Gynecomastia resident survival guide
| Gynecomastia Resident Survival Guide |
|---|
| Overview |
| Causes |
| Diagnosis |
| Treatment |
| Do's |
| Don'ts |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ifrah Fatima, M.B.B.S[2]
Overview
Gynecomastia is a benign male breast enlargement. It can be physiological, such as in infancy, puberty and old age or pathological, which is due to obesity, steroid use, pharmacologic agents, medical conditions including chronic liver and renal failure or hypogonadism. The diagnosis is primarily clinical.Laboratory investigations done are blood hormone levels, renal function tests and liver function tests and imaging such as ultrasound or mammography. Treatment is aimed at treating the underlying condition.Pharmacologic options include SERMs, androgens and aromatase inhibitors. Surgery is usually reserved for patients with either psychological stresses, extensive gynecomastia or failure of medical treatment.
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:
- Block synthesis of testosterone- Ketoconazole, Spironolactone, Metronidazole, Etomidate, Finasteride
- Antiandrogens- Bicalutamide, flutamide, Nilutamide
- 5-Alpha reductase inhibtors- Finasteride
- Cimetidine
- Hormones
- Testicular damage- Busulfan, Nitrosourea, Vincristine, Ethanol
- Other drugs
- Idiopathic[1]
- Physiologic:[1]
- Pathologic:[2]
Less Common Causes
- 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 the Endocrine Society and European Association of Andrology. ("Gynecomastia - American Family Physician".)
| Gynecomastia (Breast tissue enlargement) | |||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Newborn | Physiological; resolves within 4 weeks | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Drugs (see list above) | 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 Endocrine Society and European Association of Andrology. [4] [5] ("Gynecomastia - American Family Physician".)
| • Discontinue the causative drug • Treat the underlying cause | |||||||||||||||||||||||||||||||||||||||||
| Observe for 3 months | |||||||||||||||||||||||||||||||||||||||||
| If pain/tenderness; proceed with medical therapy | |||||||||||||||||||||||||||||||||||||||||
| Androgens and testosterone • Hypogonadism | Aromatase inhibitors in prostate cancer • Anastrazole | Selective estrogen receptor modulators (SERMs) •Tamoxifen (10-20 mg once daily for 3-9 months) •Raloxifene (60 mg once daily for 3-9 months) | Surgery if: • Persistent for > 12 months • Fibrotic gynecomastia • Failure of medical therapy | ||||||||||||||||||||||||||||||||||||||
Do's
- Always evaluate for physiological causes.
- Evaluate for drugs causing gynecomastia.
- Correct underlying causes first.
Don'ts
- Do not treat the gynecomastia without evaluating for an underlying cause.
References
- ↑ 1.0 1.1 Braunstein GD (2007). "Clinical practice. Gynecomastia". N Engl J Med. 357 (12): 1229–37. doi:10.1056/NEJMcp070677. PMID 17881754.
- ↑ 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) - ↑ Shozu M, Sebastian S, Takayama K, Hsu WT, Schultz RA, Neely K, Bryant M, Bulun SE (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.
- ↑ Kanakis GA, Nordkap L, Bang AK, Calogero AE, Bártfai G, Corona G; et al. (2019). "EAA clinical practice guidelines-gynecomastia evaluation and management". Andrology. 7 (6): 778–793. doi:10.1111/andr.12636. PMID 31099174.
- ↑ Schmoldt A, Benthe HF, Haberland G (1975). "Digitoxin metabolism by rat liver microsomes". Biochem Pharmacol. 24 (17): 1639–41. PMID doi.org/10.1210/jc.2010-1720 Check
|pmid=value (help).