World J. Surg. 22, 418–422, 1998WORLDJournal of

SURGERY© 1998 by the Societe

Internationale de Chirurgie

Adrenalectomy for Primary Aldosteronism: Long-term Follow-up Study in29 Patients

Jukka Siren, M.D.,1 Matti Valimaki, M.D.,2 Kauko Huikuri, M.D.,1 Arto Sivula, M.D.,1 Petri Voutilainen, M.D.,1

Reijo Haapiainen, M.D.1

1Department of Surgery, Helsinki University Central Hospital, Haartmaninkatu 4, SF-00290 Helsinki, Finland2Department of Medicine, Helsinki University Central Hospital, Haartmaninkatu 4, SF-00290 Helsinki, Finland

Abstract. Primary aldosteronism consists of a mixture of subgroups. Theoperative treatment is successful only in cases of aldosterone-producingneoplasia (and in rare cases of primary unilateral hyperplasia); all othercases should be treated medically. The aim of this study was to determineif aldosterone-producing neoplasia had been successfully differentiatedfrom the other subgroups and the outcome of operative treatment.Altogether 29 patients with primary aldosteronism were operated onbetween January 1, 1979 and December 31, 1993. Patient charts werereviewed retrospectively. The follow-up data were collected from thepatients’ charts, and all patients were contacted to obtain recent bloodpressure and serum potassium values. The patients were asked aboutsymptoms related to hyperaldosteronism. If any suspicion of recidivealdosteronism was present, patients were carefully reexamined by hor-monal tests and computed tomography (CT). A total of 27 patients hadunilateral adenoma, 1 patient had hyperplasia, and 1 patient had analdosterone-producing cortical carcinoma. There was no operative mor-tality or morbidity. The serum potassium level had normalized in allpatients. Mean follow-up time was 76 months. One patient died duringthe follow-up from cholangiocarcinoma; 11 patients (41%) were cured bythe operation, 10 patients (37%) have a mild but medicated hypertension,and in the remaining 22% the hypertension persisted but was wellcontrolled by the medication. Of the 29 patients, 28 were correctlydiagnosed as having an aldosterone-producing neoplasm. Basic hormonalstudies and CT can be used effectively to differentiate aldosterone-producing neoplasia from hyperplasia in most cases.

Primary aldosteronism is a syndrome characterized by hyperten-sion, hypokalemia, suppressed plasma renin activity, and elevatedserum aldosterone levels. Conn first described it 1955 [1] inassociation with adrenal cortical adenoma (Conn syndrome). Nowwe know that primary aldosteronism can be divided into at leastsix distinctive subgroups: aldosterone-producing adenoma (60–80%), aldosterone-producing adrenocortical carcinoma (1%), bi-lateral adrenocortical hyperplasia (idiopathic hyperaldosteron-ism) (20%), glucocorticoid-remediable hyperaldosteronism (,1%),renin-responsive adrenocortical adenoma (,,1%), and primaryadrenocortical hyperplasia (,,1%) [2]. Some authors also add aseventh group, “indeterminate aldosteronism,” for those rarepatients for whom the diagnosis remains uncertain. Primaryaldosteronism accounts for around 1% of all hypertensive patients[3, 4]. Operative treatment is the treatment of choice for primary

hyperaldosteronism caused by an aldosterone-producing neopla-sia (adenoma or carcinoma). Medical treatment with aldosteroneantagonists (spironolactone) seems better in most cases of hyper-plasia [3, 5]. The aim of the present study was to determine ifpreoperative diagnosis of surgically correctable aldosteronism wasaccurate and to analyze the effect of operation on hyperaldoste-ronism-related symptoms and signs in patients suspected to haveprimary aldosteronism caused by an aldosterone-producing neo-plasia.

