Hypertension and adrenal disorders

被引:21
作者
Chemaitilly, W [1 ]
Wilson, RC [1 ]
New, MI [1 ]
机构
[1] Cornell Univ, New York Presbyterian Hosp, Weill Med Coll, New York, NY 10021 USA
关键词
D O I
10.1007/s11906-003-0058-1
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
Adrenal disorders causing hypertension can be related to the dysfunction of either the adrenal cortex or the adrenal medulla. These disorders, including congenital adrenal hyperplasia (CAH), owing to 11beta-hydroxylase deficiency and to 17alpha-hydroxylase deficiency; apparent mineralocorticoid excess; familial hyperaldosteronism type 1; primary aldosteronism; Cushing's syndrome; and familial glucocorticoid resistance, primarily affect the adrenal cortex and cause low-renin hypertension. The classic disorder of the adrenal medulla resulting in hypertension is pheochromocytoma, although hypertension in obesity might also be associated with catecholamine secretion. In this review, we discuss these etiologies and the most recent advances in our knowledge of their pathophysiology, diagnosis and treatment.
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收藏
页码:498 / 504
页数:7
相关论文
共 30 条
[1]   Aldo is back: recent advances and unresolved controversies in hyperaldosteronism [J].
Auchus, RJ .
CURRENT OPINION IN NEPHROLOGY AND HYPERTENSION, 2003, 12 (02) :153-158
[2]   Pheochromocytoma - An approach to antihypertensive management [J].
Bravo, EL .
ENDOCRINE HYPERTENSION, 2002, 970 :1-10
[3]   Prenatal diagnosis and treatment of 11β-hydroxylase deficiency congenital adrenal hyperplasia resulting in normal female genitalia [J].
Cerame, BI ;
Newfield, RS ;
Pascoe, L ;
Curnow, KM ;
Nimkarn, S ;
Roe, TF ;
New, MI ;
Wilson, RC .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1999, 84 (09) :3129-3134
[4]   Extensive personal experience - Examination of genotype and phenotype relationships in 14 patients with apparent mineralocorticoid excess [J].
Dave-Sharma, S ;
Wilson, RC ;
Harbison, MD ;
Newfield, R ;
Azar, MR ;
Krozowski, ZS ;
Funder, JW ;
Shackleton, CHL ;
Bradlow, HL ;
Wei, JQ ;
Hertecant, J ;
Moran, A ;
Neiberger, RE ;
Balfe, JW ;
Fattah, A ;
Daneman, D ;
Akkurt, HI ;
De Santis, C ;
New, MI .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1998, 83 (07) :2244-2254
[5]   Commentary - Glucocorticoid-remediable aldosteronism [J].
Dluhy, RG ;
Lifton, RP .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1999, 84 (12) :4341-4344
[6]   Pheochromocytoma in the pediatric age group. [J].
Dubois, R ;
Chappuis, JP .
ARCHIVES DE PEDIATRIE, 1997, 4 (12) :1217-1225
[7]   LOCALIZATION OF THE HUMAN CYP17 GENE (CYTOCHROME-P45017-ALPHA) TO 10Q24.3 BY FLUORESCENCE INSITU HYBRIDIZATION AND SIMULTANEOUS CHROMOSOME-BANDING [J].
FAN, YS ;
SASI, R ;
LEE, C ;
WINTER, JSD ;
WATERMAN, MR ;
LIN, CC .
GENOMICS, 1992, 14 (04) :1110-1111
[8]   PHEOCHROMOCYTOMA AND PARAGANGLIOMA [J].
FONSECA, V ;
BOULOUX, PM .
BAILLIERES CLINICAL ENDOCRINOLOGY AND METABOLISM, 1993, 7 (02) :509-544
[9]   Familial/sporadic glucocorticoid resistance syndrome and hypertension [J].
Kino, T ;
Vottero, A ;
Charmandari, E ;
Chrousos, GP .
ENDOCRINE HYPERTENSION, 2002, 970 :101-111
[10]   New advances in the biochemical diagnosis of pheochromocytoma - Moving beyond catecholamines [J].
Lenders, JWM ;
Pacak, K ;
Eisenhofer, G .
ENDOCRINE HYPERTENSION, 2002, 970 :29-40