Glucocorticoids and Pheochromocytoma- a Recipe for Disaster?

Background: Pheochromocytomas are catecholamine-secreting tumors that arise from the chromaffin cells of the adrenal medulla. The catecholamine release manifests as episodic headaches, diaphoresis, and palpitations which can lead to hypertensive emergency known as a pheochromocytoma crisis(PC). This crisis can be precipitated by commonly used medications including corticosteroids, metoclopramide, and anesthetic agents like ketamine and halothane. Case report: We present a 60 year old Caucasian male with a past medical history significant for SVT on metoprolol and diltiazem and long-standing hypertension. He was admitted directly from the clinic to the ED after complaining of severe abdominal pain, multiple episodes of vomiting, and diaphoresis following prednisone intake for a presumed gout flare. He had a blood pressure of 180/100 and tachycardic to 120s on arrival. He was also found to be hypoxemic with a chest x-ray concerning for pulmonary edema along with evidence of a demand related type II NSTEMI. He underwent a CT abdomen pelvis with contrast which showed evidence of high grade distal ileum obstruction with no obstructing mass or inflammatory process. There was also 5-cm solid right adrenal mass which was initially thought to be an incidentaloma. Following stabilization, he underwent an exploratory laparotomy which did not show an obvious mechanical etiology of bowel obstruction. This raised concerns for a pheochromocytoma. Oral verapamil with doxazosin was started to provide appropriate alpha blockade. Subsequently, metoprolol was reintroduced for beta blockade. He was officially diagnosed with glucocorticoid-induced pheochromocytoma after his labs returned with elevated levels of serum metanephrines 43.7(0.00 - 0.49 nmol/L), serum normetanephrine 22.2 (0.00 - 0.89 nmol/L),), 24-hr urine epinephrine 1021 ug/g (0 - 20 ug/g), and 24-hr urine norepinephrine 838 ug/g (normal: 0 - 45 ug/g). Ultimately 3 weeks later he underwent successful R sided adrenalectomy and is doing well. Conclusion: This case demonstrates a rare but life-threatening adverse reaction associated with commonly used glucocorticoids in a patient with an undiagnosed pheochromocytoma. Pheochromocytomas are exceedingly rare and can go undiagnosed in up to 50 percent of patients (1). Failure or delays in diagnosis of PC can lead to increased morbidity and mortality. When managing a pheochromocytoma crisis, it is imperative to avoid selective beta-blockers, as it can worsen hypertension due to unopposed alpha agonism by the secreted catecholamines. This also demonstrates the importance of keeping a broad differential in order to avoid anchoring bias, particularly when there is conflicting clinical information. References: 1. Sutton MG, Sheps SG, Lie JT. Prevalence of clinically unsuspected pheochromocytoma. Review of a 50-year autopsy series. Mayo Clin Proc. 1981 Jun;56(6):354–60. PMID: 6453259.