12/05/13 Gynecomastia

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Gynecomastia
Author: George Ansstas, MD; Chief Editor: George T Griffing, MD more...

Updated: Mar 18, 2013
Practice Essentials
Gynecomastia is a benign enlargement of the male breast (usually bilateral but sometimes unilateral) resulting
from a proliferation of the glandular component of the breast. It is defined clinically by the presence of a rubbery or
firm mass extending concentrically from the nipples. Gynecomastia should be differentiated from
pseudogynecomastia (lipomastia), which is characterized by fat deposition without glandular proliferation.
Essential update: Laser-assisted lipolysis found safe and effective for gynecomastia
In a prospective study of 28 patients with bilateral gynecomastia who were treated with laser-assisted lipolysis
(LAL), Trelles et al found that LAL reduced breast volume and significantly tightened skin. At 6-month follow-up, 18
patients rated their results as very good; 6 as good; 3 as fair; and 1 as poor. Mean chest circumferences were
significantly reduced, from 117.4 11.1 cm to 103.3 7.5 cm. According to the authors, the procedure was found
to be safe, with no incidents reported in the postoperative period. LAL was performed with a 980-nm diode laser
(continuous emission, 15 W power, 8-12 kJ total energy per breast) after tumescent anesthetic infiltration.
[1]
Signs and symptoms
A thorough history should be obtained that addresses the following:
Age of onset and duration of the condition
Any recent changes in nipple size and any pain or discharge from the nipples
History of mumps, testicular trauma, alcohol use, or drug use
Family history of gynecomastia
History of sexual dysfunction, infertility, or hypogonadism
Physical examination should include the following:
Thorough examination of the breasts, with attention to size and consistency
Assessment for any nipple discharge or axillary lymphadenopathy
Testing to differentiate between true gynecomastia and pseudogynecomastia
Assessment of glandular tissue
Examination of the testicles, with attention to size and consistency, as well as nodules or asymmetry
Observation of any signs of feminization
Checking for any stigmata of chronic liver disease, thyroid disease, or renal disease
Hematoma, lipoma, male sexual dysfunction, and neurofibroma can be included in the differential diagnosis.

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See Clinical Presentation for more detail.
Diagnosis
Patients with physiologic gynecomastia do not require further evaluation. Similarly, asymptomatic and pubertal
gynecomastia do not require further tests and should be reevaluated in 6 months. Further evaluation is necessary
in the following situations:
Breast size greater than 5 cm (macromastia)
A lump that is tender, of recent onset, progressive, or of unknown duration
Signs of malignancy (eg, hard or fixed lymph nodes or positive lymph node findings)
Laboratory tests that may be considered include the following:
Serum chemistry panel
Free or total testosterone, luteinizing hormone (LH), estradiol, and dehydroepiandrosterone sulfate levels
Thyroid-stimulating hormone (TSH) and free thyroxine levels
Imaging studies that may be helpful include the following:
Mammography: Indicated if one or more features of breast cancer are apparent upon clinical examination,
[2]
followed by fine-needle aspiration or breast biopsy as appropriate
[3, 4]
Testicular ultrasonography: Indicated if the serum estradiol level is elevated and the clinical examination
findings suggest the possibility of a testicular neoplasm
Breast ultrasonography (though the positive predictive value of imaging in males is low
[5]
)
CT: Gynecomastia is often reported on CT scans
See Workup for more detail.
Management
General management considerations are as follows:
As a rule, no treatment is required for physiologic gynecomastia
Pubertal gynecomastia resolves spontaneously within several weeks to 3 years in most patients; breasts
larger than 4 cm in diameter may not regress completely
Identifying and managing an underlying primary disorder often alleviates breast enlargement
For patients with idiopathic gynecomastia or with residual gynecomastia after treatment of the primary
cause, medical or surgical treatment may be considered.
If medical therapies are used, they should be tried early in the conditions course
Pharmacologic agents used to treat gynecomastia include the following:
Clomiphene
Tamoxifen
Danazol (less frequently used)
Surgical approaches that may be considered include the following:
Reduction mammoplasty: Considered in cases of macromastia, long-standing gynecomastia, or failed
medical therapy, as well as for cosmetic reasons
More extensive plastic surgery: May be considered in cases of marked gynecomastia or excessive sagging
of the breast tissue from weight loss
Endoscopic subcutaneous mastectomy, without skin excision
[6]
Surgical complications may include the following:
Sloughing of tissue due to a compromised blood supply
Contour irregularity
Hematoma or seroma formation
Permanent numbness in the nipple-areolar area
See Treatment and Medication for more detail.
