CHAPTER I INTRODUCTION

The adrenal glands are approximately two and half by one inch long yellowishorange colored glands that are found just above the kidneys. Adrenal glands provide a very important function in protecting the body against stress. This function is carried out by secretion of a number of different types of hormones by the adrenal glands.1 As for the term adrenal tumor one can refer to several benign and malignant neoplasms of the adrenal gland, several of which are notable for their tendency to overproduce endocrine hormones. Adrenal cancer specifically refers to malignant adrenal tumors, which include neuroblastoma, adrenocortical carcinoma, and a minority of adrenal pheochromocytomas. Most adrenal pheochromocytomas and all adrenocortical adenomas are benign tumors, which do not metastasize or invade nearby tissues, but which may still cause significant health problems by giving rise to hormonal imbalances. These cases are rare. About 3 to 4 of them are reported each year. Adrenal tumors may present in a CT scan performed and the evaluation of the abdomen has become widespread, an unsuspected swelling of the adrenal gland is frequently detected in many patients and also production of symptoms due to over secretion of hormones from the tumor. 2 The treatment for adrenal tumors can be observation with no surgery, laparoscopic adrenalectomy, open adrenalectomy and laparoscopic removal of both adrenal glands.

CHAPTER II LITERATURE REVIEW

2.1.DEFINITION Tumors of the adrenal glands arise from the cortex or the medulla part of the adrenal gland. Adrenal tumors commonly present because symptoms from excess secretion of hormones by the tumor. The tumors from the adrenal cortex produce excess secretion of steroid hormones and aldosterone and tumors from the adrenal medulla produce excessive amounts of catecholamines.3 Adrenal tumors can be benign (non-cancerous) or malignant (cancer). Often this separation is difficult to make and long term close follow up is necessary after removal to detect recurrences early in patients who have adrenal cancer. An adrenal gland tumor can sometimes overproduce hormones. When it does, the tumor is called a functioning tumor. An adrenal gland tumor that does not produce hormones is called a nonfunctioning tumor. A tumor can start in an adrenal gland (called a primary adrenal tumor) or it can begin in another organ, such as the lungs, and then metastasize to the adrenal glands. The symptoms and treatment of an adrenal gland tumor depend on whether the tumor is functioning or nonfunctioning, and what hormone is overproduced, and whether the tumor is a primary adrenal gland tumor or metastases from cancer of another organ.4 Adrenal masses (AMs) are often discovered incidentally and are then termed adrenal incidentalomas (AIs). They are often discovered after an imaging procedure is performed that is unrelated to the adrenal gland. Usually, the patient has no signs of hormonal excess or obvious underlying malignancy.3 The most common tumor of the adrenal gland is actually a benign tumor called an adrenal adenoma. In most patients, these benign tumors never cause a patient to have any symptoms and do not need to be treated. They are usually found when a patient has a CT (or CAT) scan of the body for an unrelated reason, and are thus sometimes called incidentalomas. The most common malignant tumors found in the adrenal gland are tumors that come from cancer cells that have metastasized (or spread) from other parts of the body to the adrenal gland through the blood stream. Several different types of cancer may spread to the adrenal glands, most

commonly melanomas, lung cancers, and breast cancers. The adrenal glands are the fourth most common site in the body for cancer cells to metastasize to, after the lungs, liver, and bone.5 2.2. ETIOLOGY The biochemical mechanisms depend on the underlying cell type. The cellular mechanisms for primary adrenocortical tumorigenesis are just beginning to be understood. Some studies report an association with chromosomal and genetic abnormalities (genes coding for p53 and p57). Tumor markers are also present in other syndromes.4 The multiple endocrine neoplasia (MEN1) gene is linked to multiple endocrine neoplasia type 1 MEN1 and MEN2 are very rare conditions caused by an inherited faulty gene. MEN1 is associated with adrenal adenomas, and MEN2 is associated with phaeochromocytoma (which can be malignant). The

