Clinical Presentation, Diagnosis, and Management of Primary Aldosteronism and Pheochromocytoma

Abstract

Primary hyperaldosteronism (PA) or Conn’s syndrome and pheochromocytoma (Pheo) are functioning tumors from the adrenal glands that can cause secondary hypertension.[1,2] Conn’s syndrome is the excess production of the hormone aldosterone from the zona glomerulosa of the adrenal glands. The prevalence of PA has been reported to range from 4.6 to 9.5% among hypertensive individuals.[3,4] The high circulating aldosterone results in hypokalemia which leads to weakness, tingling, muscle spasms, and periods of temporary paralysis.[4,5] Bilateral adrenal hyperplasia and aldosterone-producing adrenal tumor are the most common causes of PA.[6] Pheochromocytoma (Pheo) is a rare adrenomedullary tumor with an incidence of 0.1–0.6%.[1,7] About 0.05–0.1% of Pheo cases are undiagnosed in autopsy studies.[8] These tumors can synthesize, metabolize, store, and secrete catecholamines and their metabolites.[9] Pheos originate from adrenomedullary chromaffin cells that commonly produce epinephrine, norepinephrine, and dopamine. Chromaffin cells evolve into 80–85% Pheos and 15–20% are paragangliomas.[10] A high index of clinical suspicion remains the pivotal point to initiate biochemical studies, particularly in those patients with a certain pattern of spells, blood pressure elevation (paroxysmal or alternating with hypotension), drug-resistant hypertension, Abstract