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Image library
Adolescent gynecomastia.
Background
Gynecomastia is a benign enlargement of the male breast resulting from a proliferation of the glandular component
of the breast (see the image below). Gynecomastia is defined clinically by the presence of a rubbery or firm mass
extending concentrically from the nipples. Although the condition is usually bilateral, it can be unilateral. The
condition known as pseudogynecomastia, or lipomastia, is characterized by fat deposition without glandular
proliferation. (See Etiology, Presentation, and Workup.)
Adolescent gynecomastia.
Patient education
Reassure patients with physiologic gynecomastia regarding the benign nature of their condition, and inform them
that most cases spontaneously resolve. (See Prognosis.)
Counsel patients regarding the various treatment modalities available for gynecomastia, and highlight the risks,
adverse effects, success rates, and benefits of each modality. For patient education information, see the Men's
Health Center. (See Treatment and Medication.)
Etiology
Gynecomastia results from an altered estrogen-androgen balance, in favor of estrogen, or from increased breast
sensitivity to a normal circulating estrogen level.
[7]
The imbalance is between the stimulatory effect of estrogen and
the inhibitory effect of androgen. (The normal production ratio of testosterone to estrogen is approximately 100:1;
the normal ratio of testosterone to estrogen in the circulation is approximately 300:1.)
Estrogens induce ductal epithelial hyperplasia, ductal elongation and branching, proliferation of the periductal
fibroblasts, and an increase in vascularity. The histologic picture is similar in male and female breast tissue after
exposure to estrogen.
[8]
Estrogen production in males results mainly from the peripheral conversion of androgens (testosterone and
androstenedione) to estradiol and estrone, which occurs through the action of the enzyme aromatase (mainly in
muscle, skin, and adipose tissue). The testes secrete only 6-10 mg of estradiol and 2.5 mg of estrone per day.
Since this only comprises a small fraction of estrogens in circulation (ie, 15% of estradiol and 5% of estrone), the
remainder of estrogen in males is derived from the extraglandular aromatization of testosterone and
androstenedione to estradiol and estrone. Thus, any cause of estrogen excess from overproduction to peripheral
aromatization of androgens can initiate the cascade to breast development.
Increased estrogen production and/or action can occur at the testicular level or at the periphery and is
characterized as follows:
From the testes - Can be due to testicular tumors or to ectopic production of human chorionic gonadotropin
(hCG), as is reported with carcinoma of lung, kidney, gastrointestinal (GI) tract, and extragonadal germ cell
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tumors
From peripheral conversion - Can be due to increased substrate or increased activity of aromatase, as in
chronic liver disease, malnutrition, hyperthyroidism, adrenal tumors, and familial gynecomastia
Gynecomastia can be physiologic or pathologic.
[9, 10]
Physiologic gynecomastia is seen in newborn infants,
pubescent adolescents,
[11, 12]
and elderly individuals.
Gynecomastia in adults is often multifactorial. Increased aromatization of testosterone to estradiol and the gradual
decrease of testosterone production in the aging testes most often account for gynecomastia in adult males. Older
men are also more likely to take medications associated with gynecomastia than are younger men.
Rarely, hyperprolactinemia may lead to gynecomastia through its effects on the hypothalamus to cause central
hypogonadism.
[13, 14]
Prolactin has also been reported to decrease androgen receptors and increase estrogen and
progesterone receptors in breast cancer cells, which can lead to male gynecomastia. Prolactin itself stimulates
milk production in breast tissue that has been primed by estrogen and progesterone, but it does not directly cause
gynecomastia itself.
Pathologic gynecomastia
Pathologic gynecomastia can be caused by an increase in the production and/or action of estrogen, by a
decrease in the production and/or action of testosterone accompanied by increased aromatization and high
estrogen, or by drug use. However, gynecomastia can also be idiopathic.
[7]
Pathologic decrease of androgen or increase of estrogen can be illustrated as following:
Decreased androgen action
Decreased production
Increased sex-hormone binding globulin (SHBG) binds testosterone > estrogen favoring greater peripheral
estrogen action
Androgen receptor antagonism
Increased estrogen action
Increased aromatization of androgens to estrogens
Increased androgenic precursors (dehydroepiandrosterone [DHEA] and androstenedione)
Increased SHBG binds testosterone > estrogen favoring greater peripheral estrogen action
Estrogen receptor agonism
Conditions that result in primary or secondary hypogonadism can lead to gynecomastia in different mechanisms.
