Enlargement of the ductal, stromal, and adipose components of the male breast.
What is pseudogynecomastia?
Enlargement of the adipose tissue of the male breast; often seen in obesity.
In what three age distributions does gynecomastia peak?
Neonatal, pubertal, and adult.
What is the incidence of gynecomastia in each age group?
Neonates: 60% to 90%
Adults: 30% to 65%
Overall incidence is 35%.
What is the Simon classification of gynecomastia?
I: Small but visible breast development, no skin redundancy.
IIa: Moderate breast development, no skin redundancy.
IIb: Moderate breast development with skin redundancy.
III: Severe breast development with large skin redundancy.
Name the hallmark location and clinic chest examination findings of gynecomastia.
Concentric mass directly beneath the nipple. Often described as a palpable, tender, firm, mobile, disc-like mound.
Florid—increase in vascularity and ductal tissues, early finding <4 months.
Fibrous—fewer ducts and stromal fibrosis, typically present after 1 year.
Intermediate—Mixture of the two as Florid transitions to Fibrous
What is the normal average areolar diameter in the male nipple areola complex?
25 to 30 mm.
What is the most common male nipple areola complex shape and location?
Oval and 20 cm from the sternal notch.
What is symptomatic gynecomastia?
Breast pain and tenderness.
What is the incidence and cause of newborn gynecomastia?
60%; transplacental passage of estrogens.
Name the four clinical etiologies of gynecomastia.
Physiologic (neonatal, pubertal, senescent),
What is pathologic gynecomastia?
Gynecomastia secondary to underlying disease, that is,
• adrenal tumors
• hypogonadism (acquired or congenital)
• liver disease
How is familial gynecomastia genetically transmitted?
What are the clinical characteristics of pubertal gynecomastia?
Glandular tissue is greater than 4 cm in diameter, resembling early female breast development.
What is the pathogenesis of pubertal gynecomastia?
Imbalance of androgen to estrogen ratio, often occurring in early puberty.
Commonly seen in midpuberty with Tanner stage 3 to 4 pubic hair and testicular volumes of 5 to 10 mL bilaterally.
Male: Prepubertal genitalia
Female: Prepubertal genitalia, no glandular breast tissue; areola follows chest wall
Pubic Hair: Vellus pubic hair, no sexual hair
Male: Genital enlargement and change in skin texture
Female: Breast budding
Pubic Hair: Sparse, long, pigmented downy hair
Male: Growth in penile length and circumference
Female: Continued breast enlargement, no separation of contour
Pubic Hair: Darker, coarser, curlier
Male: Penis enlarged in length and circumference. Enlarged testes
Female: Areolar and papillae elevation and secondary mound formation
Pubic Hair: Adult in quality but decreased distribution
Male: Adult genitalia
Female: Mature female breasts
Pubic Hair: Adult in quality, may spread onto medial thighs
What is the typical course of pubertal gynecomastia?
Self-limited in 75% to 90% of adolescents, regressing over 1 to 3 years.
What is the pathogenesis of senescent gynecomastia?
Primary testicular failure resulting in hypogonadism, and increased adipose tissue, leading to increased production of estrogens by aromatase.
Which drugs are strongly associated with gynecomastia?
• Anabolic steroids
What is the pathogenesis of drug-induced gynecomastia?
Administration of exogenous estrogens (i.e., prostate cancer hormone therapy, topical estrogen creams)
Reduction of serum testosterone (i.e., ketoconazole, alkylating agents)
Direct gonadal suppression, (i.e., chemotherapy agents)
Blockade of androgen action (i.e., cimetidine, spironolactone, marijuana)
Luteinizing hormone (LH) and human chorionic gonadotropin (HCG).
How does primary testicular failure cause increased estrogen to androgen ratio and gynecomastia?