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The Journal of Clinical Endocrinology & Metabolism Vol. 82, No. 11 3570-3573
Copyright © 1997 by The Endocrine Society

Original Studies

Evaluation of the Dexamethasone Suppression Test for the Diagnosis of Glucocorticoid-Remediable Aldosteronism1

W. Reid Litchfield, Maria I. New, Caroline Coolidge, Richard P. Lifton and Robert G. Dluhy

Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School (W.R.L., C.C., R.G.D.), Boston, Massachusetts 02115; the Department of Medicine, New York Hospital and Cornell Medical Center (M.I.N.), New York, New York 10021; and the Departments of Medicine and Genetics, Boyer Center for Molecular Medicine (R.P.L.), Yale University School of Medicine, New Haven, Connecticut 06510

Address all correspondence and requests for reprints to: Dr. W. Reid Litchfield, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, 221 Longwood Ave RFB-2, Boston, Massachusetts 02115.


   Abstract
Top
 Abstract
Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
Glucocorticoid-remediable aldosteronism (GRA) is a rare form of inherited hypertension caused by a characteristic gene duplication. With the advent of definitive genetic testing for GRA, the performance of the traditional screening test for GRA, the dexamethasone suppression test (DST), can be evaluated. We compared the DST to direct genetic testing in 24 patients referred for genetic screening for GRA (12 GRA positive and 12 GRA negative) based on clinical and biochemical findings, DST, and family history. Plasma aldosterone was measured before and after oral dexamethasone administration to determine the extent to which aldosterone was suppressed by glucocorticoids in each patient group. The results of the DST in these subjects were also compared to those in 19 historical patients with primary aldosteronism [4 bilateral hyperplasia and 15 aldosterone-producing adenoma (APA)] reported previously. The DST differentiated GRA-positive from GRA-negative patients with 92% sensitivity and 100% specificity. Cutoffs based on the post-DST plasma aldosterone level (<4 ng/dL) or percent suppression compared to baseline (>80%) were equally effective in correctly diagnosing GRA (only one GRA-positive patient would have been incorrectly diagnosed). However, DST in 15 APA patients revealed that 33% had greater than 80% suppression of aldosterone, and 1 had aldosterone levels below 4 ng/dL.

We conclued that a post-DST aldosterone level below 4 ng/dL will correctly diagnose GRA patients with high sensitivity and specificity. Suppression compared to baseline can be misleading, as evidenced by the results in APA patients and referred subjects who genetically screened negative.


   Introduction
Top
 Abstract
 Introduction
Subjects and Methods
 Results
 Discussion
 References
 
GLUCOCORTICOID-remediable aldosteronism (GRA) is a rare form of primary aldosteronism in which aldosterone secretion is solely under the control of ACTH (1, 2). GRA is caused by a chimeric gene in which the ACTH-responsive 5'-promoter of the 11ß-hydroxylase gene is fused to coding sequences of the aldosterone synthase gene (3, 4). This results in ectopic expression of aldosterone synthase activity in zona fasciculata cells of the adrenal cortex under the regulation of ACTH, with resultant hyperaldosteronism and suppression of angiotensin II-stimulated aldosterone production in the zona glomerulosa. Although direct genetic testing is 100% sensitive and specific for the diagnosis of GRA, many clinicians continue to rely on dexamethasone suppression testing (DST) as a screening and/or diagnostic test for GRA. However, the DST has never been prospectively studied as a diagnostic test for GRA, nor is there a standardized protocol for its use. This study compared the DST with genetic testing in patients suspected of having GRA based on their family history, biochemical or clinical findings, and DST.


   Subjects and Methods
Top
 Abstract
 Introduction
 Subjects and Methods
Results
 Discussion
 References
 
Subjects

Retrospective review of the records of patients that had been genetically screened for GRA by the International Registry for Glucocorticoid-Remediable Aldosteronism revealed 24 individuals that had prior DST with baseline and post-DST plasma aldosterone levels. These patients were referred for genetic testing based on the clinical setting, family history, or results of DST (3, 4). Twelve subjects tested positive (GRA+), and 12 tested negative (GRA-).

The results of DST in these patients were compared to results in patients with primary hyperaldosteronism reported previously [15 patients with aldosterone-producing adenomas (APA) (5, 6) and 4 patients with idiopathic hyperaldosteronism (IHA) (7)]. APA patients were diagnosed on the basis of biochemical testing alone (n = 2) or biochemical testing and adrenal venous sampling (n = 5), surgery (n = 6), or adrenal venography (n = 2). IHA was diagnosed on the basis of biochemical findings and adrenal scintigraphy (n = 3) or postmortem examination (n = 1). Genetic testing was not performed in these historical controls.

