Epidemiology
Etiology
Physiological gynecomastia
- Neonatal: Maternal estrogen.
- Pubertal gynecomastia
- Occurs in ∼ 50% of adolescent boys (typically occurs in patients aged 10–14 years)
- Caused by pubertal estrogen/androgen imbalance
- Clinical features
- Small, mobile, firm plaques of breast tissue in the subareolar region that develop during puberty
- Can be tender, unilateral/bilateral, and associated with fatty development around the nipple
- Spontaneously resolves (usually by 17 years of age)
- Elderly: ↓ Testosterone production.
Pathological gynecomastia
- Endocrine Disorders:
- Primary Hypogonadism (Testicular failure → ↓ testosterone, ↑ LH)
- Secondary Hypogonadism (Pituitary/hypothalamic failure → ↓ LH, ↓ testosterone)
- Tumors (e.g., prolactinoma), trauma, infiltrative disease.
- Tumors: hCG-producing (choriocarcinoma), Leydig/Sertoli cell, adrenal tumors.
- Systemic Disease:
- Cirrhosis: ↓ Estrogen breakdown.
- Chronic Kidney Disease: Uremic hypogonadism.
- Obesity: ↑ Peripheral aromatization in adipose tissue.
- Drug-induced
| Drug | Mechanism |
|---|
| Estrogens | Direct stimulation of ductal epithelial hyperplasia |
| Antiandrogens (e.g., flutamide, bicalutamide) | Competitive inhibition of testosterone receptor |
| 5-alpha reductase inhibitors (e.g., finasteride) | ↓ Conversion of testosterone to dihydrotestosterone |
| Spironolactone | ↓ Testosterone synthesis & inhibition of testosterone receptor |
| Ketoconazole | ↓ Synthesis of steroid hormones (↓ androgen > ↓ estrogen) |
| Cimetidine | Inhibition of testosterone receptor |
| Androgen-anabolic steroids | Aromatization of androgens to estrogen |
Pathophysiology
Clinical features
Diagnostics
Treatment