Adrenal incidentalomas: Surgical treatment in 28 patients and update of the literature
A.B. Porcaro, G. Novella, V. Ficarra, P. Curti, S. Zecchini Antoniolli, H.S. Suangwoua & G. Malossini Department of Urology, University Hospital, Verona, Italy
Abstract. Introduction: Adrenal masses discovered by imaging techniques for reasons unrelated to adrenal diseases are called adrenal incidentalomas (AI). The aim of this study was to find out the clinical outcome of 28 patients operated for incidentally discovered adrenal mass and to update the literature concerning this topic. Patients and methods: From September 1976 to December 1999 we operated on 28 patients for adrenal incidentaloma. Adrenal masses were unilateral in 25 cases and bilateral in 5. Average age was 57 years (range 10- 73). Hormonal study was performed in all patients. All patients underwent adrenalectomy by the transabdominal subcostal approach. Results: Histopathology assessed the adrenal masses as primary in 19 patients and secondary in 9. 24-hour urinary vanillylmandelic acid (VMA) excretion was elevated in 2 patients. Adrenal insufficiency was detected in 1 case. Average tumor diameter resulted 5.8 cm (range 2-17). Histopathologic features of primary adrenal masses included pheochromocytoma in 5 cases, cysts in 4, myelolipomas in 3, nodular hyperplasia in 2, tuberculous mass in 1, cortical adenoma in 1, extra-bone marrow hemopoiesis in 1, cortical carcinoma in 1 and neuroendocrine tumor of the adrenal medulla in 1. The 9 adrenal metastasis resulted by renal cell carcinoma in 7 patients, urothelial carcinoma of the upper urinary tract in 1 and primary renal lymphoma in 1. Average follow-up was 68 months (range 6-246). Patients alive were 18 (64%), deal 10 (36%). Of the 19 patients with primary adrenal tumors 16 (84%) were alive and disease free and 3 (16%) died (1 for disease and 2 for reasons unrelated to the primary tumor). Of the 9 patients with adrenal metastasis 2 (22%) were alive (1 disease free and 1 with progression of the disease) and 7 (78%) died for disease. Replacement therapy for adrenocortical hormones was given 5 patients. Conclusions: Management of AI need CT or MRI and hormonal investigation in order to detect malignancy and subclinical hypersecretory syndromes. Subclinical functional adrenal masses, single adrenal metastasis and primary nonhypersecretory adrenal tumors sized 4 cm are treated by surgery. A close morpho-functional follow-up is indicated for primary adrenal incidentalomas when nonhypersecretory and smaller than 4 cm.
Key words: Adrenal, Incidentaloma
Introduction
Adrenal masses discovered by imaging techniques for reasons unrelated to adrenal diseases are called adrenal incidentalomas (AI) [1, 2]. This defini- tion includes a heterogeneous spectrum of pathologic entities [3]. Prevalence ranges between 0.35% to 4.4% in computerized tomography (CT) and between 1.4% to 5.7% in autopsy series. Bilateral incidenta- lomas are discovered in 10% of cases. Prevalence of adrenal nodules increases with age. The likelihood of finding an incidentaloma is greater in females and in
individuals with hypertension. Adrenal metastasis in oncology patients ranges between 32% to 73% [3- 5]. The aim of this study was to find out the clinical outcome of 28 patients operated for AI and to update the literature concerning this topic.
Patients and methods
From September 1976 to December 1999 we operated on 28 patients for adrenal incidentaloma. Adrenal masses were unilateral in 25 cases and bilateral in 5.