aldosynthase/11-beta hydroxylase hybrid gene is associated with glucocorticoidremediable hyperaldosteronism.3 While the mutation-induced inactivation of tumor suppressor genes appears to be a plausible mechanism for AC development, other potential mechanisms, including activation of various protooncogenes (eg, ras, PKC), inhibition of apoptosis, or changes in various adrenocortical tissue-specific factors (eg, the steroidogenic acute regulatory protein [StaR]) are possible. Potential mechanisms for adrenocortical tumorigenesis are as follows: 3. Activation of various protooncogenes -Ras, PKC, C myc, C fos, G proteins, G protein-coupled receptors (eg, for vasoactive intestinal peptide [VIP], gastricinhibitory peptide [GIP], luteinizing hormone [LH], and catecholamines). 4. Inactivation of tumor suppressor genes (antioncogenes) -TP53, TP57, TP16, H19, retinoblastoma gene, APC gene, various DNA repair enzyme genes. 5. Inhibition of senescence and/or apoptosis - Mutations involving telomerase and/or BCL-2 genes. 6. Changes in adrenocortical tissue-specific factors - Mutations involving the genes for StaR, SF-1 (steroidogenic factor), and Dax-1 transcription factor.

7. Aberrant expression of receptors to normal adrenocortical trophic agents and ligands - Adrenocorticotropic hormone, angiotensin 2, catecholamines, and endorphins. 8. Ectopic expression of receptors on adrenocortical cells to atypical trophic factors and ligands - Cytokines, growth factors, and neurotransmitters.6 2.3. EPIDEMIOLOGY 2.3.1. Mortality/Morbidity7
1. 2. 3.

Prognosis varies depending on the underlying disease. Approximately 80% of AAs are nonfunctioning and benign. Twenty percent of AAs are either functioning or malignant and require further evaluation and treatment to avoid medical complications.

2.3.2. Race7 No racial predilection has been reported. 2.3.3. Sex7,8 AIs have a female sex predilection, probably reflecting the sex distribution of imaging procedures. Autopsy studies, however, show no sex preference for AAs. 2.3.4. Age7,9 Prevalence increases with age; the rate is less than 1% for patients younger than 30 years and is 7% for patients 70 years or older. 2.3.5. Etiology8,9
1. 2.

Chromosomal and genetic abnormalities (genes coding for p53 and p57). The multiple endocrine neoplasia (MEN1) gene is linked to multiple endocrine neoplasia type 1.

3.

The aldosynthase/11-beta hydroxylase hybrid gene is associated with glucocorticoid-remediable hyperaldosteronism.

2.4. PATHOPHYSIOLOGY Aldosterone synthase cytochrome P-450(human P-450aldo) was detected in the tumour portion of aldosterone-producingadenoma, but not in the normal control adrenals, at the proteinlevel. Neither the activities nor the amounts of other P-450sin the tumour portion of aldosterone-producing adenoma weresignificantly different from those in the non-tumour portionin the adenoma and the normal control adrenals. The aldosteronecontent was significantly elevated, while the androstenedionecontent was significantly decreased in the tumour portion ofthe adenoma compared with that in the normal control adrenals.In Cushing's syndrome, both the activities and amounts of P-45017 and P-450c21 were significantly elevated in the tumour portioncompared with the non-tumour portion of the adenoma and thenormal control adrenals, while those of P-450scc and P-45011in the tumour portion were not significantly different fromthe normal control adrenals. The cortisol content was significantlyelevated, while the amounts of aldosterone and 18hydroxydeoxycorticosteronein the tumour portion of the adenoma were significantly decreasedcompared with those in the normal control adrenals. These resultsdemonstrate that overexpression of P-450aldo in aldosteroneproducingadenoma, and those of P-45017 and P-450c21 in cortisolproducingadenoma may play some role in the pathogenesis of primary aldosteronismand Cushing's syndrome, respectively.10 2.5. SIGNS AND SYMPTOMS The adrenocortical adenomas are yellow tumors surrounded by thin or welldeveloped capsules, and most weigh less than 30 gm. Their morphology is identical to that of nonfunctional adenomas and of adenomas associated with hyperaldosteronism. Microscopically, they are composed of cells that are similar to those encountered in the normal zona fasciculata. The carcinomas, by contrast, tend to be larger than the adenomas. The prevalence of adrenal adenomas increases with increasing age.11

Figure 2.1. Spherical left adrenal tumor is observed as compared with the normal right adrenal.11

