Abstract
Megestrol acetate (MA) is a synthetic progestin with both antineoplastic and orexigenic properties. In addition to its effects on the progesterone receptor, MA also binds the glucocorticoid receptor. Some patients receiving MA therapy have been reported to develop clinical features of glucocorticoid excess, while others have experienced the clinical syndrome of cortisol deficiency—either following withdrawal of MA therapy or during active treatment. We describe a patient who presented with clinical and biochemical features of central adrenal insufficiency. Pituitary function was otherwise essentially normal, and the etiology of the isolated ACTH suppression was initially unclear. The use of an exogenous glucocorticoid was suspected but was initially denied by the patient; ultimately, the culprit medication was uncovered when a synthetic steroid screen revealed the presence of MA. The patient's symptoms improved after she was switched to hydrocortisone. Clinicians should be aware of the potential effects of MA on the hypothalamic-pituitary-adrenal (HPA) axis.
Highlights
When evaluating a patient who presents with central adrenal insufficiency, it is important to assess recent exposure to exogenous glucocorticoids, as this is the most common etiology of a suppressed hypothalamic-pituitary-adrenal (HPA) axis
Megestrol acetate (MA) is a synthetic progestin approved in the United States for the palliative treatment of advanced breast and endometrial cancers and for the treatment of anorexia or weight loss in patients with AIDS
MA was discontinued and she is being followed in the endocrinology clinic, with the plan to gradually taper her off the glucocorticoid replacement therapy. She is being continued on potassium citrate; her proximal renal tubular acidosis (RTA) was felt to be related to her antiretroviral therapy. This patient presented to the hospital with symptomatic central adrenal insufficiency, as manifested by fatigue, dizziness, and anorexia in the context of very low serum cortisol and plasma Adrenocorticotropic hormone (ACTH) levels
Summary
When evaluating a patient who presents with central adrenal insufficiency, it is important to assess recent exposure to exogenous glucocorticoids, as this is the most common etiology of a suppressed hypothalamic-pituitary-adrenal (HPA) axis. In addition to systemic oral glucocorticoids, one must screen for the use of injectable and topical agents and for antifungal therapies (e.g., ketoconazole), opiates, and other drugs that may impair HPA axis function [1]. In addition to being a potent activator of the progesterone receptor, MA activates the glucocorticoid receptor, with a binding affinity almost twice that of cortisol. Patients receiving MA therapy are susceptible to developing clinical dysfunction of the hypothalamic-pituitary-adrenal axis, similar to that seen with exogenous glucocorticoids
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