GYNECOMASTIA
Some degree of mammary hypertrophy is normally found in the male breast during adolescence. In two-thirds of all boys between the ages of 14 and 17 years, a button-shaped plaque of mammary tissue is palpated beneath the nipple. This is known as the puberty node. Although gynecomastia is usually bilateral, it can be unilateral. Normally, this involutes before the age of 21. Rarely, this adolescent growth of tissue may be two or three times its normal size and may be persistent. Sometimes it has been found so discrete and firm that the observers classified the enlargement as a benign fibroadenoma. Fat deposition without glandular proliferation is termed pseudogynecomastia.
Gynecomastia most frequently happens
in newborn, pubertal, and older males. On palpation, the enlarged mammary gland
may be the seat of increased tissue, both mammary and adipose, feeling like the
normal female breast. Often a discrete, firm mass is felt, which is composed
microscopically of increased amounts of periductal connective tissue surrounding
mammary ducts containing hyperplastic epithelium.
Growth of the mammary gland during
puberty is explained by changes in the endocrine environment characteristic of
this age. Gynecomastia generally results from an imbalance in the
estrogen–androgen balance, in favor of estrogen (stimulatory) over androgen
(inhibitory), or increased breast sensitivity to a normal circulating estrogen
level. Estrogens induce ductal epithelial hyperplasia, ductal elongation and
branching, proliferation of the periductal fibroblasts, and an increase in
vascularity just as they do in the female breast: the histologic picture is
similar in male and female breast tissue after exposure to estrogen. The Leydig
cells of the testes, long accepted to be the source of the androgens, also
secrete estrogens. Most estrogen production in males is from the peripheral
conversion of androgens (testosterone and androstenedione to estradiol and
estrone, respectively) through the action of aromatase, mainly in muscle, skin,
and adipose tissue. For this reason, overweight adolescent boys are more likely
to undergo these changes or to have more marked changes than those of normal
weight. The overall prevalence of adolescent gynecomastia ranges from 4% to
69%.
Gynecomastia in late adolescence and
in the adult is, in many instances, associated with clinical endocrine
disorders that result in estrogen excess or decreased androgens. Any endocrine
disorder that results in hypogonadism, either primary, such as Klinefelter
syndrome (46, XXY), or secondary, such as hypopituitarism due to an adenoma,
can result in gynecomastia. Other causes include testicular and feminizing
adrenal neoplasms. Hyperthyroidism is also associated with gynecomastia, which
is thought to be related to a relative decrease in circulating free
testosterone due to thyroid stimulated increases in sex hormone binding
globulin as well as increased peripheral aromatization. Genetic causes of
gynecomastia include complete and incomplete forms of androgen insensitivity as
well as certain types of congenital adrenal hyperplasia.
Gynecomastia in adult males is often
multifactorial. Increased peripheral aromatization of testosterone to estradiol
and the gradual decrease of testosterone production in the aging testes
probably accounts for gynecomastia in older men. There are a number of medications associated with gynecomastia,
including hormones like estrogen, some antibiotics like metronidazole,
antihypertensives like spironolactone, antiulcer medications such as
ranitidine, and psychoactive drugs like phenothiazines. Alcohol, especially if
associated with cirrhosis, marijuana, methadone and amphetamines, has also been
associated with gynecomastia.
Rather frequently, gynecomastia is
found in patients with testicular tumors (especially chorioepithelioma but also
teratoma and interstitial cell tumors).
Testicular deficiency in all its
forms may be accompanied by gynecomastia of varying degrees. Mammary
hypertrophy has been originally described as an integral part of Klinefelter
syndrome. Only when the underlying hyalinization process of the tubular
apparatus of the testes in this condition starts late in puberty is
gynecomastia a frequent but not obligatory phenomenon.
Simple mastectomy, performed through
a curved incision following the margin of the areola, remains the most satisfactory treatment.
