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Hypertension in Cushing's syndrome: from pathogenesis to treatment

Maria Verena Cicala1, Franco Mantero

  • 1Division of Endocrinology, University of Padua, Padua, Italy.

Neuroendocrinology
|September 11, 2010
PubMed

Insights

Hypertension is common in Cushing's syndrome (CS) due to excess cortisol. Effective treatments focus on mineralocorticoid receptor antagonists, Ang II blockers, and ACE inhibitors, while some drugs are ineffective.

Area of Science:

  • Endocrinology
  • Cardiovascular Medicine

Background:

  • Hypertension is a hallmark of endogenous Cushing's syndrome (CS), affecting 80% of adults and 47% of children.
  • Hypertension in CS is linked to hypercortisolism duration and involves complex mechanisms affecting plasma volume, vascular resistance, and cardiac output.

Purpose of the Study:

  • To review the pathophysiological mechanisms of hypertension in Cushing's syndrome.
  • To discuss effective and ineffective pharmacological treatments for hypertension in CS patients.

Main Methods:

  • Literature review of studies on hypertension in Cushing's syndrome.
  • Analysis of the mechanisms by which glucocorticoids induce hypertension.
  • Evaluation of antihypertensive drug efficacy in CS.

Main Results:

  • Glucocorticoids cause hypertension via mineralocorticoid activity, renin-angiotensin system activation, enhanced vasoactive substances, and suppressed vasodilatory systems.
  • Mineralocorticoid receptor antagonists, Ang II blockers, and ACE inhibitors are effective antihypertensive options in CS.
  • Thiazides, furosemide, adrenergic blockade, and calcium channel antagonists are generally ineffective.

Conclusions:

  • Treating hypertension in CS is challenging, requiring tailored pharmacological approaches.
  • Mineralocorticoid receptor antagonists, Ang II blockers, and ACE inhibitors represent key therapeutic options.
  • Further research is needed to optimize management and reduce associated morbidity and mortality.

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