Gynecomastia is the benign enlargement of the glandular tissue of the male breast. It is clinically defined by the presence of a mass extending concentrically beneath the nipple and is usually bilateral. Gynecomastia is categorized as physiological (during infancy, puberty, older age) or pathological (hypogonadism, liver disease, hyperthyroidism, drug-related). The glandular changes are the same, regardless of the etiology, with the degree of glandular proliferation depending on the duration and intensity of the inciting factor.
Histologically, gynecomastia has 3 stages. The initial stage (florid stage) is present during the first 6 months and is highlighted by ductal epithelial hyperplasia, increase in periductal connective tissue, and periductal inflammation.1 After a period of 12 months, the breast tissue typically transitions into the late or quiescent stage, during which there is stromal fibrosis, with resolution of the inflammatory reaction (fibrotic stage).1 There is an intermediate stage during the transition between these 2 phases; the histologic feature of this stage is similar to that of a female breast after exposure to estrogen, although terminal alveolar development is not seen, as progesterone concentrations in men are low.2
Enlargement of the male breast that is solely due to fat deposition, known as pseudogynecomastia (or lipomastia), is often seen in overweight and obese men. It is important to differentiate gynecomastia and lipomastia from breast carcinoma, which is a relatively rare condition in men. This chapter provides an overview of the epidemiology and pathophysiology of gynecomastia, its diagnostic evaluation, and current treatment options.
EPIDEMIOLOGY AND PATHOPHYSIOLOGY OF GYNECOMASTIA
Physiological gynecomastia is common in newborns, pubertal adolescents, and older men.
Pathological causes of gynecomastia include hypogonadism, obesity, medications, drugs of abuse, liver and renal disease, hyperthyroidism, estrogen or human chorionic gonadotropin–producing tumors, hereditary causes, and unintended exposure to estrogens.
Physiological gynecomastia can be a common finding in healthy men of all ages, but its incidence has 3 distinct peaks: infancy, puberty, and after 50 years of age. These peaks are thought to be related to physiological states of imbalance between estrogen and androgen action in the mammary glandular tissue.2 During infancy and puberty, this estrogen-to-androgen imbalance is transient, while in older men it could be persistent.
The first peak of physiological gynecomastia occurs in infants, with 60% to 90% of male newborns experiencing transient gynecomastia.3 This is thought to be related to placental aromatization of maternal and fetal androgens into estrogens, which enter the fetal circulation and stimulate mammary glandular proliferation. Neonatal gynecomastia usually resolves spontaneously within a few weeks after delivery, although it may persist for up to 6 months in some babies.3
The second peak occurs with the onset of puberty, with up to 65% of boys between 10 and 16 years of age presenting with some degree of breast ...