Abstract
Primary hyperaldosteronism, or Conn’s syndrome, results from an aldosterone-producing adenoma of the adrenal cortex. It presents with features of mineralocorticoid excess — increased secretion of aldosterone, hypertension, hypernatraemia, increased exchangeable sodium, hypokalemia, low exchangeable potassium, and reduced plasma concentrations of renin and angiotensin II [1–3]. Removal of the tumour corrects the aldosterone excess, reverses the electrolyte abnormality, and often restores normal blood pressure [2]. Clinicians and pathologists have little difficulty in accepting the disease as an entity.
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Lasaridis, A. et al. (1983). Is Idiopathic Hyperaldosteronism a Variant of Essential Hypertension or of Conn’s Syndrome?. In: Kaufmann, W., Wambach, G., Helber, A., Meurer, KA. (eds) Mineralocorticoids and Hypertension. International Boehringer Mannheim Symposia. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-69081-5_14
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DOI: https://doi.org/10.1007/978-3-642-69081-5_14
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