Materials and Methods

At Helsinki University Central Hospital, from January 1979through December 1993, a total of 29 patients with primaryaldosteronism were operated on. Primary aldosteronism wassuspected in hypertensive patients with hypokalemia, inappropri-ately high urinary excretion of potassium (.30 mmol/24 hr), andsuppressed plasma renin activity together with a normal or highserum aldosterone level. When appropriate hyperaldosteronismwas ascertained by showing high urinary excretion of aldosterone(.13 nmol/24 hr) during volume load [6]. The indication foroperative treatment was a suspicion of aldosterone-producingneoplasia (adenoma) in all cases. The distinction between unilat-eral neoplasia and bilateral hyperplasia was made using computedtomography (CT) (n 5 29), 131l-6-b-iodomethyl norcholesterolscan (n 5 13) with dexamethasone suppression, and a posturaltest during volume load (n 5 18) [6]. Venography or adrenalvenous sampling were not used.

Patients’ charts were reviewed retrospectively and the relevantdata collected. The follow-up data were obtained from thepatients’ charts and by a letter (and if necessary by a telephonecall) to the patient and to the patient’s primary physician. Onepatient had died, and the cause of death was verified from thenational register of death causes. If recent blood pressure andserum potassium measurements were not available, the patientwas instructed to obtain them, and the values were recorded. Thepatient was reexamined if any indication of persistent hyperaldo-steronism was present (CT and postural test during volume load).

Because no systematic analysis of symptoms had been per-Correspondence to: J. Siren, M.D.

formed preoperatively, all patients were asked to report theirpreoperative symptoms and the symptoms they had after theoperation. The symptoms asked about were headache, weakness,fatigue, nocturia, polydipsia, chest pain, numbness, and musclecramps.

The results were analyzed statistically. The paired t-test wasused to compare pre- and postoperative blood pressures andserum potassium levels. McNemars test was used to comparepreoperative with postoperative symptoms. Conventional regres-sion analysis was used to determine if the duration of hyperten-sion was associated with the postoperative blood pressure.

Results

Altogether 29 patients with primary aldosteronism were operatedon; 18 were women (62%), and 11 were men. The mean age was48 years (range 29–71 years). All patients were hypertensive, andall but one had a low serum potassium level (mean 2.9 mmol/L,range 2.2–3.6 mmol/L). The hypertension was generally not ingood control. The mean duration of hypertension was 105 months(range 1–360 months). The finding that primarily had led to thesuspicion of primary aldosteronism was poorly controlled hyper-tension with low serum potassium in most cases. Clinical symp-toms, such as headache, weakness, and fatigue, were cited as theleading indication for hormonal analysis in only two cases, al-though these patients also had hypertension and hypokalemia.There was a statistically significant difference between the re-ported symptoms preoperatively and postoperatively only forheadache (p 5 0.003).

The postural test during volume load could be reliably inter-preted in 18 cases. There was a clear decline in plasma aldoste-rone level (a finding suggestive of adenoma) from 8 a.m./recum-bent to 12 p.m./supine in 16 cases (15 adenomas, 1 adenoma withmicronodular hyperplasia). The result was inconclusive in onecase (adenoma), and the plasma aldosterone level increased (afinding suggestive of hyperplasia) in 1 case (adenoma).

The CT scan was done and localized the tumor in every case.131I-6-b-Iodomethyl-norcholesterol scan with dexamethasonesuppression was used in 13 cases (all solitary adenomas), and thelocalization was accurate in 12 cases (92%). In one case there wasa bilateral take-up. A tumor was seen by CT on the left side andat operation the left adrenal was removed; the right gland wasbiopsied even though macroscopically normal. The left adrenalcontained an adenoma; the biopsy of the right adrenal wasmicroscopically normal. This patient was cured by the operation.

