Primary hyperaldosteronism natural history, complications and prognosis: Difference between revisions
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*Improvements are not as significant as after unilateral adrenalectomy for lateralizing lesions. | *Improvements are not as significant as after unilateral adrenalectomy for lateralizing lesions. | ||
'''Patients with FH-I undergoing treatment with glucocorticoid medications''' | '''Patients with FH-I undergoing treatment with glucocorticoid medications''' | ||
*Hypertension in familial hyperaldosteronism type I (FH-I) is usually of early onset and may be severe enough to cause early death, usually from hemorrhagic stroke, unless specifically treated. | *Hypertension in familial hyperaldosteronism type I (FH-I) is usually of early onset and may be severe enough to cause early death, usually from hemorrhagic stroke, unless specifically treated.<ref name="pmid9483237">{{cite journal |vauthors=Stowasser M, Gartside MG, Gordon RD |title=A PCR-based method of screening individuals of all ages, from neonates to the elderly, for familial hyperaldosteronism type I |journal=Aust N Z J Med |volume=27 |issue=6 |pages=685–90 |year=1997 |pmid=9483237 |doi= |url= |issn=}}</ref> | ||
*Treatment with glucocorticoids, given in low doses is usually effective in controlling hypertension and consequently preventing stroke. | *Treatment with glucocorticoids, given in low doses is usually effective in controlling hypertension and consequently preventing stroke. | ||
==References== | ==References== | ||
Revision as of 19:55, 18 July 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]
Overview
If left untreated, patients with primary hyperaldosteronism may progress to develop stroke, coronary artery disease, and renal insufficiency with associated proteinuria. APAs continue to grow slowly over time. The aldosterone production likely correlates with the size of the adenoma. Primary hyperladosteronism can be progressive leading to increased severity of disease. Common complications of primary hyperaldosteronism include left ventricular hypertrophy due to chronic hypertension, atrial fibrillation, myocardial infarction, stroke, proteinuria and metabolic syndrome.
Natural History
- The natural history of primary hyperaldosteronism other than familial hyperaldosteronism type I (FH-I) is for progressive increase in disease severity, ebentually leading to involvement of both adrenals.[1]
- If left untreated, patients with primary hyperaldosteronism may progress to develop severe resistant hypertension leading to stroke, coronary artery disease, and renal insufficiency with associated proteinuria.[2]
Complications
Primary aldosteronism is characterized by the development of the following complications:[3][4][5][6]
Cardiovascular complications
- Left ventricular hypertrophy
- Myocardial infarction
- Atrial fibrillation
Neurological complications
- Stroke
- Hypertensive encephelopathy
Renal complications
- Proteinuria including microalbuminuria
- Renal cysts
Metabolic complications
- Metabolic syndrome
- Diabetes mellitus
Prognosis
- The prognosis of primary hyperaldosteronism is good with treatment. Without treatment, primary hyperaldosteronism will result in hypertension with resultant hypertension-related complications, which may be a major cause of morbidity and mortality among patients.
- Adrenalectomy lowers long-term all-cause mortality from primary hyperaldosteronism.[7][8][9]
Patients undergoing unilateral adrenalectomy for unilateral adenoma
- Adrenalectomy leads to cure of HTN in 50% to 60% of patients.[10][11]
- Blood pressure typically becomes normal after 1 to 6 months of the procedure.[12]
- Treatment leads to a significant increase in quality of life and improved cardiovascular outcomes.
Patients receiving aldosterone antagonist medications
- Hypertension is controlled in majority of the patients.[10][11]
- Improvements are not as significant as after unilateral adrenalectomy for lateralizing lesions.
Patients with FH-I undergoing treatment with glucocorticoid medications
- Hypertension in familial hyperaldosteronism type I (FH-I) is usually of early onset and may be severe enough to cause early death, usually from hemorrhagic stroke, unless specifically treated.[13]
- Treatment with glucocorticoids, given in low doses is usually effective in controlling hypertension and consequently preventing stroke.
References
- ↑ Gordon RD (1997). "Primary aldosteronism: a new understanding". Clin. Exp. Hypertens. 19 (5–6): 857–70. PMID 9247760.
- ↑ "Cardiovascular complications in patients with primary aldosteronism - ScienceDirect".
- ↑ Nishimura M, Uzu T, Fujii T, Kuroda S, Nakamura S, Inenaga T, Kimura G (1999). "Cardiovascular complications in patients with primary aldosteronism". Am. J. Kidney Dis. 33 (2): 261–6. PMID 10023636.
- ↑ Giacchetti G, Turchi F, Boscaro M, Ronconi V (2009). "Management of primary aldosteronism: its complications and their outcomes after treatment". Curr Vasc Pharmacol. 7 (2): 244–49. PMID 19356005.
- ↑ Reincke M, Meisinger C, Holle R, Quinkler M, Hahner S, Beuschlein F, Bidlingmaier M, Seissler J, Endres S (2010). "Is primary aldosteronism associated with diabetes mellitus? Results of the German Conn's Registry". Horm. Metab. Res. 42 (6): 435–9. doi:10.1055/s-0029-1246189. PMID 20119885.
- ↑ Hanslik G, Wallaschofski H, Dietz A, Riester A, Reincke M, Allolio B, Lang K, Quack I, Rump LC, Willenberg HS, Beuschlein F, Quinkler M, Hannemann A (2015). "Increased prevalence of diabetes mellitus and the metabolic syndrome in patients with primary aldosteronism of the German Conn's Registry". Eur. J. Endocrinol. 173 (5): 665–75. doi:10.1530/EJE-15-0450. PMID 26311088.
- ↑ "Long term outcome of Aldosteronism after target treatments | Scientific Reports".
- ↑ "Treatment strategy and outcome with primary aldosteronism: a nationwide longitudinal cohort based study".
- ↑ Celen O, O'Brien MJ, Melby JC, Beazley RM (1996). "Factors influencing outcome of surgery for primary aldosteronism". Arch Surg. 131 (6): 646–50. PMID 8645073.
- ↑ 10.0 10.1 Stowasser M, Gordon RD, Gunasekera TG, Cowley DC, Ward G, Archibald C, Smithers BM (2003). "High rate of detection of primary aldosteronism, including surgically treatable forms, after 'non-selective' screening of hypertensive patients". J. Hypertens. 21 (11): 2149–57. doi:10.1097/01.hjh.0000098141.70956.53. PMID 14597859.
- ↑ 11.0 11.1 Stowasser M, Gordon RD (2004). "Primary aldosteronism--careful investigation is essential and rewarding". Mol. Cell. Endocrinol. 217 (1–2): 33–9. doi:10.1016/j.mce.2003.10.006. PMID 15134798.
- ↑ Stowasser M, Gordon RD, Rutherford JC, Nikwan NZ, Daunt N, Slater GJ (2001). "Diagnosis and management of primary aldosteronism". J Renin Angiotensin Aldosterone Syst. 2 (3): 156–69. doi:10.3317/jraas.2001.022. PMID 11881117.
- ↑ Stowasser M, Gartside MG, Gordon RD (1997). "A PCR-based method of screening individuals of all ages, from neonates to the elderly, for familial hyperaldosteronism type I". Aust N Z J Med. 27 (6): 685–90. PMID 9483237.