| Hormones | Plasma | 24 h/urine |
|---|---|---|
| Cortisol | 3.9-25 ng/dl | 25-120 ng/24 h |
| ACTH | 39-25 pmol/l | |
| Aldosterone | 0.08-0.044 nmol/l | 50-235 nmol/24 h |
| PRA | 1.1-20.2 pg/ml | |
| DHEA-S | 300-3000 ng/ml | |
| Testosterone | <1.2 ng/ml | |
| 17-OHP | ||
| Norepinephrines | 215-475 pg/ml | |
| Epinephrines | <95 pg/ml | |
| Metanephrines | 15 ng/24 h | |
| VMA | 8 ng/24 h | |
| Dopamina | <136 pg/ml | |
| Omovanillic acid | 10.10-35.35 nmol/24 h |
Clinical records of the patients were retrospectively evaluated. The study excluded patients with severe or paroxysmal hypertension, hypokaliemia, Cushing’s syndrome, hyperandrogenism and previous or concurrent history of primary malignancies. Patients included 17 males and 11 females. Average age was 57 years (range 10-73). AI were detected by sonography in 25 cases and intravenous pyelography in 3. The diagnosis was assessed by computed tomography (CT) in 27 patients and by magnetic resonance imaging (MRI) in 1 patient. Hormonal study was performed in all patients and included urinary free cortisol, plasma ACTH, serum dehydroepiandrosterone sulfate (DHEA-S), serum 17-hydroxyprogesterone (17- OHP), serum testosterone, upright plasma aldosterone and PRA, serum testosterone, plasma cathecolamines, serum free cortisol, 24-hour urinary metanephrines and vanillylmandelic acid, 24-hour urinary free cortisol and 17-ketosteroid (Table 1). All patients underwent adrenalectomy by the transabdominal subcostal approach. Postoperative follow-up included sonography every 6 months and CT once yearly for the first 2 years. After ultrasound was performed once yearly. Hormone assays were analyzed once yearly for the first 2 years.
Results
Histopathology assessed the adrenal masses as primary in 19 patients and secondary in 9. Urinary VMA excretion was elevated in 2 patients. Adrenal insufficiency was detected in 1 patient. Average tumor
| Primary | Secondary | Total | |
|---|---|---|---|
| Mean | 6.3 | 5.1 | 5.8 |
| Range | 2-17 | 2.5-12 | 2-17 |
| <3 | 6 | 6 | 12 |
| >3<6 | 5 | 4 | 9 |
| >6<10 | 3 | 3 | 6 |
| >10 | 5 | 1 | 6 |
diameter resulted 5.8 cm (range 2-17) (Table 2). Primary adrenal masses were all unilateral and histo- pathologic features included pheochromocytoma in 5 cases, cysts in 4, myelolipomas in 3, nodular hyper- plasia in 2, tuberculous mass in 1, cortical adenoma in 1, extra-bone marrow hemopoiesis in 1, cortical carcinoma in 1 and neuroendocrine tumor of the adrenal medulla in 1 (Table 3). The 9 adrenal meta- stasis resulted by renal cell carcinoma in 7 patients, urothelial cell carcinoma of the upper urinary tract in 1 and primary renal lymphoma in 1 (Table 3). The metastasis were monolateral in 4 patients and bilateral in 5. Unilateral adrenal metastasis were by renal cell carcinoma in 3 cases and urothelial cancer of the upper urinary tract in 5. Bilateral metastasis were by renal cell carcinoma in 4 patients and renal lymphoma in 1. Average follow-up was 68 months (range 6- 246). Patients alive were 18 (64%), dead 10 (36%). Of the 19 patients with primary adrenal tumors 16 (84%) were alive and disease free and 3 (16%) died (2 for reasons unrelated to the primary tumor and 1 for disease). Of the 9 patients with adrenal metastasis 2 (22%) were alive (1 disease free and 1 in progression) and 7 (78%) died for disease. Replacement therapy for adrecortical hormones was given 5 patients.
Discussion
Most frequently, pathology of AI include adenomas (36-94%), pheochromocytomas (1.5-23%), cysts and pseudicysts (4-22%), metastasis (0-21%), nodular hyperplasia (7-17%), myelolipomas (7-15%), car- cinomas (1.2-11%), lipomas (0-11%), ganglioneur- omas (0-6%), hematoma and hemorrhage (0-4%) [3-5]. Primary tuberculous adrenal mass has also been reported [6]. In case of incidentaloma the first concern is a nonfunctional pheochromocytoma (15%), and the
| Primary | No. | % | Secondary | No. | % |
|---|---|---|---|---|---|
| Pheochromocytoma | 5 | 19 | Renal cell carcinoma | 7 | 25 |
| Cyst | 4 | 14 | Urothelial carcinoma | 1 | 3.5 |
| Myelolipoma | 3 | 11 | Primary renal lymphoma | 1 | 3.5 |
| Nodular hyperplasia | 2 | 7 | |||
| Tuberculous mass | 1 | 3.5 | |||
| Adenoma | 1 | 3.5 | |||
| Ectopic hemopoiesis | 1 | 3.5 | |||
| Carcinoma | 1 | 3.5 | |||
| Neuroendocrine carcinoma | 1 | 3.5 | |||
| Total | 19 | 68 | 9 | 32 |
less common occurrence is adrenocortical carcinoma (2%) [7].
