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Author: Fawzi Ali, MB, BCh, Staff Physician, Department of Surgery, Division of Plastic Surgery, McMaster University

Coauthor(s): James Bain, MD, MSc, FRCS(C), Program Director, Head of Service, Associate Professor, Department of Surgery, Division of Plastic Surgery, McMaster University Health Sciences

Editors: Christian Paletta, MD, FACS, Professor, Division Chief and Program Director, Department of Plastic and Reconstructive Surgery, St Louis University School of Medicine; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Saleh M Shenaq, MD†, Former Director and Founder, The International Brachial Plexus Institute; Former Chief, Section of Plastic Surgery, Methodist Hospital, Houston; Nicolas (Nick) G Slenkovich, MD, Practice Director, Colorado Plastic Surgery Center at Swedish Medical Center; Al Aly, MD, FACS, Consulting Surgeon, Iowa City Plastic Surgery

Author and Editor Disclosure

Synonyms and related keywords: male breast enlargement, female-like breasts, feminization, male feminization, mastectomy, liposuction-assisted mastectomy, reduction mammaplasty, male breast lesion, male breast abnormality, male breast anomaly, feminized male breast, breast mass, male breast mass, congenital anorchia, Klinefelter syndrome, Klinefelter's syndrome, testicular feminization, hermaphroditism, hermaphrodite, adrenal carcinoma, adrenal cancer, liver disorder, hepatic disorder, liver disease, hepatic disease, malnutrition, testosterone deficiency

Gynecomastia is the growth of glandular tissue in male breasts. The term comes from the Greek words gyne and mastos, meaning female and breasts (feminine form), respectively, and roughly translating to femalelike breasts. It is a benign condition that accounts for more than 65% of male breast abnormalities. Gynecomastia is clearly differentiated from pseudogynecomastia, which is an accumulation of excess fat in a male breast.

History of the Procedure

Galen introduced the term gynecomastia in the second century AD. He defined gynecomastia as an unnatural increase in the breast fat of males. Although Galen was aware that glandular enlargement of the male breast occurred as a separate entity, he did not consider this gynecomastia.

The first recorded description of a reduction mammaplasty was by Paulas and Aegina in the seventh century AD, and the intention of the procedure was to correct large breasts in males. Several medical and surgical treatments of gynecomastia were described in the 1800s.

In 1976, Letterman and Schurter and Simon and Hoffman wrote extensive reviews of gynecomastia. The surgical technique of subcutaneous mastectomy for the treatment of the gynecomastia was first developed by Thorek and then later by Webster. Subcutaneous mastectomy was the treatment of choice until the early 1980s. Teimourian and Pearlman introduced liposuction-assisted mastectomy in 1984, and ultrasonic liposuction was developed in the late 1990s.

Frequency

Gynecomastia is a benign condition that accounts for 60% of all disorders of the male breast and 85% of male breast masses. It can occur in persons of any age, but 40% of cases occur in adolescent boys aged 14-15.5 years. Approximately 40% of healthy men and up to 70% of hospitalized men have palpable breast tissue. The prevalence rate increases to more than 60% in those in the seventh decade of life.

Etiology

Gynecomastia can be classified based on etiology. Idiopathic gynecomastia accounts for approximately 75% of cases.

Physiologic gynecomastia occurs primarily in newborns and in adolescents at puberty. In the newborn, the neonatal breast results from the action of maternal estrogens, placental estrogens, or both in concert. The increased breast tissue usually disappears in a few weeks. Adolescent gynecomastia is common during puberty. The median age of onset is 14 years. Breast tissue growth is often asymmetrical, and the breasts are frequently tender. Adolescent gynecomastia usually regresses by age 20 years. However, residual gynecomastia may be present in one or both breasts.

Pathologic gynecomastia is due to testosterone deficiency, increased estrogen production, or increased conversion of androgens to estrogens. The pathological conditions associated with gynecomastia include congenital anorchia, Klinefelter syndrome, testicular feminization, hermaphroditism, adrenal carcinoma, liver disorders, and malnutrition.

Many pharmacological agents can cause gynecomastia. These drugs can be categorized by their mechanisms of action. The first type is drugs that act exactly like estrogens, such as diethylstilbestrol, birth control pills, digitalis, and estrogen-containing cosmetics. The second type is drugs that enhance endogenous estrogen formation, such as gonadotropins and clomiphene. The third type is drugs that inhibit testosterone synthesis and action, such as ketoconazole, metronidazole, and cimetidine. The final type is drugs that act by unknown mechanisms, such as isoniazid, methyldopa, captopril, tricyclic antidepressants, diazepam, and heroin.

