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mineralocorticoid excess

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 - spironolactone - triamterene - amiloride

Related

mineralocorticoid

Specific

hyperaldosteronism

General

genetic disease of the endocrine system

Database Correlations

OMIM 218030

References

  1. OMIM :accession 218030
  2. Medical Knowledge Self Assessment Program (MKSAP) 15, 17. American College of Physicians, Philadelphia 2009, 2015,
  3. 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: 23610123 Free Article
  4. 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: 22932914