eMedicine Specialties > Endocrinology > Adrenal Gland

Adrenal Adenoma

Author: George T Griffing, MD, Professor of Medicine, St Louis University School of Medicine
Contributor Information and Disclosures

Updated: Aug 17, 2009

Introduction

Background

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. Incidence has been increasing proportionally to the use of radiographic imaging.1 (See images below and Images 5-7.)

Left adrenal mass discovered incidentally.

Left adrenal mass discovered incidentally.

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Left adrenal mass discovered incidentally.

Left adrenal mass discovered incidentally.



Close-up of the left adrenal incidentaloma from t...

Close-up of the left adrenal incidentaloma from the above image.

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Close-up of the left adrenal incidentaloma from t...

Close-up of the left adrenal incidentaloma from the above image.



Left adrenal mass.

Left adrenal mass.

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Left adrenal mass.

Left adrenal mass.


Less commonly, AMs are discovered as part of the clinical workup for suspected adrenal disease (eg, Cushing syndrome). Much of the following discussion is on the clinical conundrum of the incidentally discovered AM. The term adrenal adenoma (AA) is used in the following discussion when nonadrenal sources occupying the adrenal area can be excluded. The term AM is used when a nonadrenal space-occupying structure cannot be excluded.

Pathophysiology

The 2 main concerns with regard to an AI are (1) whether it is hormonally active and (2) whether it is malignant. The treatment for a hormonally active adrenal tumor is surgery. The treatment for a malignancy depends on the cell type, spread, and location of the primary tumor.2

Frequency

United States

The autopsy prevalence for AMs is 2-9% (see Table 1). Approximately 1-10% of CT scans and MRIs detect AIs that are 5 mm or larger.

Table 1. Prevalence of AMs

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Table
AuthorMethodSample SizePrevalence, %
Russl (1941)Autopsy (>1 cm)131/90001.5
Kokko (1967) 3 Autopsy (>5 mm)21/14951.5
Hedeland (1967)Autopsy (>2 mm)64/7398.7
Glazer (1982) 4 CT scan16/22000.7
Abecassis (1985) 5 CT scan19/14591.3
Belldegrun (1986) 6 CT scan88/120000.7
Herrera (1991) 7 CT scan259/610540.4
AuthorMethodSample SizePrevalence, %
Russl (1941)Autopsy (>1 cm)131/90001.5
Kokko (1967) 3 Autopsy (>5 mm)21/14951.5
Hedeland (1967)Autopsy (>2 mm)64/7398.7
Glazer (1982) 4 CT scan16/22000.7
Abecassis (1985) 5 CT scan19/14591.3
Belldegrun (1986) 6 CT scan88/120000.7
Herrera (1991) 7 CT scan259/610540.4


Mortality/Morbidity

  • 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.

Race

No racial predilection has been reported.

Sex

AIs have a female sex predilection, probably reflecting the sex distribution of imaging procedures. Autopsy studies, however, show no sex preference for AAs.

Age

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.

Clinical

History

  • Pheochromocytomalike symptoms include episodic attacks, palpitations, sweats, headaches, and abdominal pain.
  • Primary hyperaldosteronism includes hypertension and unprovoked hypokalemia.
  • Adrenal carcinoma patients report weight loss, virilization, and feminization.
  • Cushing syndrome includes weight gain, weakness, depression, and bruising.
  • Evidence of hormonal excess includes the following:
    • Cushing syndrome for cortisol-secreting adenomas
    • Hypertension and hypokalemia for hyperaldosteronism
    • Labile hypertension and spells for pheochromocytoma
    • Virilization in women for androgen-secreting tumors
    • Feminization in men for estrogen-secreting tumors
  • If clinical evidence manifests, perform diagnostic hormonal testing (see Table 2). Table 2. Evaluation of AM Syndromes

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    Table
    DiagnosisFeaturesBiochemical Tests
    PheochromocytomaHigh blood pressure, catechol symptomsUrine- and plasma-free metanephrines
    Primary aldosteronismHigh blood pressure, low K+, low PRA*Plasma aldosterone-to-renin ratio
    Adrenocortical carcinomaVirilization or feminizationUrine 17-ketosteroids
    Cushing or "silent" Cushing syndromeCushing symptoms or normal examination resultsOvernight 1-mg dexamethasone test
    DiagnosisFeaturesBiochemical Tests
    PheochromocytomaHigh blood pressure, catechol symptomsUrine- and plasma-free metanephrines
    Primary aldosteronismHigh blood pressure, low K+, low PRA*Plasma aldosterone-to-renin ratio
    Adrenocortical carcinomaVirilization or feminizationUrine 17-ketosteroids
    Cushing or "silent" Cushing syndromeCushing symptoms or normal examination resultsOvernight 1-mg dexamethasone test
    *Plasma renin activity
  • Evidence of systemic disease, such as carcinoma, amyloidosis, or granulomatous disease, may be present.
  • Often, no clinical clues can be found and other information is needed for diagnosis.

