mineralocorticoid excess
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Etiology
- consumption of large amounts of liquorice can lead to apparent mineralocorticoid excess & hypertension
- genetic defects
Pathology
- activation of the mineralocorticoid receptor by cortisol
- Na+ retention
Genetics
- autosomal recessive
- associated with defects in HSD11B2 gene
Clinical manifestations
- severe juvenile hypertension
- sequellae of Na+ retention
Laboratory
- serum K+: hypokalemia
- serum bicarbonate: metabolic acidosis
- plasma renin: low
- plasma aldosterone: low
Complications
- nephrocalcinosis
- potentially fatal
Management
- avoid liquorice
- thiazide diuretics
- aldosterone antagonist, potassium-sparing diuretic
More general terms
More specific terms
Additional terms
References
- ↑ OMIM https://mirror.omim.org/entry/218030
- ↑ Medical Knowledge Self Assessment Program (MKSAP) 15, 17. American College of Physicians, Philadelphia 2009, 2015,
- ↑ Zennaro MC, Rickard AJ, Boulkroun S. Genetics of mineralocorticoid excess: an update for clinicians. Eur J Endocrinol. 2013 Jun 1;169(1):R15-25. Review. PMID: https://www.ncbi.nlm.nih.gov/pubmed/23610123 Free Article
- ↑ Melcescu E, Phillips J, Moll G, Subauste JS, Koch CA. 11Beta-hydroxylase deficiency and other syndromes of mineralocorticoid excess as a rare cause of endocrine hypertension. Horm Metab Res. 2012 Nov;44(12):867-78. Review. PMID: https://www.ncbi.nlm.nih.gov/pubmed/22932914