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PubMed2007

[Diagnosis of primary hyperaldosteronism].

Primary hyperaldosteronism is the most common secondary form of hypertension. Diagnosis of this entity is recommended in hypokalemic hypertension, in therapy-resistant hypertension (at least three 3 drugs and RR > 140/90 mmHg), and in adrenal incidentalomas (= incidentally discovered adrenal tumors). For screening, the ratio between plasma aldosterone (PAC) and plasma renin concentration (PRC) should be measured. In the assessment of PAC/PRC ratio, the discontinuation of some antihypertensive medication and assay-specific cutoff values must be noticed. After a positive screening test, saline infusion test should be done as confirmatory test. In contraindications/impracticability of this test, 24-h urine collection for aldosterone-18-glucuronide under high-sodium diet can be used as alternative confirmatory test. After confirmation of primary hyperaldosteronism, differential diagnosis between aldosterone-producing adenoma and idiopathic hyperaldosteronism has to be done. For this approach, adrenal CT or MRT, posture test and adrenal vein catheterization as gold standard test are available. Whereas therapy of aldosterone-producing adenoma is surgery, idiopathic hyperaldosteronism is to be treated medically by spironolactone.

Adenoma↗
PubMed2006

[Modern pharmacological aspects of hyperaldosteronism therapy].

The prevalence of primary hyperaldosteronism is 5-10% of all hypertensive patients, and clearly above the estimated prevalence in the past. In nearly 30% of patients with therapy resistant hypertension, primary hyperaldosteronism is detected if they are investigated thoroughly. This will result in 1.5 to 2.5 million people in Germany suffering from primary hyperaldosteronism. Besides efficient diagnostic procedures, an effective treatment is of increasing importance. The aldosterone-producing adenoma (Conn's syndrome) is primarily cured by operation, in most cases performed endoscopically. Bilateral hyperplasia, which is found in two-thirds of primary hyperaldosteronism, is treated primarily by mineralocorticoid receptor antagonist: 12.5-50 mg/day spironolactone (in case of anti-androgenic side-effects alternatively by 50-100 mg/day eplerenone). If the blood pressure can not be lowered by this first-line treatment, an additional treatment with potassium-sparing diuretics, calcium-antagonists, ACE-inhibitors or angiotensin-2-antagonists is necessary. The start of medication should be closely monitored by serum electrolyte and creatinine controls.

Adrenal Hyperplasia, Congenital↗
PubMed1983

Reversal of diuretic-induced secondary hyperaldosteronism and hypokalemia by enalapril (MK-421): a new angiotensin-converting enzyme inhibitor.

The study reported here prospectively evaluated the prevention of diuretic-induced secondary hyperaldosteronism and hypokalemia by a converting enzyme inhibitor, enalapril (MK 421). Eighteen normal subjects were randomized into three groups: (1) a HCTZ group (hydrochlorothiazide (HCTZ) 50 mg/day); (2) a MK-421 group (MK-421 10 mg/day); and (3) a HCTZ + MK-421 group [HCTZ 50 mg/day plus MK-421 10 mg/day]. Following a five-day control and a 28-day treatment period, the HCTZ group demonstrated an attenuated but persistent secondary hyperaldosteronism and hypokalemia, the MK-421 group manifested a gradual decline in aldosterone secretion, and the HCTZ + MK-421 group had a delayed but effective correction of secondary hyperaldosteronism and hypokalemia at 28 days but not before. In conclusion, MK-421 reversed diuretic-induced secondary hyperaldosteronism and hypokalemia after 28 days of hydrochlorothiazide therapy. Therefore, converting enzyme inhibitors, such as enalapril, provide useful adjunctive therapy in diuretic-treated patients, but potassium supplementation may be required before the start of four weeks of combined therapy.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2006

Primary hyperaldosteronism associated with hypertensive emergencies.

There is growing awareness of primary hyperaldosteronism as a cause of secondary hypertension. Usually, it manifests as hypertension and hypokalemia, or as resistant hypertension. Much less often, primary hyperaldosteronism may be detected after a hypertensive emergency has developed. We highlight this association by reporting on eight patients with a clinical diagnosis of primary hyperaldosteronism whose course was complicated by a hypertensive crisis. In all patients, an elevated serum aldosterone, was accompanied by a suppressed plasma renin activity despite the presence of a hypertensive crisis. A good outcome was obtained either with laparoscopic adrenalectomy (1 patient) or with an antihypertensive drug regimen that included an antialdosterone agent (7 patients). The differential diagnosis of hypertensive emergencies should include primary hyperaldosteronism.