Twenty-five patients were operated on via anterior laparotomy,three patients via lumbotomy, and one patient via dorsal incision.Twenty-five patients had a unilateral solitary adenoma withotherwise normal adrenal histology. The mean size of the adeno-mas was 15 mm (range 8–32 mm). Fourteen adenomas were onthe left side and eleven on the right. One patient had analdosterone-producing cortical carcinoma, 11 cm in diameter,with no lymph node involvement or distant metastases. Onepatient had macronodular hyperplasia. The largest nodule (10mm) was seen on CT; the contralateral gland appeared normal onCT and at laparotomy. Two patients had an encapsulated ade-noma (15 and 25 mm in diameter) but also micronodular hyper-plasia. In one of these cases a hormonal analysis of culturedadrenal cells had been carried out, and only the adenoma cells

produced aldosterone. The cells of micronodular hyperplasiawere inactive.

There were no operative or postoperative complications ormortality. The serum potassium level was normalized in allpatients during the first postoperative week. The blood pressurelevels at the time of discharge (mean 140/90 mmHg) weresignificantly lower than preoperatively (mean 183/113 mmHg)(p , 0.001). Only three patients had a diastolic blood pressure.100 mmHg, although the effect could be partly due to periop-erative antihypertensive treatment.

The mean follow-up time was 76 months (range 9–154 months).One patient died during the follow-up period, 21 months postop-eratively, owing to cholangiocarcinoma with distant metastases.The patient operated for the adrenocortical carcinoma has mildmedicated hypertension and has no signs of recurrent disease 36months postoperatively. The effect of the operation on hyperten-sion in 27 living patients with benign disease was estimated by thepatient and her or his doctor at the end of the follow-up. Thehypertension was totally cured, and no antihypertensive medica-tion was needed in 11 cases (41%). In 10 cases (37%) thehypertension after the operation was mild and responded well tomedication. In the remaining 6 cases (22%) the blood pressurevalues did not respond to the operation, although the hyperten-sion is better controlled by the medication. The duration ofpreoperative hypertension did predict the outcome of surgery(Fig. 1), although the difference between groups 2 and 3 is notclear.

In two patients (solitary adenomas) the serum potassium leveldropped below normal during the follow-up (3.4 and 3.5 mmol/L).One of them was reexamined 8 years after the operation, but alltest results were normal (urine aldosterone 52 nmol/24 hr, plasmarenin 0.8 mg/L/hr), and no signs of recidive hyperaldosteronismcould be found. The remaining adrenal gland appeared normal onCT examination. The other patient was reexamined 116 monthspostoperatively. CT examination of the remaining gland wasnormal, and hormonal studies were all normal (in postural testsduring volume loading: urine aldosterone 4 nmol/24 hr; plasmarenin at 08:00 a.m. 0.3 mg/L/hr and at 12:00 p.m. 0.6 mg/L/hr;serum aldosterone at 8:00 a.m. and 12:00 a.m. 132 pmol/L and 159pmol/L, respectively). There were no signs of persistent hyperal-dosteronism.

Discussion

Having first described primary aldosteronism in 1955 [1] Conn etal. published a series of 145 cases in 1964 [7] and suspected theprevalence of primary aldosteronism in the hypertensive popula-tion to be as high as 20% [8]. Today the generally acceptedprevalence among hypertensive patients is less than 1% [3, 4],although a prevalence as high as 2.2% has been reported [9]. Themost recent studies in Australia among hypertensive normokale-mic population suggest that the incidence of primary aldosteron-ism could be as high as 10% [10].

The main issues in the evaluation of primary aldosteronism areto differentiate adenomas from hyperplasia and to localize ade-nomas. Glucocorticoid suppressible hyperaldosteronism is rareand typically diagnosed in young adults with a family history ofhypokalemia-associated hypertension [11]. It is identified by adexamethasone suppression test and, if found, treated by glu-cocorticoids. Renin-responsive adrenocortical adenoma has been

Siren et al.: Adrenalectomy for Aldosteronism 419

considered to be a rare disease; but this might not be the case, andrenin-responsive adenoma could be a common finding among thehypertensive normokalemic population [10]. Primary adrenocor-tical hyperplasia is a rare condition [2].

