Datasets:

---

Recag

/

Rp_CommonC_264

like 0

ERROR: type should be string, got "https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMTI3MDgwLXRyZWF0bWVudA==\nDrugs & Diseases > Endocrinology\nPrimary Aldosteronism Treatment & Management\nAuthor: Gabriel I Uwaifo, MD; Chief Editor: Romesh Khardori, MD, PhD, FACP more...\nPrimary Aldosteronism\nSections Primary Aldosteronism\nScreening (First-Tier) Tests\nConfirmatory (Second-Tier) Tests\nDetermination of Primary Aldosteronism Subtype (Third-Tier) Tests\nCT Scanning and MRI\nNP-59 Iodo-methyl-norcholesterol Scintigraphy\nAdrenal Venous Sampling\nHydroxycorticosterone and Oxocortisol-Hydroxycortisol Assays\nFludrocortisone Suppression Test\nDexamethasone Suppression Test\nMetoclopramide (Reglan) Test\nAdditional Laboratory Studies\nAngiotensin-II infusion test\nHistological Findings\nPharmacologic Therapy\nAdrenal Surgery\nAldosterone Antagonists, Selective\nPotassium-Sparing Diuretics\nThiazide Diuretics\nAngiotensin II Receptor Blockers\nAmong the major goals of therapy for primary aldosteronism are (1) normalization of blood pressure, (2) normalization of levels of serum potassium and other electrolytes, and (3) normalization of serum aldosterone levels. [22, 41]\nThe appropriate treatment for primary aldosteronism depends on its cause. Although hypertension (HTN) is frequently cured after unilateral adrenalectomy in patients with primary aldosteronism secondary to an adrenal aldosteronoma, the mean HTN cure rate is only 19% after unilateral or even bilateral adrenalectomy in patients with idiopathic adrenal hyperplasia (IAH). Therefore, medical management is the treatment of choice for the IAH variant of primary aldosteronism. (See the chart below.)\nEffects of main antihypertensives on the renin-angiotensin system.\nView Media Gallery\nIn patients with an aldosteronoma, medical therapy is used preoperatively to control blood pressure and correct hypokalemia, thus decreasing surgical risk. Medical therapy is also administered to patients with persistent HTN postoperatively, poor surgical candidates, and patients who refuse surgery.\nIn patients with heart failure who have secondary aldosteronism, aldosterone antagonism by spironolactone and eplerenone has been demonstrated to confer survival benefit. [42]\nBy inhibiting the intracellular calcium flux in the adrenocortical cells, the dihydropyridine calcium channel blockers reduce the production of aldosterone in response to a variety of stimulants, including potassium, corticotropin, and angiotensin-II.\nNifedipine is the most extensively studied of these medications; however, although nifedipine causes a significant improvement in patients with hypertension (HTN), it does not address the pathophysiology of the condition. The plasma renin activity (PRA), aldosterone levels, plasma volume, and serum potassium concentrations remain essentially unchanged while using nifedipine.\nMineralocorticoid antagonists\nMineralocorticoid antagonists, such as spironolactone, are inhibitory ligands to the mineralocorticoid receptor (MR). They achieve remarkable blood pressure control and normalization of plasma volume and serum potassium concentrations, particularly in patients with aldosteronomas. [43]\nThe salutary effects of spironolactone appear to be due mainly to its impact on salt and water balance rather than to its antagonism of aldosterone in the kidney. The combination of spironolactone and thiazides often provides even better blood pressure control than does spironolactone alone.\nBecause of the estrogenlike adverse effects of spironolactone, including impotence and gynecomastia, the incentive to develop a similarly effective antialdosterone agent without these adverse effects is considerable. Eplerenone is a selective antialdosterone agent that may fulfill this promise, because it is a specific aldosterone receptor antagonist that does not have the additional antiandrogen effects associated with spironolactone.