Gynecomastia is the proliferation of benign male glandular breast tissue. It may be unilateral or bilateral, painful, or asymptomatic.
Gynecomastia results from relative estrogen excess or relative testosterone deficiency resulting in a high estrogen-to-testosterone ratio.
Physiologic gynecomastia occurs in the newborn period, during puberty, and with aging and obesity.
Many drugs, environmental exposures, illnesses, and some genetic conditions increase the risk for gynecomastia. Treatment may improve gynecomastia, especially if it is of recent onset.
Most cases require no specific treatment. Therapies for persistent pain or embarrassment include anti-estrogen therapy, androgen replacement if proven testosterone deficiency, or surgery (liposuction or mammoplasty).
Gynecomastia is the benign enlargement of the male breast with firm tissue extending concentrically beyond the nipple. Histologically, gynecomastia is the benign proliferation of breast ducts and duct epithelial hyperplasia accompanied by varying amounts of inflammation, edema, stroma, and fibrosis. Male breast enlargement entirely due to adipose tissue is called pseudogynecomastia.
History and exam
Key diagnostic factors
- palpable breast tissue
- newborn age
- pubertal age
- older adult age
- accidental medication exposure in children
- chemical substance abuse
- acne in adult males
- breast pain
- small or soft testicles
Other diagnostic factors
- erectile dysfunction or decreased libido
- nutritional supplements
- past history of abnormal sexual differentiation
- delayed secondary sex characteristics
- precocious puberty
- weight loss and malnutrition
- signs or symptoms of hypothalamic or pituitary disease
- signs or symptoms of liver failure (e.g., jaundice, ascites, spiders)
- signs or symptoms of hyperthyroidism (e.g., heat intolerance, weight loss, goiter)
- decreased body hair
- painless or enlarging testicular mass
- diminished strength or muscle atrophy
- anabolic steroid usage
- occupational exposure to embalming fluid or oral contraceptives
- contact with environmental phytoestrogens or phthalates
- prostate cancer
- gender identity disorder
- renal failure
- drugs that reduce testosterone synthesis
- drugs that impair testosterone action
- drugs that increase estrogen levels or stimulate estrogen receptors
- drugs with complex or unknown mechanisms
1st investigations to order
- serum TSH
- serum creatinine
- serum LFTs
Investigations to consider
- serum total testosterone
- serum LH
- serum estradiol
- serum sex hormone binding globulin (SHBG)
- serum free testosterone
- serum beta hCG
- serum dehydroepiandrosterone-sulfate (DHEAS)
- serum prolactin
- breast ultrasound
- core biopsy of breast (if cancer suspected)
- Testicular ultrasound
pubertal idiopathic gynecomastia
infantile and prepubertal gynecomastia
Catherine B. Niewoehner, MD
Professor of Medicine
University of Minnesota
CBN is an author of a number of references cited in this topic.
Dennis Styne, MD
Professor of Pediatrics
Rumsey Chair of Pediatric Endocrinology
University of California
DS declares that he has no competing interests.
Harold Carlson, MD
Professor of Medicine and Head of Endocrinology
Stony Brook University
HC is an author of a reference cited in this topic.
Glenn Braunstein, MD
Professor and Chairman
Department of Medicine
Cedars-Sinai Medical Center
GB declares that he has no competing interests.
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