Abstract
Background: Hypocortisolism can develop in patients with a pituitary mass because of hypopituitarism and is appropriately managed with steroid replacement. However, these patients often have co-existing endocrine derangements that can become clinically evident after administration of steroids. Clinical Case: A sixty-year-old Caucasian female with known non-small cell lung cancer on chemoimmunotherapy was admitted for management of an enlarging suprasellar mass. Her symptoms included nausea, vomiting and multiple syncopal episodes over the preceding three weeks. At the time of admission, physical examination was unremarkable. She was noted to be hypotensive with systolic blood pressure in the high 70s and was treated with intravenous fluids. Laboratory evaluation showed low random cortisol (0.99 ug/dL, n: 0.4-22.6 ug/dL), undetectable ACTH (<5 pg/mL, n: 7.2-63 pg/mL), low free thyroxine (1.01 ug/dL, n: 0.93-1.7 ug/dL), low free T3 (1.6 pg/mL, n: 2-4.4 pg/mL) and low TSH (0.023 ug/dL, n: 0.27-4.2 ug/dL), consistent with central hypothyroidism and secondary adrenal insufficiency. Importantly, she was normonatremic and normokalemic at admission. She was started on stress dose hydrocortisone (100 mg IV q8h) for presumed adrenal crisis. Following institution of steroid replacement therapy, the patient rapidly became polyuric while simultaneously developing hypernatremia. Her daily urine output peaked at 4400 mL corresponding temporally to a maximum serum sodium of 160 mmol/L. A single dose of 0.5 mg of desmopressin resulted in immediate lowering of daily urine output to 750 mL and appropriate improvement in urine osmolality from 147 mOsm/kg to 565 mOsm/kg, confirming a diagnosis of central diabetes insipidus (cDI). Conclusion: Hypocortisolism is known to impair free water excretion by stimulating arginine vasopressin (AVP) secretion through renal sodium loss and consequent volume depletion as well as direct feedback stimulation of corticotrophin releasing hormone (CRH) and AVP within the hypothalamus. Conversely steroid replacement leads to loss of feedback stimulation, unmasking cDI. This unique convergence of cDI with hypocortisolism is most often encountered in patients with hypopituitarism. Hence patients with secondary adrenal insufficiency should be carefully monitored for cDI after initiation of steroid replacement therapy.
Glycometabolic Alterations in Secondary Adrenal Insufficiency: Does Replacement Therapy Play a Role?
