Gynecomastia

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Chapter 19 GYNECOMASTIA

Theodore X. O’Connell

General Discussion

Gynecomastia, the occurrence of mammary tissue in the male, is a common condition. True gynecomastia, the presence of glandular breast tissue, should be distinguished from pseudogynecomastia, which is simply adipose tissue seen in overweight boys. Gynecomastia is considered the result of an imbalance between estrogens and androgens.

Gynecomastia occurs in three distinct peaks throughout the life cycle. The first is found in the neonatal period, in which palpable breast tissue transiently develops in 60% to 90% of all newborns because of the transplacental passage of estrogens. The effect disappears in a few weeks. The second peak occurs during puberty, when approximately two thirds of boys develop various degrees of subareolar hyperplasia of the breasts. A rise is seen beginning at approximately the age of 10 and peaks between the ages of 13 and 14, followed by a decline during the late teenage years. Tenderness of the breast is common but transitory. Spontaneous regression may occur within a few months, and gynecomastia rarely persists longer than 2 years. The last peak is found in the adult population, with the highest prevalence among 50- to-80-year-olds.

Benign, self-limited, and usually transitory gynecomastia has been reported in prepubertal children during the initiation of therapy with human growth hormone (HGH). Occasionally, breast development may mimic female breast development and fails to regress, as has been reported in familial gynecomastia. Asymmetric gynecomastia is common, and unilateral gynecomastia may actually represent a stage in the development of bilateral disease.

Prepubertal gynecomastia is uncommon, so an exogenous source of estrogens must be sought. Pathologic causes should be considered. However, a specific cause is rarely identified, and in 90% of patients, prepubertal gynecomastia is labeled idiopathic. Accidental or therapeutic exposure to small amounts of exogenous estrogens by inhalation, percutaneous absorption, or ingestion may cause gynecomastia. Gynecomastia has been observed in children with congenital virilizing adrenal hyperplasia, with Leydig cell tumors of the testes, and with feminizing tumors of the adrenal gland. Gynecomastia also occurs in patients with Klinefelter syndrome, certain types of male pseudohermaphroditism, androgen insensitivity syndromes, and 17-ketosteroid reductase defect.

In patients with Klinefelter syndrome, the risk of breast cancer is 16 times higher than in other men. Male breast cancer is rare, and it is even rarer in the adolescent population but warrants mention. Male breast cancer usually presents as a unilateral eccentric mass, hard or firm, that is fixed to the underlying tissues. It may be associated with dimpling of the skin, retraction or crusting of the nipple, nipple discharge, or axillary lymphadenopathy.

Key Historical Features

Pain or tenderness

Medical history

Key Physical Findings

Differentiate pseudogynecomastia (fatty tissue) from true gynecomastia

• The patient is placed in the supine position. Then the examiner grasps the breast between the thumb and forefinger and gently moves the two digits toward the nipple. If gynecomastia is present, a firm or rubbery, mobile, disklike mound of tissue arising concentrically from beneath the nipple and areolar region will be appreciated. If the enlargement is due to adipose tissue deposition, no such disk of tissue will be apparent.

Examination of the testes

Evidence of systemic disease, such as thyrotoxicosis, liver disease, or adrenal disease

Suggested Work-up

Neonatal gynecomastia develops in 60% to 90% of all newborns because of the transplacental passage of estrogens; the effect disappears in a few weeks, and no evaluation is necessary.

Painful, tender gynecomastia appearing during mid-to-late puberty requires only a history and physical examination, including careful palpation of the testicles. If the results are normal, reassurance may be provided and periodic follow-up scheduled. In most boys, the condition resolves spontaneously within 1 to 2 years. No further evaluation is necessary.

Prepubertal gynecomastia is rare and should always be considered pathological, prompting a search for an exogenous or endogenous source of estrogen. In 90% of cases, an underlying cause is not identified. The following is a suggested evaluation:

Figure 19-1 Interpretation of serum hormone levels and recommendations for further evaluation of patients with gynecomastia.

Thyroid-stimulating hormone (TSH)	To evaluate for hyperthyroidism
Luteinizing hormone	See Figure 19-1
Testosterone level	See Figure 19-1
Estradiol level	To evaluate for testicular Leydig-cell tumor or feminizing adrenocortical neoplasm
Human chorionic gonadotropin (hCG) level	To evaluate for testicular germ cell tumor, extragonadal germ cell tumor, or hCG-secreting nontrophoblastic neoplasm
	See Figure 19-1
Serum electrolytes	To evaluate for adrenal disease
Blood urea nitrogen (BUN) and creatinine	To evaluate for renal disease
Liver function tests	To evaluate for liver disease

Additional Work-up

Prolactin level	If gynecomastia is associated with galactorrhea to evaluate for prolactinoma
HIV test	If HIV infection is suspected or the patient has risk factors for infection
Testicular ultrasonongraphy	If testicular examination is abnormal or if estradiol is increased with a decreased or normal luteinizing hormone
Adrenal computed tomography (CT) or magnetic resonance imaging (MRI)	If adrenal neoplasm is suspected

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2. Einav-Bachar R., Phillip M., Aurbach-Klipper Y., Lazar L. Prepubertal gynaecomastia: aetiology, course, and outcome. Clin Endocrinol (Oxf). 2004;61:55–60.

3. Henley D.V., Lipson N., Korach K.S., Bloch C.A. Prepubertal gynecomastia linked to lavender and tea tree oils. N Engl J Med. 2007;356:479–485.

4. Rapaport R. Gynecomastia. In Behrman R.E., Kliegman R.M., Jenson H.B., editors: Nelson Textbook of Pediatrics, 17th ed., Philadelphia: WB Saunders, 2004.

5. Wilson J.D. Endocrine disorders of the breast. In: Isselbacher K.J., Braunwald E., Wilson J.D., editors. Harrisons’s Textbook of Internal Medicine. 13th ed. New York: McGraw-Hill; 1994:2037–2039.

6. Wise G.J., Roorda A.K., Kalter R. Male breast disease. J Am Coll Surg. 2005;200:255–269.

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