Pathophysiology

In boys, the main sex hormone is testosterone, which is secreted by the testes. In girls, the main sex hormone is estrogen, which is secreted by the ovaries. However, both hormones are secreted in both sexes. Some production of estrogen occurs in the testes, and some production of testosterone occurs in the ovaries. Gynecomastia has long been considered the result of an imbalance between estrogens, which stimulate breast tissue, and androgens, which antagonize this effect. An alteration in the normal ratio of estrogen to androgen has been found in patients with gynecomastia in association with many different etiological factors.

Estradiol is the growth hormone of the breast, and an excess of estradiol leads to the proliferation of breast tissue. Under normal circumstances, most estradiol in men is derived from the peripheral conversion of testosterone and adrenal estrone. The basic mechanisms of gynecomastia are a decrease in androgen production, an absolute increase in estrogen production, and an increased availability of estrogen precursors for peripheral conversion to estradiol (see Image 1).

Clinical

Patients present with an increase in breast tissue, which is unilateral in one third of cases. Tenderness may also be noted in a third of patients. Enlargement is usually central and symmetric, although occasionally it is eccentric. Idiopathic and drug-induced gynecomastia is usually unilateral; however, in pubertal and hormonal cases, the changes are often bilateral.

In 1934, Webster classified gynecomastia into 3 types. The first is glandular. Patients with a glandular component require surgical removal of the gland. The second is fatty glandular. With the fatty glandular form, surgery combined with liposuction allows good contouring. The third is simple fatty. In the cases that are primarily fatty in nature, liposuction alone provides good results.

Another classification described by Simon in 1973 groups the patients into categories according to the size of the gynecomastia. Group 1 is minor but visible breast enlargement without skin redundancy. Group 2A is moderate breast enlargement without skin redundancy. Group 2B is moderate breast enlargement with minor skin redundancy. Group 3 is gross breast enlargement with skin redundancy that simulates a pendulous female breast. Patients in groups 1 and 2 require no skin excision, but the breast development associated with group 3 is so marked that excess skin must be removed.



Generally, gynecomastia is a benign condition. The patient is usually satisfied with a simple explanation of the condition and reassurance that the condition is benign, particularly if the enlargement is minimal.

Surgical intervention is typically reserved for diagnostic purposes or for patients who request treatment. Most patients who visit a plastic surgeon request treatment for psychological reasons. These patients seek treatment because they find the condition embarrassing. They wear loose clothes and avoid exposure in showers and swimming pools, which greatly inhibits their activities of daily living.



The plastic surgeon must know the anatomy of the breast and be able to differentiate between the fat tissue and the glandular tissue. Ideally, in a liposuction-assisted mastectomy, the surgeon primarily targets the glandular breast tissue and the deep layer of subcutaneous fat. Liposuction of the superficial layer increases the chance of contour irregularities and skin retraction.



Although liposuction-assisted mastectomy for gynecomastia patients could be performed under local anesthesia, general anesthesia is usually required. Any significant medical problems, such as heart disease, lung disease, or diabetes, must be excluded before the procedure is performed.



Lab Studies

  • History and physical examinations are key elements used when considering the diagnosis of gynecomastia.
  • Blood work should include liver function tests and assays for follicle-stimulating hormone, luteinizing hormone, human chorionic gonadotropin, thyroid-stimulating hormone, thyroxine, estrogen, estradiol, and testosterone levels (see Image 2).
  • A sex chromatin study should be performed to exclude Klinefelter syndrome.
  • Elevated estrogen and 17-ketosteroid levels in urine indicate the presence of a feminizing adrenal tumor.

Imaging Studies

  • If indicated by the patient's history, physical examination, and laboratory results, include an ultrasound examination of the testes and breasts, computed tomography scan of adrenal glands, magnetic resonance imaging of sella turcica, and mammography.

Other Tests

  • Excisional biopsy or fine-needle aspiration of breast tissue should be performed if suspicion of a breast tumor exists.
  • All tissue removed should be sent for histological examination to exclude malignancy. Approximately 1% of all primary breast tumors are found in men, and breast cancer accounts for 0.7% of all male cancers.

Histologic Findings

Gynecomastia has 3 recognized pathological patterns.