\nIn the subgroup of patients with glucocorticoid-remediable aldosteronism (GRA), the treatment of choice is the administration of the lowest possible dose of glucocorticoid that can be used to achieve adequate blood pressure control. Because of the potential adverse effects that can result from even subtle glucocorticoid excess, using short-acting glucocorticoids, such as prednisone and hydrocortisone (rather than dexamethasone), is generally best.\nACE inhibitors and angiotensin receptor blockers (ARBs) are also potential treatment options. Less ideal medical treatment options include potassium-sparing diuretics, such as triamterene and amiloride, that are not mineralocorticoid antagonists. Amiloride acts at the level of the distal convoluted tubule but does not bind to mineralocorticoid receptors.\nA few reports of the use of percutaneous injection of ethanol or acetic acid into aldosteronomas as a treatment modality exist; in these cases, the treatment was usually administered to patients for whom surgery was contraindicated. [44] This technique is neither popular nor well validated. Furthermore, it requires the technical expertise of a highly skilled interventional radiologist.\nNonsurgical therapy is also a viable treatment option in patients who have lateralizable disease but who are poor surgical candidates because of other coexisting comorbidities. It is also a viable treatment option in the rare setting of bilateral functional adrenal adenomas that would otherwise require bilateral adrenalectomy.\nSurgery is the treatment of choice for the lateralizable variants of primary aldosteronism, including typical aldosteronomas, renin-responsive adenomas (RRAs), and primary adrenal hyperplasia (PAH).\nPreoperatively, once the biochemical and anatomic diagnoses are made and confirmed, the patient should be started on a 3- to 5-week course of spironolactone. This serves as an additional diagnostic tool (in confirming the diagnosis of primary aldosteronism) and as a means of predicting the blood pressure response that can be expected postsurgery.\nAn adrenalectomy can be performed via a formal laparotomy or by using a laparoscopic technique (with performance of the latter becoming increasingly common). The laparoscopic option now makes it possible to offer surgical therapy to relatively frail patients who would be unable to withstand a formal laparotomy. Ongoing studies are systematically evaluating the place of adrenal-conserving operations versus total unilateral adrenalectomy in these patients. [45]\nAmong the options being studied are (1) partial adrenalectomy, in which a wedge resection of the gland with the adenoma is performed along with aldosteronoma enucleation, and (2) medulla-sparing adrenalectomy, in which an attempt is made to retain the adrenal medullary tissue while removing the cortex.\nAbout 60-70% of patients are rendered normotensive following curative surgery for aldosteronomas when evaluated 1 year postoperatively. Hypertension (HTN) typically does not resolve immediately postoperatively but, rather, over 3-6 months. (Although following surgery, virtually all patients with an aldosteronoma have significant reductions in aldosterone secretion and blood pressure and also demonstrate a correction of hypokalemia. [46, 47, 48, 49, 50] )\nA retrospective study of 168 patients with primary aldosteronism who underwent an adrenalectomy found that HTN was cured or controlled in 77% of patients with a unilateral adenoma and in 68% of patients with aldosteronism who had no adenoma, but whose aldosterone-to-cortisol ratio was at least 5 times higher on the dominant side than on the nondominant side. [48]\nThe percentage of patients who remain normotensive 5 years postoperatively is about 53%. The resolution of HTN following adrenalectomy invariably occurs in the setting of a family history in which HTN is absent and/or when there has been preoperative use of 2 or fewer antihypertensives by the patient.