Cortisol produces subclinical Cushing syndrome occurs when the adrenal adenoma autonomously secretes cortisol at levels high enough to suppress corticotropin but too low to produce Cushing stigmata. Patients do not have increased rates of hypertension or diabetes mellitus, but they may have features of metabolic syndrome, including hypertension, dyslipidemia, and impaired glucose tolerance. Patients may have reduced bone density and osteoporosis. Patients are prone to adrenal insufficiency once the cortisolsecreting tumor is removed. This postoperative adrenal insufficiency is caused by corticotropin suppression and adrenal cortical atrophy of the contralateral adrenal gland.12 With time, the more characteristic centripetal distribution of adipose tissue becomes apparent, with resultant truncal obesity, "moon" facies, and accumulation of fat in the posterior neck and back ("buffalo hump"). The catabolic effects on proteins cause loss of collagen and resorption of bone. Thus, the skin is thin, fragile, and easily bruised; cutaneous striae are particularly common in the abdominal area.14 Bone resorption results in the development of osteoporosis, with consequent increased susceptibility to fractures. Because glucocorticoids suppress the immune response, patients are also at increased risk for a variety of infections. Additional manifestations include hirsutism and menstrual abnormalities, as well as a number of mental disturbances, including mood swings, depression, and frank psychosis.12

Figure 2.2. A woman with Cushings syndrome due to a right adrenal cortical adenoma. A. One month prior to surgery, age 20. B. One year after surgery.15

Clinical manifestations in school-age children may be very florid, with very characteristic presentation and with no doubt in diagnosis; however, in other patients the clinical signs may be evident by growth failure and obesity, delaying the diagnosis.11 Cushings syndrome with the full moon characteristics of the face, hirsutism, acneiform lesions in the chest and arms, as well as a hump and bulging of the superior segment (trunk) in the cervicodorsal region.14

Figure 2.3. Full moon face, hisutism, acne and buffalo hump were observed in the lateral sequence.14

General signs are central obesity and gynecomastia. The cutoff criterion for suspicion of malignancy ranges from 3-6 cm in diameter. The best hope for a surgical cure is a lower cutoff, but this means a greater number of benign tumors will be removed unnecessarily. A 4-cm cutoff is estimated to result in an acceptable ratio of 1 cancerous to 8 benign tumors.11 Adrenal adenomas often manifest on CT scans as smooth,well defined, homogeneous, smaller than 4 cm in diameter, and low in attenuation. Several reports in the literature indicate that an adrenal mass with a value of 10 Hounsfield units (HU) or fewer on unenhanced CT scan is likely to be an adenoma.13 The low attenuation of these lesions is attributed to their rich lipid content. CT can detect adrenal masses >5 mm in diameter. Of these, nonfunctioning adrenocortical adenomas are the most common. They are usually homogeneous, round and small, have smooth borders and well delineated margins that separate them from adjacent structures. Larger adenomas may distort the body, medial or lateral limbs of the adrenal. Lipid-rich adenomas have an unenhanced CT attenuation <10 Hounsfield units (HU). However, some 2530% of adenomas are lipid poor and have unenhanced CT attenuation values >10 HU.13

Figure 2.4. Lipid-rich adenoma. (A) Unenhanced CT of the abdomen showing a left adrenal mass with a HU measurement of K6 HU (arrow). (B) Contrast-enhanced CT acquired 60 s after administration of i.v. contrast shows enhancement of the adrenal mass to 50 HU. (C) On delayed CT, acquired 15 min after administration of i.v. contrast, the mass measures 15 HU. These measurements provide an absolute contrast enhancement washout of 63% and a relative contrast washout of 70% proving a lipid-rich adenoma. 13

On MRI, adenomas appear homogeneous on all sequences. Their contrast enhancement is mild; they have low or equal signal intensity to the liver on T2- weighted images and may appear of lower signal intensity than the rest of the adrenal gland.13

Table2.1. Imaging in Differentiating Benign From Malignant Adrenal Masses.13

2.6. DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS 2.6.1. Diagnosis There are many tests to diagnose a tumour and to see if it is cancerous and metastasis has occurred. This diagnosis is important as well for determining the treatment and management of the tumour. To diagnose an adrenal gland tumour, blood and urine tests are done to look for certain substances that may indicate that cancer is present. If there is no evidence that the cancer has spread to the adrenal gland from another part of the body, the diagnosis can be made with a computed tomography (CT or CAT) scan or a magnetic resonance imaging (MRI) scan.16 Imaging tests may also be used to find out whether the cancer has metastasized. These are the main tests that can be done to diagnose adrenal tumour:
1.

