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Primary hyperaldosteronism history and symptoms

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Overview

Overview

The hallmark of primary hyperaldosteronism is resistant hypertension. A positive history of spontaneous or unprovoked hypokalemia and treatment-resistant (refractory) hypertension are suggestive of primary hyperaldosteronism. The most common symptoms of primary hyperaldosteronism include headaches, facial flushing, vision changes, and weakness.

History and Symptoms

History and Symptoms

Primary hyperaldosteronism may be suspected in the following scenarios:

Patients with profound hypokalemia report fatigue, muscle weakness, cramping, headaches, and palpitations. They can also have polydipsia and polyuria from hypokalemia-induced nephrogenic diabetes insipidus. Long-standing HTN may lead to cardiac, retinal, renal, and neurologic problems, with all the associated symptoms and signs. Patients with primary hyperaldosteronism may have subclinical systolic dysfunction, more bradycardia, higher blood pressure, and vascular resistance values than those with the secondary hyperaldosteronism. Plasma renin activity has been found to be lower in primary than in secondary hyperaldosteronism.

Common Symptoms

Common symptoms of primary hyperaldosteronism (PA) include:[1][2][3][4][5][6]

Less Common Symptoms

Less common symptoms of Conn’s syndrome (primary hyperaldosteronism) include:[7][8]

References

References

  1. Rubidge CJ, O’Dowd PB, Powell SJ (1973). “Difetarsone in the treatment of Trichuris trichiura infections”. S. Afr. Med. J. 47 (23): 991–2. PMID 4714286.
  2. Mattsson C, Young WF (2006). “Primary aldosteronism: diagnostic and treatment strategies”. Nat Clin Pract Nephrol. 2 (4): 198–208, quiz, 1 p following 230. doi:10.1038/ncpneph0151. PMID 16932426.
  3. Di Tullio M, Alli C, Avanzini F, Bettelli G, Colombo F, Devoto MA, Marchioli R, Mariotti G, Radice M, Taioli E (1988). “Prevalence of symptoms generally attributed to hypertension or its treatment: study on blood pressure in elderly outpatients (SPAA)”. J Hypertens Suppl. 6 (1): S87–90. PMID 3216243.
  4. Unwin RJ, Luft FC, Shirley DG (2011). “Pathophysiology and management of hypokalemia: a clinical perspective”. Nat Rev Nephrol. 7 (2): 75–84. doi:10.1038/nrneph.2010.175. PMID 21278718.
  5. Bautista J, Gil-Neciga E, Gil-Peralta A (1979). “Hypokalemic periodic paralysis in primary hyperaldosteronism. Subclinical myopathy with atrophy of the type 2A muscle fibers”. Eur. Neurol. 18 (6): 415–20. PMID 546663.
  6. Bortolotto LA, Cesena FH, Jatene FB, Silva HB (2003). “Malignant hypertension and hypertensive encephalopathy in primary aldosteronism caused by adrenal adenoma”. Arq. Bras. Cardiol. 81 (1): 97–100, 93–6. PMID 12908077.
  7. Moeller J, Muniz B (1967). “[Hypokalemic ileus and aldosteronism]”. Med Klin (in German). 62 (52): 2019–24. PMID 5596496.
  8. Failor RA, Capell PT (2003). “Hyperaldosteronism and pheochromocytoma: new tricks and tests”. Prim. Care. 30 (4): 801–20, viii. PMID 15024897.

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