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Fecal Glucocorticoid Analysis: Non-invasive Adrenal Monitoring in Equids
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Fecal Glucocorticoid Analysis: Non-invasive Adrenal Monitoring in Equids

Published on: April 25, 2016

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

Insights

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.

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.

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.

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