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Concurrent hypercortisolism and hypermineralocorticoidism

M J Hogan, M Schambelan, E G Biglieri

    The American Journal of Medicine
    |May 1, 1977
    PubMed
    Summary
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    Patients with Cushing's syndrome can experience hypertension and hypokalemia. This case highlights excess deoxycorticosterone as a cause of low renin hypertension in Cushing's syndrome.

    Area of Science:

    • Endocrinology
    • Nephrology
    • Oncology

    Background:

    • Cushing's syndrome is characterized by hypertension and hypokalemia, often with normal aldosterone and variable plasma renin activity.
    • A normal aldosterone level with suppressed plasma renin activity suggests mineralocorticoid excess.
    • Adrenocortical adenomas are a common cause of Cushing's syndrome.

    Observation:

    • The patient presented with Cushing's syndrome secondary to an adrenocortical adenoma.
    • The patient exhibited low renin hypertension, defined by suppressed renin and normal aldosterone levels.
    • Elevated deoxycorticosterone was identified as the excess mineralocorticoid responsible for renin suppression.

    Findings:

    • The adrenocortical adenoma produced normal levels of aldosterone, while deoxycorticosterone excess suppressed plasma renin activity.

    Related Experiment Videos

  • Following adenoma removal, suppressed contralateral adrenal function (zona glomerulosa and fasciculata) was observed.
  • Gradual restoration of normal adrenal function occurred post-surgery.

    • Implications:

    • Excess deoxycorticosterone can cause low renin hypertension in Cushing's syndrome.
    • Understanding mineralocorticoid excess is crucial for managing hypertension in endocrine disorders.
    • This case underscores the importance of assessing specific mineralocorticoids beyond aldosterone in certain hypertensive conditions.