Genetic testing

Total genomic DNA was extracted from 10–20 mL peripheral venous blood as previously described (8). The chimeric 11ß-hydroxylase/aldosterone synthase gene was identified using a previously reported Southern blotting technique (4). Genetic testing was performed without prior knowledge of the response to DST.

DST

Most subjects underwent low dose DST based on that originally described by Liddle et al. (9, 10). Dexamethasone (0.75–2.0 mg/day) was administered orally for at least 2 days. Plasma aldosterone was measured before and after the DST.

Statistical analysis

The two patient groups were compared using an unpaired t test with an {alpha} level of 0.05. Results are expressed as the mean ± SEM. Sensitivity, specificity, positive predictive value, and negative predictive value were calculated for DST using genetic testing as the definitive test. Baseline and post-DST aldosterone levels and percent suppression of aldosterone were compared in these patient groups.


   Results
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
Discussion
 References
 
Genetically screened subjects

The GRA+ subjects (n = 12) were similar to the GRA- subjects (n = 12) with respect to gender, systolic blood pressure, diastolic blood pressure, baseline serum aldosterone, and PRA (Table 1Go). GRA+ and GRA- subjects differed significantly with respect to age (mean age, 21.2 ± 3.6 and 36.4 ± 4.2 yr, respectively; P = 0.02). The median plasma aldosterone/PRA ratio for both groups was 141.5, consistent with a diagnosis of primary aldosteronism where the ratio usually exceeds 30 (11).


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  		Table 1. Clinical and biochemical characteristics of the 24 subjects referred for genetic screening for the chimeric gene who had dexamethasone suppression tests

 
Both dose (mean, 1.7 ± 0.13 mg/day; range, 0.75–2 mg/day) and duration of dexamethasone treatment (mean, 4.5 ± 0.73 days; range, 1–15 days) varied widely for all subjects. Although the two groups did not differ significantly in terms of dexamethasone dose or duration, GRA- patients showed a trend toward a longer duration of DST (P = 0.06; Table 1Go).

Although all subjects had aldosterone measured during the DST, pre- and post-DST cortisol levels were measured in only 7 of 12 GRA+ patients and in 3 of 12 GRA- patients. Post-DST cortisol levels indicated that the dexamethasone dose was sufficient to suppress cortisol levels to less than 5 ng/dL in these subjects (data not shown). Of those subjects without post-DST cortisol measurements, all had been given dexamethasone at doses that have been previously shown to suppress morning cortisol levels in normal subjects.

Baseline aldosterone levels tended to be higher, but were not significantly different, in the GRA- compared to the GRA+ group (54.2 ± 13.9 vs. 26.0 ± 3.6 ng/dL, respectively; P = 0.06; Fig. 1AGo). However, post-DST aldosterone levels were significantly lower in GRA+ patients compared to GRA- subjects (2.4 ± 0.44 and 22.0 ± 5.5 ng/dL, respectively; P < 0.002). In addition, the percent suppression of aldosterone vs baseline was significantly greater in GRA+ subjects (88 ± 3% vs. 54 ± 4%; P < 0.0001; Fig. 1BGo).



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  		Figure 1. A, Mean (±SEM) plasma aldosterone pre- and post-DST in 24 subjects genetically screened for GRA (GRA+, n = 12; GRA-, n = 12). Post-DST aldosterone levels were significantly lower in GRA+vs. GRA- subjects. B, Percent suppression (±SEM) of plasma aldosterone vs. baseline post-DST in these same subjects. After DST, GRA+ subjects showed a significantly greater percent suppression of aldosterone than did GRA subjects. *, P < 0.002; {ddagger}, P < 0.0001.

 
Comparison of DST to genetic testing showed good discrimination between GRA+ and GRA- when either the post-DST plasma aldosterone (GRA+, <4 ng/dL) or the percent suppression of aldosterone vs. baseline (GRA+, >80% suppression) end points were employed. The sensitivity and specificity were, respectively, 91.7% and 100%, with positive and negative predictive values of 100% and 99.1% for both tests (the latter assumes a 20% prevalence of disease in our study population, which approximates that seen in patients referred for genetic testing). The use of either end point resulted in correct identification of all GRA- subjects and a misclassification of one GRA+ subject.