Primary hypogonadism can be related to a congenital abnormality such as Klinefelter syndrome, an enzymatic
defect in testosterone biosynthesis, infection, infiltrative disorders, testicular trauma, or aging. The associated
reduction in testosterone production leads to a decrease in the serum testosterone concentration and a
compensatory rise in leuteinizing hormone (LH) release. The excess LH results in enhanced Leydig cell
stimulation with inhibition of the 17,20-lyase and 17-hydroxylase activities and increased aromatization of
testosterone to estradiol; the net effect is an increase in estradiol relative to testosterone secretion.
[15]
Secondary hypogonadism due to a hypothalamic or pituitary abnormality may also be associated with
gynecomastia. In these patients, the production of LH is deficient, resulting in a low testosterone production rate
and low estradiol production from the testes. However, the adrenal cortex continues to produce estrogen
precursors that are aromatized in extraglandular tissue; the result is an estrogen/androgen imbalance.
The following are some of the conditions associated with gynecomastia:
Klinefelter syndrome
Congenital anorchia
Testicular trauma
Viral orchitis
Kallmann syndrome: A form of hypogonadotropic hypogonadism, Kallmann syndrome is usually associated
with varying degrees of abnormality in olfactory perception; this results from the defective migration of
gonadotropin-releasing hormonesecreting cells (which co-migrate with the cells of the olfactory epithelium)
during embryogenesis.
Pituitary tumors or abnormalities such as the ones that lead to either hypersecretion or hyposecretion of LH
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Malignancies that increase the serum level of hCG (eg, large cell lung cancer, gastric carcinoma, renal cell
carcinoma, hepatoma)
[7]
Renal failure: Men with end-stage renal disease may have reduced testosterone and elevated gonadotropin
values. This apparent primary testicular failure may then lead to increased breast development.
[7]
Hyperthyroidism: Gynecomastia seen with hyperthyroidism is due to increased aromatase activity and
increased levels of SHBG. SHBG binds androgens more avidly than estrogen, allowing for higher free levels
to act on peripheral tissues such as the breast.
Malnutrition: Gynecomastia seen with malnutrition and starvation is probably due to reduced gonadotropin
and testosterone levels relative to estrogen and may worsen with refeeding, owing to a rise in estradiol
production that outpaces the increases in gonadotropin and testosterone.
Environmental pollutants: The most likely mechanism is through estrogen receptor binding and activation.
Androgen insensitivity syndrome
Aromatase excess syndrome: Familial prepubertal gynecomastia is a rare autosomal dominant inherited
disorder that results in an excess estrogen state due to increased aromatase activity. This disorder
appears to be due to heterozygous inversion or polymorphisms of the P450 aromatase gene. The
phenotypic picture was described in an 8-year-old boy with accelerated growth and bone maturation with
severe feminization and gynecomastia due to high rate conversion of plasma androstenedione to
estrone.
[16]
Various drugs are implicated in gynecomastia and can be classified into categories (although drugs in the same
class do not all cause gynecomastia to the same extent).
[17, 18]
Of note, the pathophysiologic mechanism for some drugs, such as estrogens or antiandrogens, is quite clear.
However, for others such as spironolactone, the mechanism is more complex. Spironolactone can increase the
aromatization of testosterone to estradiol, decrease testosterone production by the testes, increasing the rate of
testosterone clearance by displacing it from SHBG, and also binding to androgen receptors leading to
gynecomastia through estrogen/testosterone imbalance. Another example is tea tree oil, which possesses weak
estrogenic and antiandrogenic activities that may contribute to an imbalance in estrogen and androgen pathway
signaling. Estrogenic or antiandrogenic activities have been reported for other essential oils and some of their
monoterpene constituents.