Acute Disease↗
PubMed2004

[Cardiac consequences of primary hyperaldosteronism].

The activation of the renin-angiotensin system is associated with vascular and cardiac hypertrophy. But there are few data on the renal and cardiac consequences of the hypersecretion of aldosterone. In the experimental setting, hyperaldosteronism leads to an excess of fibrous interstitial tissue and cardiac hypertrophy. In man, these consequences are those of hyperaldosteronism. The aim of this study was to assess the cardiac consequences of hyperaldosteronism in a series of 31 patients with a documented Conn adenoma, in comparison with a matched population of 31 patients with primary hypertension. For the same level of blood pressure, cardiac hypertrophy is more prominent in hyperaldosteronism and there is a positive correlation between the level of plasma aldosterone and left ventricular wall thickness. Left ventricular hypertrophy is of the concentric type. In addition, an increase in myocardial fibrosis (that can now be quantified by echocardiography) is observed, with a positive correlation between plasma aldosterone and reflected ultrasound which might correspond to increased myocardial collagen. These anatomic modifications of myocardial structure result in diastolic dysfunction. Overall, Conn adenoma is associated in accelerated disease, which is partly independent of the level of blood pressure.

Adenoma↗
PubMed1994

Restoration by corticosteroids of the hyperaldosteronism in hyponatraemic rats with panhypopituitarism.

1. In the syndrome of inappropriate secretion of antidiuretic hormone, hyponatraemia is associated with a normal bicarbonate concentration despite dilution. This normal bicarbonate concentration is related to the development of a hyperaldosteronism, which is attributed to a direct stimulation of the zona glomerulosa by the hyponatraemic state. Some workers have suggested that, to develop this hyperaldosteronism requires the presence of a pituitary factor. To determine whether the pituitary gland plays a role in this hyponatraemia-induced hyperaldosteronism, water intoxication was performed for 24 h in normal and in panhypopituitaric rats. 2. In normal rats, hyponatraemia (108 mmol/l), induced by the administration of 1-desamino-8-D-arginine vasopressin and 2.5% D-glucose-0.45% NaCl by gavage (15% body weight) was associated with a mild increase in bicarbonate concentration, and blood acid-base equilibrium showed a mixed metabolic and respiratory alkalosis (pH 7.57, partial pressure of CO2 29 mmHg, base excess +5.5 mmol/l), and aldosterone concentration was increased 3-fold as compared with the control value. When hyponatraemia (110 mmol/l) was induced in a similar manner in panhypopituitaric rats, we observed a very low aldosterone concentration (< 50 pg/ml) and a compensated respiratory alkalosis (pH 7.45, partial pressure of CO2 30 mmHg, base excess -2.6 mmol/l). The restoration of a hyperaldosteronaemic state in this group of rats was related essentially to corticosteroid intake. 3. These data suggest that corticosteroids play a critical role in the development of hyponatraemia-related hyperaldosteronism, a phenomenon not necessarily dependent on a pituitary factor.

Acid-Base Equilibrium↗
PubMed2000

Insulin action in primary hyperaldosteronism before and after surgical or pharmacological treatment.

The relationship between arterial hypertension and insulin resistance has long been established. We used primary hyperaldosteronism as a model of the relationship between secondary hypertension and insulin sensitivity. Our group consisted of 9 patients with arterial hypertension caused by primary hyperaldosteronism. Five of these patients with aldosterone producing adenoma were operated on and four patients with idiopathic hyperaldosteronism were treated with spironolactone. Hyperinsulinaemic euglycaemic clamp technique was performed before and at least 6 months following the treatment to evaluate the insulin action. Significantly lower glucose disposal rate (M), insulin sensitivity index (M/I) and decreased metabolic clearance rate of glucose (MCR(G)) were found in patients before treatment as compared to healthy controls. In both treated groups the blood pressure and plasma potassium concentrations returned to normal values, whereas plasma aldosterone levels were normalised only after surgical removal of the adenoma. Significantly improved insulin action (M/I: 30.2 +/- 5.9 vs. 51.4 +/-12.2 micromol.kg(-1).min(-1) per mU.l(-1) x 100, p = 0.017) was observed in patients after operation of aldosterone producing adenoma. In contrast, spironolactone treatment of patients with idiopathic hyperaldosteronism did not significantly influence insulin action (M/I: 24.5 +/- 7.3 vs. 18.7 +/- 7.6 micromol.kg(-1).min(-1) per mU.l(-1) x 100, p = 0.198). Since plasma aldosterone concentrations have been normalised only in patients after removal of the adenoma whereas they remained increased in spironolactone treated group, we suppose that aldosterone itself could play a role in the development of impaired insulin action.