Historical subjects with primary aldosteronism (5, 6, 7)

Compared to our study subjects, the historical patients had been given a greater mean dose of dexamethasone (2.1 ± 0.2 mg/day; P = 0.02) and a shorter mean duration of treatment (2.2 ± 0.1 days; P < 0.01). DST in 15 APA patients resulted in mean baseline plasma aldosterone levels (50.0 ± 7.3 ng/dL) declining to 23.1 ± 5.2 ng/dL (49 ± 9% suppression). Basal and post-DST plasma aldosterone levels and percent suppression of plasma aldosterone in APA patients were significantly different from those in GRA+ subjects (P values 0.01, 0.02, and 0.001, respectively), but not from those in GRA- subjects (Fig. 2Go).



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  		Figure 2. Plasma aldosterone levels post-DST in GRA+ (n = 12) and GRA- (n = 12) subjects referred for genetic screening and historical data of aldosterone-producing adenoma (APA) patients (n = 15) (5, 6). Open symbols = individual data points; closed symbols = mean ± SD.

 
A post-DST plasma aldosterone measurement below 4 ng/dL resulted in 14 of 15 APA patients being correctly classified as GRA-. However, only 10 of 15 APA patients would be correctly classified as GRA- if 80% suppression vs. baseline was used. The small group of 4 patients with IHA did not exhibit a significant reduction in aldosterone levels post-DST (pre-DST, 23.2 ± 3.9 ng/dL; post-DST, 24.9 ± 5.7; 0 ± 6% suppression). Table 2Go summarizes the results of DST in all 4 patient groups.


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  		Table 2. Results of dexamethasone suppression testing in 24 subjects genetically screened for the chimeric gene and 19 subjects with primary aldosteronism reported in the literature

 

   Discussion
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
References
 
The identification of the genetic basis of GRA by Lifton et al. (4) and the recent development of a simple PCR test (12, 13) have permitted the diagnosis of GRA using direct genetic testing. However, many clinicians continue to perform a DST to determine who should be genetically screened or use it in lieu of genetic testing altogether. Although the DST has been used to diagnose GRA since the syndrome was first described by Sutherland et al. (14), there is no consensus as to the how the test should be performed. Doses ranging from 2–8 mg/day for 2 days to 4 weeks have been used (15, 16, 17, 18, 19, 20). Finally, it appears that clinicians are uncertain how they should interpret the results of DST in the differential diagnosis of patients with biochemically established primary aldosteronism.

The present study represents a retrospective review of patients referred for genetic testing to the International Registry for Glucocorticoid-Remediable Aldosteronism. Of 24 subjects with pre- and post-DST aldosterone measurements (12 GRA positive and 12 GRA negative), the DST proved to be accurate in correctly diagnosing GRA if the proper suppression criteria were applied. Cut-offs based on absolute aldosterone levels (<4 ng/dL) or percent suppression of aldosterone (>80%) were equally effective in correctly diagnosing GRA, with only 1 subject that was GRA+ being misclassified. This subject’s plasma aldosterone level fell from 14.3 to 6.4 ng/dL (55% suppression) after the administration of 0.5 mg dexamethasone every 6 h for 3 days. However, treatment compliance could not be confirmed because cortisol was not measured post-DST. This underscores the importance of measuring both aldosterone and cortisol concurrently when performing DST to ensure that noncompliance with dexamethasone administration does not result in a false negative test.

In considering the differential diagnosis of GRA, there are a number of mineralocorticoid excess states in which the elevation in blood pressure may be glucocorticoid responsive (1). These include congenital and acquired 11ß-hydroxysteroid dehydrogenase deficiency as well as congenital adrenal hyperplasia due to 11ß-hydroxylase or 17{alpha}-hydroxylase deficiency. Although lowering blood pressure with DST in these syndromes is similar to that seen in GRA, these low renin syndromes can be distinguished because the mineralocorticoid excess state is caused by a steroid other than aldosterone (e.g. cortisone in 11ß-hydroxysteroid deficiency). However, DST in patients with the more common etiologies of primary aldosteronism, such as APA and IHA, could cause confusion, because dexamethasone-induced suppression of aldosterone is a well documented and often not appreciated finding in APA (5, 6, 7, 21, 22, 23).

As the final diagnosis was unknown in our subjects who genetically screened negative for GRA, we reviewed the literature for the plasma aldosterone response to DST in patients with primary aldosteronism. When the above DST diagnostic criteria were applied to 15 patients with APA (5, 6), the post-DST aldosterone level was more accurate than the percent suppression in correctly classifying these patients as GRA-; 14 of 15 APA subjects had post-DST aldosterone levels above 4 ng/dL. On the other hand, one third of the APA patients had more than 80% suppression of aldosterone levels post-DST (5, 6). Thus, even though APA patients often show clear-cut dexamethasone suppressibility of aldosterone, the post-DST aldosterone level is usually higher than those seen in GRA patients.

