Gynecomastia can be classified based on etiology. Idiopathic gynecomastia accounts for over 85% of cases that require surgical intervention.
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. Neonatal gynecomastia is not a problem that requires surgical intervention.
Adolescent gynecomastia, by definition, is initiated during puberty. The median age of onset is 13 years. Breast tissue growth is often asymmetrical, and the breasts are frequently tender. Adolescent gynecomastia usually regresses by the latter teen years. Note that the normal course during puberty is for a palpable, often visible, mass below the areola that begins to resolve in the mid teen years. While continued visible enlargement in the size of the breast is not normal in a teenager, residual palpable gynecomastia may be present in one or both breasts through the mid teen years. The authors would stress that the norm would be progressive diminution of any visible or palpable deformity through this period. In each case, the clinician must evaluate the degree of tissue present, the clinical presentation, and the physical and psychological effects on the patient.
Pathologic gynecomastia may be 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 tumors, liver disorders, pituitary tumors, and malnutrition.
Many pharmacological agents have been linked to gynecomastia.5 These drugs can be categorized by their mechanisms of action. The first type is drugs that act exactly like estrogens (eg, diethylstilbestrol, birth control pills, digitalis, estrogen-containing cosmetics). The second type is drugs that enhance endogenous estrogen formation (eg, gonadotropins, progesterone, clomiphene). The third type is drugs that inhibit testosterone synthesis and action (eg, ketoconazole, metronidazole, and cimetidine). The final type is drugs that act by unknown mechanisms (eg, isoniazid,6 methyldopa, captopril, tricyclic antidepressants, diazepam, marijuana, heroin). While heavy marijuana use has been linked to gynecomastia in rats, the relationship in humans is at best poorly documented. Chronic alcohol abuse may result in hepatocellular destruction and scarring which may result in gynecomastia. Adult patients should be routinely questioned about alcohol abuse or addiction.
A link between testicular atrophy, Klinefelter syndrome, and breast cancer has been noted. Longstanding, stable gynecomastia in an otherwise healthy male does not require an extensive medical workup.