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Original Studies |
Endocrine-Diabetes Center, Departments of Medicine and Radiology, St. Luke’s Medical Center, Milwaukee, Wisconsin 53215
Address correspondence and requests for reprints to: Dr. Steven B. Magill, Endocrinology and Diabetes, 2801 West Kinnickinnic River Parkway, Suite 245, Milwaukee, Wisconsin 53215. E-mail: steven_magill{at}aurora.org
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Abstract |
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The diagnosis of primary aldosteronism was made in 62 patients based on an elevated plasma aldosterone to PRA ratio and an elevated urinary aldosterone excretion rate. Thirty-eight patients had CT imaging and successful bilateral adrenal vein sampling and were included in the final analysis. AVS was considered the gold standard in determining the specific subtype of primary aldosteronism.
There were 15 patients with APA, 21 patients with BAH, and 2 patients with primary adrenal hyperplasia. Plasma aldosterone was significantly higher in patients with APA (46.3 ± 8.5 ng/dL; 1284 ± 235 pmol/L) than in those with BAH (29.3 ± 2.4 ng/dL; 813 ± 11 pmol/L; P < 0.05). Plasma potassium was significantly lower in patients with APA (3.1 ± 0.1 mmol/L) than in patients with BAH (3.5 ± 0.1 mmol/L; P < 0.02). There was considerable overlap in the other biochemical indices (e.g. PRA and urinary aldosterone) in patients with the different subtypes.
In patients with APA proven by AVS, eight had concordant findings with CT imaging, four had discordant findings, and three had normal CT imaging. In patients with BAH proven by AVS, four had concordant findings with CT imaging, eight had discordant findings, and nine had normal CT imaging. Compared with AVS, CT imaging was either inaccurate or provided no additional information in 68% of the patients with primary aldosteronism.
We conclude that adrenal CT imaging is not a reliable method to differentiate primary aldosteronism. Adrenal vein sampling is essential to establish the correct diagnosis of primary aldosteronism.
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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The appropriate treatment of primary aldosteronism depends on the correct differential diagnosis. Of the various subtypes of primary aldosteronism, aldosterone-producing adenomas (APA) and bilateral adrenal hyperplasia (BAH), also known as idiopathic aldosteronism, account for over 95% of all cases. Primary adrenal hyperplasia (PAH) or unilateral hyperplasia is an unusual subtype that physiologically and biochemically mimics APA (7). Glucocorticoid-remediable aldosteronism is a rare familial subtype with an autosomal dominant inheritance pattern (8, 9). Primary aldosteronism has uncommonly been associated with adrenal carcinoma (10).
APAs are typically amenable to unilateral adrenalectomy, which corrects the hypokalemia and can attenuate the hypertension (11). Medical management of BAH is generally recommended, as total or subtotal adrenalectomy results in cure rates of only 20–38% (11, 12).
After the diagnosis of primary aldosteronism, imaging of the adrenal glands with computed tomography (CT) is recommended to help delineate the subtype (13). Magnetic resonance is a promising technique in subtype evaluation, but is not as cost-effective as CT (14). With improved spatial resolution of CT imaging, an increasing number of adrenal abnormalities are being detected (15).
Adrenal vein sampling (AVS) was initially described in the 1960s and appeared useful in the delineation of primary aldosteronism (16). The technique fell into disfavor due to the technical difficulty of cannulating both adrenal veins (17). With improved radiological and angiographic techniques, AVS has reemerged and is considered the gold standard in determining the etiology of hyperaldosteronism (17, 18). Other methods, including saline suppression testing, posture studies, captopril challenge, and the use of biochemical markers, lack the requisite sensitivity necessary to differentiate the etiology of hyperaldosteronism (2). [6-ß-131I]Iodomethyl-19-norcholesterol scanning, an alternate method of differentiating the cause of hyperaldosteronism (19), is not universally available and lacks sensitivity if the adrenal nodule is less than 1–1.5 cm in diameter (20). Adrenal venography has essentially been abandoned because of the high risk of adrenal hemorrhage from the contrast load (18).
The current study compared CT imaging with bilateral adrenal vein sampling in the differentiation of primary aldosteronism. We hypothesize that CT imaging is not a dependable approach in the differential diagnosis of primary aldosteronism.
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Subjects and Methods |
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This was a retrospective analysis of patients who were referred for evaluation of suspected primary aldosteronism from 1987–1997. The patients had a history of poorly controlled hypertension, which was often, but not always, associated with hypokalemia. Many of the patients were taking two or more antihypertensive agents and potassium supplements. Patients taking spironolactone or amiloride were switched to other antihypertensive agents at least 4 weeks before evaluation.