The approach to AI is focused on assessing the masses as benign, malignant, nonhypersecreting and hormone secreting [2, 5, 8]. Exclusion of malignancy from diagnosis should be of primary importance for oncology patients because it might affect staging and therapy of the primary cancer. An optimal diagnostic approach to AI should consider the results of the biochemical tests and a review of the anatomical qualities depicted on CT or MRI while taking into account the previous clinical epidemiological data [8]. Choosing the most direct and cost-effective diagnostic approach to AI are common dilemmas in clinical practise [9, 10].
Clinical evaluation is focused on evaluating a history of extra-adrenal malignancy, granulomatous infections (fungal and tuberculosis) or familial syndromes [3, 5]. Pheochromocytomas may be asso- ciated with neurofibromatosis, medullary thyroid carcinoma, hyperparathyroidism and the von Hippel- Lindau syndrome. Physical examination will assess the presence of hypertension, obesity, stria, myopathy, hirsutism in a female patient or feminization in a male patient. The prevalence of hypertension in patients with adrenal incidentaloma is higher than in the general population (41% versus 20%) [5]. Clinically silent hypercortisolism is not completely asympto- matic [11].
Most frequently AI are nonhypersecretory (67% to 94%) adenomas, but some may retain minor endocrine abnormalities or subclinical hyperfunc- tion. Endocrine evaluation is the first step in the evaluation of AI [1-4, 10]. Subclinical autonomous
cortisol secretion may suppress the controlateral adrenal gland and may be associated with abnor- malities in the hypothalamic-pituitary adrenal axis that may persist for several months after adrenalec- tomy. Subclinical hypersecretion of cortisol occurs in 10-15% of patients with adrenal incidentaloma [1, 11, 12]. Bone mass and metabolism are altered in adrenal incidentaloma patients with subclinical hyper- cortisolism [13-15]. In adenomas with autonomous cortisol secretion the GH response to GNRH is blunted due to increased somatostatinergic tone as it may be restored to normal by pretreatment with the functional somatostatin antagonist arginine [16, 17]. An increased response to 17-hydroxyiprogesterone to ACTH stimulation has been observed in adrenal incidentaloma and linked to an impairment of either 21-hydroxylase or of 11-betahydroxylase activity [18, 19]. Endocrine findings for subclin- ical hypercortisolism include high-borderline free cortisol excretion, impaired cortisol rhythm, partial cortisol suppression with dexamethasone, low plasma adrenocorticotropic hormone (ACTH) and unrespon- siveness to corticotropin-releasing hormone (CRH) [20-22]. Endocrine findings for aldosterone - produc- ing adenomas are suppressed plasma renin activity, elevated plasma aldosterone and hypokaliemia. The acute saline suppression test (2 liter of 0.9% NaCl solution infused intravenously in 4 hours) or the fluorohydrocortisone suppression test (0.4 mg of 9- alpha-fluorohydrocortisone every day for 4 days) should be performed [3]. The prevalence of primary aldosteronism in AI adenomas ranges between 0% to 7% [1, 3, 10]. Low dehydroepiandrosterone (DHEAS) levels are frequently observed in patients with subclin-
ical Cushing’s syndrome and adrenocortical adenomas [4]. Elevated plasma levels of DHEAS, andros- tenedione and testosterone are frequently detected in androgen-secreting neoplasms that quit often are adrenocortical carcinomas rather than adenomas. An exaggerated 17-OH-progesterone (17-OHP) response to the ACTH test in present in 17% to 71% of cases of adrenal incidentaloma [3, 10]. The prevalence of clin- ically silent pheochromocytomas ranges from 1.5% to 13%. Pheochromocytoma hormones are screened by resting plasma cathecolamines, plasma dopamine, 24-hour urinary excretion of cathecolamine, metha- nephrine and urinary vanillymandelic acid [1-3, 23]. A 24-hour urine collection is not convenient for out- patients [24]. Selective analysis of adrenomedullary hormonal function is the most cost-effective strategy [10].
Imaging is focused on evaluating size and morphology of AI, although it lacks the specificity to distinguish benign from malignant lesions [1, 3, 25]. Size is an important feature of malignancy. The risk increases with increasing lesion diameter. The cut- off value for malignancy ranges from 3 to 6 cm. A reasonable cut-off value is 4 cm [1, 3]. Size criteria alone often do not permit differentiation of benign and malignant tumors. Malignant tumors may present as small masses (lesser than 2.5 cm). Many adrenal lesions may appear as large masses [3].