Thus, DST can be used to correctly diagnose almost all patients with GRA if appropriate post-DST aldosterone criteria are applied. We believe that DST is best accomplished by administering 0.5 mg dexamethasone, orally, every 6 h for 2 days; concurrent measurement of cortisol with aldosterone is recommended to document adequate suppression of ACTH. Longer duration of DST (>1 week), as has been performed by some investigators (20, 25), is not recommended because this may result in reactivation of the renin-angiotensin system in GRA patients, possibly yielding false negative results. Although a cut-off of more than 80% suppression of aldosterone after DST would clearly have misclassified some patients with APA, a post-DST aldosterone level less than 4 ng/dL was seen in less than 7% of APA patients. Thus, there was overlap in the post-DST aldosterone levels in the GRA+ and APA groups. As the DST cannot definitively distinguish APA from GRA+, direct genetic testing still appears to be the definitive confirmatory test (100% sensitivity and 100% specificity). This is underscored by a report of autonomous aldosterone production with failure to suppress after DST in an established GRA family (24).

When should the DST be administered? GRA is rare and has a low prevalence, even among patients with biochemical primary hyperaldosteronism. It is, therefore, important to stress that the routine use of the DST as part of the initial diagnostic evaluation of patients with primary hyperaldosteronism is inappropriate. Rather, we propose that the DST be used in patients with biochemical primary hyperaldosteronism, who have a suggestive clinical history (i.e. early-onset hypertension in the proband and in first degree relatives) and negative computed tomography imaging of the adrenals. Finally, a positive DST should not displace the primacy of direct genetic testing in the diagnosis of GRA.

The fall in aldosterone to nearly undetectable levels after DST in GRA is expected and reflects the sole control of aldosterone by ACTH in this disorder. The significant suppression of aldosterone levels after DST in APA reflects the well recognized regulation of aldosterone by ACTH in this disorder (16, 17, 24, 25, 26). However, autonomous production of aldosterone by the neoplasm accounts for the failure of aldosterone levels to fall to very low or nearly undetectable levels. It was with these observations in mind that the late Dr. Stanley Ulick favored the term GRA over dexamethasone-suppressible hyperaldosteronism for the disorder that he biochemically characterized by the measurement of unique steroid metabolites (6). These data underscore his penetrating contributions and insights.


   Footnotes
 
1 This work was supported by General Clinical Research Center Grant 5-MO1-RR-002635, NIH Grant 5-RO1-HL-53693, and NIH Grant T32-HL-07609. Back

Received May 9, 1997.

Accepted July 17, 1997.


