title: Management of hypertension and heart failure in patients with Addison's disease.
abstract: Addison's disease may be complicated by hypertension and less commonly by heart failure. We review the pathophysiology of the renin-angiotensin-aldosterone axis in Addison's disease and how this is altered in the setting of hypertension and heart failure. An essential first step in management in both conditions is optimizing glucocorticoid replacement and considering dose reduction if excessive. Following this, if a patient with Addison's disease remains hypertensive, the fludrocortisone dose should be reviewed and reduced if there are clinical and/or biochemical signs of mineralocorticoid excess. In the absence of such signs, where the renin is towards the upper end of the normal range or elevated, an angiotensin II (AII) receptor antagonist or angiotensin converting enzyme (ACE) inhibitor is the treatment of choice, and the fludrocortisone dose should remain unchanged. Dihydropyridine calcium channel blockers are clinically useful as second line agents, but diuretics should be avoided. In the setting of heart failure, there is an increase in total body sodium and water; therefore, it is appropriate to reduce and rarely consider ceasing the fludrocortisone. Loop diuretics may be used, but not aldosterone antagonists such as spironolactone or eplerenone. Standard treatment with ACE inhibitors, or as an alternative, AII receptor antagonists, are appropriate. Measurements of renin are no longer helpful in heart failure to determine the volume status but plasma levels of brain natriuretic peptide (BNP/proBNP) may help guide therapy.
authors.affiliation: Department of Diabetes and Endocrinology, Princess Alexandra Hospital and University of Queensland, Brisbane, Qld, Australia.
authors.forename: Warrick J
authors.initials: WJ
authors.lastname: Inder
authors.affiliation: Department of Endocrinology and Diabetes, St Vincent's Hospital, Melbourne, Vic., Australia.
authors.forename: Caroline
authors.initials: C
authors.lastname: Meyer
authors.affiliation: Department of Endocrinology, Christchurch Hospital and University of Otago, Christchurch, New Zealand.
authors.forename: Penny J
authors.initials: PJ
authors.lastname: Hunt
mesh_terms: D000224:Addison Disease / Q000097:blood / Q000150:complications / Q000175:diagnosis / Q000188:drug therapy; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D054796:Drug Dosage Calculations; D016903:Drug Monitoring; D005260:Female; D005938:Glucocorticoids / Q000494:pharmacology*; D006333:Heart Failure / Q000175:diagnosis / Q000188:drug therapy / Q000209:etiology; D006801:Humans; D006973:Hypertension / Q000175:diagnosis / Q000188:drug therapy / Q000209:etiology; D054539:Medication Therapy Management; D008875:Middle Aged; D000451:Mineralocorticoid Receptor Antagonists / Q000494:pharmacology*; D020097:Natriuretic Peptide, Brain / Q000097:blood; D012083:Renin / Q000097:blood*; D063189:Symptom Assessment
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D005938:Glucocorticoids; D000451:Mineralocorticoid Receptor Antagonists; D020097:Natriuretic Peptide, Brain; D012083:Renin