Blood and urine tests Blood tests can measure the amounts of natural hormones produced during stress, such as catecholamines and metanephrines, which can detect a functional tumour. A patient may be asked to take a pill on the evening before the blood and urine tests, which helps detect the normal suppression of production of the hormone cortisol. A 24-hour urine sample, which requires the collection of all urine during that timeframe for laboratory testing, may also be needed. This track how quickly various hormones are produced. 16

2.

Biopsy A biopsy is the removal of a small amount of tissue for examination under a microscope. For an adrenal tumour, a hollow needle is used to collect the tissue. If the it is suspected to be adrenal cancer, a biopsy of the adrenal gland is not recommended because it could help the cancer to spread. However, if the doctor suspects that cancer has spread to the adrenal gland from another area of the body where the cancer started, a biopsy may be done to determine

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the type of cancer, which can help the doctor plan treatment. The sample removed during the biopsy is analyzed by a pathologist.16
3.

CT scan A CT scan creates a three-dimensional picture of the inside of the body with an x-ray machine. A computer then combines these images into a detailed, cross-sectional view that shows any abnormalities or tumours. Sometimes, a contrast medium is injected into a patients vein to provide better detail.16

4.

MRI An MRI uses magnetic fields, not x-rays, to produce detailed images of the body. A contrast medium is injected into a patients vein to provide better detail.16

5.

Metaiodobenzylguanidine (MIBG) scan MIBG is a chemical similar to adrenaline that will collect in a neuroendocrine tumour. A MIBG scan can show a tumour of the adrenal medulla that may not appear in an x-ray. The scan takes place over two consecutive days. On the first day, an injection of MIBG is given in the arm. Several hours later, pictures are taken with a special camera that can detect if or where in the body the MIBG has collected. The following morning, more pictures are taken, and the process may be repeated if needed.16 2.6.2. Differential Diagnosis Adrenal tumour has many common symptoms as many other diseases hence making adrenal tumour have many differential diagnoses. These are some known differential diagnoses of adrenal tumour16: 1.Addison Disease 2.Adrenal Carcinoma 3.Adrenal Crisis

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4.Adrenal Haemorrhage 5.Breast Cancer 6.Cryptococcosis 7.Cushing Syndrome 8.Hyperaldosteronism, Primary 9.Lung Cancer, Non-Small Cell 10.Lung Cancer, Oat Cell (Small Cell) 11.Lymphoma, B-Cell 12.Lymphoma, Cutaneous T-Cell 13.Lymphoma, Diffuse Large Cell 14.Lymphoma, Follicular 15.Lymphoma, Lymphoblastic 16.Neuroblastoma 17.Pheochromocytoma 18.Teratoma, Cystic 19.Tuberculosis

2.7. SUPPORTIVE EXAMINATION 2.7.1. Laboratory Because adrenal adenoma (AA) may be hormonally silent, biochemical screening is warranted. Biochemical screening for Cushing syndrome, pheochromocytomas and primary hyperaldosteronism are discussed. 17 Cushing syndrome Frequently, cortisol produces subclinical Cushing syndrome. This occurs when the AA autonomously secretes cortisol at levels high enough to suppress corticotrophin but too low to produce Cushing stigmata. Patients do not have increased rates of hypertension or diabetes mellitus, but they may have features of metabolic syndrome, including hypertension, dyslipidemia, and impaired glucose tolerance. Patients may have reduced bone density and osteoporosis. Patients are prone to adrenal insufficiency once the cortisol-secreting tumor is removed. This postoperative adrenal insufficiency is caused by corticotrophin suppression and adrenal cortical atrophy of the contralateral adrenal gland. Because urinary free

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cortisol levels may be within the reference range, a 1-mg overnight dexamethasone suppression test is needed to diagnose subclinical Cushing syndrome.17,18 Pheochromocytoma The most important hormonally silent AA is pheochromocytoma.

