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The Pathophysiology and Treatment of Hypertension in Patients With Cushing's Syndrome

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Specialty Endocrinology
Date 2019 Jun 6
PMID 31164868
Citations 22
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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.

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References
1.
Guemes M, Murray P, Brain C, Spoudeas H, Peters C, Hindmarsh P . Management of Cushing syndrome in children and adolescents: experience of a single tertiary centre. Eur J Pediatr. 2016; 175(7):967-76. DOI: 10.1007/s00431-016-2727-5. View

2.
Pecori Giraldi F, Moro M, Cavagnini F . Gender-related differences in the presentation and course of Cushing's disease. J Clin Endocrinol Metab. 2003; 88(4):1554-8. DOI: 10.1210/jc.2002-021518. View

3.
Bailey M, Mullins J, Kenyon C . Mineralocorticoid and glucocorticoid receptors stimulate epithelial sodium channel activity in a mouse model of Cushing syndrome. Hypertension. 2009; 54(4):890-6. DOI: 10.1161/HYPERTENSIONAHA.109.134973. View

4.
Daffara F, De Francia S, Reimondo G, Zaggia B, Aroasio E, Porpiglia F . Prospective evaluation of mitotane toxicity in adrenocortical cancer patients treated adjuvantly. Endocr Relat Cancer. 2008; 15(4):1043-53. DOI: 10.1677/ERC-08-0103. View

5.
Heaney A, Fernando M, Yong W, Melmed S . Functional PPAR-gamma receptor is a novel therapeutic target for ACTH-secreting pituitary adenomas. Nat Med. 2002; 8(11):1281-7. DOI: 10.1038/nm784. View