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Abstract: PO1096

A Rare Case of Acquired 11-Beta-Hydroxysteroid Dehydrogenase Deficiency

Session Information

Category: Fluid, Electrolyte, and Acid-Base Disorders

  • 901 Fluid, Electrolyte, and Acid-Base Disorders: Basic


  • Elharrif, Khalid, Kern Medical Center, Bakersfield, California, United States
  • Alhosainat, Nidal, The University of Texas Medical Branch at Galveston, Galveston, Texas, United States
  • Alex, Mica, The University of Texas Medical Branch at Galveston, Galveston, Texas, United States
  • Greti, Petersen, Kern Medical Center, Bakersfield, California, United States
  • Kassem, Hania, The University of Texas Medical Branch at Galveston, Galveston, Texas, United States

11-Beta Hydroxysteroid Dehydrogenase (HSD11B) is an enzyme that is involved in steroid hormone physiology. HSD11B enzyme exists in two isoforms, HSD11B-type 1 and type 2. Type 2 isozyme is responsible for converting cortisol to inactive cortisone. Plasma concentration of cortisol is approximately 100-fold higher than aldosterone and activation of mineralocorticoid receptors by cortisol is normally limited due to its conversion to inactive cortisone at the sites of aldosterone action by the enzyme HSD11B-type 2. We are presenting a rare case of HSD11B deficiency in a patient taking herbal supplementation.

Case Description

A 73-year-old female with PMH of hypertension, hyperlipidemia and chronic pain was admitted to the hospital with fatigue and shortness of breath. She denied any history of diarrhea or recent use of diuretics or laxatives. She has a history of using some herbal supplements in large quantities for pain control. Initial blood pressure was 140/80 mmHg. EKG showed sinus bradycardia with PVCs and bigeminy. The lab results are summarized in table A. She received aggressive potassium supplementation and spironolactone with subsequent improvement of her condition.


HSD11B deficiency is either congenital or acquired by ingestion of licorice or its derivatives (glycyrrhizic and glycyrrhetinic acids). The deficiency results in a decreased conversion to cortisone and accumulation of cortisol. The effect of cortisol on the mineralocorticoid receptor results in hypokalemia, metabolic alkalosis, and low aldosterone and renin activity. The diagnosis requires careful history and identification of specific clinical features and biochemical abnormalities.