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Apparent mineralocorticoid excess.

John W Funder1

  • 1Hudson Institute of Medical Research and Monash University, Clayton 27-31 Wright Street, Clayton, Victoria 3168, Australia.

The Journal of Steroid Biochemistry and Molecular Biology
|March 10, 2016
PubMed
Summary
This summary is machine-generated.

Apparent mineralocorticoid excess syndrome results from impaired 11β-hydroxysteroid dehydrogenase Type 2 activity. Diagnosis involves hypertension, hypokalemia, and abnormal urinary cortisol/cortisone ratios, with treatment varying by severity.

Keywords:
11βhydroxysteroid dehydrogenase type 2AldosteroneCortisolMineralocorticoid receptorsUrinary steroid metabolites

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Area of Science:

  • Endocrinology
  • Genetics
  • Nephrology

Background:

  • Apparent mineralocorticoid excess (AME) is a rare genetic disorder.
  • It stems from mutations in the HSD11B2 gene, impairing 11β-hydroxysteroid dehydrogenase Type 2 (11β-HSD2) enzyme activity.
  • This enzyme normally inactivates cortisol in mineralocorticoid-target tissues.

Purpose of the Study:

  • To describe the clinical presentation, diagnosis, and management of apparent mineralocorticoid excess.
  • To highlight the role of 11β-HSD2 in mineralocorticoid receptor selectivity.
  • To underscore the concept of reverse translation in understanding physiological mechanisms.

Main Methods:

  • Clinical case review and biochemical analysis.
  • Measurement of plasma aldosterone and urinary cortisol/cortisone ratios.
  • Genetic testing for HSD11B2 mutations.

Main Results:

  • Patients present with hypertension, hypokalemia, and suppressed plasma renin/aldosterone.
  • An elevated urinary free cortisol to free cortisone ratio is a key diagnostic marker.
  • Severity correlates with residual 11β-HSD2 activity, impacting treatment strategies.

Conclusions:

  • Apparent mineralocorticoid excess diagnosis requires a combination of clinical and biochemical findings.
  • Prompt and aggressive treatment is crucial for severe neonatal/infantile forms.
  • Understanding AME pathogenesis has elucidated aldosterone's role in mineralocorticoid receptor activation.