Gynecomastia is an abnormal enlargement of one or both breasts in men. Milk production may or may not be present.
Gynecomastia is fairly common. It is a physiologic phenomenon that occurs during puberty, when at least half of males experience enlargement of one or both breasts. Pubertal hypertrophy is characterized by a tender discoid enlargement of the breast tissue beneath the areola and usually subsides spontaneously within a year.
Gynecomastia also is common among elderly men, particularly when there is associated weight gain.
This condition is usually temporary and benign. It may be caused by hormonal imbalance, medication with estrogens or steroidal compounds, or failure of the liver to inactivate circulating estrogen, as in alcoholic cirrhosis.
It tends to remit spontaneously but, if marked, may be corrected surgically for cosmetic or psychological reasons.
It can be the first sign of a serious disorder such as a testicular tumor. Medical evaluation is always indicated when breast enlargement occurs.
Less commonly, gynecomastia may be caused by a hormone-secreting tumor of the breast, lung, or other organ. Biopsy may be performed to rule out the presence of cancer.
It is more common, however, in patients with Klinefelter’s syndrome.
Pseudogynecomastia is breast enlargement due to fat accumulation.
Pseudogynecomastia can be distinguished by physical examination. The examiner places the thumb and forefinger at opposite margins of the breast. The fingers are then brought slowly together along the nipple line. Enlarged glandular tissue can be recognized as a rubbery to firm disk of tissue concentric to and beneath the areolar area. The tissue often is freely mobile and may be exquisitely tender to palpation during the acute phase of development of gynecomastia.
The causes of gynecomastia are multiple. A search for a common mechanism has not been successful. A number of researchers believe that in many cases (but not all), an altered androgen/estrogen ratio causes changes in cellular elements in breast tissue. This could be due to:
- decrease in production of androgen
- increase in estrogen formation
- decrease in sensitivity of breast tissue to androgens
Certain medications can promote breast growth. They interact with the natural levels of testosterone and estrogen, and upset the balance in some manner. Gynecomastia is a common consequence of estrogen treatment in patients with prostate cancer. Drugs that may cause gynecomastia include:
- Hormones (androgens, anabolic steroids, estrogen agonists)
- Antiandrogens or androgen-synthesis inhibitors
- Antibiotics (isoniazid, ketoconazole, metronidazole)
- Anti-ulcer medications such as cimetidine
- Cancer chemotherapeutics, especially alkylating agents
- Cardiovascular drugs, such as captopril and digitoxin
- Psychoactive agents, such as diazepam and tricyclic antidepressants
- Recreational drugs, such as alcohol and marijuana
Alcohol and drugs can cause gynecomastia by mimicking estrogen and stimulating androgen production. Steroids and other excess androgens are sometimes converted by the body into estrogens and consequently cause male breast problems.
To reverse breast growth, it may be possible to change medications.
Men over the age of 50 tend to produce fewer androgens such as testosterone or gain fat tissue that converts androgen into estrogen. In 3 percent of reported cases, gynecomastia can signal lung, liver, or adrenal cancer. Tumors can secrete estrogen, upsetting the hormonal balance.
Gynecomastia And Peptic Ulcer Therapy
Gynecomastia has been frequently associated as a side effect of cimetidine (Tagamet) and has been less commonly associated with omeprazole (Prilosec) treatment. Another common ulcer treatment, ranitidine (Zantac), has also been associated with gynecomastia in a single case report.
To estimate the risk of gynecomastia with various drugs used for the treatment of peptic ulcer, a British research group studied men who received such prescriptions from their general practitioners over a four-year period. More than 81,000 men received at least one prescription for cimetidine, misoprostol, omeprazole or ranitidine. Men were excluded from the study who had a history of gynecomastia, testicular cancer, breast cancer, liver disease, or androgen therapy.
During the case study, gynecomastia developed in 153 men. The majority (84 percent) of cases were self-reported by patients, and in 43 percent of patients, gynecomastia was unilateral. In 46 percent of patients, the condition regressed, and in an additional 18 percent, partial regression occurred.
The researchers calculated that the risk of gynecomastia was substantially increased with cimetidine use but not with the other three drugs. The period of greatest risk was between the 7th and 12th month of cimetidine treatment and was influenced by daily dosage. The greatest risk occurred with dosages of more than 1,000 mg daily. Patients who followed such regimens were estimated to have a 40-fold risk, compared with patients who did not take cimetidine.
Choices of treatment for gynecomastia depend on several factors. The first is the cause of the disorder. If the gynecomastia is drug-induced, discontinuance of the agent may be all that is needed.
If it is pubertal, watchful waiting is in order, since in most patients the condition will resolve spontaneously.
Gynecomastia due to hyperthyroidism, acute hepatic disorders, or a recent onset of hypogonadism may remit in response to therapy for the underlying disorder.
The second consideration is whether the gynecomastia is an incidental finding, detected only by the physician, or is brought to the attention of the physician by the patient himself. Mild asymptomatic gynecomastia detected only through physical examination requires no therapy other than treatment of the underlying cause.
A third factor to consider is the length of time the gynecomastia has been present. A number of histologic studies have shown that gynecomastia present for less than six months usually demonstrates an active, or florid, histologic picture, characterized by marked ductal epithelial hyperplasia, proliferation of the periductal mesenchymal tissue, and periductal edema.
In general, the indications for treatment include: marked pain and tenderness, severe embarrassment or emotional disturbance. The most uniformly effective therapy at any stage is surgical removal of the glandular tissue through a periareolar incision. In patients with a large amount of adipose tissue in the subglandular area, suction-assisted lipectomy may be performed at the time of surgery to improve the cosmetic results.
Is it gynecomastia or pseudogynecomastia?
What is the cause?
Is it a hormonal problem?
Can you rule out a serious disorder such as testicular or breast cancer?
Is it related to male hypogonadism or hyperthyroidism?
Is the gynecomastia drug-related?
Under what circumstances would surgical correction be indicated?