Prevalence and characteristics of the metabolic syndrome in primary aldosteronism.

CONTEXT Patients with hypertension have a high prevalence of concurrent metabolic abnormalities, including obesity, dyslipidemia, and hyperglycemia. Clustering of these cardiovascular risk factors, defined as metabolic syndrome, causes a more pronounced target organ damage. Aldosterone excess has been found to be associated with glucose disorders and may contribute to cardiovascular damage. OBJECTIVE The aim of our study was to assess the prevalence and the characteristics of the metabolic syndrome in a group of patients with hypertension due to primary aldosteronism compared with patients with essential hypertension. METHODS The National Cholesterol Education Program Adult Treatment Panel III definition of the metabolic syndrome was used. Eighty-five patients with primary aldosteronism and 381 patients with essential hypertension were studied. Most patients were not receiving antihypertensive therapy during the investigation. RESULTS Blood glucose and systolic blood pressure were higher (P < 0.05 and P < 0.01, respectively) and duration of hypertension was longer (P < 0.05) in primary aldosteronism than in essential hypertension. The prevalence of metabolic syndrome was higher in primary aldosteronism than in essential hypertension (41.1% vs. 29.6%; P < 0.05). Distribution of single components of the metabolic syndrome other than hypertension showed a higher prevalence of hyperglycemia in primary aldosteronism than in essential hypertension (27.0% vs. 15.2%; P < 0.05). CONCLUSIONS Our findings confirm a negative effect of aldosterone excess on glucose metabolism and suggest that the recently reported higher rates of cardiovascular events in primary aldosteronism than in essential hypertension might be due to increased prevalence of the metabolic syndrome in the former condition.

[1]  M. Cassader,et al.  The metabolic syndrome and high C‐reactive protein: prevalence and differences by sex in a southern‐European population‐based cohort , 2005, Diabetes/metabolism research and reviews.

[2]  G. Leoncini,et al.  Metabolic syndrome is associated with early signs of organ damage in nondiabetic, hypertensive patients , 2005, Journal of internal medicine.

[3]  P. Milliez,et al.  Evidence for an increased rate of cardiovascular events in patients with primary aldosteronism. , 2005, Journal of the American College of Cardiology.

[4]  M. Boscaro,et al.  Aldosterone as a cardiovascular risk factor , 2005, Trends in Endocrinology & Metabolism.

[5]  M. Boscaro,et al.  Diagnosis of primary aldosteronism: from screening to subtype differentiation , 2005, Trends in Endocrinology & Metabolism.

[6]  R. Carey,et al.  The renin–angiotensin–aldosterone system, glucose metabolism and diabetes , 2005, Trends in Endocrinology & Metabolism.

[7]  A. Fornoni,et al.  Metabolic syndrome and endothelial dysfunction , 2005, Current hypertension reports.

[8]  N. Sonino,et al.  Adiponectin, insulin resistance, and left ventricular structure in dipper and nondipper essential hypertensive patients. , 2005, American journal of hypertension.

[9]  G. Lip,et al.  Plasma von Willebrand factor and the development of the metabolic syndrome in patients with hypertension. , 2004, The Journal of clinical endocrinology and metabolism.

[10]  F. Magrini,et al.  Metabolic syndrome and target organ damage in untreated essential hypertensives , 2004, Journal of hypertension.

[11]  E. Mannarino,et al.  Prognostic value of the metabolic syndrome in essential hypertension. , 2004, Journal of the American College of Cardiology.

[12]  T. Ludwig,et al.  Human Endothelium: Target for Aldosterone , 2004, Hypertension.

[13]  W. Young,et al.  Increased Diagnosis of Primary Aldosteronism, Including Surgically Correctable Forms, in Centers from Five Continents , 2004 .

[14]  G. Mancia,et al.  Cardiovascular risk profile and blood pressure control in Italian hypertensive patients under specialist care , 2004, Journal of hypertension.

[15]  B. Howard,et al.  Comparison of cardiac structure and function in American Indians with and without the metabolic syndrome (the Strong Heart Study). , 2004, The American journal of cardiology.

[16]  Daniel W. Jones,et al.  Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. , 2003, Hypertension.

[17]  A. Gederlini,et al.  Primary Aldosteronism and Hypertensive Disease , 2003, Hypertension.

[18]  Daniel W. Jones,et al.  The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. , 2003, JAMA.

[19]  M. Tuck,et al.  The effect of aldosterone on glucose metabolism , 2003, Current hypertension reports.

[20]  P. Raskin,et al.  Report of the expert committee on the diagnosis and classification of diabetes mellitus. , 1999, Diabetes care.

[21]  R. Schmieder,et al.  Aldosterone-induced cardiac damage: focus on blood pressure independent effects. , 2003, American journal of hypertension.

