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Glucocorticoid excess and hypertension.

Smita Baid1, Lynnette K Nieman

  • 1National Institute of Child Health and Human Development, National Institutes of Health, Building 10, Room 9D42 MSC 1583, 10 Center Drive, Bethesda, MD 20892-1583, USA. NiemanL@nih.gov

Current Hypertension Reports
|November 6, 2004
PubMed
Summary

Cushing's syndrome, marked by excess glucocorticoids, frequently causes hypertension. This review explores mechanisms behind this high blood pressure and its persistence even after treatment.

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Diagnosis of Cushing's Disease.

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Area of Science:

  • Endocrinology
  • Cardiovascular Medicine
  • Nephrology

Background:

  • Cushing's syndrome involves chronic excess glucocorticoid exposure.
  • Hypertension is a key feature, affecting 80% of patients.
  • Associated cardiovascular risks significantly increase mortality.

Purpose of the Study:

  • To review pathogenetic mechanisms of glucocorticoid-induced hypertension.
  • To discuss the role of sodium/water and mineralocorticoid excess.
  • To examine vascular and renal involvement in hypertension.

Main Methods:

  • Literature review of pathogenetic mechanisms.
  • Analysis of glucocorticoid effects on cardiovascular system.
  • Discussion of treatment implications.

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Main Results:

  • Hypertension is a prevalent complication of Cushing's syndrome.
  • Glucocorticoids impact sodium/water balance, mineralocorticoid activity, vasculature, and kidneys.
  • Antihypertensive treatment offers moderate success; 30% experience persistent hypertension post-cure.

Conclusions:

  • Understanding glucocorticoid-induced hypertension mechanisms is crucial.
  • Effective management strategies are needed for persistent hypertension.
  • Further research into long-term cardiovascular outcomes is warranted.