Background: Cushing's syndrome is a constellation of signs and symptoms commonly characterized by weight gain, round (moon) facies, truncal obesity, hypertension, hyperglycemia, and abdominal striae. Causes include pituitary and adrenal tumors, ectopic foci of ACTH or cortisol production, and exogenous glucocorticoid administration. We present the case of a patient referred for evaluation of Cushingoid body habitus who was found to have Cushing's syndrome from exogenous glucocorticoids.
Case Report: A 40 year-old woman with a past medical history significant for refractory hypertension, mild asthma, dyslipidemia, and many self-reported allergies was referred to an endocrinologist for evaluation of hypertension, central obesity, a dorsal hump, and hyperglycemia noted during a recent Emergency Department visit. She expressed frustration at being obese, stating that it had developed over many years and prohibited her from working in her chosen vocation as a choreographer. A chart review revealed an extensive past lab workup notable for normal urine and serum catecholamines, normal thyroid function tests, and persistently low cortisol levels. Physical examination revealed lipodystrophy at C7, vague abdominal striae, and round facies. Her hemoglobin A1c returned elevated at 6.3%. ACTH stimulation was normal; salivary and urine cortisol levels were low. The patient denied taking exogenous steroids. In light of a workup inconsistent with the patient's history and exam, serum prednisone, dexamethasone, and prednisolone concentrations were sent. Her serum prednisolone returned at 3.4 mcg/dL (normal range undetectable); 2 weeks later a follow-up concentration was also elevated at 2.2 mcg/dL. The patient insisted on further workup of her Cushingoid body habitus, but vehemently denied any knowledge of exogenous steroid exposure. Further chart review revealed no documented use of steroid therapy for treatment of her asthma in the preceding 10 years.
Discussion: Glucocorticoids, a common therapy for a variety of illnesses, are a well-known etiology of Cushing's syndrome. Factitious Cushing's syndrome is less common, however case reports support its existence. Additional case reports underscore its gravity, with glucocorticoid withdrawal and deaths secondary to opportunistic infections both reported. This case highlights the importance of a careful review of available data--in this case across multiple institutions--in uncovering this often difficult to diagnose disorder.
Conclusion: Toxicologists and endocrinologists should be aware of surreptitious administration of glucocorticoids as a hidden cause of Cushing's syndrome.