Adenoma↗
PubMed1998

Establishment of an adrenocortical carcinoma xenograft with normotensive hyperaldosteronism in vivo.

We established a xenograft line of human adrenocortical carcinoma (ADR-1), and analyzed the hyperaldosteronism induced by the xenograft in vivo. Adrenocortical carcinoma specimens from a 25-year-old woman were subcutaneously inoculated into nude mice (BALB/c-nu/nu) followed by serial passages in vivo. ADR-1 retained the histopathological features (trabecular and sinusoid nests) seen in the primary carcinoma. The patient showed hyperaldosteronism (serum aldosterone >4000 pg/ml) and hypokalemia (serum K 2.1 mEq/l), but did not show hypertension. The nude rat (F344-rnu/rnu) bearing ADR-1 showed hyperaldosteronism (serum aldosterone 3320+/-1420 pg/ml; control 191+/-130 pg/ml) and hypokalemia (serum K 3.4+/-0.4 mEq/l; control 5.2+/-1.0 mEq/l) in vivo, and hypertension was not obvious. ADR-1 was shown immunohistochemically to retain production of human-specific corticosteroid synthetase. The xenograft ADR-1 will be useful to elucidate the regulatory mechanism of normotensive hyperaldosteronism.

Adrenal Gland Neoplasms↗
PubMed2006

Is primary hyperaldosteronism a risk factor for aortic dissection?

Primary hyperaldosteronism is a rare (<1%) and underdiagnosed cause of secondary hypertension. We present a case of aortic dissection in a patient with primary hyperaldosteronism. To our knowledge, there are six other reported cases of aortic dissection in patients with primary hyperaldosteronism. Our case strengthens the hypothesis that primary hyperaldosteronism is a potential independent risk factor for aortic dissection.

Aortic Dissection↗
PubMedDate not supplied

Primary hyperaldosteronism in childhood due to unilateral macronodular hyperplasia. Case report.

We present the first report of primary hyperaldosteronism in childhood due to unilateral macronodular hyperplasia. A 10-year-old white boy with severe hypertension (150/100 mm Hg), hypokalemia (1.4 mEq/liter), and suppressed plasma renin activity (PRA) (less than 0.1 ng/ml/hr) demonstrated fixed PRA and aldosterone (aldo) levels that did not change with alteration of dietary sodium. The paradoxical decrease in serum aldo on assumption of upright posture suggested a tumor. Prolonged ACTH administration produced a continuous rise in blood pressure, but a transient rise in aldo. A minimal decrease in urinary aldo during dexamethasone administration was noted, excluding dexamethasone-suppressible hyperaldosteronism. Blood pressure normalized with spironolactone. Computerized transaxial tomography, iodocholesterol scanning, and adrenal venography were not diagnostic of a discrete adrenal lesion. Although hyperplasia is more common than an adenoma as a cause of hyperaldosteronism in childhood, a tumor was predicted, since adrenal vein hormone sampling with ACTH stimulation lateralized aldosterone secretion unequivocally to the left adrenal gland. However, left adrenalectomy revealed macronodular hyperplasia. Postoperatively, there was reversal of hypertension, hypokalemia, and hyperaldosteronism. Thus, in childhood, unilateral hypersecretion of aldosterone may result from nodular hyperplasia, rather than a discrete adenoma.

Adrenal Glands↗
PubMed1978

Increased adrenal sensitivity to angiotensin II in idiopathic hyperaldosteronism.

Plasma aldosterone increases briskly during upright posture in patients with idiopathic hyperaldosteronism, despite only small increases in PRA and presumably small increases in angiotensin II. To examine the postulate that small increments in angiotensin II mediate these brisk increases in aldosterone, we infused graded doses of angiotensin II into normal subjects and patients with idiopathic hyperaldosteronism and compared the changes in levels of plasma aldosterone in the two groups. Supplemental sodium and dexamethasone were given before the infusion to minimize the influence of endogenous angiotensin II and ACTH. In response to the infusion of angiotensin II, increases in the levels of plasma aldosterone of patients with idiopathic hyperaldosteronism were significantly greater than those of normal subjects. In addition, levels of plasma aldosterone increased at a lower rate of infusion of angiotensin II in patients than in normal subjects. It is concluded that patients with idiopathic hyperaldosteronism have increased adrenal sensitivity to angiotensin II. This increased sensitivity may explain the brisk increases in aldosterone that occur during upright posture in these patients.

