Abstract: TH-PO1100

Hyperkalemia and Megestrol Acetate: Related?

Session Information

Category: Fluid, Electrolytes, and Acid-Base

  • 704 Fluid, Electrolyte, Acid-Base Disorders

Authors

  • Agrawal, Nikhil, Beth Israel Deaconess Medical Center, Brookline, Massachusetts, United States
  • Netravali, Ilka A, Beth Israel Deaconess Medical Center, Brookline, Massachusetts, United States
  • Mitra, Shimontini, None, Brookline, Massachusetts, United States
  • Lecker, Stewart H., Beth Israel Deaconess Medical Center, Brookline, Massachusetts, United States
  • Hoenig, Melanie P., Beth Israel Deaconess Medical Center, Brookline, Massachusetts, United States
Background

Megestrol acetate (MGA) is a synthetic progestin widely used as an appetite stimulant for patients with cancer. MGA binds to the glucocorticoid receptor with nearly twice the affinity as cortisol and can cause symptoms of glucocorticoid excess while suppressing endogenous glucocorticoid production. We report a case of concomitant mineralocorticoid deficiency in a patient taking MGA with evidence of glucocorticoid deficiency.

Methods

A 51-year-old woman with allogenic stem cell transplant 2 years prior for AML and subsequent relapse was admitted for a line infection. She was noted to have a refractory hyperkalemia a week after admission that required repeated interventions with insulin, dextrose, IV fluids, furosemide, and sodium polystyrene.
She reported 3 cups of tomato juice daily and a history of hypokalemia. Medications: atovaquone, ciprofloxacin, daptomycin, famotidine, folic acid, ondansetron, posaconazole, valacyclovir, cefepime and allopurinol. Two days prior to admission, her MGA was increased from 400 to 800mg daily. She denied fatigue, weakness, or hyperpigmentation. She was normotensive and her examination was unremarkable.
She had pancytopenia without evidence of tumor lysis.
Serum chemistry showed Na 139, K 6.2, Chloride 110, Bicarb 21, BUN 21, Cr 0.8
Early am cortisol: 0.8 mg/dl (increased to 8.8mg/dl at one hour with high dose ACTH stimulation). ACTH <5 pg/mL (6-50). Renin 2.79 ng/mL/hr (0.25-5.82), Aldosterone 1.0 ng/dL (supine 3-16).
A low potassium diet was begun but potassium remained high. Urine potassium excretion was low. MGA discontinued, and fludrocortisone and hydrocortisone were begun. Potassium normalized within 24 hr. Within 5 days, she became hypokalemic, and fludrocortisone was discontinued.

Conclusion

This is the first reported case of hyperkalemia in association with MGA. Although MGA is a well-known cause of adrenal insufficiency, this is usually restricted to the glucocorticoid axis. Here low ACTH level suggests secondary adrenal insufficiency which is typically not associated with defects in the mineralocorticoid axis. Yet low aldosterone level in the setting of hyperkalemia without suppression of renin and with reduced renal potassium excretion is consistent with mineralocorticoid deficiency. Since this resolved with discontinuation of MGA, this suggests that MGA may have an additional effect on the mineralocorticoid axis.