Operative treatment is curative for aldosterone-producing ad-enomas (and for renin-responsive adenomas), but patients withbilateral adrenal hyperplasia are generally best treated withspironolactone. Hypokalemia, alkalosis, plasma aldosterone, andsuppression of plasma renin seem to be greater in patients withadenomas, and this feature has been used successfully in math-ematic analysis to distinguish between adenoma and hyperplasia[12]. We have not used this method.

The aldosterone secretion of adenomas is sensitive to adreno-corticotrophic hormone (ACTH), unlike aldosterone secretionfrom hyperplastic adrenocortical tissue, which is regulated by therenin-angiotensin axis. ACTH excretion follows a circadianrhythm, where the ACTH level (and in case of an adenoma thealdosterone level as well) is decreased during the forenoon [13].This fall in plasma aldosterone level can be shown by measuringits concentration at 8 a.m. after overnight recumbency and atnoon after 4 hours of ambulation. The accuracy of this posturaltest is about 75% in collected literature [14], and in our series itwas accurate in 89%. The postural test is negative not only inpatients with hyperplasia but also in patients with renin-sensitive

cortical adenomas, which can be a diagnostic problem if theincidence of these adenomas is as high as recently suggested [10].

In skillful hands the most accurate test differentiating adeno-mas from hyperplasia is selective adrenal venous sampling foraldosterone measurement [15]. It is invasive, the technique isdifficult, and the failure rate for catheterization of the rightadrenal vein is 26% [5]. Hence it is not used widely. Venoussampling is also the best test for localizing aldosterone-producingadenomas. CT seems also to be accurate, with a sensitivity of 88%,specificity of 83%, and accuracy of 86% [16].

Doppman et al. compared the efficacy of CT and adrenalvenous sampling in a series of 24 patients [17] and reported thatvenous sampling was significantly more sensitive (100% vs. 71%)and specific (67% vs. 33%) than CT. The most common error wasdiagnosis of hyperplasia based on the presence of bilateralnodules on CT scans.

In our series all adenomas were correctly localized with CT,although a hyperplastic nodule gave a false-positive result in onecase. This patient with macronodular hyperplasia may representthe rare unilateral hyperplasia. However, we do not know if someadenomas were missed owing to the limitations of CT. Iodocho-lesterol scintigraphy during dexamethasone inhibition can also beused, but it does not seem to have advantages over CT scans, andthe accuracy is 72% to 92% [5]. Magnetic resonance imaging(MRI) has also been used as a localization method but has notbeen better than CT [5]. Despite of the limitations of thesensitivity and specificity of CT, we continue to use it as a primarylocalization method and consider a unilateral adrenal mass to bean indication for operative treatment.

The treatment of choice for patients with aldosterone-produc-ing adenoma is laparoscopic unilateral adrenalectomy [18, 19].Adrenalectomy through the posterior approach was the methodof choice before laparoscopic surgery came into wide use and canstill be used by surgeons not familiar with laparoscopic methods.The anterior approach (laparotomy) should be avoided because itseems to increase the duration of the hospital stay, morbidity, andmortality [20].

In the collected literature, calculated from 694 cases [5], thelong-term cure rate of operatively treated aldosterone-producingadenomas was 69%. Most patients have improved blood pressurecontrol after operation. In our series 41% were without antihy-pertensive medication, and 37% had a mild hypertension wellcontrolled by mild medication. The blood pressure level in theremaining 22% did not decrease but is better controlled bymedication. The long duration of the hypertension preoperativelyis believed to cause adaptive and irreversible vascular changes thatmaintain hypertension [21]. The present study shows that theduration of hypertension can predict the outcome of surgery tosome extent, but there is considerable overlap between thegroups. Obara et al. estimated the risk factors for postoperativepersistent hypertension by univariate analysis in 100 patients [22].They showed that only age and sex, and not the duration ofhypertension, were independent risk factors. The serum potas-sium level normalizes in almost all cases.

