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Related Experiment Videos

Spontaneous hypercortisolism without Cushing's syndrome.

A C Vingerhoeds, J H Thijssen, F Schwarz

    The Journal of Clinical Endocrinology and Metabolism
    |November 1, 1976
    PubMed
    Summary
    This summary is machine-generated.

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    A patient with high cortisol production and elevated ACTH, despite lacking Cushing's syndrome symptoms, suggests a possible genetic hyposensitivity to cortisol. This finding was also observed in one of his children.

    Area of Science:

    • Endocrinology
    • Genetics
    • Internal Medicine

    Background:

    • Elevated cortisol production rate (CPR) and plasma ACTH can indicate endocrine disorders.
    • Hypertension and hypokalemia are key symptoms that warrant investigation into cortisol regulation.
    • Cushing's syndrome is a common consideration, but its absence necessitates exploring other etiologies.

    Purpose of the Study:

    • To investigate the cause of hypercortisolism in a patient presenting with hypertension and hypokalemia without Cushing's syndrome.
    • To explore the potential genetic basis of the observed endocrine abnormalities.
    • To differentiate the condition from Conn's syndrome and enzymatic defects in steroidogenesis.

    Main Methods:

    • Measurement of cortisol production rate (CPR) and plasma ACTH levels.

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  • Clinical evaluation for symptoms and signs of Cushing's syndrome.
  • Diagnostic workup to rule out Conn's syndrome and steroidogenesis defects.
  • Family history and screening of offspring for similar conditions.

    • Main Results:

    • The patient exhibited very high CPR and elevated plasma ACTH, indicative of pituitary-dependent hypercortisolism.
    • No clinical features of Cushing's syndrome were present, even after 36 months of follow-up.
    • One of the patient's children also presented with hypertension and hypercortisolism.
    • Conn's syndrome and enzymatic defects were excluded.

    Conclusions:

    • The findings suggest a possible genetically determined hyposensitivity to the glucocorticoid action of cortisol.
    • Pituitary-dependent hypercortisolism can occur without the typical clinical manifestations of Cushing's syndrome.
    • Further research into genetic factors influencing cortisol sensitivity is warranted.