Breast Disorders and Gynecomastia
Alison M. Moody
Jessica L. Buicko
EMBRYOLOGY
At the 5th or 6th week of fetal development, 2 mammary ridges (bands of thickened ectoderm) form. These extend form the axilla to the inguinal region bilaterally. Paired breasts develop along these ridges.1
Breasts develop when an ingrowth of ectoderm forms a primary tissue bud in the mesenchyme.1
At birth, breasts are identical in males and females.1
RELEVANT ANATOMY
Breasts are composed of 15 to 20 lobes, each of which is composed of several lobules. Each lobe of the breast terminates in a major (lactiferous) duct (2-4 mm in diameter), which opens through a constricted orifice (0.4-0.7 mm in diameter) into the ampulla of the nipple.1
Cooper suspensory ligaments are fibrous bands of connective tissue that travel through the breast and insert perpendicularly into the dermis to provide structural support.1
The epidermis of the nipple-areola complex is pigmented and variably corrugated. The areola contains sebaceous glands, sweat glands, and accessory glands. The dermal papilla at the tip of the nipple contains numerous sensory nerve endings.1
EPIDEMIOLOGY AND ETIOLOGY
Incidence: Gynecomastia affects up to 65% to 70% of adolescent males.2
Three different age groups experience gynecomastia: neonates (secondary to transplacental transfer of maternal estrogen), pubertal males, and senescent males.3
This chapter will focus on pubertal gynecomastia. Onset occurs between ages 10 and 12 years with peak pathology occurring between ages 13 and 14 years. Gynecomastia develops at least 6 months after the development of secondary sexual characteristics, when Tanner stages 3 to 5 in sexual development are reached.3 (Figure 41.1).
At the onset of puberty, the pituitary gland stimulates the testes to secrete testosterone only at night. As puberty advances, testosterone begins to be secreted during the day.
Gynecomastia usually resolves by age 17 years when adult androgen/estrogen ratios are achieved.3
Positive family history of gynecomastia is present 50% of the time2 (Figure 41.2).
Pathogenesis: imbalance between estrogens that stimulate proliferation of breast tissue and androgens, which function as estrogen antagonists.2 This imbalance can occur from an increase in free estrogen secretion (from adrenals or testes), a decrease in androgen secretion from the testes, altered metabolism, or increased binding of androgens relative to estrogens by sex hormone-binding globulin. Androgen receptor abnormalities and competitive displacement of androgens from their receptors by certain drugs can also lead to gynecomastia.3
Hyperprolactinemia can indirectly contribute to the development of gynecomastia because high prolactin levels induce a hypogonadal state and may lead to secondary testicular failure.3
Leptin may play a role in development of gynecomastia.2
Etiology: Broadly defined, gynecomastia can be caused by endocrine disorders, systemic illnesses, and medications, or defined as an idiopathic condition.2
Endocrine causes of gynecomastia include the following:
Hypogonadism: primary testicular failure or secondary gonadal insufficiency can occur secondary to hypothalamic-pituitary disease3
Klinefelter syndrome: testosterone levels are low and luteinizing hormone (LH) levels are subsequently increased secondary to loss of testosterone inhibition3
Defects in testosterone synthesis or action3
Hermaphroditism: both ovarian and testicular tissue are present3
Adrenal disorders: Adrenocorticotropic hormone deficiency (results in lack of corticosteroid feedback and upregulation of LH), congenital adrenal hyperplasia (results in increased production of androstenedione, which is aromatized to estrogen)3Stay updated, free articles. Join our Telegram channel
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