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Primary Hyperaldosteronism: Screening, Diagnosis, and Management for the Clinician Eugene T Archives of Diabetes and Endocrine System ISSN 2638-4981 Volume 1, Issue 2, 2018, PP:39-48 Primary Hyperaldosteronism: Screening, Diagnosis, and Management for the Clinician Eugene T. Van, DO1, Winnie Nhan, DO2*, Kristyn Perry, DO3, Azadeh Brumand, DO4 Serena Shen, DO5, Kelvin L. Tran, DO6, Quang T. Nguyen, DO, FACP, FACE, FTOS7 1, 2, 3, 4, 6 5 Department of Internal Medicine, Valley Hospital Medical Center, Las Vegas, NV. 7 Department of Family Medicine, Valley Hospital Medical Center, Las Vegas, NV. Medical Director, Las Vegas Endocrinology, Clinical Associate Professor, Clinical Education, AZCOM, and *Corresponding Author: Winnie Nhan, DO, Department of Internal Medicine, Valley Hospital Medical Center, Las Adjunct Associate Professor of Endocrinology, Touro University Nevada. Vegas, NV, USA. Abstract Primary hyperaldosteronism (PA) is the most common secondary, non-iatrogenic cause of hypertension. This condition is associated with significant risk of morbidity and mortality, yet it is often unrecognized and undiagnosed in the primary care setting. Screening with the aldosterone to renin ratio (ARR) should be considered in patients with resistant hypertension, defined as blood pressure >140/90 mmHg despite the use of three different classes of antihypertensive medications, including a diuretic. The goal of this review is to inform the primary care clinician of the current guideline recommendations for screening, confirming, subtyping, and treating primary hyperaldosteronism. Introduction hypertension is frequently recognized and treated Hypertension affects up to 75 million adults in America, in the primary care setting, secondary hypertension with an estimated cost of $46 billion in annual health is often overlooked and remains untreated. The care utilization, prescription medications, and missed most common cause of secondary hypertension work days (11). Patients with hypertension are at an is hyperaldosteronism and evidence suggests it is increased risk for heart disease and stroke, which are associated with higher risk of cardiac disease, renal the first and third leading cause of death in the United failure as well as cerebrovascular accidents compared Table 1. Overview of secondary causes of hypertension States, respectively (4). Although primary or essential to essential hypertension alone (Table 1) (12). Secondary causes of Hypertension OCP, Pseudoephedrine, NSAID, TCA, SSRI, Glucocorticoid, Medications, Illicit drug use Decongestants, Weight loss agents, Methylphenidate, Methamphetamine, Cocaine. Most common etiology is bilateral idiopathic adrenal hyperplasia, followed by aldosterone-producing adenoma, and primary Primary hyperaldosteronism adrenal hyperplasia. Rare causes include aldosterone-producing adrenocortical carcinoma, ectopic aldosterone-producing adenomas, and familial hyperaldosteronism. Exogenous mineralocorticoid use, nephrotic syndrome, pregnancy, renovascular disease (fibromuscular dysplasia in children and Secondary hyperaldosteronism atherosclerosis including renal artery stenosis in adults), renin- Archives of Diabetes and Endocrine Systemsecreting V1 . I2 tumor. 2018 39 Primary Hyperaldosteronism: Screening, Diagnosis, and Management for the Clinician Blood pressure fluctuates due to a significant increase in Obstructive sleep apnea (OSA) sympathetic activity during sleep. Patients with OSA often retain sodium and fail to respond to anti-hypertensive drug therapy (10). Rare but fatal, caused by a functional adrenal mass. Patients Pheochromocytoma present with paroxysmal hypertension. Exogenous steroid use, adrenal masses, adrenal hyperplasia, and Cushing’s syndrome ectopic sources abnormally increase the level of glucocorticoid. Congenital disease with unknown pathophysiology. Patients Coarctation of the aorta present with hypertension in upper extremities and low or unobtainable arterial blood pressure in the lower extremities. Hyperthyroidism has been shown to increase systolic ambulatory blood pressure compared to euthyroid patients (8). Patients have Hyperthyroidism increased heart rate, decreased systemic vascular resistance, and increased cardiac output and stroke volume. Positive correlation between serum TSH levels and blood pressure Hypothyroidism specifically increased diastolic pressure and causing an increase systemic vascular resistance (22). 