequent investigations, dexamethasone was changed to hydrocortisone accordingly for hypocortisolism cover. His serum and CSF tumour markers so far have been negative and we are awaiting for decision to proceed for biopsy. The likely cause being inflammatory or lymphoma is high on list in view of the serendipitous improvement in clinical picture following glucocorticoid therapy. In this case, we want to highlight for discussion this rare presentation of AVP-D, potential challenges in managing inpatient fluid balance, and steroid use when clinically indicated but risking interfering with the diagnostic investigations.