\nAdrenalectomy has very little utility in the setting of idiopathic adrenal hyperplasia (IAH). In reported cases in which surgery has unintentionally been performed on patients with IAH, the effects on blood pressure, hypokalemia, and aldosterone hypersecretion have been minimal, further underpinning the necessity of making a correct diagnosis before making a case for adrenalectomy.\nPersistence of HTN following apparent surgical treatment of lateralizable disease is most common in patients older than 45 years, in those who had HTN for more than 5 years prior to surgery, and in persons who did not respond preoperatively to spironolactone. [48, 49]\nPersistent HTN may be related to resetting of baroreceptors, established hemodynamic changes, structural changes in the blood vessels, or coincidental essential HTN.\nAnother possibility to consider in persistent HTN is an incomplete resection of the adenoma, with remaining remnant hyperplastic tissue. The coexistence of hypertensive nephrosclerosis in some patients with persistent HTN is also a distinct possibility. The coexistence of other secondary causes of HTN needs to be considered as well; renal artery stenosis is an important consideration.\nPreoperative and postoperative care\nPrior to surgery, patients should receive at least 8-10 weeks of medical therapy in order to decrease blood pressure and to correct the metabolic syndromes that are often associated with primary aldosteronism.\nPostoperatively, metabolic profiles should be closely monitored. Most patients do not develop permanent hypomineralocorticoidism and therefore do not require fludrocortisone replacement.\nFor patients who develop hypoaldosteronism, the symptoms may persist for a long time and may be akin to the delay observed in adrenal glucocorticoid recovery following chronic corticotropin suppression by exogenous steroids. However, if significant hyperkalemia develops, potassium supplements should be discontinued, and the patient can be started on furosemide at doses of 80-160 mg daily.\nA low-salt diet, although helpful in achieving blood pressure control in primary aldosteronism, may be associated with false-negative results on biochemical testing.\nA high-salt diet makes the achievement of blood pressure control more difficult and may cause false-positive results on biochemical testing.\nRossi GP, Ragazzo F, Seccia TM, Maniero C, Barisa M, Calò LA, et al. Hyperparathyroidism can be useful in the identification of primary aldosteronism due to aldosterone-producing adenoma. Hypertension. 2012 Aug. 60(2):431-6. [Medline].\nDluhy RG, Lifton RP. Glucocorticoid-remediable aldosteronism. Endocrinol Metab Clin North Am. 1994 Jun. 23(2):285-97. [Medline].\nFunder JW. The genetic basis of primary aldosteronism. Curr Hypertens Rep. 2012 Apr. 14(2):120-4. [Medline].\nChoi M, Scholl UI, Yue P, et al. K+ channel mutations in adrenal aldosterone-producing adenomas and hereditary hypertension. Science. 2011 Feb 11. 331(6018):768-72. [Medline]. [Full Text].\nYoung DB. Quantitative analysis of aldosterone's role in potassium regulation. Am J Physiol. 1988 Nov. 255(5 Pt 2):F811-22. [Medline].\nStowasser M, Klemm SA, Tunny TJ, et al. Plasma aldosterone response to ACTH in subtypes of primary aldosteronism. Clin Exp Pharmacol Physiol. 1995 Jun-Jul. 22(6-7):460-2. [Medline].\nLitchfield WR, New MI, Coolidge C, et al. Evaluation of the dexamethasone suppression test for the diagnosis of glucocorticoid-remediable aldosteronism. J Clin Endocrinol Metab. 1997 Nov. 82(11):3570-3. [Medline]. [Full Text].\nMulatero P, Stowasser M, Loh KC, Fardella CE, Gordon RD, Mosso L, et al. Increased diagnosis of primary aldosteronism, including surgically correctable forms, in centers from five continents. J Clin Endocrinol Metab. 2004 Mar. 89(3):1045-50. [Medline].\nKayser SC, Deinum J, de Grauw WJ, et al. Prevalence of primary aldosteronism in primary care: a cross-sectional study. Br J Gen Pract. 