In boys, the main sex hormone is testosterone, which is secreted by the testes. In girls, the main sex hormone is estrogen, which is secreted by the ovaries. However, both hormones are secreted in both sexes. Some production of estrogen occurs in the testes, and some production of testosterone occurs in the ovaries. Gynecomastia has long been considered the result of an imbalance between estrogens, which stimulate breast tissue, and androgens, which antagonize this effect. An alteration in the normal ratio of estrogen to androgen has been found in patients with gynecomastia in association with many different etiological factors.7, 8

Estradiol is the growth hormone of the breast in women, and an excess of estradiol leads to the proliferation of breast tissue. Under normal circumstances, most estradiol in men is derived from the peripheral conversion of testosterone and adrenal estrogen. The basic mechanisms of physiologic gynecomastia have been postulated to represent a decrease in androgen production, an absolute increase in estrogen production, and an increased availability of estrogen precursors for peripheral conversion to estradiol. See the image below.

Pathophysiology of gynecomastia

The etiology of most cases of gynecomastia remains unknown. The number of breast malignancies does not appear to be increased in patients with idiopathic gynecomastia. Patients who present with gynecomastia and have Klinefelter syndrome do exhibit an increased incidence of breast malignancies. Pensler et al noted that patients with Klinefelter syndrome exhibited elevated estrogen and progesterone receptors in their breast tissue.9 The presence of elevated estrogen and progesterone receptors in patients with Klinefelter syndrome provides a potential mechanism by which these patients may develop breast neoplasms. By contrast, patients with idiopathic gynecomastia did not demonstrate an increased number of estrogen or progesterone receptors. Also, the binding affinity of the receptors in both groups were not affected. The absence of elevated progesterone or estrogen receptors in patients with idiopathic gynecomastia helps to explain why these patients rarely manifest breast malignancy.

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