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Cushing's disease: evaluation of mineralocorticoid-induced hypertension
G Yasuda1, H Shionoiri, S Hayashi
1Second Department of Internal Medicine, Yokohama City University School of Medicine.
Insights
This study reviews a patient with Cushing's syndrome, highlighting how high deoxycorticosterone levels contributed to hypertension and hypokalemia. Normalization occurred after surgery, suggesting deoxycorticosterone's role in the patient's endocrine and blood pressure abnormalities.
Area of Science:
- Endocrinology
- Cardiovascular Medicine
- Nephrology
Background:
- Cushing's syndrome, often caused by pituitary adenomas, can lead to complex hormonal imbalances.
- Hypertension and hypokalemia are significant comorbidities requiring thorough etiological investigation.
Observation:
- A 32-year-old female patient presented with Cushing's syndrome, hypertension, and hypokalemia.
- Endocrinological evaluation revealed low plasma renin activity, low plasma aldosterone, and elevated plasma deoxycorticosterone.
- Enhanced blood pressure response to exogenous angiotensin II was noted.
Findings:
- Post-surgical withdrawal of cortisol replacement normalized hormonal levels, including deoxycorticosterone.
- Hypertension and hypokalemia resolved, alongside a reduced blood pressure response to angiotensin II.
- These changes indicate deoxycorticosterone's potential contribution to the observed clinical and biochemical abnormalities.
Implications:
- Deoxycorticosterone may play a crucial role in the pathogenesis of hypertension and hypokalemia in specific endocrine disorders.
- Understanding these mechanisms is vital for accurate diagnosis and effective management of patients with complex hormonal imbalances.
- This case underscores the importance of comprehensive endocrinological assessment in managing resistant hypertension and electrolyte disturbances.
Abstract:
A patient (32-year-old female) with Cushing's syndrome due to pituitary adenoma and hypertension with hypokalemia is reviewed. Endocrinological studies demonstrated low plasma renin activity, low plasma aldosterone concentration and high plasma deoxycorticosterone concentration. Blood pressure response to exogenous angiotensin II was enhanced. After the withdrawal of cortisol replacement following surgery, her abnormal endocrinological findings, hypertension and serum potassium level returned to normal and her blood pressure response to exogenous angiotensin II was reduced. These results suggest that in this case deoxycorticosterone might have contributed to the development and maintenance of her hypertension accompanied with hypokalemia.