[22]  Jukka T Salonen,et al.  The metabolic syndrome and total and cardiovascular disease mortality in middle-aged men. , 2002, JAMA.

[23]  D. Calhoun,et al.  Hyperaldosteronism Among Black and White Subjects With Resistant Hypertension , 2002, Hypertension.

[24]  L. Niskanen,et al.  Metabolic syndrome and development of diabetes mellitus: application and validation of recently suggested definitions of the metabolic syndrome in a prospective cohort study. , 2002, American journal of epidemiology.

[25]  F. Veglio,et al.  Drug Effects on Aldosterone/Plasma Renin Activity Ratio in Primary Aldosteronism , 2002, Hypertension.

[26]  A. Baron,et al.  Vascular function, insulin resistance and fatty acids , 2002, Diabetologia.

[27]  C. Stier,et al.  Pathophysiological effects of aldosterone in cardiovascular tissues , 2001, Trends in Endocrinology & Metabolism.

[28]  H. Raff,et al.  Comparison of adrenal vein sampling and computed tomography in the differentiation of primary aldosteronism. , 2001, The Journal of clinical endocrinology and metabolism.

[29]  J. Widimský,et al.  Insulin action in primary hyperaldosteronism before and after surgical or pharmacological treatment. , 2012, Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association.

[30]  J. Henquin,et al.  Triggering and amplifying pathways of regulation of insulin secretion by glucose. , 2000, Diabetes.

[31]  A. Rantala,et al.  Prevalence of the metabolic syndrome in drug‐treated hypertensive patients and control subjects , 1999, Journal of internal medicine.

[32]  Bruce Neal,et al.  1999 World Health Organization-International Society of Hypertension Guidelines for the Management of Hypertension. Guidelines Subcommittee. , 1999, Journal of hypertension.

[33]  M. Boscaro,et al.  Diagnosis of glucocorticoid-remediable aldosteronism in primary aldosteronism: aldosterone response to dexamethasone and long polymerase chain reaction for chimeric gene. , 1998, The Journal of clinical endocrinology and metabolism.

[34]  E. Ferrannini,et al.  Insulin resistance and hypersecretion in obesity. European Group for the Study of Insulin Resistance (EGIR). , 1997, The Journal of clinical investigation.

[35]  H. Okayama,et al.  Left ventricular hypertrophy precedes other target-organ damage in primary aldosteronism. , 1997, Hypertension.

[36]  P. Palatini,et al.  Changes in left ventricular anatomy and function in hypertension and primary aldosteronism. , 1996, Hypertension.

[37]  G. Reaven,et al.  Pathophysiology of insulin resistance in human disease. , 1995, Physiological reviews.

[38]  B. Kasiske,et al.  Effects of Antihypertensive Therapy on Serum Lipids , 1995, Annals of Internal Medicine.

[39]  Y. Miyazaki,et al.  Does insulin resistance participate in an impaired glucose tolerance in primary aldosteronism? , 1994, Journal of human hypertension.

[40]  G. Reaven.  Syndrome X: 6 years later. , 1994, Journal of internal medicine. Supplement.

[41]  M. Alderman,et al.  Role of Preclinical Cardiovascular Disease in the Evolution From Risk Factor Exposure to Development of Morbid Events , 1993, Circulation.

[42]  J. Mckenney,et al.  Summary of the second report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II) , 1993, JAMA.

[43]  A. Rantala,et al.  Multiple metabolic syndrome: aspects of genetic epidemiology and molecular genetics. , 1992, Annals of medicine.

[44]  A. Ribeiro,et al.  Hypokalemia, glucose intolerance, and hyperinsulinemia during diuretic therapy. , 1992, Hypertension.

[45]  T. Rosenthal,et al.  Insulin resistance in secondary hypertension. , 1992, American journal of hypertension.

[46]  H. Lithell.  Effect of Antihypertensive Drugs on Insulin, Glucose, and Lipid Metabolism , 1991, Diabetes Care.

[47]  N. Kaplan.  The Deadly Quartet: Upper-Body Obesity, Glucose Intolerance, Hypertriglyceridemia, and Hypertension , 1989 .

[48]  G. Reaven.  Role of Insulin Resistance in Human Disease , 1988, Diabetes.

[49]  S. Haffner,et al.  Hyperinsulinemia, upper body adiposity, and cardiovascular risk factors in non-diabetics. , 1988, Metabolism: clinical and experimental.

[50]  H. Halkin,et al.  Hyperinsulinemia. A link between hypertension obesity and glucose intolerance. , 1985, The Journal of clinical investigation.

[51]  C. Gomez-Sanchez,et al.  Further evaluation of saline infusion for the diagnosis of primary aldosteronism. , 1984, Hypertension.

[52]  J. Conn.  Hypertension, the potassium ion and impaired carbohydrate tolerance. , 1965, The New England journal of medicine.