Ultrasonography may detect adrenal masses greater than 2 cm with low costs and risks, but it does not allow to assess accurately size and morphology of the lesion. Ultrasound may be used for follow-up evaluation of adrenal masses [1, 2, 26]. Laparoscopic ultrasound accurately localizes adrenal tumors, helps define their relationship to adjacent structures, and provides confirmation that larger tumors are amenable to laparoscopic resection [27, 28].
Computed tomography (CT) estimates size and morphological features of adrenal lesions [1, 2]. CT may underestimate tumor size [3, 29]. Benign AI appear as a smooth homogeneous masses of low density with little contrast enhancement. Malignant lesions appear as large masses, exhibit irregular margins and non-homogeneous density marked with dynamic contrast enhancement. Tumor progression shows mass enlargement and images of malignancy. Adrenocortical adenomas appear as small, homo- geneous round masses with smooth margins, with relatively low density and without enhancement after intravenous contrast. The presence of a fatty adrenal mass is diagnostic of myelolipoma, a usually nonfunc-
tioning tumor composed of fat and bone marrow elements in various proportions. Nevertheless, atyp- ical radiological features may occur in the presence of high bone marrow to fat ratio, hemorrhage, or calcifi- cation in the tumor. Adrenal metastases vary consid- erably in diameter. They are smaller than primary adrenal carcinomas and larger than adenomas. Meta- stasis, often bilateral, have irregular margins, are not very homogeneous and show a thick irregular enhanc- ing rim after contrast. A threshold of 10 Housfield units (HU) and a threshold of 24 HU with a 14-minute delay on a contrast-enhanced CT scan are used as the cut-off values to distinguish between adenomas and metastasis. CT is accurate in assessing the spread of the tumor into tissues such as liver, lymph nodes, lung and inferior vena cava.
The characterization of an adrenal mass can be made with high sensitivity and specificity using MR imaging. The increased reliance on MR imaging seems to be based mainly on findings from chemical- shift and dynamic gadolinium-enhanced studies. Benign lesions have isointense or low signal intensity on both T1 and T2-weighted images. Malignant masses show intermediate or increased signal intensity on T2-weighted images. After gadolinium administra- tion, they show strong contrast enhancement and slow washout [1, 3, 30, 31]. Benign and malignant masses may show necrosis, hemorrhage and calcifications. About 30% masses are not reliably distinguished on the T2 weighted images. MRI evaluates small adrenal lesions better than CT. Pheochromocytoma typically is isointense to liver on T1-weighted images and hyper- intense on T2-weighted images. Adrenal carcinoma and metastatic nodules present with hyperintensity on T2-weighted images. After gadolinium administra- tion, adenomas show rapid contrast enhancement and rapid washout.
Adrenocortical scintigraphy provides information concerning cortical function and anatomic localiza- tion of the adrenal glands as discrimination between benign and malignant lesions. The ability to map differential adrenal cortical function has great clin- ical utility and demonstrable cost-effectiveness in the evaluation of adrenocortical disease and in distin- guishing benign from malignant lesions in patients with incidentally discovered adrenal masses [1-3, 9, 10, 32, 33]. Adrenocortical scintigraphy uses radiocholesterol such as 131-I-6-beta-iodomethyl-19- norcholesterol (NP59) or 75-Se-methylnorcholesterol. The 131-I-6-beta-iodomethylnorcholesterol (NP-59) scintigraphy is the most cost-effective diagnostic tool
for evaluating adrenal incidentalomas over wide range of malignancy rates. Adrenocortical scintigraphy shows radiocholesterol uptake patterns for hyper- secreting tumors (cortisol, aldosterone and androgen secreting adenomas) and nonhypersecreting adenomas and cold nodules for primary and secondary malignan- cies. Primary and secondary malignant lesions show a discordant scintigraphic pattern such as decreased or absent radiocholesterol uptake by the affected adrenal gland. A typical pattern of cortical adenoma is unilateral adrenal visualization with virtual absence of the controlateral adrenal gland. Well-differentiated carcinomas with radiotracer up-take have sometimes been described. A discordant scan can also point to a silent pheochromocytoma.