The first type, the florid type, is characterized by an increase in the number and length of ducts, proliferation of ductal epithelium, periductal edema, a highly cellular fibroblastic stroma and hypervascularity, and the formation of pseudolobules. The florid type is the most common in patients with gynecomastia of less than 4 months' duration.

The second type, the fibrous type, is characterized by dilated ducts with minimal proliferation of epithelium, an absence of periductal edema, and an almost acellular fibrous stroma without adipose tissue. The fibrous type is the most common in patients with gynecomastia that lasts for 4-12 months.

The third type, the intermediate type, is an overlapping pattern of both the florid and the fibrous types.



Medical Therapy

Medical management is most successful when the gynecomastia is of recent onset and is caused by testosterone deficiency. Testosterone administration has inconsistent effects in persons with Klinefelter syndrome, but it can cause dramatic improvement in those with other forms of testicular failure (eg, anorchia, viral orchitis). Testosterone therapy involves an element of uncertainty because testosterone can serve as substrate for extraglandular estrogen formation. Under some circumstances (eg, patient with liver disease), androgen therapy can cause a disproportionate increase in plasma estrogen levels.

Various drug regimens have been tried for the treatment of gynecomastia, with varying degrees of success. These drugs include the antiestrogens tamoxifen and clomiphene, the aromatase inhibitor testolactone, and danazol (a weak androgen that inhibits gonadotropin secretion and causes a decrease in plasma testosterone). Treatment with dihydrotestosterone, which cannot be aromatized to estrogen, has also been reported to cause significant symptomatic improvement in persons with gynecomastia. However, to the authors' knowledge, no controlled studies have been conducted to study the clinical effectiveness of any of these regimens. The clinical efficacy of each regimen is not established.

Radiation

Several studies have shown that prophylactic breast irradiation reduces the risk of gynecomastia in patients with prostate cancer who are undergoing long-term estrogen or anti-androgen therapy.

Surgical Therapy

The objectives of surgical management for breast gynecomastia are (1) to restore the normal male breast contour and (2) to correct deformity of the breast, nipple, or areola. The 2 surgical options for the patient with gynecomastia are mastectomy and liposuction-assisted mastectomy.

Surgical resection (subcutaneous mastectomy)

The choice of surgical technique depends on the likelihood of skin redundancy after surgery. Generally, skin shrinkage is greater in younger individuals than in older individuals. Many different incisions are described for the excision of male breasts. The most common approach is the intra-areolar incision, or Webster incision. The Webster incision extends along the circumference of the areola, and the length of the incision varies.

The Webster intra-areolar incision is placed in the inferior hemisphere (see Image 3). This incision may be enlarged by lateral and medial extensions (see Image 4). The transverse nipple-areola incision is quite popular, but it is associated with limited exposure (see Image 5). The triple-V incision appears to offer maximum exposure (see Image 6). The transaxillary incision has been recommended because of its advantage of scars on the chest wall, but its disadvantage is that it causes glandular resection to be more difficult.

In moderate gynecomastia, skin resection and nipple transposition techniques are necessary. The most common type is the Letterman technique (see Image 7). After the skin is resected, the nipple-areola complex is rotated superiorly and medially based on a single dermal pedicle.

Sometimes, in massive gynecomastia, an en bloc resection of excessive skin and breast tissue and free nipple grafting can be performed (see Image 8).

Preoperatively, outline the incision and estimate the thickness and depth of fat and breast tissue to be removed. Extend the dissection to the pectoralis major fascia; excise the fat and breast tissue from this fascia. Achieve hemostasis, and, possibly, insert a catheter to prevent postoperative hematoma.

Liposuction-assisted mastectomy

Teimourian, Pearlman, and Courtiss first introduced liposuction with surgical resection in the 1980s. Recently, the advent of ultrasonic liposuction has improved the results of gynecomastia correction. In liposuction-assisted mastectomy, less compromise of the blood supply, nipple distortion, saucer deformity, and areola slough occur. In addition, the postoperative complications (eg, hemorrhage, infection, hematoma, seroma, necrosis) are fewer with this technique than with open surgical resection. However, liposuction-assisted mastectomy is not always effective when correcting pure glandular gynecomastia.

Preoperative Details

Explain all the possible postoperative complications of the surgery to the patient. In all patients, the extent of the palpable enlargement of the breast tissue is preoperatively outlined on the skin.

