Adrenal Adenoma

8/13/2019 Adrenal Adenoma

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CHAPTER I

INTRODUCTION

The adrenal glands are approximately two and half by one inch long yellowish-

orange 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.



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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



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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 glucocorticoid-

remediable 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], gastric-

inhibitory 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.



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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. Prognosis varies depending on the underlying disease.

2. Approximately 80% of AAs are nonfunctioning and benign.

3. 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. Chromosomal and genetic abnormalities (genes coding for p53 and p57).

2. 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.



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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-45011βin the tumour portion

were not significantly different fromthe normal control adrenals. The cortisol

content was significantlyelevated, while the amounts of aldosterone and 18-

hydroxydeoxycorticosteronein the tumour portion of the adenoma were

significantly decreasedcompared with those in the normal control adrenals.

These resultsdemonstrate that overexpression of P-450aldo in aldosterone-

producingadenoma, and those of P-45017 and P-450c21 in cortisol-

producingadenoma 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 well-

developed 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



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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 cortisol-

secreting 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



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Figure 2.2. A woman with Cushing’s 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 Cushing’s 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

A B



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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 benigntumors 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, non-

functioning 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 25 – 30% of adenomas are lipid poor and have unenhanced CT

attenuation values >10 HU.13



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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

A B C



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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 patient’s 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 patient’s 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 tumour 16:

1.Addison Disease

2.Adrenal Carcinoma

3.Adrenal Crisis

http://emedicine.medscape.com/article/116467-overview








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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.Thetest of choice is an upright plasma aldosterone – to – renin ratio. A plasma

aldosterone concentration – to – plasma 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 T2-

weighted 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.

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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. Long-

standing, 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. A corticotropin test with 60-minute cortisol levels helps rule out the diagnosis.

3. If found, suspect granulomatous disease, hemorrhage, or lymphoma.

4. A 21-hydroxylase deficiency can also be diagnosed with a 60-minute post-

corticotropin 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 metanephrine – to – creatinine ratio, and a renin-to-aldosterone

ratio.

2. If found, surgical removal is usually indicated.

3. 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. Metastatic disease is managed according to the type of primary cancer.

6. 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. FOLLOW UP AND PROGNOSIS21

2.9.1. 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 folloe-

up 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 well-

developed 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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Adrenal Adenoma