History and exam
Key diagnostic factors
common
palpable breast tissue
The patient should be examined in the supine position.[11][27]
Thumb and forefinger are placed on the outer and inner breast margins and are brought together in a pincer movement along the chest wall until they reach a mound of firm breast tissue located concentrically under the nipple/areola.
The diameter is measured with a ruler or measuring tape.
A diameter 2 cm or less is considered normal in an adult.
newborn age
Newborns have high estrogen levels derived from the mother and placenta.
pubertal age
In puberty there is a physiologic response to the increase in testosterone fueled by marked increases in growth hormone, insulin-like growth factor-1, follicle-stimulating hormone, and luteinizing hormone. Testosterone increases 30-fold, and estrogen increases 3-fold but peaks earlier than testosterone.
older adult age
Decrease in free testosterone and increase in adipose tissue with aging.
accidental medication exposure in children
Opportunities for children to obtain adult medications (including contraceptives) should be reviewed.
substance use disorder
acne in adult males
The triad of marked muscle development, small testicles, and adult acne suggests exogenous androgen usage.
obesity
Testosterone is converted to estrogen by aromatase in fat tissue.
uncommon
breast pain
Symptomatic men are more likely to note irritation than pain, with chafing of the breast.
small or soft testicles
Sign of low testosterone.
Decreased body hair, female fat distribution, decreased strength, or small or soft testicles suggest hypogonadism.
The triad of marked muscle development, small testicles, and adult acne suggests exogenous androgen usage.
Other diagnostic factors
common
erectile dysfunction or decreased libido
May be due to low testosterone, although there are many other causes.
uncommon
nutritional supplements
Exposure to estrogenizing substances may result from supplement ingestion, some of which may be adulterated with anabolic steroids.
differences in sex development (DSD)
Gynecomastia can result from genetic factors (e.g., testicular feminization, Klinefelter syndrome [47, XXY]).
delayed secondary sex characteristics
Low testosterone leading to gynecomastia can result from orchitis, hemochromatosis, chemotherapy or radiation therapy, spinal cord injury, or trauma.
precocious puberty
Any history of abnormal sexual development may be related to imbalance of the testosterone-to-estrogen ratio.
weight loss and malnutrition
In severe physiologic stress testosterone decreases more than estrogen and takes longer to rebound.
Weight loss may also be an indicator of hyperthyroidism.
signs or symptoms of hypothalamic or pituitary disease
May include headache or visual loss.
Gynecomastia can result from low follicle-stimulating hormone and luteinizing hormone (LH), leading to low Leydig cell stimulation and testosterone production.
High prolactin suppresses the gonadotropin-releasing hormone pulse generator needed for normal LH production.
signs or symptoms of liver failure (e.g., jaundice, ascites, spiders)
There may be a history of alcohol use or hepatitis. Other signs and symptoms include Dupuytren contracture or hepatosplenomegaly. Because of decreased testosterone catabolism in the face of hepatic insufficiency, more testosterone is available for conversion to estrogen.
signs or symptoms of hyperthyroidism (e.g., heat intolerance, weight loss, goiter)
Other signs and symptoms include sweating, stare or lid lag, exophthalmos, pretibial myxedema, palpitations, and tremor.
Hyperthyroidism results in high sex hormone binding globulin and increased estrogen production.
decreased body hair
Sign of low testosterone. Decreased body hair, female fat distribution, decreased strength, or small or soft testicles suggest hypogonadism.
painless or enlarging testicular mass
Gynecomastia can result from human chorionic gonadotropin-producing testicular tumors and estrogen-producing Leydig cell tumors.
diminished strength or muscle atrophy
Sign of low testosterone.
Risk factors
strong
anabolic steroid usage
prostate cancer
Estrogen and antiandrogen therapy in the treatment of prostate cancer may contribute to breast enlargement.[34]
hormone therapy for gender dysphoria
Estrogen and antiandrogen therapy for gender dysphoria (e.g., in male-to-female transgender individuals) may contribute to breast enlargement.[35]
drugs that reduce testosterone synthesis
Include the following: gonadotropin-releasing hormone (GnRH) agonists (which down-regulate pituitary luteinizing hormone production); cancer chemotherapeutic agents; ketoconazole; metronidazole; spironolactone (reduces synthesis more than eplerenone; also impairs testosterone action); some antipsychotics (increase prolactin, which suppresses GnRH pulses).[22][36][37]
drugs that impair testosterone action
Include the following: androgen receptor blockers (bicalutamide, flutamide); spironolactone (which also reduces testosterone synthesis); 5-alpha reductase inhibitors (e.g., finasteride); H2 antagonists (e.g., cimetidine); proton-pump inhibitors (impair less than H2 antagonists).[28][29][30][31][38]
weak
occupational exposure to embalming fluid or oral contraceptives
contact with environmental phytoestrogens or phthalates
Environmental phytoestrogens (plant estrogens) and other compounds activating estrogen receptors include shampoos, creams and cosmetics, tea tree oil, or lavender oil.[45][46][47] Phthalates are industrial compounds found in many cosmetic products and plastics.[48] Children are particularly vulnerable.
hyperthyroidism
renal failure
Multifactorial mechanisms may lead to gynecomastia.
cirrhosis
Androgen catabolism is reduced, so there is greater availability of androgens for conversion to estrogen.[51]
drugs with complex or unknown mechanisms
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