page_title: Gynecomastia
section_title: Pathophysiology
hierarchical_section_title: Gynecomastia / Pathophysiology
caption_attribution_description: English: Intermediate magnification micrograph of gynecomastoid hyperplasia, also gynecomastia and gynaecomastia. H&amp;E stain. Histologic changes: Moderate hyperplasia. Budding of cells into the duct lumen. Stromal palor. These changes may be seen in females. Related images Low mag. Intermed. mag. High mag. Very high mag. Low mag. Intermed. mag. High mag. Very high mag.
context_page_description: Gynecomastia is an endocrine system disorder in which a noncancerous increase in the size of male breast tissue occurs. Psychological distress or dysphoria may occur.
  The development of gynecomastia is usually associated with benign pubertal changes. However, 75% of pubertal gynecomastia cases resolve within two years of onset without treatment. In rare cases, gynecomastia has been known to occur in association with certain disease states. The pathologic causes of gynecomastia are diverse and may include Klinefelter syndrome, certain cancers, endocrine disorders, metabolic dysfunction, various medications, or may occur due to a natural decline in testosterone production. Disturbances in the endocrine system that lead to an increase in the ratio of estrogens/androgens are thought to be responsible for the development of gynecomastia. This may occur even if the levels of estrogens and androgens are both appropriate, but the ratio is altered. Diagnosis is based on signs and symptoms.
  The condition commonly resolves on its own and conservative management of gynecomastia is often all that is necessary.
context_section_description: The causes of common gynecomastia remain uncertain, but are thought to result from an imbalance between the actions of estrogen and androgens at the breast tissue. Breast prominence can result from enlargement of glandular breast tissue, chest adipose tissue (fat) and skin, and is typically a combination. As in females, estrogen stimulates the growth of breast tissue in males. In addition to directly stimulating male breast tissue growth, estrogens indirectly decrease secretion of testosterone by suppressing luteinizing hormone secretion, resulting in decreased testicular secretion of testosterone. Furthermore, estrogens can increase blood levels of the protein sex hormone-binding globulin (SHBG), which binds free testosterone (the active form) leading to decreased action of testosterone in male breast tissue.
  Primary hypogonadism (indicating an intrinsic problem with the testes in males) leads to decreased testosterone synthesis and increased conversion of testosterone to estradiol potentially leading to a gynecomastic appearance. Klinefelter syndrome is a notable example of a disorder that causes hypogonadism and gynecomastia, and has a higher risk of breast cancer in males (20–50 times higher than males without the disorder). Central hypogonadism (indicating a problem with the brain) leads to decreased production and release of luteinizing hormone (LH, a stimulatory signal for endogenous steroid hormone synthesis) which leads to decreased production of testosterone and estradiol in the testes.
  Individuals who have cirrhosis or chronic liver disease may develop gynecomastia for several reasons. Cirrhotics tend to have increased secretion of the androgenic hormone androstenedione from the adrenal glands, increased conversion of this hormone into various types of estrogen, and increased levels of SHBG, which leads to decreased blood levels of free testosterone. Around 10–40% of individuals with Graves' disease (a common form of hyperthyroidism) experience gynecomastia. Increased conversion of testosterone to estrogen by increased aromatase activity, increased levels of SHBG and increased production of testosterone and estradiol by the testes due to elevated levels of LH cause the gynecomastia. Proper treatment of the hyperthyroidism can lead to the resolution of the gynecomastia.
  Medications are known to cause gynecomastia through several different mechanisms. These mechanisms include increasing estrogen levels, mimicking estrogen, decreasing levels of testosterone or other androgens, blocking androgen receptors, increasing prolactin levels, or through unidentified means. High levels of prolactin in the blood (which may occur as a result of certain tumors or as a side effect of certain medications) has been associated with gynecomastia. A high level of prolactin in the blood can inhibit the release of gonadotropin-releasing hormone and therefore cause central hypogonadism. Receptors for prolactin and other hormones including insulin-like growth factor 1, insulin-like growth factor 2, luteinizing hormone, progesterone, and human chorionic gonadotropin have been found in male breast tissue, but the impact of these various hormones on gynecomastia development is not well understood.
caption: Microscopic image showing gynecomastoid hyperplasia, the cellular changes seen in gynecomastia H&E stain
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