2018 Feb. 68 (667):e114-22. [Medline]. [Full Text].\nBorn-Frontsberg E, Reincke M, Rump LC, et al. Cardiovascular and cerebrovascular comorbidities of hypokalemic and normokalemic primary aldosteronism: results of the German Conn's Registry. J Clin Endocrinol Metab. 2009 Apr. 94(4):1125-30. [Medline].\nBernini G, Galetta F, Franzoni F, Bardini M, Taurino C, Bernardini M, et al. Arterial stiffness, intima-media thickness and carotid artery fibrosis in patients with primary aldosteronism. J Hypertens. 2008 Dec. 26(12):2399-405. [Medline].\nApostolopoulou K, Künzel HE, Gerum S, Merkle K, Schulz S, Fischer E, et al. Gender differences in anxiety and depressive symptoms in patients with primary hyperaldosteronism: A cross-sectional study. World J Biol Psychiatry. 2012 May 8. [Medline].\nMourtzinis G, Adamsson Eryd S, Rosengren A, et al. Primary aldosteronism and thyroid disorders in atrial fibrillation: A Swedish nationwide case-control study. Eur J Prev Cardiol. 2018 Jan 1. 2047487318759853. [Medline].\nOhno Y, Sone M, Inagaki N, et al. Prevalence of Cardiovascular Disease and Its Risk Factors in Primary Aldosteronism: A Multicenter Study in Japan. Hypertension. 2018 Mar. 71 (3):530-7. [Medline].\nCruz DN, Perazella MA. Hypertension and hypokalemia: unusual syndromes. Conn Med. 1997 Feb. 61(2):67-75. [Medline].\nCesari M, Letizia C, Angeli P, Sciomer S, Rosi S, Rossi GP. Cardiac Remodeling in Patients With Primary and Secondary Aldosteronism: A Tissue Doppler Study. Circ Cardiovasc Imaging. 2016 Jun. 9 (6):[Medline].\nHall JE, Granger JP, Smith MJ Jr. Role of renal hemodynamics and arterial pressure in aldosterone \"escape\". Hypertension. 1984. 6:1183.\nYokota N, Bruneau BG, Kuroski de Bold ML, et al. Atrial natriuretic factor significantly contributes to the mineralocorticoid escape phenomenon. Evidence for a guanylate cyclase-mediated pathway. J Clin Invest. 1994 Nov. 94(5):1938-46. [Medline]. [Full Text].\nVallon V, Rieg T. Regulation of renal NaCl and water transport by the ATP/UTP/P2Y2 receptor system. Am J Physiol Renal Physiol. 2011 Sep. 301(3):F463-75. [Medline]. [Full Text].\nSchiffrin EL, Chrétien M, Seidah NG, et al. Response of human aldosteronoma cells in culture to the N-terminal glycopeptide of pro-opiomelanocortin and gamma 3-MSH. Horm Metab Res. 1983 Apr. 15(4):181-4. [Medline].\nWolley MJ, Stowasser M. New Advances in the Diagnostic Workup of Primary Aldosteronism. J Endocr Soc. 2017 Mar 1. 1 (3):149-61. [Medline]. [Full Text].\n[Guideline] Funder JW, Carey RM, Fardella C, Gomez-Sanchez CE, Mantero F, Stowasser M, et al. Case detection, diagnosis, and treatment of patients with primary aldosteronism: an endocrine society clinical practice guideline. J Clin Endocrinol Metab. 2008 Sep. 93(9):3266-81. [Medline].\nQuamme GA. Control of magnesium transport in the thick ascending limb. Am J Physiol. 1989 Feb. 256(2 Pt 2):F197-210. [Medline].\nSeiler L, Rump LC, Schulte-Mönting J, Slawik M, Borm K, Pavenstädt H, et al. Diagnosis of primary aldosteronism: value of different screening parameters and influence of antihypertensive medication. Eur J Endocrinol. 2004 Mar. 150(3):329-37. [Medline].\nTzanela M, Effremidis G, Vassiliadi D, et al. The aldosterone to renin ratio in the evaluation of patients with incidentally detected adrenal masses. Endocrine. 2007 Oct. 32(2):136-42. [Medline].\nDiederich S, Mai K, Bahr V, et al. The simultaneous measurement of plasma-aldosterone- and -renin-concentration allows rapid classification of all disorders of the renin-aldosterone system. Exp Clin Endocrinol Diabetes. 2007 Jul. 115(7):433-8. [Medline].\nWu VC, Chang HW, Liu KL, et al. Primary aldosteronism: diagnostic accuracy of the losartan and captopril tests. Am J Hypertens. 2009 Aug. 22(8):821-7. [Medline].\nBurton TJ, Mackenzie IS, Balan K, Koo B, Bird N, Soloviev DV, et al. Evaluation of the sensitivity and specificity of (11)C-metomidate positron emission tomography (PET)-CT for lateralizing aldosterone secretion by Conn's adenomas. J Clin Endocrinol Metab. 