Adrenal Glands↗
PubMed1981

The plasma aldosterone response to angiotensin II infusion in aldosterone-producing adenoma and idiopathic hyperaldosteronism.

To determine if the adrenal sensitivity to angiotensin II in patients with an aldosterone-producing adenoma differs from that in patients with idiopathic hyperaldosteronism, we infused graded doses of angiotensin II into 17 patients with primary aldosteronism and measured their plasma aldosterone concentrations after each dose. At a rate of 0.5 ng angiotensin II/kg.min, the mean increase in the plasma aldosterone concentration in the 8 patients from whom an aldosterone-producing adenoma was subsequently removed was 4 +/ 2.4 ng/dl (mean +/- SE), which was significantly less (P less than 0.01) than the mean increase (23 +/- 4.8 ng/dl) in the 9 patients with idiopathic hyperaldosteronism. The threshold dose of angiotensin II in the patients with aldosterone-producing adenoma was 1.0 +/- 0.24 ng/kg.min, significantly greater (P less than 0.05) than the threshold dose (0.3 +/- 0.07 ng/kg.min) in the patients with idiopathic hyperaldosteronism. We conclude that the sensitivity of aldosterone-producing adenomas to angiotensin II is significantly less than that of the hypersecreting adrenal tissue in patients with idiopathic hyperaldosteronism. This difference in adrenal sensitivity might in part explain the difference in the response of plasma aldosterone concentrations to upright posture in these two subsets of aldosteronism with low renin activity.

Adenoma↗
PubMed1987

Long term evolution of glucocorticoid-suppressible hyperaldosteronism.

It is generally held that idiopathic hyperaldosteronism and glucocorticoid-suppressible hyperaldosteronism (GSH) are distinct entities, distinguishable by thorough investigation. We report a patient who presented in 1974 at age 15 yr with blood pressure of 240/120 mm Hg, serum K of 3.1 mM, low renin, and high normal aldosterone excretion, with findings diagnostic of GSH. After dexamethasone treatment (2 mg/day for 4 weeks), urinary aldosterone was undetectable (less than 1 microgram/24 h), associated with correction of hypertension and hypokalaemia. While untreated, plasma aldosterone increased in response to ACTH infusion at a dose that did not influence plasma cortisol. Plasma aldosterone at 0800 h while recumbent was higher than in subsequent samples taken while ambulant, consistent with ACTH dependence of aldosterone secretion. Blood pressure, renin, and potassium remained normal for 4 yr during treatment with dexamethasone (0.5-0.75 mg/day), but hypertension then slowly returned. After 7 yr, the original studies were repeated. Urinary aldosterone excretion was again in the high normal range after 3 weeks of no treatment, but both plasma renin and aldosterone consistently increased in response to upright posture. After dexamethasone treatment (2 mg/day) for 4 weeks, urinary aldosterone was not suppressed (excretion rate, 10.8, 9.2, and 5.7 micrograms/day; urinary Na, greater than 100 mmol/day; urinary cortisol, less than 1 microgram/day). At this time, dexamethasone did not alleviate hypertension or increase renin. Control of blood pressure has been readily achieved, 8-12 yr after diagnosis, with a low dose of beta-adrenergic antagonist and amiloride. Aldosterone remains incompletely suppressible during sodium loading, so that the findings now resemble those of idiopathic hyperaldosteronism. This sequence indicates that glucocorticoids may not permanently control hypertension in GSH. The transient dominance of ACTH in control of aldosterone secretion indicates that the relationship between GSH and idiopathic hyperaldosteronism merits further evaluation in long term studies.

Adolescent↗
PubMed1995

[The long-term administration of dexamethasone for the differentiation of the 4 types of hyperaldosteronism].

