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Gynecomastia is the proliferation of mammary gland tissue in male individuals, including those with Klinefelter syndrome; neonatal gynecomastia manifests in both male and female infants. Gynecomastia is caused by an increased estrogen/testosterone ratio that can be physiological (typically in neonates, during puberty, or in older adults), pathological (e.g., due to medications, liver cirrhosis, chronic kidney disease, estrogen-secreting tumors), or idiopathic. Gynecomastia is a clinical diagnosis confirmed by identifying palpable glandular tissue on physical examination. A should be performed in all patients; drug-induced gynecomastia accounts for 25% of cases. Diagnostics are not routinely recommended for individuals with physiological gynecomastia. Breast imaging may be considered to rule out differential diagnoses or if physical examination findings are inconclusive. Diagnostic workup for pathological gynecomastia should be guided by clinical evaluation and includes laboratory studies to evaluate for chronic diseases (e.g., liver chemistries, renal function tests, thyroid function tests), hypogonadism (e.g., sex hormone profile), or malignancy (e.g., tumor markers, imaging, biopsy). Pathological gynecomastia can usually be managed by treating the underlying cause. Physiological gynecomastia usually regresses spontaneously. Surgery (e.g., nipple-sparing mastectomy) may be considered for pathological gynecomastia unresponsive to treatment of the underlying cause, longstanding gynecomastia, or cosmesis.
Gynecomastia is caused by an increased estrogen/testosterone ratio (e.g., elevated estrogen levels, decreased testosterone levels, or both) but can be idiopathic in upto 25% of patients. It is the most common abnormality of the male breast. 
Physiological gynecomastia 
- Neonatal gynecomastia 
Pubertal gynecomastia 
- Occurs in ∼ 50% of adolescent boys (typically occurs in patients aged 10–14 years)
- Caused by pubertal estrogen/androgen imbalance
- Clinical features
- Pharmacotherapy or surgery can be considered for persistent pubertal gynecomastia or if symptoms cause significant distress.
- Senile gynecomastia: occurs in ∼ 50% of men > 50 years
Pathological gynecomastia 
Due to estrogen excess
- Liver cirrhosis: due to increased conversion of adrenal androgen precursors to estrogen
- Hyperthyroidism: due to
- Refeeding (after prolonged starvation) 
Due to decreased testosterone
- Klinefelter syndrome
- Chronic kidney disease 
- Testicular disorders (e.g., mumps orchitis, castration, trauma to both testes)
- Hyperprolactinemia 
Drug-induced gynecomastia accounts for up to 25% of cases. 
- Inhibitors of testosterone receptors
- Inhibitors of testosterone synthesis
- Exogenous androgens and androgenic steroids ; 
- Estrogen receptor stimulators
- cART drugs
Some Hormones Cause Fulminant Kleavage: Spironolactone, Hormones, Cimetidine, Finasteride, Ketoconazole cause gynecomastia.
General principles 
- Obtain a detailed medical history (including a ; see ).
- Perform a thorough physical examination.
- Confirm gynecomastia (i.e., palpable glandular breast tissue) on physical examination.
- Distinguish between physiological and pathological gynecomastia based on clinical evaluation.
Examine the breasts and testes in all patients with gynecomastia. Expedite further diagnostics (e.g., imaging, biopsies) if malignancy is suspected (e.g., features of breast cancer; testicular mass on palpation or imaging). 
Assess all patients with symptom onset in adulthood for pathological gynecomastia, even when an apparent cause has been identified. 
Routine studies 
- Serum prolactin levels: Elevated levels are suggestive of prolactinoma. 
Suspected estrogen-secreting tumors
- Tumor markers
Breast imaging 
- Indications and preferred first-line modalities
- Supportive findings of gynecomastia 
Consider routinely screening for breast cancer in all patients with Klinefelter syndrome who present with gynecomastia; these individuals have a significantly higher risk (16–30 times) of breast cancer than those with XY chromosomes. 
Some guidelines recommend testicular ultrasound for all individuals with gynecomastia; others recommend imaging only in the following cases: 
- Suspected testicular tumor 
- Suspected hypogonadism 
- Gynecomastia > 5 cm 
- Pathological gynecomastia of unknown etiology 
- Pseudogynecomastia 
- Male breast cancer: examination findings may include hard immobile mass, skin changes, axillary lymphadenopathy, and nipple retraction or discharge 
- Lipoma: well-defined mobile typically unilateral mass; not necessarily subareolar in location 
- Mastitis: signs of local (e.g., erythema, edema, tenderness) and systemic (e.g., fever, leukocytosis) infection
The differential diagnoses listed here are not exhaustive.
Treat the underlying cause and monitor for regression. Examples include:
- Drug-induced gynecomastia: If feasible, discontinue the causative agent.
- Hyperthyroidism: See “Treatment of hyperthyroidism.”
- Testicular tumor: See “Management of testicular cancer.”
- Confirmed hypogonadism: testosterone replacement 
Most patients with gynecomastia experience spontaneous regression or respond well to management of the underlying condition. 
After discontinuing medications or treating the underlying cause, an observation period is recommended to monitor for regression. Surgery can be considered for patients with persistent gynecomastia. 
Physiological and idiopathic gynecomastia 
Watchful waiting can be considered if no pathological cause is suspected and the patient is not disturbed by their symptoms.
- Reassurance and follow up every 6 months. 
- Provide adequate analgesia.
- Persistent gynecomastia
- Agents: (off-label): selective estrogen receptor modulators (tamoxifen, raloxifene)
- Indications (limited evidence of benefit)