   References
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 

  1. Litchfield WR, Dluhy RG. 1996 Glucorticoid-remediable aldosteronism. Curr Opin Endocrinol Diabetes3 :265–270.
  2. Litchfield WR, Dluhy RG, Lifton RP, Rich GM. 1995 Glucocorticoid-remediable aldosteronism. Comp Ther. 21:553–558.
  3. Lifton RP, Dluhy RG, Powers M, et al. 1992 Hereditary hypertension caused by chimaeric gene duplications and ectopic expression of aldosterone synthase. Nat Genet. 2:66–74.[CrossRef][Medline]
  4. Lifton RP, Dluhy RG, Powers M, et al. 1992 A chimaeric 11 beta-hydroxylase/aldosterone synthase gene causes glucocorticoid-remediable aldosteronism and human hypertension. Nature. 355:262–265.[CrossRef][Medline]
  5. Ganguly A, Chavarri M, Luetscher JA, Dowdy AJ. 1977 Transient fall and subsequent return of high aldosterone secretion by adrenal adenoma during continued dexamethasone administration. J Clin Endocrinol Metab. 44:775–779.[Abstract]
  6. Wenting GJ, Man In’t Veld AJ, Derkx FH, Brummelen PV, Schalekamp MADH. 1978 ACTH-dependent aldosterone excess due to adrenocortical adenoma: a variant of primary aldosteronism. J Clin Endocrinol Metab. 46:326–335.[Medline]
  7. Hoefnagels WH, Drayer JI, Smals AG, Benraad TJ, Kloppenborg PW. 1980 Nocturnal, daytime, and postural changes of plasma aldosterone before and during dexamethasone in adenomatous and idiopathic aldosteronism. J Clin Endocrinol Metab. 51:1330–1334.[Abstract]
  8. Bell G, Karam J, Rutler W. 1981 Polymorphic DNA region adjacent to the 5'endo of the human insulin gene. Proc Natl Acad Sci USA. 78:5759–5763.[Abstract/Free Full Text]
  9. Liddle GW. 1960 Tests of pituitary-adrenal suppressibility in the diagnosis of Cushing’s syndrome. J Clin Endocrinol Metab. 20:1539–1561.
  10. Liddle GW, Estep HL, Kendall JWJ, Williams WCJ, Townes AW. 1959 Clinical application of a new test of pituitary reserve. J Clin Endocrinol Metab. 19:875–894.
  11. Lins PE, Adamson U. 1986 Plasma aldosterone-plasma renin activity ratio. A simple test to identify patients with primary aldosteronism. Acta Endocrinol (Copenh). 113:564–569.[Abstract/Free Full Text]
  12. Stowasser M, Bachmann AW, Jonsson JR, Tunny TJ, Klemm SA, Gordon RD. 1995 Clinical, biochemical, and genetic approaches to the detection of familial hyperaldosteronism type I. J Hypertens. 13:1610–1613.[Medline]
  13. Jonsson JR, Klemm SA, Tunny TJ, Stowasser M, Gordon RD. 1995 A new genetic test for familial hyperaldosteronism type I aids in the detection of curable hypertension. Biochem Biophys Res Commun. 207:565–571.[CrossRef][Medline]
  14. Sutherland DJ, Ruse JL, Laidlaw JC. 1966 Hypertension, increased aldosterone secretion, and low plasma renin activity relieved by dexamethasone. Can Med Assoc J. 95:1109–1119.[Medline]
  15. Giebink GS, Gotlin RW, Biglieri EG, Katz FH. 1973 A kindred with familial glucocorticoid suppressible aldosteronism. J Clin Endocrinol Metab. 36:715–723.[Medline]
  16. Oberfield SE, Levine LS, Stoner E, et al. 1981 Adrenal glomerulosa function in patients with dexamethasone-suppressible hyperaldosteronism. J Clin Endocrinol Metab. 53:158–164.[Abstract]
  17. Woodland E, Tunny TJ, Hamlet SM, Gordon RD. 1985 Hypertension corrected and aldosterone responsiveness to renin-angiotensin restored by long-term dexamethasone in glucocorticoid-suppressible hyperaldosteronism. Clin Exp Pharmacol Physiol. 12:245–248.[Medline]
  18. Kato S, Haji M, Yanase T, Nawata H, Kato K, Ibayashi H. 1988 A case of glucocorticoid-suppressible hyperaldosteronism with aldosterone producing adenoma. Endocrinol Jpn. 35:311–320.[Medline]
  19. Ganguly A, Grim CE, Bergstein J, Brown RD, Weinberger MH. 1981 Genetic and pathophysiologic studies of a new kindred with glucocorticoid-suppressible hyperaldosteronism manifest in three generations. J Clin Endocrinol Metab. 53:1040–106.[Abstract]
  20. Stockigt JR, Scoggins BA. 1987 Long term evolution of glucocorticoid-suppressible hyperaldosteronism. J Clin Endocrinol Metab. 64:22–26.[Abstract]
  21. Newton MA, Laragh JH. 1968 Effects of glucocorticoid administration on aldosterone excretion and plasma renin in normal subjects, in essential hypertension and in primary aldosteronism. J Clin Endocrinol Metab. 28:1014–1022.[Medline]
  22. Schambelan M, Brust NL, Chang BCF, Slater KL, Biglieri EG. 1976 Circadian rhythm and effect of posture on plasma aldosterone concentration in primary aldosteronism. J Clin Endocrinol Metab. 43:115.[Abstract]
  23. Slaton PE, Schambelan M, Biglieri EG. 1969 Stimulation and suppression of aldosterone secretion in patients with an aldosterone producing adenoma. J Clin Endocrinol Metab. 29:239–250.[Medline]
  24. Stockigt JR, Scoggins BA. 1987 Long term evolution of glucocorticoid-suppressible hyperaldosteronism. J Clin Endocrinol Metab. 64:22–26.
  25. Connell JM, Kenyon CJ, Corrie JE, Fraser R, Watt R, Lever AF. 1986 Dexamethasone-suppressible hyperaldosteronism. Adrenal transition cell hyperplasia? Hypertension. 8:669–676.[Abstract/Free Full Text]
  26. Ulick S, Chan CK, Gill Jr JR, et al. 1990 Defective fasciculata zone function as the mechanism of glucocorticoid-remediable aldosteronism. J Clin Endocrinol Metab. 71:1151–1157.[Abstract]



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