[19]
Antiandrogen/inhibitors of androgen synthesis are as follows:
Cyproterone acetate
Flutamide, bicalutamide, nilutamide
Finasteride, dutasteride
Ketoconazole
Spironolactone
Tea tree oil
Cancer/chemotherapeutic drugs are as follows:
Alkylating agents
Methotrexate
Vinca alkaloids
Imatinib
Cardiac and antihypertensive medications are as follows:
Calcium channel blockers (verapamil, nifedipine, diltiazem)
ACE Inhibitors (captopril, enalapril)
Digoxin
Alpha-blockers
Amiodarone
Methyldopa
Reserpine
Nitrates
Hormones are as follows:
Androgens
Anabolic steroids
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Estrogens
Growth hormones
Chorionic gonadotropin
Psychoactive drugs are as follows:
Haloperidol
Diazepam
Tricyclic antidepressants
Haloperidol
Phenothiazines
Drugs for infectious diseases are as follows:
Antiretroviral therapy for HIV/AIDS (eg, indinavir)
Isoniazid
Ethionamide
Griseofulvin
Minocycline
Metronidazole
Ketoconazole
Drugs of abuse are as follows:
Amphetamines
Heroin
Methadone
Alcohol
Marijuana
Others are as follows:
Theophylline
Omeprazole
Auranofin
Diethylpropion
Domperidone
Penicillamine
Sulindac
Heparin
Methotrexate
Drugs can also be stratified depending on the evidence that supports their association with gynecomastia, as
follows:
Probable - Estrogenlike or estrogen receptor binders, verapamil with relative risk (RR) of 9.7, spironolactone
(RR of 9.3), cimetidine (RR of 7.2), finasteride, and ketoconazole
Possible - Digoxin (RR of 2.7), nifedipine (RR of 2.9), cytotoxic agents, and marijuana
Uncertain (reported but could be coincidental) - Nitrates, alfa-blockers, and diazepam
A study by Den Hond et al on the effects of pollutants on sexual maturation indicated that higher blood levels of
lead increased the risk of gynecomastia in the study's subjects, while higher serum levels of hexachlorobenzene
decreased the risk. The report involved 1679 adolescents, aged 14-15 years. The mechanism of gynecomastia is
thought to be through estrogen receptor binding and activation.
[9]
Estimates suggest the following etiologies in males seeking medical attention for gynecomastia:
Persistent pubertal gynecomastia - 25%
Drugs - 10-25%
No detectable abnormality - 25%
Cirrhosis or malnutrition - 8%
Primary hypogonadism - 8%
Testicular tumors - 3%
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Secondary hypogonadism - 2%
Hyperthyroidism - 1.5%
Chronic renal insufficiency - 1%
Epidemiology
Occurrence in the United States
Gynecomastia is the most common reason for male breast evaluation. The condition is common in infancy and
adolescence, as well as in middle-aged to older adult males. One estimate is that 60-90% of infants have transient
gynecomastia due to the high estrogen state of pregnancy.
The next peak of occurrence is during puberty,
[11, 12]
with a prevalence ranging from 4-69%. Some reports have
shown a transient increase in estradiol concentration at the onset of puberty in boys who develop gynecomastia.
Pubertal gynecomastia usually has an onset in boys aged 10-12 years. It generally regresses within 18 months,
and persistence is uncommon in men older than 17 years. The third peak occurs in older men, with a prevalence
of 24-65%. [#Clinical]
Prognosis
Other than the associated risk of breast cancer, gynecomastia does not cause any long-term complications. In
approximately 90% of cases, pubertal gynecomastia resolves within a period of months to several years. However,
macromastia seldom resolves completely and often requires surgery.
Gynecomastia that occurs secondary to an underlying, treatable cause (eg, drug-induced gynecomastia) usually
responds to treatment or removal of the primary cause. Men with Klinefelter syndrome have a 10- to 20-fold
increased risk for breast cancer.

Contributor Information and Disclosures
Author
George Ansstas, MD Instructor, Department of Internal Medicine, Washington University School of Medicine
George Ansstas, MD is a member of the following medical societies: American Medical Association
Disclosure: Nothing to disclose.
Coauthor(s)
Michael Ansstas, MD Fellow in Allergy and Immunology, Department of Internal Medicine, St Louis University
Hospital
Disclosure: Nothing to disclose.
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, International Society for Clinical
Densitometry, Southern Society for Clinical Investigation, and The Endocrine Society
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, International Society for Clinical
Densitometry, Southern Society for Clinical Investigation, and The Endocrine Society
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Disclosure: Nothing to disclose.
Additional Contributors
Mark R Allee, MD Associate Professor, Department of Medicine, University of Oklahoma College of Medicine
Mark R Allee, MD is a member of the following medical societies: American College of Physicians
Disclosure: Nothing to disclose.
Mary Zoe Baker, MD Professor, Department of Medicine, Section of Endocrinology, Metabolism and
Hypertension, University of Oklahoma College of Medicine; Medical Director, Medicine Specialty Clinic, General
Medicine Clinic and Medicine Residents' Clinic, University of Oklahoma Physicians
Mary Zoe Baker, MD is a member of the following medical societies: American Association of Clinical
Endocrinologists, American Chemical Society, and American College of Physicians-American Society of
Internal Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center
College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Reference Salary Employment
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