Coronary Artery Spasm, Hypertension, Hypokalemia and Licorice
|Ewa Konik1*, Emily Graham Kurtz1, Flora Sam2 and Douglas Sawyer1|
|1Vanderbilt University, Nashville, TN, USA|
|2Boston University School of Medicine, Boston, MA, USA|
|Corresponding Author :||Ewa Konik, MD
Nashville, TN, USA
E-mail: [email protected]
|Received March 05, 2012; Accepted May 05, 2012; Published May 14, 2012|
|Citation: Konik E, Kurtz EG, Sam F, Sawyer D (2012) Coronary Artery Spasm, Hypertension, Hypokalemia and Licorice. J Clin Case Rep 2:143. doi:10.4172/2165-7920.1000143|
|Copyright: © 2012 Konik E, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.|
Hypertension with hypokalemia, especially in a patient off diuretics, suggests a secondary hypertension due to an increase in mineralocorticoid activity, for example, primary increases in renin, aldosterone, or nonaldosterone mineralocorticoid secretion or an increased mineralocorticoid-like effect.
Mineralocorticoid Receptors (MR) preferentially bind cortisol. A mineralocorticoid effect of cortisol is avoided in some tissues by expression of 11-Beta Hydroxysteroid Dehydrogenase type 2 (11 BHSD2), the enzyme responsible for transformation of cortisol to its 11-keto derivative (cortisone), which has minimal affinity for MR receptors. Only when cortisol is converted to the inactive cortisone can aldosterone bind to the MR. Rare congenital deficiency of 11 BHSD2 or its inhibition by licorice consumption mimics hyperaldosteronic state.