How common is adrenal-based mineralocorticoid hypertension?

Current Opinion in Endocrinology and Diabetes

Volumn 7, Issue 3, 2000, Pages 143-150

  Stowasser, Michael ^a  

^a UNIVERSITY OF QUEENSLAND   (Australia)

Author keywords

[No Author keywords available]

Indexed keywords

11BETA HYDROXYSTEROID DEHYDROGENASE; ALDOSTERONE; CORTICOTROPIN; DIURETIC AGENT; FLUDROCORTISONE; RENIN; STEROID 17ALPHA MONOOXYGENASE;

ADRENAL TUMOR; ENZYME DEFICIENCY; FAMILIAL DISEASE; HUMAN; HYPERALDOSTERONISM; HYPERTENSION; LIDDLE SYNDROME; PRIMARY HYPERALDOSTERONISM; RENIN ANGIOTENSIN ALDOSTERONE SYSTEM; REVIEW; SCREENING TEST;

EID: 0034074458     PISSN: 10683097     EISSN: None     Source Type: Journal    
DOI: 10.1097/00060793-200006000-00007     Document Type: Review

References (78)

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33. 33 Young WF Jr: Primary aldosteronism: a common and curable form of hypertension. Cardiol Rev 1999, 7:207-214. This is an excellent review of the clinical features, familial varieties, diagnostic workup, and management of PAL. Improved screening methodologies were associated with a more than tenfold increase in the average annual rate of diagnosis of PAL at the Mayo Clinic during the past 8 years compared with that between 1960 and 1991.
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37. 37 Lim PO, Brennan G, Shiels P, Dow E, Hanning I, Jung RT, et al.: Unexpectedly high prevalence of primary aldosteronism in a hypertension clinic population of Dundee. (Abstract) J Endocrinol 1998, 156(suppl):P22. Aldosterone-to-PRA ratio levels were elevated in 77 (15.5%) of 495 consecutive patients referred to a hypertension unit in Dundee, UK. PAL was confirmed in 34 of the 36 who were assessed further by salt-loading and fludrocortisone-suppression tests, suggesting that the aldosterone-to-PRA ratio is highly specific for PAL.
38. 38 Lim PO, Rodgers P, Cardale K, Watson AD, MacDonald TM: Potentially high prevalence of primary aldosteronism in a primary-care population. Lancet 1999, 353:40. These authors reported confirmation of PAL in 40 (93%) of 43 patients who underwent further assessment. When they applied the aldosterone-to-PRA ratio to 125 patients with hypertension who were randomly selected from a UK family physician practice database they found high ratios in 18 (14.4%) most of whom probably had PAL.
39. 39 Rossi GP, Rossi E, Pavan E, Rosati N, Zecchel R, Semplicini A, et al.: Screening for primary aldosteronism with a logistic multivariate discriminant analysis. Clin Endocrinol 1998, 49:713-723. A 25% prevalence rate for PAL was observed among a highly selected group of 574 patients who were referred to two hypertension units in Italy. Only 13 (41%) of 32 patients who were diagnosed as having APA at one of these units were hypokalemic. A multivariate discriminant-analysis approach (incorporating supine PRA, captopril-suppressed aldosterone, and serum potassium) was reported to be superior to the supine aldosterone-PRA ratio in detecting APAs.
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53. 53 MacConnachie AA, Kelly KF, McNamara A, Loughlin S, Gates LJ, Inglis GC, et al.: Rapid diagnosis and identification of cross-over sites in patients with glucocorticoid-remediable aldosteronism. J Clin Endocrinol Metab 1998, 83:4328-4331. The authors describe a modification of the previously described long-PCR method of detecting the hybrid gene responsible for FH-I, which uses a one-tube (rather than a two-tube) method.
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60. 60 Shen WT, Lim RC, Siperstein AE, Clark OH, Scheeler WP, Hunt TK, et al.: Laparoscopic vs open adrenalectomy for the treatment of primary aldosteronism. Arch Surg 1999, 134:628-632. Patients undergoing adrenalectomy laparoscopically (n = 42) had fewer complications afterwards and were equally likely to improve in terms of blood pressure and hypokalemia as those who were operated on by the open approach (n = 38).
61. 61 McAlister FA, Lewanczuk RZ: Primary hyperaldosteronism and adrenal incidentaloma: an argument for physiological testing before adrenalectomy. Can J Surg 1998, 41:299-305. Of 18 patients with PAL plus an adrenal mass visualised on CT, only 13 had APA subsequently proven by AVS. The remaining 5 had BAH.