To elucidate the significance of long-term administration of dexamethasone in order to differentiate the 4 types of hyperaldosteronism, blood pressure, serum electrolytes, plasma renin activity (PRA) and diurnal rhythm of plasma aldosterone (PAC) were studied before and after long-term dexamethasone (Dex) administration in patients with aldosterone-producing adenoma (APA), idiopathic hyper aldosteronism (IHA), unilateral adrenal hyperplasia (UAH) and Dex suppressible hyperaldosteronism (DSH). The results were as follows: 1) In APA with ACTH-dependent aldosterone secretion, long-term Dex administration induced a significant depression of PAC associated with an elevation in serum potassium (s-K). In almost all patients with APA, the diurnal rhythm of PAC, parallel to that of ACTH, completely disappeared following Dex administration. 2) In most patients with IHA, PAC was mainly influenced by the renin-angiotensin system. Dex did not affected on s-K, but it induced a slight decrease in PAC in some patients with IHA. 3) In UAH having similar pathophysiological findings of the adrenal cortex as IHA, Dex decreased PAC. 4) In DSH, Dex at a dose of 6 mg/day decreased PAC to normal value in association with normalization of blood pressure and s-K. From these results, hyperaldosteronism inducing a decrease in PAC and an increase in s-K by Dex is possibly diagnosed as APA, while the patients with no change of s-K by Dex may be diagnosed as IHA. Even if PAC is suppressed with Dex and ACTH-independent, the hyperaldosteronism may be UAH. It may be possible that factors other than aldosterone are important to induce hypokalemia in patients with IHA. Furthermore, it is suggested that UAH is a precedent pathophysiological condition of aldosterone-producing adenoma in the adrenal cortex. It is concluded that the measurement of s-K and diurnal rhythm of PAC before and after Dex administration are useful for discriminating APA and IHA.

Adrenocorticotropic Hormone↗
PubMed1992

Urinary excretion of 19-noraldosterone, 18, 19-dihydroxycorticosterone and 18-hydroxy-19-norcorticosterone in patients with aldosterone-producing adenoma or idiopathic hyperaldosteronism.

Urinary excretion of 19-noraldosterone, 18. 19-dihydroxycorticosterone (18, 19(OH)2-B), 18-hydroxy-19-norcorticosterone (18-OH-19-nor-B), 18-hydroxycorticosterone (18-OH-B), 18-hydroxycortisol (18-OH-F) and aldosterone were measured in 25 patients with primary aldosteronism, 16 with an aldosterone-producing adenoma and 9 with idiopathic hyperaldosteronism. In patients with idiopathic hyperaldosteronism, urinary 19-noraldosterone (207 +/- 51 pmol/day), 18, 19(OH)2-B (21 +/- 4.2 nmol/day) and 18-OH-19-nor-B (879 +/- 213 pmol/day) levels were lower but not significantly different from 19-noraldosterone (263 +/- 56 pmol/day), 18, 19(OH)2-B (40 +/- 8.7 nmol/day) and 18-OH-19-nor-B (1322 +/- 267 pmol/day) seen in patients with aldosterone-producing adenoma. Urinary aldosterone did not differ significantly between patients with idiopathic hyperaldosteronism and those with aldosterone-producing adenoma. Both urinary 18-OH-B and 18-OH-F excretion were significantly higher in aldosterone-producing adenoma (39 +/- 5.2 nmol/day, 1660 +/- 318 nmol/day, respectively) compared with patients with idiopathic hyperaldosteronism (19 +/- 3.3 nmol/day, 541 +/- 93 nmol/day, respectively) (p less than 0.05). Though urinary 18-OH-F and 18-OH-B concentrations were useful markers, the mineralocorticoid steroids which we can only now measure, 19-noraldosterone, 18, 19(OH)2-B and 18-OH-19-nor-B, could not be used to distinguish the two subsets of primary aldosteronism.

18-Hydroxycorticosterone↗
PubMed1996

Relative value of computed tomography scanning and venous sampling in establishing the cause of primary hyperaldosteronism.