Physical

  • Vital signs may include findings of high blood pressure, postural hypotension, and tachycardia.
  • A fundi feature is hypertensive retinopathy.
  • Skin findings include hirsutism and striae.
  • General signs are central obesity and gynecomastia.
  • Mass size is an important predictive characteristic.
    • Larger tumors are more likely to be malignant.
    • 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 (see image below and Image 1).8


Characteristics of adrenal masses and their malig...

Characteristics of adrenal masses and their malignant potential.

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Characteristics of adrenal masses and their malig...

Characteristics of adrenal masses and their malignant potential.

Causes

  • 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.
    • The multiple endocrine neoplasia (MEN1) gene is linked to multiple endocrine neoplasia type 1.
    • The aldosynthase/11-beta hydroxylase hybrid gene is associated with glucocorticoid-remediable hyperaldosteronism.

More on Adrenal Adenoma

Overview: Adrenal Adenoma
Differential Diagnoses & Workup: Adrenal Adenoma
Treatment & Medication: Adrenal Adenoma
Follow-up: Adrenal Adenoma
Multimedia: Adrenal Adenoma
References
Further Reading
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Further Reading

Related eMedicine topics:
Adrenal Adenoma [Radiology]
Adrenal Carcinoma [Oncology]
Adrenal Carcinoma [Pediatrics: General Medicine]
Adrenal Glands
Hyperaldosteronism [Pediatrics: General Medicine]
Hyperaldosteronism [Radiology]

Clinical guidelines:
ACR Appropriateness Criteria® incidentally discovered adrenal mass.
American College of Radiology - Medical Specialty Society.  2000 (revised 2007).  8 pages.  NGC:005995

ACR Appropriateness Criteria® neuroendocrine imaging.
American College of Radiology - Medical Specialty Society.  1999 (revised 2006).  11 pages.  [NGC Update Pending] NGC:005121

Case detection, diagnosis, and treatment of patients with primary aldosteronism: an Endocrine Society clinical practice guideline.
The Endocrine Society - Disease Specific Society.  2008 Sep.  26 pages.  NGC:006766

The diagnosis of Cushing's syndrome: an Endocrine Society clinical practice guideline.
The Endocrine Society - Disease Specific Society.  2008.  29 pages.  NGC:006662

Clinical trials:
 A Study of the Efficacy and Safety of CORLUX in the Treatment of Endogenous Cushing's Syndrome (SEISMIC)

D2 Dopamine Receptor on Human Aldosterone-Producing Adenoma and Its Role in Aldosterone Secretion and Cell Proliferation

Study of Adrenal Gland Tumors

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Keywords

adrenal adenoma, adrenal glands, adrenal tumor, adrenal carcinoma, adrenal cancer, adrenal gland cancer, adrenal gland carcinoma, adrenal incidentaloma, adrenal mass, Cushing syndrome, Cushing's syndrome, pheochromocytoma, hyperaldosteronism, primary hyperaldosteronism

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Contributor Information and Disclosures

Author

George T Griffing, MD, Professor of Medicine, St Louis University School of Medicine
George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

Medical Editor

Stanley Wallach, MD, Executive Director, American College of Nutrition; Clinical Professor, Department of Medicine, New York University School of Medicine
Stanley Wallach, MD is a member of the following medical societies: American Society for Bone and Mineral Research, American Society for Clinical Investigation, American Society for Clinical Nutrition, American Society for Nutritional Sciences, Association of American Physicians, and Endocrine Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Don S Schalch, MD, Professor Emeritus, Department of Internal Medicine, Division of Endocrinology, University of Wisconsin Hospitals and Clinics
Don S Schalch, MD is a member of the following medical societies: American Diabetes Association, American Federation for Medical Research, Central Society for Clinical Research, and Endocrine Society
Disclosure: Nothing to disclose.

CME Editor

Mark Cooper, MBBS, PhD, FRACP, Head, Diabetes & Metabolism Division, Baker Heart Research Institute, Professor of Medicine, Monash University
Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD, Professor of Medicine, St Louis University School of Medicine
George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

 
 
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