A plasma aldosterone to PRA ratio (Aldo/PRA) of 20 or greater in
conjunction with a PRA less than 1.0 ng/mL·h (<0.278 ng/L·s) was
used as the initial screening criteria (2). Patients were
instructed to liberalize daily salt intake for 72 h, and a 24-h
urine collection was obtained on the third day. A urinary aldosterone
excretion rate of 14 µg/day or greater (
38.8 nmol/day) (3, 21), confirmed the diagnosis of primary aldosteronism in 62
patients. Urinary sodium excretion of 150 mmol/day or greater indicated
adequate salt loading.
CT imaging
In almost all cases, noncontrast CT imaging of the adrenal glands with contiguous 3- to 5-mm cuts were obtained. A GE 9800 scanner was used for CT imaging of adrenal glands for the majority of patients. Three patients who did not undergo AVS had CT scans completed at other institutions and were not included in the accuracy calculations.
AVS
AVS is a direct assessment of hormonal secretion and is more specific than anatomical imaging modalities. Based on extensive past literature, we defined bilaterally successful AVS as the gold standard for differentiation of subtype of hyperaldosteronism. AVS was accomplished via the femoral vein approach (17). Blood samples were obtained from the inferior vena cava (IVC) and the right and left adrenal vein. Samples for aldosterone, cortisol, and epinephrine concentrations were obtained from all three sites. Six of 15 patients with APA, 9 of 21 patients with BAH, and 0 of 2 patients with PAH received cosyntropin infusion [250 µg Cortrosyn (Organon Pharmaceuticals, West Orange, NJ) in 500 mL 5% dextrose at a rate of 100 mL/h] during AVS. Successful AVS was determined by at least a 3-fold elevation in adrenal vein epinephrine and cortisol levels compared with the IVC.
For each sample, the aldosterone concentration was divided by the cortisol concentration to correct for dilutional effects of adrenal vein drainage and herein will be referred to as normalized aldosterone. The diagnoses of APA and PAH were based on the assumption that the ratio of dominant to nondominant normalized aldosterone would be 4 or greater, and the nondominant normalized aldosterone would be less than or equal to the normalized aldosterone in the IVC. For the definition of BAH, the normalized aldosterone in each adrenal vein was equal to or greater than the normalized aldosterone from the IVC. There was no cut-off point of the ratio of dominant to nondominant normalized aldosterone in defining BAH.
Assays
Plasma aldosterone was measured by solid phase RIA
(Diagnostic Products, Los Angeles, CA). Intra- and
interassay coefficients of variation for measurement of aldosterone
were 6% and 9%, respectively (22). Plasma cortisol was
measured by an immunofluorometric method. PRA was determined by RIA of
angiotensin I generated in vitro (lower limit of detection,
0.13 ng/mL·h; 0.036 ng/L·s; INCSTAR Corp.,
Stillwater, MN). Intra- and interassay coefficients of variation for
measurement of PRA were 5% and 10%, respectively (22).
Plasma epinephrine was measured by high pressure liquid chromatography
electrochemical detection (SmithKline Beecham, Schaumburg,
IL).
Data were analyzed by unpaired t tests for comparison, with P < 0.05 considered a significant difference. Ratios of dominant to nondominant normalized aldosterone were analyzed by the Mann-Whitney test. Data are shown as the mean ± SEM.
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Sixty-two patients were identified as having primary aldosteronism based on clinical and biochemical evaluation. AVS was not performed in 13 patients. Two of these 13 patients had a well defined unilateral adrenal nodule and a normal contralateral gland with CT imaging suggestive of a clinical diagnosis of APA. Unilateral adrenalectomy confirmed the presence of adrenal cortical adenoma in these 2 patients. Both patients had an improvement in control of blood pressure after adrenalectomy. AVS could not technically be performed in 2 patients due to morbid obesity. Another patient developed chest pain just before AVS, and the procedure was aborted. Eight additional patients did not undergo AVS because they refused to undergo the procedure or were lost to follow-up before the sampling could be arranged. The 11 patients who did not undergo AVS were managed with antihypertensive therapy.