Adrenal medullary scintigraphy with 131-I- or 123-I-metaiodobenzylguanidine (MIBG) shows pheochromocytoma as focal increased adrenal uptake. Malignant pheochromocytomas and metastases are usually visualized. Adrenal medullary scintigraphy does not visualize masses lesser than 1.5 to 2 cm in diameter, and large tumors with extensive tumoral necrosis and/or hemorrhage. Imaging performed 36-48 h after metaiodobenzylguanidine (MIBG) injection is being widely used in the diagnosis of pheochromocytoma. Scans performed 7 days after MIBG injection is effective not only for finding early small pheochromocytomas and the remnants of tumors after resection, but also in diagnosing non-pheochromocytomas [34].
Positron emission tomography (PET) is a new and promising technique in studying adrenal masses [1, 3, 35-37]. PET imaging with 18-F-fluorodeoxyglucose (FDG) can metabolically characterize adrenal masses. Benign adrenal lesions do not show any uptake while adrenal metastases appear as a high uptake pattern with 100% sensitivity and specificity. Abnormally increased FDG uptake in adrenal malignancies allows one to differentiate these abnormalities from benign lesions. Whole-body PET can also reveal extra- adrenal tumor sites in patients with malignant tumors, using a single imaging technique for accurate disease staging.
Ultrasound or CT-guided fine needle aspiration (FNA) biopsy is indicated for suspected metastasis [1- 3, 9, 10, 38]. FNA has 80% to 90% specificity and 75% to 85% accuracy [3]. Fine needle aspiration does not differentiate adrenal adenomas and carcinomas. Complications such as pain, pneumothorax, renal and hepatic hematoma, septicemia have been reported in 8% to 13% of cases. The potential hormonal activity
for the AI must be assessed before performing FNA, because it could precipitate a potentially lethal hyper- tensive crisis in patients with pheochromocytoma. FNA has the advantage of real time imaging without radiation exposure and of requiring less time for patient evaluation. It also rarely misses its target.
Nonhypersecreting adrenal incidentalomas tend to remain hormonally unchanged. Adrenal hyperfunc- tion develops with incidence ranging from 0% to 16% [1, 3, 39]. Subclinical hormonal abnormalities may normalize or persist unchanged in the majority of cases, but in some patients they evolve toward endocrine hyperfunction. The likelihood of adrenal incidentalomas to evolve toward malignancy is slight. The majority of benign masses tend to remain morpho- logically unchanged. Mass enlargement may develop in 11% of patients. Another mass may appear in the controlateral adrenal gland. The adrenal mass may evolve toward reduction or disappearance [14, 17] indicating a programmed end of growth may be for factors involved in sterodogenesis regulation, cell proliferation, and/or apoptosis [23-25]. Adrenal nodules increases with age and vascular rearrange- ments have been suggested as pathogenetic mech- anism.
Risk factors for adrenal mass enlargement or hyperfunction include sex, age, obesity, hyperten- sion, diabetes, abnormal endocrine test at diagnosis, mass size, mass appearance and scintigraphic uptake pattern [39]. Abnormal endocrine tests at diagnosis have predictive value for mass enlargement. Exclusive radiocholesterol uptake by a mass of 3 cm and no visualization of the controlateral adrenal gland is suggestive of adrenal hyperfunction.
The risk of morbidity or mortality of a patient with an adrenal incidentaloma is related to hormonal hyper- secretion or malignancy. Patients with subclinical autonomous cortisol secretion are at risk to develop adrenal insufficiency after removal of the mass in 18% to 20% of cases, if the syndrome is not identified preoperatively [3, 40]. The potential morbidity asso- ciated with a missed diagnosis of pheochromocytoma may be significant [41]. Life expectancy of patients with adrenal incidentalomas is decreased by a mean of about 1 year if left undiagnosed and untreated [10].
The appropriate management of adrenal incidenta- lomas remains controversial [1, 3, 42, 43] for the risk of morbidity and mortality due to hormone hyper- secretion or malignancy, cost-to-benefit ratio, patient history, age and general health condition. Small or medium-sized adrenal incidentalomas may be ignored
| No. | Mean follow-up (months) | Alive | Dead | |
|---|---|---|---|---|
| Primary | 19 | 88 | 16 (84%) | 3 (16%) |
| Secondary | 9 | 44 | 2 (22%) | 7 (78%) |
| Total | 28 | 68 | 18 (64%) | 10 (36%) |
if MRI or other tests suggest benign pheochromo- cytoma disorder, or patients are elderly, or both [10]. We suggest an algorithm for the management of AI (Table 4).