Pheochromocytomas should be considered in all AA cases because they are more common than previously thought, the diagnosis is often overlooked, and a failure to recognize them may lead to patient death. A 24-hour urine catecholamine and metabolites evaluation remains a good test for the diagnosis of

pheochromocytoma, but it is not as sensitive as free metanephrine testing. Assume all AAs have a pheochromocytoma until proven otherwise, especially when paroxysmal hyperadrenergic symptoms are present. Exclude the presence of pheochromocytoma prior to performing a fine-needle aspiration (FNA) biopsy.17,18 Primary hyperaldosteronism Primary hyperaldosteronism is a less compelling, but nevertheless important, diagnosis. Surgical intervention can cure the hypertension and hypokalemia.The test of choice is an upright plasma aldosteronetorenin ratio. A plasma aldosterone concentrationtoplasma renin activity ratio greater than 30 and a plasma aldosterone concentration of greater than 0.5 nmol/L are suggestive of primary aldosteronism.Hyperaldosteronism is usually identified by suppressed upright plasma renin levels and concomitant elevated plasma aldosterone levels.17 Others Other secreted hormones can include estrogens, androgens, and 17-

hydroxyprogesterone.They is associated with AAs, carcinomas, and hyperplasia. They often manifest clinically and therefore do not require presumptive screening.18 2.7.2. Imaging CT scan, MRI, iodine I 131 metaiodobenzyl guanidine and positron emission tomography are used.CT scanning is preferred because it is more cost-effective

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than MRI to delineate size, shape, and appearance. A smooth homogeneous lesion smaller than 4 cm with a low attenuation value (Hounsfield units) is usually benign. A larger inhomogeneous lesion with irregular borders and a higher attenuation score should be considered for malignancy.MRI is as effective as CT scanning for distinguishing benign from malignant lesions and is superior for detecting pheochromocytomas. A benign adenoma has a T2-weighted intensity similar to liver tissue. Plain radiography, tomography, and ultrasonography are less sensitive and are used less frequently since the advent of CT scanning and MRI.Other scanning techniques include iodine I 131 metaiodobenzyl guanidine, for pheochromocytoma; iodine I 131-6-b-iodomethylnorcholesterol (NP-59 cholesterol), for adrenocortical lesions; and positron emission tomography; however, these test are not widely available and data on their clinical usefulness is insufficient.17

Pheochromocytomas Pheochromocytomas vary in size, consistency, and margins. They can be bilateral and are strongly enhanced with contrast. They show high signal intensity on T2weighted images, owing to their vascularity. 17 Adrenal carcinoma Meanwhile adrenal carcinomas are often larger than 6 cm in diameter, with an irregular margin and adrenal carcinomas demonstrate a soft tissue inhomogeneous density on CT scans, which enhances with contrast. Adrenal carcinomas are unilateral, sometimes with local invasion and lymphadenopathy and metastases. Besides that, adrenal cortical carcinomas have an intermediate increased intensity on T2-weighted MRIs. 17 Myelolipomas Myelolipomas show characteristic images of fat.17 Bilateral AMs Bilateral AMs should always raise the possibility of haemorrhage, especially in patients with coagulopathies or those on anticoagulant therapy. Diagnosis can be made with a rapid corticotrophin stimulation test demonstrating decreased cortisol reserve. 17,18

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Granulomatous diseases Granulomatous diseases like histoplasmosis and tuberculosis are characteristically homogeneous and may show calcifications.17 Others Most metastatic disease to the adrenal gland is unilateral, but lymphoma may be bilateral and can cause adrenal insufficiency. A 21-hydroxylase deficiency can produce unilateral AMs, but bilateral AMs are more common. To recognize this, measure the level of corticotrophin-stimulated plasma 17-hydroxyprogesterone.In a patient with primary hyperaldosteronism, bilateral AIs suggest bilateral adrenal hyperaldosteronism (idiopathic hyperaldosteronism). Confirm this by adrenal venous sampling to demonstrate bilateral plasma aldosterone secretion. Longstanding, corticotrophin-dependent Cushing syndrome may result in large AMs.17 2.7.3. Adrenal FNA Adrenal FNA helps identify metastatic, systemic, and hemorrhagic disease of the adrenal glands but it cannot distinguish between benign and malignant primary adrenal tumors.It should be used only when AMs cannot be diagnosed clinically or hormonally. If a metastatic lesion is found, initiate a search for the primary cancer. If adrenal tissue is found, consider surgical removal.Pheochromocytoma should always be excluded before performing FNA biopsy to avoid the potential for a hypertensive crisis.17,18 2.8.MANAGEMENT19,20 2.8.1. Medical Care Adrenal insufficiency
1.

Adrenal insufficiency should be the first consideration, especially with bilateral AMs.

