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Apparent mineralocorticoid excess type II

F Mantero1, R Tedde, G Opocher

  • 1Cattedra di Endocrinologia, University of Ancona, Italy.

Steroids
|February 1, 1994
PubMed
Summary
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Apparent mineralocorticoid excess (AME) involves impaired cortisol metabolism. A newly discovered Type II AME presents similarly but with different metabolic defects, responding to dexamethasone treatment.

Area of Science:

  • Endocrinology
  • Metabolic Disorders

Background:

  • Apparent mineralocorticoid excess (AME) results from impaired cortisol metabolism, leading to mineralocorticoid (MC) receptor overactivation.
  • This impairment typically involves reduced activity of 11 beta-hydroxysteroid dehydrogenase and 5 beta-reductase, hindering cortisol inactivation.

Observation:

  • A novel form of AME (Type II) was identified in four patients exhibiting hypertension, hypokalemia, and suppressed renin-angiotensin-aldosterone system.
  • In Type II AME, cortisol to cortisone conversion appears normal or impaired bidirectionally, unlike classic AME.

Findings:

  • Both AME types demonstrate significantly decreased cortisol turnover quotient and Ring A reduction constant.
  • Type II AME patients present with a distinct cortisol metabolic profile compared to classic AME.

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Implications:

  • The discovery of Type II AME expands the understanding of glucocorticoid metabolism disorders.
  • Dexamethasone shows efficacy in managing MC-related abnormalities in AME, with potential need for additional antihypertensives for severe hypertension.