Abstract
When hypertension, a pathology that is frequently found in the general population, presents in a young patient, secondary causes such as Cushing's syndrome (CS), a rare disease characterized by long-term elevated cortisol levels, should be considered. Present in ~80% of CS patients independently of their age and sex, hypertension is one of the pathology's most prevalent, alarming features. Its severity is principally associated with the duration and intensity of elevated cortisol levels. Prompt diagnosis and rapid initiation of treatment are important for reducing/delaying the consequences of hypercortisolism. Glucocorticoid excess leads to hypertension via a variety of mechanisms including mineralocorticoid mimetic activity, alterations in peripheral and renovascular resistance, and vascular remodeling. As hypertension in CS patients is caused by cortisol excess, treating the underlying pathology generally contributes to reducing blood pressure (BP) levels, although hypertension tends to persist in approximately 30% of cured patients. Surgical removal of the pituitary tumor remains the first-line treatment for both adrenocorticotropin hormone (ACTH) dependent and independent forms of the syndrome. In light of the fact that surgery is not always successful in curing the underlying disease, it is essential that other treatments be considered and prescribed as needed. This article discusses the mechanisms involved in the pathogenesis of CS and the pros and the cons of the various antihypertensive agents that are presently available to treat these patients.
Highlights
Cushing’s syndrome (CS) is a severe clinical condition caused by prolonged glucocorticoid excess [1]
A synergism of pathophysiological mechanisms causes the high rate of hypertension found in CS patients
The absence of nocturnal blood pressure (BP) dipping profile is a typical feature of CS and reflects the impairment in circadian cortisol secretion
Summary
Cushing’s syndrome (CS) is a severe clinical condition caused by prolonged glucocorticoid excess [1]. It has been hypothesized that glucocorticoid receptor activation is responsible for enhanced ENaC and glomerular hyperfiltration, as neither selective mineralocorticoids nor glucocorticoid receptor antagonists appears to be able to fully revert cortisol’s effects [18]. These findings may explain why CS patients display more improvement when they are receiving mifepristone, a glucocorticoid receptor antagonist, than when they are taking MR antagonists [19, 20]. Glucocorticoids enhance angiotensin II’s action as a neurotransmitter leading to elevated sympathetic nerve activity, stimulating vasopressin release, and attenuating the arterial baroreceptor reflex [14]
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