Pathophysiologic mechanisms for gynecomastia

Absolute increase in free estrogens

Direct secretion from:

Maternal-placental-fetal unit

Testes

Adrenal glands

Extraglandular aromatization of precursors

Displacement from sex hormone-binding globulin

Decreased metabolism

Exogenous estrogen administration

Decreased endogenous free androgens

Decreased secretion

Increased metabolism

Relative increase in free estrogen/free androgen ratio

Androgen insensitivity

Congenital defects in androgen receptor structure and function

Displacement of androgens from breast androgen receptors by certain drugs

Other

Estrogen-like effect of drugs

Possible enhanced sensitivity of breast tissue

Adapted from: Braunstein GD. Gynecomastia. N Engl J Med 1993; 328:490.

Graphic 53166 Version 3.0