Document Detail


Hypertension in Cushing's syndrome.
MedLine Citation:
PMID:  16980206     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Maria Alexandra Magiakou; Penelope Smyrnaki; George P Chrousos
Related Documents :
14709846 - A case of acth-producing pheochromocytoma associated with pregnancy.
6603966 - A follow-up of the "low dose suppressible" hypercortisolism.
15527696 - Glucocorticoid excess and hypertension.
8491916 - Leydig cell tumor of the testis in klinefelter syndrome: mr detection.
1666176 - Chickenpox-associated acute retinal necrosis syndrome.
6586106 - Ectropion and epiphora in mcardle's syndrome.
Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Best practice & research. Clinical endocrinology & metabolism     Volume:  20     ISSN:  1521-690X     ISO Abbreviation:  Best Pract. Res. Clin. Endocrinol. Metab.     Publication Date:  2006 Sep 
Date Detail:
Created Date:  2006-09-18     Completed Date:  2006-12-07     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101120682     Medline TA:  Best Pract Res Clin Endocrinol Metab     Country:  England    
Other Details:
Languages:  eng     Pagination:  467-82     Citation Subset:  IM    
Affiliation:
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
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
11-beta-Hydroxysteroid Dehydrogenases / physiology
Angiotensin II / physiology
Antihypertensive Agents / therapeutic use
Atherosclerosis / complications
Catecholamines / pharmacokinetics
Cushing Syndrome / complications*,  epidemiology,  surgery
Glucocorticoids / pharmacology
Humans
Hypertension / complications*,  drug therapy,  epidemiology,  etiology
Models, Biological
Renin-Angiotensin System / drug effects,  physiology
Vasoconstrictor Agents / pharmacology
Vasodilator Agents / pharmacology
Chemical
Reg. No./Substance:
0/Antihypertensive Agents; 0/Catecholamines; 0/Glucocorticoids; 0/Vasoconstrictor Agents; 0/Vasodilator Agents; 11128-99-7/Angiotensin II; EC 1.1.1.146/11-beta-Hydroxysteroid Dehydrogenases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Incidentally discovered masses in hypertensive patients.
Next Document:  Laparoscopic adrenalectomy.