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Apparent mineralocorticoid excess

R Benediktsson1, C R Edwards

  • 1University Department of Medicine, Western General Hospital, Edinburgh, UK.

Journal of Human Hypertension
|May 1, 1994
PubMed
Summary
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Apparent Mineralocorticoid Excess (AME) is a syndrome caused by a deficiency in the enzyme 11beta-hydroxysteroid dehydrogenase (11beta-OHSD). This deficiency allows cortisol to overactivate mineralocorticoid receptors, leading to hypertension.

Area of Science:

  • Endocrinology
  • Metabolic Disorders
  • Hypertension Research

Background:

  • Apparent Mineralocorticoid Excess (AME) syndrome, identified in 1979, presents with hypertension and hypokalemia.
  • It stems from a deficiency in 11beta-hydroxysteroid dehydrogenase (11beta-OHSD), an enzyme crucial for converting cortisol to cortisone.
  • This enzyme deficiency allows cortisol to inappropriately activate mineralocorticoid receptors, mimicking aldosterone's effects.

Purpose of the Study:

  • To elucidate the role of 11beta-hydroxysteroid dehydrogenase (11beta-OHSD) in Apparent Mineralocorticoid Excess (AME).
  • To explore the implications of 11beta-OHSD deficiency in various tissues and its link to essential hypertension.
  • To investigate the placental 11beta-OHSD isoform's role in fetal exposure to maternal glucocorticoids and potential hypertension risk.

Related Experiment Videos

Main Methods:

  • Clinical case review and biochemical analysis of patients with Apparent Mineralocorticoid Excess (AME).
  • Enzyme activity assays for 11beta-hydroxysteroid dehydrogenase (11beta-OHSD) in affected individuals and control groups.
  • Comparative analysis of placental 11beta-OHSD activity and fetal growth parameters in animal models.

Main Results:

  • Patients with AME exhibit a deficiency in 11beta-hydroxysteroid dehydrogenase (11beta-OHSD), leading to cortisol's mineralocorticoid receptor activation.
  • Dexamethasone treatment can normalize biochemistry by suppressing cortisol but often fails to fully resolve hypertension.
  • Deficient 11beta-OHSD activity is observed in one-third of essential hypertensive patients, suggesting a broader role in hypertension.
  • Lower placental 11beta-OHSD activity correlates with smaller fetuses and larger placentas, indicating increased fetal glucocorticoid exposure.

Conclusions:

  • 11beta-hydroxysteroid dehydrogenase (11beta-OHSD) deficiency is the primary cause of Apparent Mineralocorticoid Excess (AME), linking cortisol metabolism to mineralocorticoid receptor activity.
  • The enzyme's deficiency in tissues beyond the kidney, including the placenta, has significant implications for hypertension development.
  • Further research into 11beta-OHSD function may reveal new therapeutic targets for hypertension and related metabolic disorders.