SUN-080 Immune Checkpoint Inhibitor (ICI) hypophysitis involving the posterior pituitary with AVP deficiency presenting with Diabetic Ketoacidosis

Abstract Disclosure: B. Stanley: None. M.J. Gardner: None. G. Lastra: None. Immune Checkpoint Inhibitor (ICI) Therapy is improving cancer treatment and has lead to increased patient survival. However, it can often lead to immune-related adverse events targeting endocrine tissues. This can result in autoimmune damage to normal tissues including the thyroid, adrenal, and pancreas, with the latter leading to autoimmune diabetes. ICI therapy can lead to pituitary hypophysitis that results in anterior pituitary dysfunction. Nonetheless, it is extremely uncommon for ICI induced hypophysitis to affect posterior pituitary function leading to Arginine Vasopressin (AVP) deficiency. We present a case of a patient with ICI induced hypophysitis with central hypothyroidism/adrenal insufficiency who developed diabetic ketoacidosis (DKA). This was in the setting of untreated adrenal insufficiency and was further diagnosed with AVP deficiency during treatment. A 31-year-old female with metastatic melanoma on ICI therapy (Ipilimumab and Nivolumab) presented with fatigue, nausea, and altered mental status. Laboratory tests were consistent with DKA, with elevated serum glucose/β-hydroxy-butyrate and anion gap metabolic acidosis, as well as low serum cortisol. She was started on stress dose steroids with IV insulin/fluids and quickly developed polyuria and hypernatremia simultaneously with low urine osmolality, suggestive of AVP deficiency. Treatment with desmopressin led to >50% increase in urine osmolality with resolution of polyuria and normalization of sodium levels confirming AVP deficiency, which was believed to be unmasked by steroid therapy. MRI imaging showed loss of posterior pituitary bright spot, without metastatic lesions in the pituitary or hypothalamus. She was also later confirmed to likely have ICI induced autoimmune diabetes with GAD65 antibodies that likely led to her developing DKA. In summary, this case illustrates a spectrum of adverse effects of CPI therapy occurring in a single patient, including an extremely rare case of ICI induced hypophysitis resulting in AVP deficiency. This demonstrates the various endocrine manifestations of ICI therapy and challenges in their management when they occur simultaneously. Similarly, it suggests that AVP deficiency may be a more common complication than previously believed, and should be suspected for patients on ICI therapy. Presentation: Sunday, July 13, 2025