May be unilateral or bilateral, painful, or asymptomatic. Male breast enlargement is benign in 99% of cases.
Results from relative oestrogen excess or relative testosterone deficiency resulting in a high oestrogen-to-testosterone ratio.
Physiological gynaecomastia occurs in the newborn period, during puberty, and with ageing and obesity.
Many drugs, environmental exposures, illnesses, and some genetic conditions increase the risk for gynaecomastia.
Most cases require no specific treatment. Therapies for persistent pain or embarrassment include anti-oestrogen therapy such as tamoxifen, androgens, or surgery (liposuction or mammoplasty).
Gynaecomastia is the benign enlargement of the male breast with firm tissue extending concentrically beyond the nipple. Histologically, gynaecomastia is the benign proliferation of breast ducts and duct epithelial hyperplasia accompanied by varying amounts of inflammation, oedema, stroma, and fibrosis. Male breast enlargement entirely due to adipose tissue is called pseudo-gynaecomastia.
History and exam
- 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, goitre)
- 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 phyto-oestrogens or phthalates
- prostate cancer
- gender identity disorder
- renal failure
- drugs that reduce testosterone synthesis
- drugs that impair testosterone action
- drugs that increase oestrogen levels or stimulate oestrogen receptors
- drugs with complex or unknown mechanisms
Professor of Medicine
University of Minnesota
CBN is an author of a number of references cited in this monograph.
Professor of Pediatrics
Rumsey Chair of Pediatric Endocrinology
University of California
DS declares that he has no competing interests.
Professor of Medicine and Head of Endocrinology
Stony Brook University
HC is an author of a reference cited in this monograph.
Professor and Chairman
Department of Medicine
Cedars-Sinai Medical Center
GB declares that he has no competing interests.
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