Endocrine Abstracts

The last few decades had seen major breakthroughs in the management of Heart Failure (HF) especially in relation to the modulation of the pathogenetic mechanistic pathway. One of these is the AVP pathway antagonism via the V2R which is promising. However, the influence of the HF complex pathophysiologic pathways in the context of AVP disorder is not well defined. We present an 83-year-old man with long-standing AVP related disorder presenting with acute decompensated HF. He has a background bipolar affective disorder on Lithium treatment for more than 25 years prior to the initial presentation with osmotic symptoms. He also has long standing gynecomastia, loss of libido, and erectile dysfunction. His other past medical history includes AF, T2DM, CKD3, and recently Dementia. Examination showed slightly small testis (15 ml), normal body hair, genitalia, visual field, and bilateral gynecomastia. The initial biochemistry showed sodium of 145, plasma osmolality 304, urine osmolality 303, eGFR of 44, adjusted calcium 2.67, potassium 4.3, 9 am cortisol and testosterone of 327 and 4.6 respectively, FSH 1.9, LH 2.4, IGF-1 31.6, prolactin 214, ferritin 101, Oestradiol 85, FT4 16.9, eGFR of 54. Due to other pituitary hormone deficiency, he had a pituitary MRI which was normal and water deprivation test (WDT) showed baseline plasma osmolality of 317, urine osmolality of 317. Post-DDAVP, the urine osmolality rose to 565 (43% rise) which was interpreted as partial Cranial AVP deficiency. She was therefore started on Desmopressin 100 mg TDS which initially improved his symptoms. However, over a course of 14 years, he developed resistance requiring 600 mg per day of DDAVP to control his osmotic symptoms until his recent presentation with shortness of breath and fluid overload. He was diagnosed with acute decompensated HFpEF, and started on high dose Intravenous Furosemide which was co-administered with the DDAVP leading to difficult fluid mobilization. We weaned vasopressin to 300 mg daily with slightly improved diuresis, however, there was associated troublesome nocturia and this became difficult to manage. This patient had the possibilities of either AVP deficiency (other pituitary hormone deficiency) or AVP resistance (long-term Lithium therapy) and with an inconclusive WDT, he was treated as AVP deficiency. The case illustrates the interaction the two pathologies could have upon each other from the pathophysiologic point of view and if AVP disorder management could be a tweak for the HF treatment in patient with both disorders without use of diuretic.