Patients who had incomplete AVS
Eleven of 49 patients in whom AVS was attempted had incomplete catheterization of the adrenal glands due to anatomical variation and technical difficulties. Seven had unsuccessful right AVS, and 4 had incomplete sampling due to difficulty in cannulating the left adrenal vein. Despite the technical difficulty, AVS generated sufficient data to provide a diagnosis in 5 of 11 patients who had incomplete AVS. Four of these 11 patients underwent unilateral adrenalectomy, and final pathology demonstrated the presence of an adrenal cortical adenoma. Three of 4 patients with APA who underwent adrenalectomy had improvement or normalization of blood pressure after surgery. Another patient was diagnosed with BAH based on the incomplete AVS findings and was treated medically. Two patients with equivocal AVS results underwent unilateral adrenalectomy, and pathology demonstrated adrenal hyperplasia. These latter 2 patients had no improvement in control of blood pressure after adrenalectomy and were retrospectively thought to have BAH. Four patients had no further differentiation of hyperaldosteronism and also were treated medically. Routine postoperative or post-AVS measurement of plasma aldosterone and PRA was not performed in these patients.
Successful bilateral AVS
Thirty-eight patients had successful bilateral AVS based on the
criteria described in the methods. Fifteen patients had APA, 2 patients
had PAH, and 21 patients had BAH. Clinical characteristics and data of
the patients with APA and BAH are shown in Table 1
. There were no differences in gender or
age between the 2 groups. The majority of patients identified with
primary aldosteronism were male.
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). PRA
levels in patients with APA and BAH were similar. Plasma aldosterone
and potassium were lower in the APA group than in the BAH group.
Aldo/PRA and the urinary aldosterone excretion rate tended to be higher
in patients with APA, but the difference was not statistically
significant. Three of 15 patients with APA and 11 of 21 patients with
BAH were eukalemic (normal range for plasma potassium, 3.5–5.0 mmol/L)
at the time of biochemical evaluation. The 2 patients with PAH had
plasma potassium levels of 3.2 and 3.5 mmol/L, respectively. Both of
the patients with PAH were Caucasian. There was no significant difference in normalized aldosterone levels (from the dominant and nondominant adrenal glands) between patients with APA or BAH who did vs. those who did not receive cosyntropin infusion during bilateral AVS. In the APA group, 6 patients received cosyntropin (normalized aldosterone, 14.8 ± 4.7; range, 5.0–30.0), and 9 patients did not (normalized aldosterone, 38.1 ± 9.8; range, 3.3–86.2; P = 0.090). In the patients with BAH, 9 patients received cosyntropin (normalized aldosterone, 1.6 ± 0.2; range, 1.0–3.2), and 12 patients did not (normalized aldosterone, 2.6 ± 0.5; range, 1.1–7.0; P = 0.137).
APAs based on AVS
There was a significant difference between the mean dominant to
nondominant normalized aldosterone levels in APA vs. BAH
(Tables 2 and 3). The ratio of dominant to nondominant
normalized aldosterone was greater than 4 in all but 1 patient with APA
(Table 2). In patient 10 the dominant to nondominant normalized
aldosterone ratio was 3.8. However, the contralateral normalized
aldosterone was less than the normalized aldosterone in the IVC and
therefore met the criteria for APA. One patient had a contralateral
normalized aldosterone level equal to that in the IVC, but the dominant
to nondominant corrected aldosterone ratio was 10 (patient 9, Table 2).
This patient was found to have an adenoma with adrenalectomy and had
resolution of hypokalemia and improvement in control of blood pressure
after adrenalectomy. There was no difference in the nondominant divided
by IVC normalized aldosterone levels in APA vs. BAH.
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). For example, CT imaging
demonstrated an ipsilateral adrenal nodule and a plump contralateral
adrenal gland in patients 13 and 15 (Table 2). Aldosterone production
lateralized with AVS, and findings were discordant with the CT imaging
results in these 2 patients. Confirmation of the presence of an
adrenocortical adenoma was obtained in 13 patients who underwent
unilateral adrenalectomy. The majority of these patients had
improvement of blood pressure control after adrenalectomy (Table 2).
Ten of 13 patients with APA who underwent adrenalectomy had resolution
of hypokalemia within 1 week after surgery. Two patients with APA who
had successful sampling did not undergo surgery. One of these patients
was lost to follow-up, and it is uncertain whether adrenalectomy was
completed. Another patient refused surgery and was treated medically
(Table 2). Primary adrenal gland hyperplasia based on AVS
The ratios of dominant to nondominant normalized aldosterone were
21 and 8 in the two patients with PAH (patients 16 and 17, Table 2).
One patient had normal-appearing adrenal glands on CT. The second
patient with PAH had bilateral adrenal enlargement. Both patients
underwent unilateral adrenalectomy based on AVS, and pathology
confirmed the presence of adrenal hyperplasia. These patients had
improvement in blood pressure control and were eukalemic after surgery
(Table 2).