Conclusions

The diagnosis of primary aldosteronism is usually suspected whenthe patient presents with poorly controlled hypertension withhypokalemia. Symptoms related to hyperaldosteronism are non-

Fig. 1. Duration of hypertension (years) vs. operative result. Estimate ofmedian (Wilcoxon method), 95% confidence interval. 1: no hypertension;2: mild hypertension; 3: persisting hypertension.

420 World J. Surg. Vol. 22, No. 4, April 1998

specific and seldom suggest the diagnosis. When the diagnosis ofprimary aldosteronism is established, aldosterone-producing ade-nomas and idiopathic hyperplasia must be distinguished. CT canbe used as the primary examination; and if a clear unilateral mass($1 cm) is found, no further evaluation is indicated. Laparoscopicunilateral adrenalectomy is then performed. If both adrenals havenodules, venous sampling may be used to rule out unilateraladenoma. If no lateralization is found, the patient is considered tohave idiopathic hyperplasia and is treated medically, usually withspironolactone. Hypertension is cured or better controlled by theoperative treatment in most cases. The duration of hypertensionpredicts the outcome in some extent. The serum potassium levelnormalizes in almost all cases.

References

1. Conn, J.W.: Presidential address. Part I. Painting the background.Part II. Primary aldosteronism, a new clinical syndrome. J. Lab. Clin.Med. 43:3, 1955

2. Irony, I., Kater, C.E., Biglieri, D.G., Shackleton, C.H.L.: Correctablesubsets of primary aldosteronism: primary adrenal hyperplasia andrenin responsive adenoma. Am. J. Hypertens. 3:576, 1990

3. Scoggins, B.A., Coghlan, J.P.: Primary hyperaldosteronism. Pharma-col. Ther. 9:367, 1980

4. Berglund, G., Andersson, O., Wilhelmsen, L.: Prevalence of primaryand secondary hypertension: studies in a random population sample.B.M.J. 2:554, 1976

5. Young, W.F., Hogan, M.J., Klee, G.G., Grant, C.S., van Heerden,J.A.: Primary aldosteronism: diagnosis and treatment. Mayo Clin.Proc. 65:96, 1990

6. Vaughan, N.J.A., Jowett, T.P., Slater, J.D.H., Wiggins, R.C., Light-man, S.L., Ma, J.T.C., Payne, N.N.: The diagnosis of primary hyper-aldosteronism. Lancet 1:120, 1981

7. Conn, J.W., Knopf, R.F., Nesbit, R.M.: Clinical characteristics ofprimary aldosteronism from an analysis of 145 cases. Am. J. Surg.107:159, 1964

8. Conn, J.W.: Plasma renin activity in primary aldosteronism. J.A.M.A.190:222, 1964

9. Streeten, D.H.P., Tomycz, N., Andersson, G.H.: Reliability of screen-

ing methods for the diagnosis of primary aldosteronism. Am. J. Med.67:403, 1979

10. Gordon, R.D., Stowasser, M., Tunny, T.J., Klemm, S.A., Rutherford,J.C.: High incidence of primary aldosteronism in 199 patients referredwith hypertension. Clin. Exp. Pharmacol. Physiol. 21:315, 1994

11. Giebink, E.S., Gotlin, R.W., Biglieri, E.G., Katz, F.H.: A kindred withfamilial glucocorticoid suppressible aldosteronism. J. Clin. Endocri-nol. Metab. 36:715, 1973

12. Aitchison, J., Brown, J.J., Frazer, R., Kay, A.W., Lever, A.F., Neville,A.M., Symington, T., Robertson, J.I.S.: Quadric analysis in thepreoperative distinction between patients with and without adreno-cortical tumors in hypertension with aldosterone excess and lowplasma renin. Am. Heart J. 82:660, 1971

13. Schambelan, M., Brust, N.L., Chang, B.C.F., Slater, K.L., Biglieri,E.G.: Circadian rhythm and effect of posture on plasma aldosteroneconcentration in primary aldosteronism. J. Clin. Endocrinol. Metab.43:115, 1976