Tumors with endocrine activity, although clin- ically silent, should be removed unless there is a prohibitive surgical risk. Patients with subclinical Cushing’s syndrome require glucocorticoid therapy during and after surgery [3]. Patients with primary aldosteronism may complain postoperative hyper- kalemia for the inability of the adrenal gland to produce sufficient amounts of aldosterone. Hyper- kalemia, if severe and prolonged, needs replacement therapy with mineralocorticoids [44, 45]. Subclin- ical incidental pheochromocytoma needs preoperative medical treatment with alpha-1-adrenergic antagonists (prazosin, doxazosin). The treatment will allow the expansion of the vascular bed and plasma volume and will reduce the amount of liquids required for mainte- nance of blood pressure when the tumor is removed [1,3].
For an endocrine inactive adrenal incidentaloma the size of the mass and the imaging features of malig- nancy are the most important factors for deciding surgical resection [1-3]. Enlargement of the mass is an indication for resection. The decision will also depend on patient’s age, general medical condition, and overall clinical setting. Underestimation of the tumor size by conventional CT can delay surgery. The size threshold varies from 3 to 6 cm and usually from 3 to 4 cm. A mass larger than 4 cm should be surgically removed. In young patients adrenalec- tomy is indicated for masses sized 3 cm. Only 5% of incidentalomas sized less than 3 cm may be malignant. The appropriate surgical approach, including conven- tional open and laparoscopic adrenalectomy, must be selected [43, 46-48]. Large or malignant adrenal lesions require open adrenalectomy. In these cases the retroperitoneal approach is the preferred route. Laparoscopic adrenalectomy is the choice treatment
| Adrenal incidentalomas | ||||
|---|---|---|---|---|
| ↓ Primary | ↓ | |||
| Secondary | ||||
| V | Į | Į | ||
| Functional | Non-functional | Surgery | ||
| V | 1 V | |||
| Surgery | >4 cm | ≤4 cm | ||
| ↓ | ↓ | |||
| Surgery | Follow-up | |||
for small hormone active benign adrenal lesions [49, 50]. The specific risks of pheochromocytoma surgery are not increased by the laparoscopic approach. The majority of endoscopic adrenalectomies are performed via the transperitoneal route, but there is growing interest in the retroperitoneoscopic approach. Laparo- scopy is superior to open surgery since it is associated with less pain, a shorter hospital stay, and more rapid return to normal activities, and also yields the best cosmetic and long-term results. Partial adrenalectomy may be indicated for bilateral pheochromocytoma, and also has advantages for patients with aldosterone- producing adenomas. The feasibility of laparoscopic partial adrenalectomy has been demonstrated. Ambu- latory adrenalectomy is feasible and safe, and results in high patient satisfaction, but it should be performed by minimally invasive surgeons who have consider- able experience with laparoscopic adrenal surgery.
Successful autotransplantation of adrenal tissue in muscular pockets or omental wrapping have been reported [51].
Long-term follow-up may be the choice treatment for the majority of incidentalomas [1-3, 43]. Conser- vative management is indicated for small (less than 3 cm) nonhypersecreting and apparently benign inciden- talomas. Radiological and endocrine evaluation within 6 months and yearly thereafter for the following 3 to 4 years or longer is recommended. Anxiety from knowing about the tumor of patients under- going follow-up evaluation should be considered. Although small adrenal incidentalomas may represent early stages of cancer, malignant transformation at long-term follow-up is very low. Magnetic resonance imaging or spiral CT are recommended for long-term follow-up. Adrenal percutaneous ethanol ablation for treatment of an aldosterone producing adenoma and an adenocarcinoma has been reported [52, 53]. Percu-
taneous ethanol ablation may represent a promising treatment option for malignant tumors of the adrenal gland for patients who are not candidates for surgical resection.
Radiotherapy for adrenal gland metastasis may be a good palliative therapy sometimes it may curatively treat metastasis from lung cancer [54].
Conclusions
Management of AI need CT or MRI and hormonal investigation in order to detect malignancy and subclinical hypersecretory syndromes. Subclinical functional adrenal masses, single adrenal metastasis and primary nonhypersecretory tumors sized 4 cm are treated by surgery. A close morpho-functional follow- up is indicated for primary adrenal incidentalomas when nonhypersecretory and smaller than 4 cm.
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Address for correspondence: Dr Antonio Benito Porcaro, Divisione Clinicizzata di Urologia, Ospedale Policlinico ‘G. Rossi’, Universià degli Studi di Verona, Via della Menegone No. 10, I-37134 Verona, Italy
Phone: + 39 45 8074370 - 8074630; Fax: +39 45 8074080