gynecomastia
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Introduction
Benign proliferaton of glandular tissue in the male breast.
Etiology
- persistent pubertal gynecomastia (25%)
- idiopathic 25%
- chronic illness
- malnutrition
- hypogonadism
- hyperthyroidism
- testicular tumors (germ cell tumors)
- pharmaceutical agents
- spironlactone, cimetidine, androgen antagonists, HIV1 protease inhibitors, 5-alpha reductase inhibitors (finasteride, dutasteride), opioids
- chronic renal failure
Epidemiology
- common in infants, adolescents, older adults
Pathology
- decrease in androgens, increase in estrogens
- androgen receptor antagonism
- increased sex-hormone binding globulin
- histology changes in breasts over time
- initial phase: generally present for 6 months
- epithelial hyperplasia, proliferation & lengthening of ducts, increase in stromal & periductal connective tissue, proliferation of periductal inflammatory cells, periductal edema, stromal fibroblast proliferation
- late phase: after 12 months
- increased number of ducts, marked dilation of ducts, little or no epithelial cell proliferation, increased stroma, stromal fibrosis, no inflammation
- initial phase: generally present for 6 months
Clinical manifestations
- rubbery of firm mass extending concentrically from the nipple
Diagnostic criteria
- subareolar glandular tissue >= 0.5 cm in diameter, usually bilateral
- distorts the normally flat contour of the male nipple[3][7]
- protrusion of the nipple due to the mass of glandular tissue beneath it
Laboratory
Radiology
- mammogram
- unilateral gynecomastia in a male is a concern for breast cancer[3]
Differential diagnosis
- breast cancer
- pseudogynecomastia (fat deposits in men with obesity)[3]
Management
- prevention:
- avoid pharmaceutical agents associated with gynecomastia
- chronic, mild, asymptomatic gynecomastia in males does not warrant evaluation[3]
- treatment during active proliferative phase may be beneficial[3]
- long-standing gynecomastia is resistant to treatment due to fibrosis[3]
- pharmaceutic agents
- androgens
- testosterone, may exacerbate gynecomastia, but useful for hypogonadism
- danazol
- androgens
- estrogen antagonists (investigational -> treatment of choice)[3]
- aromatase inhibitors (investigational -> treatment of choice)[3]
- surgery
More general terms
Additional terms
References
- ↑ Harrison's Principles of Internal Medicine, 13th ed. Companion Handbook, Isselbacher et al (eds), McGraw-Hill Inc. NY, 1995, pg 830
- ↑ UpToDate 14.1 http://www.utdol.com
- ↑ 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 Medical Knowledge Self Assessment Program (MKSAP) 16, 17, 18, 19. American College of Physicians, Philadelphia 2012, 2015, 2018, 2022
Medical Knowledge Self Assessment Program (MKSAP) 19 Board Basics. An Enhancement to MKSAP19. American College of Physicians, Philadelphia 2022
Medical Knowledge Self Assessment Program (MKSAP) 20 American College of Physicians, Philadelphia 2025 - ↑ Braunstein GD. Clinical practice. Gynecomastia. N Engl J Med. 2007 Sep 20;357(12):1229-37. PMID: https://pubmed.ncbi.nlm.nih.gov/17881754
- ↑ Dickson G. Gynecomastia. Am Fam Physician. 2012 Apr 1;85(7):716-22. Review. PMID: https://pubmed.ncbi.nlm.nih.gov/22534349 Free Article
- ↑ Sansone A, Romanelli F, Sansone M, et al. Gynecomastia and hormones. Endocrine. 2017;55:37-44. PMID: https://pubmed.ncbi.nlm.nih.gov/27145756
- ↑ 7.0 7.1 Kanakis GA, Nordkap L, Bang AK, et al. EAA clinical practice guidelines - gynecomastia evaluation and management. Andrology. 2019;7:778-793. PMID: https://pubmed.ncbi.nlm.nih.gov/31099174