2012 Jan. 97(1):100-9. [Medline].\nOtsuka F, Otsuka-Misunaga F, Koyama S, et al. Hormonal characteristics of primary aldosteronism due to unilateral adrenal hyperplasia. J Endocrinol Invest. 1998 Sep. 21(8):531-6. [Medline].\nStowasser M, Bachmann AW, Tunny TJ. Production of 18-oxo-cortisol in subtypes of primary aldosteronism. Clin Exp Pharmacol Physiol. 1996 Jun-Jul. 23(6-7):591-3. [Medline].\nHamlet SM, Gordon RD, Gomez-Sanchez CE, et al. Adrenal transitional zone steroids, 18-oxo and 18-hydroxycortisol, useful in the diagnosis of primary aldosteronism, are ACTH-dependent. Clin Exp Pharmacol Physiol. 1988 Apr. 15(4):317-22. [Medline].\nMcAlister FA, Lewanczuk RZ. Primary hyperaldosteronism and adrenal incidentaloma: an argument for physiologic testing before adrenalectomy. Can J Surg. 1998 Aug. 41(4):299-305. [Medline].\nDi Martino M, Garcia Sanz I, Munoz de Nova JL, Marin Campos C, Martinez Martin M, Dominguez Gadea L. NP-59 test for preoperative localization of primary hyperaldosteronism. Langenbecks Arch Surg. 2017 Feb 21. [Medline].\nGeorgiades CS, Hong K, Geschwind JF, et al. Adjunctive use of C-arm CT may eliminate technical failure in adrenal vein sampling. J Vasc Interv Radiol. 2007 Sep. 18(9):1102-5. [Medline].\nYoung WF, Stanson AW, Grant CS, et al. Primary aldosteronism: adrenal venous sampling. Surgery. 1996 Dec. 120(6):913-9; discussion 919-20. [Medline].\nWebb R, Mathur A, Chang R, Baid S, Nilubol N, Libutti SK, et al. What is the Best Criterion for the Interpretation of Adrenal Vein Sample Results in Patients with Primary Hyperaldosteronism?. Ann Surg Oncol. 2011 Nov 3. [Medline].\nDekkers T, Prejbisz A, Kool LJ, et al. Adrenal vein sampling versus CT scan to determine treatment in primary aldosteronism: an outcome-based randomised diagnostic trial. Lancet Diabetes Endocrinol. 2016 Sep. 4 (9):739-46. [Medline].\nYoung WF, Stanson AW, Thompson GB, et al. Role for adrenal venous sampling in primary aldosteronism. Surgery. 2004 Dec. 136(6):1227-35. [Medline].\nKline G, Leung A, So B, Chin A, Harvey A, Pasieka JL. Application of strict criteria in adrenal venous sampling increases the proportion of missed patients with unilateral disease who benefit from surgery for primary aldosteronism. J Hypertens. 2018 Feb 20. [Medline].\nNaruse M, Naruse K, Yoshimoto T, et al. Dopaminergic regulation of aldosterone secretion: its pathophysiologic significance in subsets of primary aldosteronism. Hypertens Res. 1995 Jun. 18 Suppl 1:S59-64. [Medline].\nCarey RM. Primary aldosteronism. Horm Res. 2009 Jan. 71 Suppl 1:8-12. [Medline].\nHood SJ, Taylor KP, Ashby MJ, et al. The spironolactone, amiloride, losartan, and thiazide (SALT) double-blind crossover trial in patients with low-renin hypertension and elevated aldosterone-renin ratio. Circulation. 2007 Jul 17. 116(3):268-75. [Medline]. [Full Text].\nRonconi V, Turchi F, Appolloni G, di Tizio V, Boscaro M, Giacchetti G. Aldosterone, Mineralocorticoid Receptor and the Metabolic Syndrome: Role of the Mineralocorticoid Receptor Antagonists. Curr Vasc Pharmacol. 2011 Oct 21. [Medline].\nMinowada S, Fujimura T, Takahashi N, et al. Computed tomography-guided percutaneous acetic acid injection therapy for functioning adrenocortical adenoma. J Clin Endocrinol Metab. 2003 Dec. 88(12):5814-7. [Medline]. [Full Text].\nSukor N, Gordon RD, Ku YK, et al. Role of unilateral adrenalectomy in bilateral primary aldosteronism: a 22-year single center experience. J Clin Endocrinol Metab. 2009 Jul. 94(7):2437-45. [Medline].\nCelen O, O'Brien MJ, Melby JC, et al. Factors influencing outcome of surgery for primary aldosteronism. Arch Surg. 1996 Jun. 131(6):646-50. [Medline].\nWaldmann J, Maurer L, Holler J, Kann PH, Ramaswamy A, Bartsch DK, et al. Outcome of surgery for primary hyperaldosteronism. World J Surg. 2011 Nov. 35(11):2422-7. [Medline].