Case Presentation: A 33-year-old woman with metastatic breast cancer and recent subtotal resection of a suprasellar brain metastasis presented with subacute fatigue and confusion a month after her surgery.
She was oriented only to self, normotensive, with an exam notable only for mild left sided weakness, unchanged from her post-operative discharge. Admission laboratory data showed a serum sodium of 130 mmol/L and potassium of 3.8 mmol/L. A non-contrast computed tomography of the brain showed a slight increase in the peritumoral edema without significant change from baseline. She had been discharged on a post-operative steroid taper, but upon further history, had self-discontinued steroids a week prior due to weight gain.
Given concern for adrenal insufficiency vs peritumoral edema as a cause for her symptoms, dexamethasone was initiated at 6 milligrams every 6 hours. She was also placed on fluid restriction given her hyponatremia. Over the next 24 hours, she developed progressive polyuria (>2.5L) and her morning serum sodium increased to 150 mmol/L. Urine studies showed an osmolality of 204 mmol/kg and sodium of 17 mmol/L.
Her rapid sodium shift, urine studies, and polyuria despite fluid restriction were concerning for central diabetes insipidus (DI) and her hypernatremia required multiple days of treatment with both free water and arginine desmopressin before normalization. A random cortisol of 1 ug/dL and morning ACTH of 10 ng/L were consistent with adrenal insufficiency. She was eventually discharged home with a diagnosis of DI and central AI, and was managed with arginine desmopressin, a free water prescription, and glucocorticoid supplementation.
Discussion: This patient presented with a condition known as “Masked Diabetes Insipidus”, where adrenal insufficiency can mask the clinical manifestations of central diabetes insipidus. This is a rare phenomenon and, in nearly all described cases, rapid onset of polyuria occurs following the administration of high dose glucocorticoids. The etiology is imperfectly understood, but likely involves hypocortisolism-mediated hypersecretion of ADH by the remaining functional portions of the pituitary as well as ADH-independent impaired free water clearance in the setting of glucocorticoid deficiency. While rare, adrenal insufficiency and central DI can coincide leading to dangerous shifts in sodium balance. Early recognition is vital to avoid potential harm. Patients with intracranial and particularly suprasellar metastasis are at particular risk as they often receive high dose steroids and are susceptible to multiple endocrinopathies.
Conclusions: CDI should be suspected in patients who experience acute onset of polyuria after therapeutic doses of steroids and should prompt close monitoring of serum sodium levels. Rarely, CDI can be “masked” by the coincident presence of adrenal insufficiency, only becoming clinically evident with glucocorticoid replacement.