14. Granberg, P.O., Adamson, U., Cohn, K.H., Hamberger, B., Lins, P.E.:The management of patients with primary aldosteronism. WorldJ. Surg. 6:757, 1982

15. Doppman, J.L., Gill, J.R., Jr.: Hyperaldosteronism: sampling theadrenal veins. Radiology 198:309, 1996

16. Ikeda, D.M., Francis, I.R., Glazer, G.M., Amendola, M.A., Gross,M.D., Aisen, A.M.: The detection of adrenal tumors and hyperpla-sia in patients with primary aldosteronism: comparison of scintig-raphy, CT, and MR imaging. A.J.R. Am. J. Roentgenol. 153:301,1989

17. Doppman, J.L., Gill, J.R., Jr., Miller, D.L., Chang, R., Gupta, R.,Friedman, T.C., Choyke, P.L., Feuerstein, I.M., Dwyer, A.J., Jicha,D.L., Walther, M.M., Norton, J.A., Linehan, W.M.: Distinctionbetween hyperaldosteronism due to bilateral hyperplasia and unilat-eral aldosteronoma: reliability of CT. Radiology 184:677, 1992

18. Prinz, R.A.: A comparison of laparoscopic and open adrenalectomies.Arch. Surg. 130:489, 1995

19. Horgan, S., Sinanan, M., Helton, S., Pellegrini, C.A.: Use of laparo-scopic techniques improves outcome from adrenalectomy. Am. J.Surg. 173:371, 1997

20. Russell, C.F., Hamberger, B., van Heerden, J.A., Edis, A.J., Ilstrup,D.M.: Adrenalectomy: anterior or posterior approach? Am. J. Surg.144:322, 1982

21. Folkow, B.: Physiological aspects of primary hypertension. Physiol.Rev. 62:347, 1982

22. Obara, T., Ito, Y., Fujimoto, Y.: Textbook of Endocrine Surgery.Philadelphia, Saunders, 1997

Invited Commentary

William F. Young, Jr., M.D.

Division of Endocrinology, Metabolism, and Internal Medicine, Schoolof Medicine, Mayo Clinic, Rochester, Minnesota, USA

Siren and colleagues focus on two major issues: (1) the efficacy ofadrenal computed tomography (CT) for subtype evaluation ofprimary aldosteronism, and (2) the long-term cure rate of hyper-tension following surgery for aldosterone-producing adenomas(APAs) detected by CT. For the last 40 years much debate andcontroversy have surrounded the optimal diagnostic approach tothe subtype evaluation in primary aldosteronism [1–3]. During thelast decade of this century it has become clear that, beyondhistorical interest, there are limited or nonexistent roles for many oftests that have been default standards for subtype evaluation (e.g.,[6b-131I]iodomethyl-19-norcholesterol scintigraphy, posture stimula-tion test, and serum 18-hydroxycorticosterone concentration) [4].

Today, subtype evaluation of primary aldosteronism may re-quire one or more tests, the first of which is imaging the adrenalwith CT. The report from Siren and colleagues supports theapproach that when a solitary unilateral macroadenoma (. 1 cm)and normal contralateral adrenal morphology are found on CT ina patient with primary aldosteronism, unilateral adrenalectomy isa reasonable therapeutic option. Adrenal CT can accuratelydiagnose APAs that are macroadenomas.

However, Siren and colleagues did not address the large groupof patients with primary aldosteronism with ambiguous findingson adrenal CT. CT imaging may reveal normal-appearing adre-nals, minimal unilateral adrenal limb thickening, unilateral mi-croadenomas (# 1 cm), or bilateral macroadenomas. In thesecases additional testing is required to determine the source ofexcess aldosterone secretion. Small APAs may be labeled incor-rectly as idiopathic hyperaldosteronism (IHA) on the basis of CTfindings of bilateral nodularity or normal-appearing adrenals [5].Also, apparent adrenal microadenomas may represent areas ofhyperplasia, and unilateral adrenalectomy would be inappropriate[6]. Patients with APAs have more severe hypertension, more