Intraoperative Details

Surgical resection

The technique used depends on the degree of gynecomastia. If gynecomastia is small or moderate, the Webster intra-areolar incision is the most appropriate. For a higher grade of gynecomastia, the concentric circle incision provides better exposure for the resection. For massive breast gynecomastia, more skin removal and deeper excision are necessary. With an accurate estimation of the extent of the hypertrophied tissue and the thickness of the fat on the chest wall, the dissection may reach the pectoralis major muscle fascia very near to the preoperatively estimated breast limits. The hypertrophied tissue is then excised from pectoralis major fascia. Hemostasis is secured, and a surgical drain is placed. Subcutaneous tissues are reapproximated, and the skin is closed subcuticularly.

Liposuction-assisted mastectomy

Liposuction-assisted mastectomy is the most popular method used for pseudogynecomastia. Through a 1-cm supra-areolar incision, parenchymal and glandular tissues are suctioned out. Preareolar and lateral suction are completed to remove fat. For small and moderate gynecomastia, suction lipectomy is extended to the clavicle, to the sternum, to 2 cm below the inframammary crease, and to the anterior axillary fold. For large gynecomastia, suction lipectomy is extended to the postaxillary fold and the iliac crest.

Postoperative Details

Compression garments are applied for at least 2 weeks. Dressings are changed as needed for the first 2 weeks. A small amount of blood, injection fluid, and liquified fat may leak from the incision sites for approximately 24 hours. The patient may resume his physical activities within few days.

Follow-up

Patients are usually seen 2 weeks postoperatively and once a month for the first 6 months. The final results are not fully appreciated for up to a year (see Image 9).



Complications of mastectomy for gynecomastia include the following:

  • Hematoma (most common)
  • Breast asymmetry
  • Nipple or areola necrosis
  • Nipple or areola inversion
  • Infection
  • Sensory changes
  • Painful scar
  • Contour deformity
  • Conspicuous scar
  • Skin redundancy



Regardless of the etiology of gynecomastia, the prognosis is excellent. Studies have shown that 90% of physiological gynecomastia involutes spontaneously within 2 years. In pathological-induced gynecomastia, medical or surgical treatment of the cause regresses gynecomastia, in most cases. In drug-induced gynecomastia, withdrawal of the medication leads to regression in 60% of patients. If the gynecomastia is of long duration, it is unlikely to spontaneously regress.



Drug-induced gynecomastia and gynecomastia due to long-term exposure to estrogen are believed by some to increase a patient's risk for breast cancer. However, numerous clinical studies have failed to show the relationship between breast cancer and gynecomastia. The only study which shows clear association between gynecomastia and male breast cancer is with Klinefelter syndrome; patients who have gynecomastia and Klinefelter syndrome are at about 50% increased risk of male breast cancer. Drug-induced gynecomastia is the second most common cause of gynecomastia. Significant studies have been conducted to research the effects of the drugs that cause gynecomastia.

In general, the management of gynecomastia is not controversial; its benign nature and the indications for medical and surgical management are well known.



Media file 1:  Pathophysiology of gynecomastia. Estradiol is the growth hormone of the breast, and an excess of estradiol leads to the proliferation of breast tissue. Under normal circumstances, most estradiol in men is derived from the peripheral conversion of testosterone and adrenal estrone. The basic mechanisms of gynecomastia are a decrease in androgen production, an absolute increase in estrogen production, and an increased availability of estrogen precursors for peripheral conversion to estradiol.
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Media type:  Graph

Media file 2:  Flow chart of the workup to determine the etiology of gynecomastia.
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Media type:  Graph

Media file 3:  The Webster intra-areolar incision is placed in the inferior hemisphere.
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Media type:  Image

Media file 4:  The Webster intra-areolar incision may be enlarged by lateral and medial extensions.
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Media type:  Image

Media file 5:  The transverse nipple-areola incision.
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Media type:  Image

Media file 6:  The triple-V incision offers maximum exposure.
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Media type:  Image

Media file 7:  The most common technique for skin resection and nipple transposition is the Letterman technique.
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Media type:  Image

Media file 8:  In massive gynecomastia, an en bloc resection of excessive skin and breast tissue and free nipple grafting can be performed using an elliptical incision with a nipple-areola graft.
Click to see larger pictureClick to see detailView Full Size Image
Media type:  Image

Media file 9:  Before (left) and after (right) photographs of liposuction-assisted mastectomy.
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Media type:  Photo



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Gynecomastia excerpt

Article Last Updated: Jun 9, 2006