Bilateral adrenal hyperplasia based on AVS
The ratio of dominant to nondominant normalized aldosterone
was less than 4 in all but three patients with BAH (Table 3). Eleven
patients had equivalent normalized aldosterone levels between the left
and right adrenal glands. In the three patients who had a dominant to
nondominant normalized aldosterone ratio of 4 or greater (patients 7,
9, and 21, Table 3), the ipsilateral and contralateral normalized
aldosterone was greater then the normalized aldosterone in the IVC;
therefore, these patients met the criteria for BAH. Patient 21 was
inappropriately referred for unilateral adrenalectomy based on a
dominant to nondominant corrected aldosterone of 4 or more. Two
additional patients underwent unilateral adrenalectomy despite evidence
of bilateral aldosterone production (patients 3 and 11, Table 3). None
of these three patients had improvement in blood pressure control or
resolution of hypokalemia after surgery. These outcomes suggest that
the patients did indeed have bilateral aldosterone production,
confirming the validity of AVS.
Of the patients with BAH, 8 of 21 had discordance between CT imaging
and AVS (patients 14–21, Table 3). For example, patient 17 had a
2.4-cm diameter left adrenal nodule, but AVS demonstrated bilateral
aldosterone production consistent with BAH. Another 9 patients with BAH
had normal adrenal glands based on CT imaging. After AVS, 18 of 21
patients with BAH were treated medically with spironolactone or
amiloride in combination with other antihypertensive agents. These
patients had improvement in control of blood pressure with diuretic
therapy and did not undergo further evaluation of PRA or plasma
aldosterone.
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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38.8
nmol/day) obtained during a 3-day high salt diet or salt loading
confirms the diagnosis of primary aldosteronism (3, 21). Adrenal imaging with CT or magnetic resonance is typically performed after confirmation of the diagnosis. CT imaging reportedly has a sensitivity of 58–75% in detecting adrenal adenomas (26, 27). More recent literature suggests that high resolution CT scanning has a sensitivity approaching 80–85% in distinguishing between APA and BAH (28).
Most previous studies demonstrated superiority of AVS over CT scanning in correctly differentiating hyperaldosteronism. In experienced hands, AVS is highly accurate and rarely yields false positive or negative results. Direct comparison of the two methods in one study found only 67% sensitivity with CT imaging and 92% sensitivity using AVS (28). The same group did report one instance in which the AVS falsely suggested the presence of an APA. After adrenalectomy, PRA was persistently suppressed, and plasma aldosterone was elevated, indicating the presence of BAH (28). Another group reported a sensitivity of 70% with CT imaging and 96% with AVS in correctly determining the subtype of hyperaldosteronism (26). Gleason and colleagues determined the correct differential diagnosis of hyperaldosteronism and found 84% sensitivity with CT scanning and 92% sensitivity with AVS (29). Sheaves et al. advocate using CT alone for differentiation of primary aldosteronism based on the reported 100% sensitivity with that modality. They suggest reserving AVS for cases in which there are no adrenal abnormalities identified with CT scanning (30). On the other hand, another group recently found a high degree of inaccuracy with CT imaging. AVS altered management in one third of the cases in this study and was recommended for routine management of primary aldosteronism (31).
Patients with APA are thought to have more dramatic biochemical abnormalities and severe hypertension than patients with BAH (25). However, the present study found a surprising degree of overlap between these groups. The only statistically significant differences were lower plasma potassium and higher plasma aldosterone concentrations in the patients with APA compared with those with BAH. Thirty-seven percent of all patients and 52% of the patients with BAH had normokalemia. Based on these data, screening of patients suspected as having primary aldosteronism should be considered even in the presence of normokalemia.
We found no statistical difference between APA and BAH in control of blood pressure, PRA, Aldo/PRA ratio, or urinary aldosterone excretion rates. Furthermore, there was no particular cut-off level in these indices to separate one subtype of hyperaldosteronism from another. The lack of difference in biochemical features makes the determination of subtypes even more difficult.
Thirty-eight of 49 patients referred for selective catheterization had successful bilateral AVS (78%). Even though bilaterally successful adrenal vein catheterization was not achieved in 11 of 49 patients, interpretable data from unilateral AVS in 5 patients allowed determination of the subtype of primary aldosteronism. Therefore, 88% of patients who underwent AVS in our study had correct differentiation of hyperaldosteronism. Recently, investigators at the Mayo Clinic reported successful bilateral adrenal vein catheterization in 33 of 34 patients evaluated for primary aldosteronism (23). Other groups have reported successful bilateral AVS rates of 63% (32) and 75% (30), respectively, in evaluation of hyperaldosteronism.
