Hypertension in Cushing's syndrome.
Cushing's syndrome can be exogenous, resulting from the administration of glucocorticoids or adrenocorticotrophic hormone (ACTH), or endogenous, secondary to increased secretion of cortisol or ACTH. Hypertension is one of the most distinguishing features of endogenous Cushing's syndrome, as it is present in about 80% of adult patients and in almost half of children and adolescents patients. Hypertension results from the interplay of several pathophysiological mechanisms regulating plasma volume, peripheral vascular resistance and cardiac output, all of which may be increased. The therapeutic goal is to find and remove the cause of excess glucocorticoids, which, in most cases of endogenous Cushing's syndrome, is achieved surgically. Treatment of Cushing's syndrome usually results in resolution or amelioration of hypertension. However, some patients may not achieve normotension or may require a prolonged period of time for the correction of hypercortisolism. Therefore, therapeutic strategies for Cushing's-specific hypertension (to normalise blood pressure and decrease the duration of hypertension) are necessary to decrease the morbidity and mortality associated with this disorder. The various pathogenetic mechanisms that have been proposed for the development of glucocorticoid-induced hypertension in Cushing's syndrome and its management are discussed.
Magiakou
Maria Alexandra
MA
Unit of Endocrinology, Metabolism and Diabetes, First Department of Pediatrics, University of Athens Medical School, Agia Sophia Children's Hospital, 11527 Goudi, Athens, Greece. mmayakou@med.uoa.gr
Smyrnaki
Penelope
P
Chrousos
George P
GP
D042842:11-beta-Hydroxysteroid Dehydrogenases / Q000502:physiology; D000804:Angiotensin II / Q000502:physiology; D000959:Antihypertensive Agents / Q000627:therapeutic use; D050197:Atherosclerosis / Q000150:complications; D002395:Catecholamines / Q000493:pharmacokinetics; D003480:Cushing Syndrome / Q000150:complications* / Q000453:epidemiology / Q000601:surgery; D005938:Glucocorticoids / Q000494:pharmacology; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000188:drug therapy / Q000453:epidemiology / Q000209:etiology; D008954:Models, Biological; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
D000959:Antihypertensive Agents; D002395:Catecholamines; D005938:Glucocorticoids; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D000804:Angiotensin II; D042842:11-beta-Hydroxysteroid Dehydrogenases