Abstract
Objective: Primary hyperaldosteronism was initially considered a rarity, but has proven to be, according to more recent data, a more common cause of secondary hypertension (HTN). When sought, it may occur in greater percentages among patients with resistant HTN. More recent epidemiological work showed that most cases are usually associated with bilateral adrenal hyperplasia in the absence of the classically reported adenoma. Design and method: We present the case of 55 years old male diabetic patient, presenting to the emergency department with frequent hypertensive urgencies during the past year. He had been diagnosed 5 years prior with HTN and received treatment with an ACE inhibitor, a calcium channel blocker and a low-dose diuretic. Despite proper life style changes and appropriate adherence to therapy, the 24 h ambulatory blood pressure measurement showed significantly elevated blood pressure (BP) levels – mean systolic BP 175/94 mmHg with a non-dipping profile. In the course of investigations for secondary causes of hypertension we performed nocturnal polysomnography, duplex ultrasound of renal arteries and tested for cortisol levels – all with negative findings. Remarkable findings were a persistent moderate hypokalemia (∼ 3 mmol/L), mild hypernatremia (143 mmol/L) despite low-sodium diet and urinary potassium excretion increased at 37 mmol/24 h. Further, the abdominal CT scan showed bilateral adrenal hyperplasia, with no adenomas. The patient was switched to high-dose verapamil and high-dose doxazosin for 4 weeks, and the endocrinology profile showed high plasma aldosterone levels (suppressed after oral 50 mg of captopril), high plasma aldosterone/plasma renin activity ratio, with a negative postural test, thus confirming primary hyperaldosteronism. The patient was switched to initial antihypertensive therapy adding 50 mg spironolactone, which conferred a better BP control confirmed at 1-month re-evaluation. Results: The diagnostic of primary hyperaldosteronism is challenging, but it presence significantly affects BP control, especially in selected populations, such as resistant HTN patients. Considering recent trials (PATHWAY) showed that adding spironolactone to the triple therapy in resistant HTN achieves BP control in most patients, it may remain an open debate whether cases without evidence of adenoma actually benefit from performing the full diagnostic algorithm.
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