We used a normalized aldosterone from each adrenal gland to correct for venous dilution from the right and left adrenal veins during AVS (27). A normalized aldosterone in the dominant divided by the nondominant adrenal gland of 4 or more was used to define the presence of APA or PAH. Fourteen of 15 patients met these criteria for APA. The remaining patient had a dominant to nondominant adrenal, normalized aldosterone ratio of 3.8, and was found to have an adenoma after adrenalectomy. Two patients with APA or PAH had contralateral normalized aldosterone levels equal to that in the IVC, indicating incomplete suppression of contralateral aldosterone production by the APA. In each of these cases, the dominant to nondominant aldosterone ratio was well above the diagnostic cut-point of 4, however. These 2 patients had improvement in blood pressure control and were eukalemic after adrenalectomy.
Doppman et al. used a dominant to nondominant normalized aldosterone ratio of 5 or greater to define APA (28). Young et al. found that 14 of 17 patients with APA had normalized aldosterone ratios of 5 or greater. The remaining 3 patients had normalized aldosterone ratios between 3 and 5 (23).
We found the ratio of dominant to nondominant normalized aldosterone was 4 or more in 3 of 21 patients with BAH, and this could be interpreted as consistent with presence of APA. However, these 3 patients each had nondominant normalized aldosterone levels greater than the corrected aldosterone in the IVC. This is consistent with bilateral autonomous aldosterone production with relative overproduction by 1 dominant adrenal gland. Three of the patients categorized as BAH underwent unilateral adrenalectomy based on slight lateralization of normalized aldosterone. Pathology confirmed the presence of adrenal hyperplasia in each case. Because these patients did not have an improvement in blood pressure after surgery, we retrospectively concluded that these patients did not have PAH, but, rather, BAH. Bilateral adrenalectomy would have had to be performed to actually prove this point.
Previous groups have recommended synthetic ACTH infusion before and during AVS to minimize the pulsatile variation in aldosterone release (17, 33). A potential weakness of the present study is that routine use of cosyntropin infusion during AVS was not instituted in our institution until 1996. Any patient who underwent AVS before that date did not receive cosyntropin infusion. However, the use of synthetic ACTH in the present study did not significantly improve the differentiation of hyperaldosteronism, contrary to previous reports (17, 33).
Fifty-five percent of the patients in this study had a final diagnosis of BAH, 40% had APA, and 5% had a diagnosis of PAH. None of the patients we evaluated had onset of hypertension in the first or second decade of life or a characteristic family history suggestive of glucocorticoid-remediable aldosteronism. Recent literature suggests that BAH accounts for 25–43% of all cases of primary aldosteronism (2, 30). PAH has been reported to represent 1–6% of all cases of hyperaldosteronism (18, 23, 34), and APA constitutes the majority. The higher percentage of patients with BAH in the current study may have been influenced by referral bias. Patients with an obvious unilateral adrenal nodule and dramatic features of primary aldosteronism may undergo adrenalectomy without having AVS or evaluation by an endocrinologist. On the other hand, bilateral adrenal hyperplasia may be recognized more frequently. This may be especially true if patients with milder forms of the disease, such as those with normokalemia, are properly screened for primary aldosteronism.
In this study CT imaging was concordant with pathology results after
adrenalectomy in two patients with APA who did not undergo AVS. CT
imaging was concordant with AVS in 5 of 11 patients who had
unilaterally successful catheterization and 12 of 38 patients who had
bilaterally successful AVS. This yields an accuracy of 37% overall for
CT scanning in the present study. Adrenal imaging with CT provided no
additional information or discordant findings in 68% of the patients
who underwent bilaterally successful AVS. The presence of a unilateral
adrenal nodule did not preclude a diagnosis of BAH in the present study
(patients 14, 17, and 19–21; Table 3). All of these patients could
have been mistakenly diagnosed with APA based on CT imaging, but AVS
indicated bilateral aldosterone production consistent with BAH. There
is no definable size criterion for unilateral adrenal nodules that
absolutely indicates the presence of APA. Despite improved resolution,
CT is an insensitive test to define the subtype of primary
aldosteronism in the majority of cases.
In conclusion, these results indicate that CT imaging is unreliable in the differentiation of primary aldosteronism. CT imaging has a discordance rate of 34% and can lead to improper therapy of hyperaldosteronism. For complete diagnostic certainty, AVS is essential to define the specific subtype of primary aldosteronism so that appropriate treatment can be recommended.
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Footnotes |
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Received November 11, 1999.
Revised June 8, 2000.
Revised November 15, 2000.
Accepted November 17, 2000.
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