Gynecomastia

From Greek: gyne meaning "woman" and mastos meaning "breast." In practical terms, this means abnormally large male breasts.

Gynecomastia can be emotionally devastating. A boy or man with gynecomastia struggles with anxiety over such simple acts as taking off his shirt in public. For many men, the best solution is surgery. However, a full history, examination and laboratory evaluation is necessary prior to surgery. Step two is a psychological redress.

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. Generally, the swollen breast tissue regresses within two to three weeks after birth.

The next peak of occurrence is during puberty, with a prevalence ranging from 4-69%. Some reports have shown a transient increase in estradiol concentration at puberty in boys who develop gynecomastia. Pubertal gynecomastia usually has an onset in boys aged 10-12 years. 90% of the time it regresses within 18 months, and persistence is seen in approximately 10% of patients over the age of than 17 years. The latter group often have a family history: father, brother, uncle or grandfather and no clear cause is usually found.

The third peak occurs in older men, with a peak incidence over 50. At least one-quarter of men are affected during this time. Gynecomastia in adults is often multi-factorial. 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. Approximately 25% of men will lack a definitive cause for adult onset gynecomastia. Another 25% will have a drug related cause, including:

a. drugs of unclear mechanism such as isonicotinic acid hydrazide, methyldopa, busulfan, tricyclic antidepressants, diazepam, heroin, penicillamine, omeprazole, phenothiazines, calcium channel blockers, marijuana, angiotensin-converting enzyme (ACE) inhibitors, antiulcer therapy: antihistamines and proton pump inhibitors, antiretroviral therapy (HAART) with efavirenz more commonly associated with gynecomastia than other HIV medications and amphetamines

b. drugs that enhance estrogen synthesis, such as gonadotropins, clomiphene, phenytoin, alcohol and exogenous testosterone. Most anabolic steroids also have a androgenic effect as well as a estrogenic. The greater the testosterone level rises the more your estrogen level will increase as well.

c. drugs that inhibit testosterone synthesis or action, such as ketoconazole, metronidazole, alkylating agents, cisplatin, spironolactone, cimetidine, flutamide, finasteride, and etomidate

d. Anti-androgens used to treat prostate enlargement or cancer and some other conditions. Examples include cyproterone, flutamide, finasteride and spironolactone.

e. drugs that mimic estrogens in activity: digitalis, diethylstilbestrol, as well as estrogen-contaminated food and estrogen-containing cosmetics

The remaining 25% of cases are related to various disease states described below: Cirrhosis, chronic liver disease or malnutrition (8%); Chronic renal insufficiency (1%); Hypogonadism (10%) Any of the conditions that interfere with normal testosterone production, such as castration, Klinefelter syndrome or pituitary insufficiency, can be associated with gynecomastia; Hyperthyroidism (1.5%); Tumors may be associated with gynecomastia (3 %): specifically testicular, lung, liver, or adrenal cancer.

Pseudogynecomastia, refers to a fat deposition in the subareolar area, in obese men. Men over the age of 50 tend to produce fewer androgens such as testosterone or gain fat tissue that converts androgen into estrogen. This is not pathologic or physiologic. Patients with pseudogynecomastia will typically have bilateral deposition of fat, and over time, these deposits will not change in shape or size. A careful history may reveal that the lesions have remained unchanged over a span of several years. If mammography demonstrates no evidence of malignancy, a treatment option would be observation alone.

It can be seen from the above that a through history and physical examination and in certain patients an endocrine laboratory work-up should be performed prior to surgery.

Surgical Options

The most popular recent technique for the surgical treatment of gynecomastia is liposuction. Liposuction alone is indicated when the skin tone is adequate for retraction into a favorable position following removal of breast and fatty tissue. Liposuction may be performed in any number of ways: hand held cannulae and tumescent technique, laser assisted emulsification/subcutaneous tightening, ultrasonic emulsification and finally with an oscillating intracannular fat cutting curette. However, liposuction alone has it’s limitations. In individuals with dense breasts, passing a liposuction cannulae through this tissue is often very difficult and as a result there may be an under-correction. In individuals with loose skin, a worsening of the ptosis (drooping) may occur, if liposuction alone is performed.

In common with mastopexy and breast reduction techniques, when the breast tissue is significantly ptotic and lax, some type of skin resection is needed in order to lift the nipple areola and to restore skin tone. Many choices have been described in respective order of increasing complexity: superior crescent mastopexy, superior crescent mastopexy with lateral limb extensions of elliptical skin resection, peri-areolar mastopexy, tear drop mastopexy, formal anchor incision Wise pattern inferior pedicle reduction and nipple areola free graft after a horizontal elliptical breast resection to the infra-mammary crease.

It has been my experience that the majority of patients with gynecomastia, after liposuction alone, feel there has been an under-correction. I prefer to perform a formal subcutaneous mastectomy using a superior periareola incision and then I perform liposuction peripheral to the subcutaneous mastectomy in order to create a more natural contour.

In cases where the nipple is clearly ptotic, a crescent of skin is removed above the original incision and the areola is lifted into a higher position, termed superior crescent mastopexy.

However, if the degree of ptosis and laxity is quite excessive and a large amount of skin and breast/fatty tissue must be removed in the vertical dimension, I prefer to remove a horizontal wedge of skin and breast/fat, then bring the upper incision downwards onto the lower incision at the infra-mammary crease, where it becomes less visible and then place the nipple areola onto the chest wall as a skin graft.