Pubertal gynecomastia, the glandular enlargement
of breast tissue in males, is a common complaint. Gynecomastia,
which occurs transiently in 40% to 60% of 10-
to 16-year-old boys and peaks in incidence at SMR 2 to SMR 4 (age
14 years), results from a decreased ratio of androgen to estrogen
and a change in end-organ receptor sensitivity. The breast tissue
is frequently firm, tender, and often asymmetric. Spontaneous resolution
occurs in 90% of boys within 3 years. Rare causes of gynecomastia
include endogenous states of estrogen excess, such as testicular,
adrenal, or pituitary tumors; hyperthyroidism and hypothyroidism;
hepatic disorders; refeeding poststarvation; endogenous androgen
deficiency states such as hypogonadism, Klinefelter syndrome, renal hemodialysis,
and congenital adrenal hyperplasia; and specific drugs, including
estrogen, testosterone, anabolic steroids, human chorionic gonadotropins,
tricyclic antidepressants, insulin, alcohol, marijuana, amphetamines,
methadone, cimetidine, digitalis, and cytotoxic agents among others. Pseudogynecomastia (fatty
tissue or muscle development), frequently confused with true gynecomastia
(glandular enlargement), can be distinguished by comparing the consistency
of the breast tissue with that of adipose tissue in the anterior
axillary fold.