\nLetavernier E, Peyrard S, Amar L, et al. Blood pressure outcome of adrenalectomy in patients with primary hyperaldosteronism with or without unilateral adenoma. J Hypertens. 2008 Sep. 26(9):1816-23. [Medline].\nMilsom SR, Espiner EA, Nicholls MG, et al. The blood pressure response to unilateral adrenalectomy in primary aldosteronism. Q J Med. 1986 Dec. 61(236):1141-51. [Medline].\nGiacchetti G, Turchi F, Boscaro M, Ronconi V. Management of primary aldosteronism: its complications and their outcomes after treatment. Curr Vasc Pharmacol. 2009 Apr. 7(2):244-49. [Medline].\nAmar L, Baguet JP, Bardet S, et al. SFE/SFHTA/AFCE primary aldosteronism consensus: Introduction and handbook. Ann Endocrinol (Paris). 2016 Jun 14. [Medline]. [Full Text].\nBaguet JP, Steichen O, Mounier-Vehier C, Gosse P. SFE/SFHTA/AFCE consensus on primary aldosteronism, part 1: Epidemiology of PA, who should be screened for sporadic PA?. Ann Endocrinol (Paris). 2016 Apr 15. 86 (20):1002-8. [Medline]. [Full Text].\nDouillard C, Houillier P, Nussberger J, Girerd X. SFE/SFHTA/AFCE Consensus on Primary Aldosteronism, part 2: First diagnostic steps. Ann Endocrinol (Paris). 2016 May 10. [Medline]. [Full Text].\nReznik Y, Amar L, Tabarin A. SFE/SFHTA/AFCE consensus on primary aldosteronism, part 3: Confirmatory testing. Ann Endocrinol (Paris). 2016 Jun 15. [Medline]. [Full Text].\nBardet S, Chamontin B, Douillard C, et al. SFE/SFHTA/AFCE consensus on primary aldosteronism, part 4: Subtype diagnosis. Ann Endocrinol (Paris). 2016 Mar 29. [Medline]. [Full Text].\nZennaro MC, Jeunemaitre X. SFE/SFHTA/AFCE consensus on primary aldosteronism, part 5: Genetic diagnosis of primary aldosteronism. Ann Endocrinol (Paris). 2016 Jun 14. [Medline]. [Full Text].\nSteichen O, Amar L, Chaffanjon P, Kraimps JL, Menegaux F, Zinzindohoue F. SFE/SFHTA/AFCE consensus on primary aldosteronism, part 6: Adrenal surgery. Ann Endocrinol (Paris). 2016 Jun 10. [Medline]. [Full Text].\nPechère-Bertschi A, Herpin D, Lefebvre H. SFE/SFHTA/AFCE consensus on primary aldosteronism, part 7: Medical treatment of primary aldosteronism. Ann Endocrinol (Paris). 2016 Jun 14. [Medline]. [Full Text].\n[Guideline] Funder JW, Carey RM, Mantero F, et al. The Management of Primary Aldosteronism: Case Detection, Diagnosis, and Treatment: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2016 May. 101 (5):1889-916. [Medline]. [Full Text].\n[Guideline] Romero DG, Yanes Cardozo LL. Clinical Practice Guideline for Management of Primary Aldosteronism: What is New in the 2016 Update?. Int J Endocrinol Metab Disord. 2016. 2 (3):[Medline]. [Full Text].\nMagnetic resonance imaging (MRI) scan in a patient with Conn syndrome showing a left adrenal adenoma.\nScintigram obtained by using iodine-131-beta-iodomethyl-norcholesterol (NP-59) in a 59-year-old man with hypertension shows fairly intense radionuclide uptake in the right adrenal tumor. At surgery, a Conn tumor was confirmed.\nPotential causes of primary aldosteronism.\nTransitional zone adrenocortical steroids.\nAlgorithm for screening for potential primary aldosteronism.\nAlgorithm for confirmation of primary aldosteronism.\nAlgorithm for distinguishing subtypes of primary aldosteronism.\nGabriel I Uwaifo, MD Associate Professor, Section of Endocrinology, Diabetes and Metabolism, Louisiana State University School of Medicine in New Orleans; Adjunct Professor, Joint Program on Diabetes, Endocrinology and Metabolism, Pennington Biomedical Research Center in Baton Rouge\nGabriel I Uwaifo, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians-American Society of Internal Medicine, American Diabetes Association, American Medical Association, American Society of Hypertension, Endocrine Society\nNicholas J Sarlis, MD, PhD, FACP Vice President, Head of Medical Affairs, Incyte Corporation\nNicholas J Sarlis, MD, PhD, FACP is a member of the following medical societies: American Association for the Advancement of Science, American Association