2. 3. 4.

A corticotropin test with 60-minute cortisol levels helps rule out the diagnosis. If found, suspect granulomatous disease, hemorrhage, or lymphoma. A 21-hydroxylase deficiency can also be diagnosed with a 60-minute postcorticotropin plasma 17-hydroxyprogesterone level.

Hormonal excess

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1.

Use the 1-mg overnight dexamethasone suppression test, urinary free cortisol test, a urinary metanephrinetocreatinine ratio, and a renin-to-aldosterone ratio.

2. 3.

If found, surgical removal is usually indicated. Exceptions that do not warrant surgery include bilateral adrenal diseases such as corticotropin-dependent Cushing disease or bilateral hyperaldosteronism.

4.

If no hormonal excess is found and the corticotropin test results were unremarkable, FNA helps distinguish between adrenal and metastatic disease.

5. 6.

Metastatic disease is managed according to the type of primary cancer. Adrenal disease should be removed if the diameter is greater than 6 cm. Otherwise, follow up with repeat CT scans at periodic intervals.

2.8.2. Surgical Care 1. No randomized trials have compared laparotomy versus laparoscopic adrenalectomy; however, abdominal laparotomy is preferred for bilateral disease and pheochromocytoma. 2. Fiberoptic laparoscopy is used for visualization, biopsy, and removal. 3. A transthoracic approach is faster than fiberoptic laparoscopy but has a longer postoperative recovery period. 4. Other experimental approaches, including a laparoscopic robot and augmented-reality visualization of the surgical field, have been described. 2.8.3. Consultations An endocrinologist should be consulted to review the results of endocrine testing. 2.8.4. Diet No specific diet recommendations are necessary. 2.8.5. Activity No specific diet recommendations are necessary. 2.8.6. Medication No specific medical therapy is required except treating the underlying disease.

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2.9. 2.9.1.

FOLLOW UP AND PROGNOSIS21 Follow Up

1. Follow up important for patient who do not have an adrenalectomy by detect interval changes in tumor size or the abnormality in hormon production. It can be done by repeated CT scanning every 6-12 months baceuse most tumors remain unchanged or decreased in size, but 5-25% still have possibilities to enlarged. Decreased size tumors do not recommended for further testing. 2. Measurement of hormones production can be done by: a. Overnight 1 mg dexamethasone suppresion testing b. Renin-to-aldosterone ratio testing c. Urine catecholamine and metabolite measurements 3. Hypercortisolism is the most hormonal disorder that occur during folloeup period instead hyperaldosteronism or excessive catecholamines. Hypercortisolism usually subclinical, thats why periodic measurement is recommended. 4. Adrenal insufficiency may occur in bilateral adrenal disease such as lymphoma. Hypocortisolism result from corticotropin deficiency from a cortisol-secreting adenoma that causing contralateral adrenal atrophy. 5. Postoperative course for patient with contralateral atrophy is prolonged physiologic cortisol replacement. 6. Patient should be educated about the sign of adrenal insufficiency. 2.9.2. Prognosis

Prognosis depend on the type of underlying adrenal disease. For adrenal adenoma the prognosis is usually excellent, but poor clinical outcomes for patient with adrenal cortical carcinomas. Patient should be very aware of adrenal insufficiency.

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CHAPTER III SUMMARY

1. Tumors of the adrenal glands arise from the cortex or the medulla part of the adrenal gland. Adrenal tumors commonly present because symptoms from excess secretion of hormones by the tumor. 2. The adrenocortical adenomas are yellow tumors surrounded by thin or welldeveloped capsules, and most weigh less than 30 gm. Their morphology is identical to that of nonfunctional adenomas and of adenomas associated with hyperaldosteronism. Adrenal adenomas often manifest on CT scans as smooth,well defined, homogeneous, smaller than 4 cm in diameter, and low in attenuation 3. The diagnosis of adrenal adenoma is derived from the blood and urine test, biopsy, and imaging. These examinations also help to exclude other possible differential diagnosis. 4. Management of adrenal adenoma includes medical care, surgical care, and referral if it is indicated. 5. Follow up is needed in patient not undergo surgery to measure hormone production and education about adrenal insufficiency is important. 6. Prognosis depends on the case. For adrenal adenoma the prognosis is excellent, but for adrenal cortical carcinoma the prognosis is bad.

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