The purpose of this study was to evaluate the relative merits of the postural stimulation test, adrenal computed tomography (CT) and venous sampling in the differential diagnosis of patients presenting with primary hyperaldosteronism. The records of 20 patients presenting with primary hyperaldosteronism were reviewed retrospectively. There were 15 patients with a unilateral aldosterone-producing adenoma (APA), four patients with idiopathic hyperaldosteronism (IHA) and one patient with primary adrenal hyperplasia (PAH). The postural stimulation test was based on measurements of plasma aldosterone and renin activity at 08.00 h and at noon after 4 h of ambulation. The CT scans of the adrenals were reviewed by a single radiologist. Bilateral venous sampling of adrenal veins was attempted in all patients and blood collected for aldosterone and cortisol assay. Plasma aldosterone concentration increased after 4 h of standing in all cases of hyperplasia but was also demonstrated in 10/15 patients with a surgically-proven APA. If one defines a significant postural rise as being greater than 30%, then 8/15 patients with APA can be considered as being posturally responsive. Computed tomography scanning correctly identified all 15 cases of APA and also classified correctly the remaining five cases of hyperplasia (four cases of IHA and one case of PAH). Venous sampling failed technically in 4/15 cases of APA and in one case of IHA: a total of 5/20 (25%,). A correct diagnosis of APA or IHA was established in all the remaining cases. However, the one case of PAH was treated successfully by adrenalectomy following venous sampling, which suggested a unilateral adrenal lesion: this one result was the only instance where venous sampling altered clinical decision-making. Computed tomography scanning may be used alone to confirm the cause of hyperaldosteronism where postural studies suggest an adrenal adenoma, and such patients may be considered for early surgery. Venous catheterization studies are not necessary routinely. but may still be useful in selected patients, particularly when CT scanning shows no clear lesion.

Adenoma↗
PubMed2005

The utility of three different methods for measuring urinary 18-hydroxycortisol in the differential diagnosis of suspected primary hyperaldosteronism.

OBJECTIVE: Urine 18-hydroxycortisol (18-OHF) measurements are claimed to discriminate between primary hyperaldosteronism due to Conn's syndrome/adrenal adenoma or idiopathic bilateral adrenal hyperplasia (BAH), and also to identify cases of glucocorticoid-suppressible hyperaldosteronism (GSH). We have evaluated three urine 18-OHF methods using a panel of urine samples from patients with hypertension. DESIGN: Clinical methods comparative study. METHODS: Urine samples from patients with primary hyperaldosteronism due to either adenoma (n = 6), BAH (n = 6), GSH (n = 9), or essential hypertension (n = 38) were analysed without knowledge of the diagnosis using three different methods in different laboratories. These included 'in-house' radioimmunoassay (RIA), 'in-house' time-resolved fluorometric assay (DELFIA), and gas chromatography mass spectrometry (GC-MS). RESULTS: The three assays showed good correlation, but there were large bias differences: RIA bias was greater than DELFIA which was greater than GC-MS. Discrimination between adenoma and BAH patients was best for the DELFIA method, with no overlap between results for these two groups. All three methods gave significantly elevated results for the GSH group compared with the BAH and essential hypertension groups. No assay distinguished BAH from essential hypertension. CONCLUSION: Measurement of urine 18-OHF may be a useful additional test in the differential diagnosis of primary hyperaldosteronism. The clinical diagnostic value of urinary 18-OHF measurements is method-dependent with the DELFIA assay having the best discriminatory value.

Adenoma↗
PubMed2003

CT of primary hyperaldosteronism (Conn's syndrome): the value of measuring the adrenal gland.

OBJECTIVE: The objectives of our study of patients with primary hyperaldosteronism (Conn's syndrome) were to determine whether the adrenal glands are larger in patients with bilateral adrenal hyperplasia than in those with aldosterone-producing adenomas or in healthy control subjects; and whether a CT criterion based on adrenal gland size can be developed to positively diagnose bilateral adrenal hyperplasia. MATERIALS AND METHODS: A retrospective study of CT scans of 28 patients with primary hyperaldosteronism was performed. The means of two observers' measurements of adrenal gland size were recorded and compared with published normal values. In addition, a radiologist experienced in adrenal imaging and unaware of the cause of the primary hyperaldosteronism diagnosed either bilateral adrenal hyperplasia or aldosterone-producing adenoma by visual inspection. RESULTS: The adrenal glands in patients with bilateral adrenal hyperplasia were significantly (p < 0.05) larger than those in patients with aldosterone-producing adenoma or in healthy control subjects. A sensitivity of 100% was achieved when a mean limb width of greater than 3 mm was used to diagnose bilateral adrenal hyperplasia, and a specificity of 100% was achieved when the mean limb width was 5 mm or greater. Receiver operating characteristic curve analysis showed that the overall performance of the radiologist and the mean adrenal limb width in detecting bilateral adrenal hyperplasia were equivalent. CONCLUSION: In patients with primary hyperaldosteronism, adrenal limb measurements on CT can aid in differentiating bilateral adrenal hyperplasia from aldosterone-producing adenoma because the adrenal glands in bilateral adrenal hyperplasia are larger.

Adrenal Glands↗