62. 62 Lim PO, Jung RT, MacDonald TM: Raised aldosterone to renin ratio predicts antihypertensive efficacy of spironolactone: a prospective cohort follow-up study. Br J Clin Pharmacol 1999, 48:756-760. Spironolactone was a highly effective antihypertensive agent in 27 patients with hypertension who demonstrated a raised aldosterone-to-PRA ratio, failure of plasma aldosterone to suppress with salt loading and fludrocortisone-suppression testing, and absence of an adrenal mass on CT scan imaging and FH-I on genetic testing.
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64. 64 Stowasser M, Bachmann AW, Huggard PJ, Rossetti TR, Gordon RD: Severity of hypertension in familial hyperaldosteronism type I: relationship to gender and to degree of biochemical disturbance. J Clin Endocrinol Metab (In press). In a series of 26 patients with FH-I, hypertension was more severe among men. The degree of hybrid gene-induced aldosterone overproduction may have contributed to hypertension severity.
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70. 70 Torpy DJ, Gordon RD, Lin J-P, Huggard PR, Taymans SE, Stowasser M, et al.: Familial hyperaldosteronism type-II: description of a large kindred and exclusion of the aldosterone synthase (CYP11B2) gene. J Clin Endocrinol Metab 1998, 83:3214-3218.
71. 71 Iida A, Blake K, Tunny T, Klemm S, Stowasser M, Hayward N, et al.: Allelic losses on chromosome 11q13 in aldosterone-producing adrenal tumors. Genes Chromosoma Cancer 1995, 12:73-75.
72. 72 Takeda Y, Furukawa K, Inaba S, Miyamori I, Mabuchi H: Genetic analysis of aldosterone synthase in patients with idiopathic hyperaldosteronism. J Clin Endocrinol Metab 1999, 84:1633-1637. No hybrid gene mutations or other mutations within the coding region of the aldosterone synthase gene (CYP11B2) were found in DNA extracted from mononuclear leukocytes from patients with BAH or APA. However, both aldosterone synthase activity and CYP11B2 expression were greater in mononuclear leukocytes from patients with BAH than those with APA or controls, raising the possibility that factors leading to enhanced expression of CYP11B2 (perhaps mutations within the regulatory regions of the gene itself) may cause PAL in BAH.
73. 73 Pilon C, Mulatero P, Barzon L, Veglio F, Garrone C, Boscaro M, et al.: Mutations in CYP11B1 gene converting 11β-hydroxylase into an aldosterone-producing enzyme are not present in aldosterone-producing adenomas. J Clin Endocrinol Metab 1999, 84:4228-4231. Point mutations in exons 5 and 6 of the 11β-hydroxylase gene (CYP11B1) that have been shown to confer aldosterone synthase activity to the gene product in vitro were sought but not found among DNA extracted from APAs.
74. 74 Hampf M, Widimsky J, Bernhardt R: Aldosterone synthase gene in patients suffering from hyperaldosteronism. Endocr Res 1998, 24:877-880. Examination of the promoter region of CYP11B2 in DNA from patients with BAH revealed no evidence of mutations that might have been responsible for PAL in those subjects.
75. 75 Klemm SA, Ballantine DM, Tunny TJ, Stowasser M, Gordon RD. PCR-SSCP analysis of the angiotensin II type 1 receptor gene in patients with aldosterone-producing adenomas. Clin Exper Pharmacol Physiol 1995, 22:457-459.
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78. 78 Davies E, Holloway CD, Ingram MC, Inglis GC, Friel EC, Morrison C, et al.: Aldosterone excretion rate and blood pressure in essential hypertension are related to polymorphic differences in the aldosterone synthase gene CYP11B2. Hypertension 1999, 33:703-707. Two bialleleic polymorphic sites (C-344T and a CYP11B2/1 conversion within intron 2) within the CYP11B2 gene demonstrated a significant association with hypertension in a study of 138 patients with hypertension and matched controls. For one of these sites (C-344T) the allele that was overrepresented in patients with hypertension was also associated with higher tetrahydroaldosterone excretion rates among a sample of 486 subjects.