Conn Syndrome Treatment & Management

  • Author: Serge A Jabbour, MD; Chief Editor: George T Griffing, MD   more...
 
Updated: Dec 13, 2011
 

Approach Considerations

In patients with primary hyperaldosteronism, the goal of treatment is to prevent the morbidity and mortality associated with hypertension and hypokalemia. The appropriate treatment depends on the cause (Conn syndrome vs IHA). Although hypertension is frequently cured after unilateral adrenalectomy in patients with Conn syndrome, the mean cure rate is only 19% after unilateral or bilateral adrenalectomy in patients with IHA, in whom treatment is primarily medical.

In the case of APA, medical therapy is used preoperatively to control blood pressure and correct hypokalemia, thus decreasing surgical risk. Medical therapy is administered to patients with persistent hypertension postoperatively, poor surgical candidates, and patients who refuse surgery.

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Adrenalectomy

Surgery is the main therapy for Conn syndrome. A laparoscopic adrenalectomy is favored, when possible.[6, 9] In patients with Conn syndrome, the blood pressure response to spironolactone preoperatively is a predictor of the blood pressure response to unilateral adrenalectomy.

Surgical risk can be decreased by correcting the patient’s hypokalemia and controlling his or her blood pressure by administering spironolactone for at least 1-2 weeks (preferably 6 wk) before surgery.

Hypertension typically does not resolve immediately postoperatively but, rather, over 3-6 months; however, almost all patients have improved blood pressure control after surgery. Long-term cure rates with unilateral adrenalectomy for Conn syndrome average 69%.

A retrospective study of 168 patients with primary hyperaldosteronism who underwent an adrenalectomy found that hypertension was cured or controlled in 77% of patients with a unilateral adenoma and in 68% of patients with hyperaldosteronism but no adenoma.[10] Persistent hypertension may be related to resetting of baroreceptors, established hemodynamic changes, structural changes in the blood vessels, or coincidental essential hypertension.

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Contributor Information and Disclosures
Author

Serge A Jabbour, MD  Associate Professor, Department of Medicine, Division of Endocrinology, Jefferson Medical College of Thomas Jefferson University

Serge 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

Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD  Professor of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Additional Contributors

Arthur 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

Arthur 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

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

References

  1. Born-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. Apr 2009;94(4):1125-30. [Medline].

  2. Bernini G, Galetta F, Franzoni F, et al. Arterial stiffness, intima-media thickness and carotid artery fibrosis in patients with primary aldosteronism. J Hypertens. Dec 2008;26(12):2399-405. [Medline].

  3. Bravo EL. Primary aldosteronism: new approaches to diagnosis and management. Cleve Clin J Med. Sep-Oct 1993;60(5):379-86. [Medline].

  4. Mulatero P, Stowasser M, Loh KC, Fardella CE, Gordon RD, Mosso L. Increased diagnosis of primary aldosteronism, including surgically correctable forms, in centers from five continents. J Clin Endocrinol Metab. Mar 2004;89(3):1045-50. [Medline].

  5. Seiler L, Rump LC, Schulte-Monting J, et al. Diagnosis of primary aldosteronism: value of different screening parameters and influence of antihypertensive medication. Eur J Endocrinol. Mar 2004;150(3):329-37. [Medline].

  6. Funder JW, Carey RM, Fardella C, et al. Case detection, diagnosis, and treatment of patients with primary aldosteronism: an endocrine society clinical practice guideline. J Clin Endocrinol Metab. Sep 2008;93(9):3266-81. [Medline].

  7. Webb R, Mathur A, Chang R, et al. What is the best criterion for the interpretation of adrenal vein sample results in patients with primary hyperaldosteronism?.

  8. Doppman JL, Gill JR Jr. Hyperaldosteronism: sampling the adrenal veins. Radiology. Feb 1996;198(2):309-12. [Medline].

  9. Carey RM. Primary aldosteronism. Horm Res. Jan 2009;71 Suppl 1:8-12. [Medline].

  10. Letavernier E, Peyrard S, Amar L, et al. Blood pressure outcome of adrenalectomy in patients with primary hyperaldosteronism with or without unilateral adenoma. J Hypertens. Sep 2008;26(9):1816-23. [Medline].

  11. Wu VC, Chang HW, Liu KL, et al. Primary aldosteronism: diagnostic accuracy of the losartan and captopril tests. Am J Hypertens. May 14 2009;[Medline].

  12. Al Fehaily M, Duh QY. Clinical manifestation of aldosteronoma. Surg Clin North Am. Jun 2004;84(3):887-905. [Medline].

  13. Capricchione A, Winer N, Sowers JR. Adrenocortical hypertension. Curr Hypertens Rep. Jun 2004;6(3):224-9. [Medline].

  14. Gill JR. Primary aldosteronism: Strategies for diagnosis and treatment. The Endocrinologist. 1991;1:365-9.

  15. Hirohara D, Nomura K, Okamoto T, et al. Performance of the basal aldosterone to renin ratio and of the renin stimulation test by furosemide and upright posture in screening for aldosterone-producing adenoma in low renin hypertensives. J Clin Endocrinol Metab. Sep 2001;86(9):4292-8. [Medline].

  16. Jabbour SA, De Papp AE. Pitfalls in the diagnosis and management of primary hyperaldosteronism. The Endocrinologist. 1999;9:395-8.

  17. Montori VM, Schwartz GL, Chapman AB, et al. Validity of the aldosterone-renin ratio used to screen for primary aldosteronism. Mayo Clin Proc. Sep 2001;76(9):877-82. [Medline].

  18. Rose BD, Kaplan NM. Approach to the patient with hypertension and hypokalemia. UpToDate [CD-ROM and online]. 1997;1-8.

 
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Magnetic resonance imaging (MRI) scan in a patient with Conn syndrome showing a left adrenal adenoma.
Scintigram obtained by using iodine-131-6β-iodomethylnorcholesterol (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.
 
 
 
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