for Cancer Research, American Association of Clinical Endocrinologists, American College of Physicians, American Federation for Medical Research, American Head and Neck Society, American Medical Association, American Society for Radiation Oncology, American Thyroid Association, Endocrine Society, New York Academy of Sciences, Royal Society of Medicine, Association for Psychological Science, American College of Endocrinology, European Society for Medical Oncology, American Society of Clinical Oncology\nDisclosure: Received salary from Incyte Corporation for employment; Received ownership interest from Sanofi-Aventis for previous employment; Received ownership interest/ stock & stock option (incl. rsu) holder from Incyte Corporation for employment.\nRomesh Khardori, MD, PhD, FACP Professor of Endocrinology, Director of Training Program, Division of Endocrinology, Diabetes and Metabolism, Strelitz Diabetes and Endocrine Disorders Institute, Department of Internal Medicine, Eastern Virginia Medical School\nRomesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, Endocrine Society\nArthur B Chausmer, MD, PhD, FACP, FACE, FACN, CNS, Professor of Medicine (Endocrinology, Adj), Johns Hopkins School of Medicine; Affiliate Research Professor, Bioinformatics and Computational Biology Program, School of Computational Sciences, George Mason University; Principal, C/A Informatics, LLC\nArthur B Chausmer, MD, PhD, FACP, FACE, FACN, CNS is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Endocrinology, American College of Nutrition, American College of Physician Executives, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Medical Informatics Association, American Society for Bone and Mineral Research, American Society of Law, Medicine &Ethics, Endocrine Society, and International Society for Clinical Densitometry\nSerge A Jabbour, MD Associate Professor, Department of Medicine, Division of Endocrinology, Jefferson Medical College of Thomas Jefferson University\nSerge A Jabbour, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians-American Society of Internal Medicine, American Diabetes Association, American Medical Association, American Thyroid Association, Endocrine Society, and Pennsylvania Medical Society\nFrederick H Ziel, MD Associate Professor of Medicine, University of California, Los Angeles, David Geffen School of Medicine; Physician-In-Charge, Endocrinology/Diabetes Center, Director of Medical Education, Kaiser Permanente Woodland Hills; Chair of Endocrinology, Co-Chair of Diabetes Complete Care Program, Southern California Permanente Medical Group\nFrederick H Ziel, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Endocrinology, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Diabetes Association, American Federation for Medical Research, American Medical Association, American Society for Bone and Mineral Research, California Medical Association, Endocrine Society, andInternational Society for Clinical Densitometry\nencoded search term (Primary Aldosteronism) and Primary Aldosteronism\nEpidemiology of Hypertension\nPathophysiology of Hypertension\nHypertensive Emergencies\nHypertension and Pregnancy\nHypertensive Heart Disease\nHypertension Medication for Specific Comorbidities\nWomen Have Steeper, Earlier BP Increases Over Lifetime\nWomen Have Lower Risk for Gout Than Men at Comparable Uric Acid Levels\nTop News From TCT 2019: Slideshow\nAccording to Endocrinologists\nIntermittent Fasting Promotes Weight Loss, Improves Lipids\nFDA Investigating Metformin for Possible Carcinogen\nMelatonin: Magic Potion or Unregulated Danger?\nHigh-Protein Diet Could Be Harmful, Even for Healthy Kidneys\nMediterranean Diet Repeats as Best Overall of 2020\n2001 /viewarticle/923981 News\nNews Women Have Steeper, Earlier BP Increases Over Lifetime\nNews Primary Aldosteronism Can Present as Atrial Fibrillation\nDiseases & Conditions Epidemiology of Hypertension\nDiseases & Conditions Hypertension"