Siren et al.: Adrenalectomy for Aldosteronism 421

profound hypokalemia (, 3.0 mEq/L), higher plasma (. 25 ng/dl) and urinary (. 30 mg/24 hr) levels of aldosterone, and youngerage (, 50 years) than those with IHA [2]. Patients fitting thesedescriptors are considered to have a “high probability of APA.”Improved methods and advances in catheter technology havegreatly enhanced the overall success rate of adrenal venoussampling [7]; we have found a unilateral APA in 36% of thosewith clinically “high probability” APA who had normal findings orunilateral adrenal limb thickening on CT [8].

The treatment goal in patients with primary aldosteronism is toprevent morbidity and mortality associated with hypertension andhypokalemia. The cause of the primary aldosteronism determinesthe appropriate treatment. Siren and colleagues found a hyper-tension cure rate of 41% and a major improvement in bloodpressure control in 37% of patients. The persistent hypertensionfollowing unilateral adrenalectomy for APA was correlated in partwith the duration of hypertension. Age has also been shown to bea predictor of cure of hypertension following unilateral adrenal-ectomy [9]. This type of information is useful when deciding whichpatients are the best candidates for surgery.

In conclusion, Siren and colleagues confirm the concept thatadrenal CT is a reasonable initial test for subtype evaluation ofprimary aldosteronism. When a unilateral adrenal macroadenomais found with CT, ipsilateral adrenalectomy can cure or markedlyimprove the hypertension in approximately 78% of patients.Patients who have a high probability of APA based on clinicalpredictors and lack a macroadenoma on adrenal CT should beconsidered for adrenal venous sampling.

References

1. Sheaves, R., Goldin, J., Reznek, R.H., Chew, S.L., Dacie, J.E., Lowe,D.G., Ross, R.J., Wass, J.A., Besser, G.M., Grossman, A.B.: Relativevalue of computed tomography scanning and venous sampling inestablishing the cause of primary hyperaldosteronism. Eur. J. Endocri-nol. 134:308, 1996

2. Melby, J.C., Spark, R.F., Dale, S.L., Egdahl, R.H., Kahn, P.C.: Diag-nosis and localization of aldosterone-producing adenomas by adrenal-vein catheterization. N. Engl. J. Med. 277:1050, 1967

3. Blumenfeld, J.D., Sealey, J.E., Schlussel, Y., Vaughan, E.D., Jr., Sos,T.A., Atlas, S.A., Muller, F.B., Acevedo, R., Ulick, S., Laragh, J.H.:Diagnosis and treatment of primary aldosteronism. Ann. Intern. Med.121:877, 1994

4. Young, W.F., Jr.: Primary aldosteronism: update on diagnosis andtreatment. Endocrinologist 7:213, 1997

5. Doppman, J.L., Gill, J.R., Jr., Miller, D.L., Chang, R., Gupta, R.,Friedman, T.C., Choyke, P.L., Feuerstein, I.M., Dwyer, A.J., Jicha,D.L.: Distinction between hyperaldosteronism due to bilateral hyper-plasia and unilateral aldosteronoma: reliability of CT. Radiology184:677, 1992

6. Radin, D.R., Manoogian, C., Nadler, J.L.: Diagnosis of primaryhyperaldosteronism: importance of correlating CT findings with endo-crinologic studies. Am. J. Radiol. 158:553, 1992

7. Doppman, J.L., Gill, J.R., Jr.: Hyperaldosteronism: sampling theadrenal veins. Radiology 198:309, 1996

8. Young, W.F., Jr., Stanson, A.W., Grant, C.S., Thompson, G.B., vanHeerden, J.A.: Primary aldosteronism: adrenal venous sampling. Sur-gery 120:913, 1996

9. Celen, O., O’Brien, M.J., Melby, J.C., Beazley, R.M.: Factors influenc-ing outcome of surgery for primary aldosteronism. Arch. Surg. 131:646,1996

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