MON-046 ACUTE MYELOID LEUKEMIA ASSOCIATED ARGININE VASOPRESSIN DEFICIENCY

Abstract Disclosure: A. Arif: None. N. Sharifi: None. S. Sun: None. Arginine vasopressin deficiency (AVP-D) associated with acute myeloid leukemia (AML) is extremely rare, with barely understood pathomechanics and it points to an overall poor prognosis.We are reporting a case of middle-aged women diagnosed with AML and concurrent AVP-D. Case Presentation: A 53-year-old woman admitted with cough and shortness of breath was diagnosed with AML (MECOM rearrangement with inv 3 and monosomy 7). During her hospital stay, she reported new-onset excessive thirst and urination. She denied a history of brain trauma, surgery, or radiation, as well as a family history of pituitary disorders. Additionally, no identifiable cause of AVP-R was found. An MRI of the pituitary gland showed a normal pituitary gland.On examination, she appeared euvolemic, with a heart rate of 92 bpm and blood pressure of 118/75 mmHg She reported drinking approximately 3-4 liters of water daily due to thirst and dry mouth.Laboratory findings on admission revealed a sodium level of 136 mmol/L, which later increased to 151 mmol/L (reference range: 135-145 mmol/L). The patient started normalizing her sodium levels during her hospital stay by drinking ample fluids. Further evaluation with a water deprivation test demonstrated an increase in serum sodium (> 145 mmol/L) and serum osmolality (>300 mOsm/kg) while urine osmolality remained low, however, we were unable to give DDAVP to complete the test due to the patient’s limitation. The diagnosis of AVP-D was made as per the above results. Desmopressin was started and led to the resolution of symptoms. Discussion: AML is one of the most common leukemia in adulthood. The association with AVP-D is increasingly recognized but still rare. The cytogenetic abnormalities chiefly seen are monosomy of chromosome 7 and inversion of chromosome 3 (q21q26). A subset of cases showed MECOM overexpression which is also a consequence of chromosome 3 inversion.The timing of AVP-D is usually concomitant with AML diagnosis although few exceptions were reported. The diagnosis is made in a similar fashion although the imaging abnormalities are frequently absent.The underlying mechanism is not completely understood. It was previously hypothesized to be tumor infiltration vs. infection, although complete resolution of AVP-D with AML treatment points against this. As vasopressin is platelet-bound, some literature suggests dysmegakaryopoiesis is the primary culprit.Treatment with DDAVP leads to improvement in symptoms in 90% of patients. Most patients show decreased requirement of DDAVP and even complete resolution of AVP-D following AML treatment. The AML-associated AVP-D confers a poor prognosis due its cytogenetic abnormalities, not related to AVP-D.Most patient compensates for fluid losses by drinking excess water, although treatment of AVP-D will lead to a better quality of life and avoid hypernatremia in a setting of acute illness. Presentation: Monday, July 14, 2025