Gynecomastia resident survival guide
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ifrah Fatima, M.B.B.S[2]
Overview
This section provides a short and straight to the point overview of the disease or symptom. The first sentence of the overview must contain the name of the disease.
Causes
Life-threatening Causes
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. There are no known life-threatening causes of gynecomastia.
Common Causes
- Drugs:[1][2][3][4]
- Block synthesis of testosterone- Ketoconazole, Spironolactone, Metronidazole, Etomidate, Finasteride
- Antiandrogens- Bicalutamide, flutamide, Nilutamide
- 5-Alpha reductase inhibtors- Finasteride
- Cimetidine
- Hormones
- Testicular damage- Busulfan, Nitrosurea, Vincristine, Ethanol
- Other drugs
- Idiopathic[2][5]
- Physiologic:[2][6]
- Pathologic:[7][6][8][9]
Less Common Causes[10]
- Aromatase overexpression
- Androgen insensitivity syndrome
- Drugs
- Kallmann syndrome
- Testosterone pathway defects
- Tumors
To review a complete list of gynecomastia causes, click here.
Genetic Causes
Diagnosis
Shown below is an algorithm summarizing the diagnosis of gynecomastia according to American Family Physicians. ("Gynecomastia - American Family Physician".)
| Gynecomastia (Breast tissue enlargement) | |||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Newborn | Physiological; resolves within 4 weeks | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Drugs (see list here) | Discontinue implicated drug | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Pseudogynecomastia | Weight loss | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Features of malignancy | Mammography; Breast USG; Biopsy | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Testicular mass | Testicular USG | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
| True Gynecomastia | |||||||||||||||||||||||||||||||||||||||||||||||||||||||
| • Testosterone • Estradiol(E2) • Luteinizing hormone (LH) • Prolactin • Follicle Stimulating Hormone (FSH) • Beta- hCG | • Thyroid function tests • Liver function tests • Renal function tests | If deranged,correct underlying disease | |||||||||||||||||||||||||||||||||||||||||||||||||||||
| • Low testosterone • High LH | • Low testosterone • Low LH | • High Estradiol • Low LH | • High Prolactin | • High beta-hCG | |||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary hypogonadism | Secondary hypogonadism | Testicular USG | MRI head for • Pituitary adenoma • Empty sella • Panhypopituitarism | Testicular USG | |||||||||||||||||||||||||||||||||||||||||||||||||||
| Sertoli or Leydig cell tumor | Evaluate for •Adrenal neoplasm • Exogenous estrogen use • Obesity (excess aromatase) | Germ cell tumor | If normal; evaluate for • Extragonadal germ cell tumor • Non-trophoblastic beta hCG secreting tumors | ||||||||||||||||||||||||||||||||||||||||||||||||||||
Treatment
Evaluation of Gynecomastia
❑ Obtain a detailed history Obtain laboratory tests ❑ Testosterone Treat underlying disorders ❑ Follow the algorithm for diagnosis to treat the underlying disorder or tumor | |||||
Shown below is an algorithm summarizing the treatment of gynecomastia according to the American Family Physicians. ("Gynecomastia - American Family Physician".)
guidelines.
| Box 1 in Row 1 | |||||||||||||||||||||||||||||||||||||||
| Box 2 in Row 2 | |||||||||||||||||||||||||||||||||||||||
| {{{ ,}}} | |||||||||||||||||||||||||||||||||||||||
| {{{ }}} | |||||||||||||||||||||||||||||||||||||||
Do's
- Always evaluate for physiological causes.
- Evaluate for drugs causing gynecomastia.
- Correct underlying causes first.
Don'ts
- The content in this section is in bullet points.
References
- ↑ Deepinder F, Braunstein GD (2012). "Drug-induced gynecomastia: an evidence-based review". Expert Opin Drug Saf. 11 (5): 779–95. doi:10.1517/14740338.2012.712109. PMID 22862307.
- ↑ 2.0 2.1 2.2 Braunstein GD (2007). "Clinical practice. Gynecomastia". N Engl J Med. 357 (12): 1229–37. doi:10.1056/NEJMcp070677. PMID 17881754.
- ↑ Lainscak M, Pelliccia F, Rosano G, Vitale C, Schiariti M, Greco C; et al. (2015). "Safety profile of mineralocorticoid receptor antagonists: Spironolactone and eplerenone". Int J Cardiol. 200: 25–9. doi:10.1016/j.ijcard.2015.05.127. PMID 26404748.
- ↑ Henley DV, Lipson N, Korach KS, Bloch CA (2007). "Prepubertal gynecomastia linked to lavender and tea tree oils". N Engl J Med. 356 (5): 479–85. doi:10.1056/NEJMoa064725. PMID 17267908.
- ↑ Vandeven H, Pensler J. PMID 28613563. Missing or empty
|title=(help) - ↑ 6.0 6.1 De Groot LJ, Chrousos G, Dungan K, Feingold KR, Grossman A, Hershman JM, Koch C, Korbonits M, McLachlan R, New M, Purnell J, Rebar R, Singer F, Vinik A, Swerdloff RS, Ng J. PMID 25905330. Vancouver style error: initials (help); Missing or empty
|title=(help) - ↑ Ladizinski B, Lee KC, Nutan FN, Higgins HW, Federman DG (2014). "Gynecomastia: etiologies, clinical presentations, diagnosis, and management". South Med J. 107 (1): 44–9. doi:10.1097/SMJ.0000000000000033. PMID 24389786.
- ↑ Wagner MS, Wajner SM, Maia AL (2008). "The role of thyroid hormone in testicular development and function". J Endocrinol. 199 (3): 351–65. doi:10.1677/JOE-08-0218. PMC 2799043. PMID 18728126.
- ↑ Cavanaugh J, Niewoehner CB, Nuttall FQ (1990). "Gynecomastia and cirrhosis of the liver". Arch. Intern. Med. 150 (3): 563–5. PMID 2310274.
- ↑ 10.0 10.1 Shozu M, Sebastian S, Takayama K, Hsu WT, Schultz RA, Neely K; et al. (2003). "Estrogen excess associated with novel gain-of-function mutations affecting the aromatase gene". N Engl J Med. 348 (19): 1855–65. doi:10.1056/NEJMoa021559. PMID 12736278.