21-hydroxylase deficiency is the most common and causes impaired synthesis of glucocorticoid and mineralocorticoid leading to downstream androgen overproduction (16). Congenital adrenal hyperplasia (CAH) 17α-hydroxylase deficiency is rare, but causes increase in mineralocorticoids from excess conversion of upstream precursors (2). An autosomal dominant condition characterized by over-activity Liddle’s Syndrome of the epithelial sodium channel (ENaCs) leading to the triad of hypertension, hypokalemia, and metabolic alkalosis. PHPT is associated with hypertension, studies show a correlation between hypercalcemia and hypertension (9). However, the Primary hyperparathyroidism (PHPT) etiology is unknown in multiple endocrine neoplasia as treatment does not improve hypertension (23). Prevalence of hypertension is 46% in this population. Growth hormone has antinatriuretic actions which leads to sodium Acromegaly retention, resulting in volume expansion, increased systolic a output, and increased heart rate (24). The Endocrine Society recommends screening s they may have hypertension from other causes for primary hyperaldosteronism in patients who including renal parenchymal or vascular disease. The have sustained hypertension resistant to three purpose of screening is to identify those patients who antihypertensive medications, including a diuretic, or can potentially benefit from ameliorative or curative in patients with controlled hypertension on four or surgical and/or medical intervention to significantly more antihypertensive medications (6). Additionally, reducePrimary cardiovascular Hyperaldosteronism morbidity. other patients who should be screened include those with hypertension and hypokalemia, an adrenal incidentaloma, sleep apnea, patients <40 years old Primary hyperaldosteronism is characterized by with a cerebrovascular accident, or patients who have a unregulated aldosterone production. The most common first degree relative with primary hyperaldosteronism cause of primary hyperaldosteronism is bilateral (6). More extensive workup should be done in young adrenal hyperplasia, and the second most common, adults (age < 30 years old) presenting with resistant representing approximately 40% of cases, are due hypertension,Archives of Diabetes without andrisk Endocrinefactors or Systemfamily history, V1 . I2 . 2018to aldosterone-producing adrenocortical adenomas.40 Primary Hyperaldosteronism: Screening, Diagnosis, and Management for the Clinician Other rare etiologies include unilateral adrenal axis. Aldosterone is created in response to the hyperplasia, aldosterone-secreting adrenocortical body’s need for sodium retention, which plays a carcinomas, ectopic aldosterone-producing tumors, pivotal role for water and sodium homeostasis and familial hyperaldosteronism (6). Of the secondary (5). Aldosterone exerts its action on the principle causes of hypertension, primary hyperaldosteronism cells of the late distal convoluted tubules and renal was previously cited as having a prevalence of less than collecting ducts to promote the action of sodium/ 1% of patients with hypertension. However, newer potassium-ATPase, leading to increased sodium studies with cross-sectional and prospective data reabsorption and potassium secretion. Aldosterone suggest that this may actually be falsely understated secretion is regulated by the renin-angiotensin and is present in greater than 10% of hypertensive system (RAS) via stimulation from angiotensin II patients (6, 3). Up to 23% of patients with resistant in response to low perfusion states (figure 1). In hypertension carry a diagnosis of hyperaldosteronism (15). primary hyperaldosteronism, aldosterone secretion Aldosterone is a mineralocorticoid that is produced is increased independently from the RAS, leading to by the zona glomerulosa of the adrenal cortex as an increased sodium reabsorption and thereby increased end-product of the renin-angiotensin-aldosterone extracellular fluid volume and blood pressure (18). Figure 1. Renin-angiotensin-aldosterone system in normal physiologic state Clinical Presentation hypokalemia likely more prevalent in more severe cases (6). Hypokalemia may also be accompanied Clinical symptoms of primary hyperaldosteronism by metabolic alkalosis, excessive urinary sodium are nonspecific, though in general patients may excretion, and hypernatremia. Patients with primary report a history of fatigue, muscle weakness, hyperaldosteronism have higher cardiovascular polyuria, polydipsia and constipation. Despite morbidity and mortality than age- and sex-matched the increase in aldosterone, only a minority of patients with essential hypertension and same patients with primary hyperaldosteronism have degree of blood pressure elevation (18). Patients hypokalemia, with a reported prevalence of 9-37%. could have symptoms of progressive heart failure and Therefore, normokalemic hypertension constitutes imaging may reveal left ventricular hypertrophy and theArchives most commonof Diabetes presentation and Endocrine of the System disease, V1 with . I2 . 2018myocardial fibrosis (15). 41 Primary Hyperaldosteronism: Screening, Diagnosis, and Management for the Clinician Figure 2. Clinical manifestations
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