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Male Breast -Gynaecomastia.

Gynecomastia: Enlargement of the Male Breast

Gynecomastia ~(guy-ne-co-mast-ear) is a harmless enlargement of the male breast resulting from a growth of the glandular tissue of the breast. 

Gynecomastia is defined clinically by the presence of a rubbery or firm mass extending from the nipples. Although gynecomastia  usually affects both sides, it can be unilateral.

Pseudogynecomastia, or lipomastia, is characterized by fat deposition without glandular swelling and is much more common in overweight men.

In pseudogynecomastia, there is only fat deposition, found across the chest. This is not a disease, just excess fat deposited on the chest. Patients with pseudogynecomastia will typically have bilateral deposition of fat, and over time, these deposits will not change in shape or size. Simply losing weight is the treatment of choice.

Cause of True Gynaecomastia.

Gynecomastia results from an altered hormone oestrogen (female)-androgen(male) balance, in favour of oestrogen, or from increased breast sensitivity to a normal circulating oestrogen level.

The imbalance is between the stimulatory effect of oestrogen and the inhibitory effect of androgen. Oestrogens induce ductal growth, elongation and branching, with proliferation of the periductal fibroblasts, and an increase in vascularity. 

Oestrogen production in males results mainly from the conversion of androgens (testosterone ) — through the action of the enzyme aromatase, mainly in muscle, skin, and adipose tissue — to oestradiol and oestrone.


Gynecomastia is the most common reason for male breast evaluation. The condition is common in infancy and adolescence, as well as in middle-aged to older adult males. 

Peak of occurrence is during puberty .Pubertal gynecomastia usually has an onset in boys aged 10-14 years. It generally regresses within 18 months, and persistence is uncommon in men older than 17 years. 

Gynecomastia in adults is often multifactorial. Increased conversion of testosterone to Oestradiol and the gradual decrease of testosterone production in the aging testes most often account for gynecomastia in adult males. Older men are also more likely to take medications associated with gynecomastia than are younger men.

Estimates suggest the following causes in males seeking medical attention for gynecomastia:

Persistent pubertal gynecomastia – 25%
Drugs – 10-25% prescribed from your GP.
No detectable abnormality – 25%
Liver disease – 8%
Testicular failure– 8%
Testicular tumours – 3%
Hyperthyroidism - 1.5%
Chronic renal insufficiency – 1%

Clinical Causes

Gynecomastia can be physiologic or pathologic

Physiologic gynecomastia is seen in newborn infants, pubescent adolescents,and elderly individuals.
Pathologic gynecomastia can be caused by a decrease in the production and/or action of testosterone, by an increase in the production and/or action of oestrogen, or by drug use; however, gynecomastia can also be idiopathic (f unknown cause)

Conditions that result in primary or secondary testicular failure and cause decreased testosterone production and/or action include the following:

Testicular trauma
Testicular torsion (twisting) 
Viral orchitis (eg mumps infection
Pituitary tumors
Malignancies (rare) that increase the serum human chorionic gonadotropin (hCG) (eg, large cell lung cancer, gastric carcinoma, renal cell carcinoma, hepatoma)
Kidney failure
Over active thyroid gland

Increased oestrogen production and/or action can occur at the testicular level or at the periphery.

From the testes, which can be due to testicular tumors or to ectopic production of hCG as is reported with carcinoma of lung, kidney, GI tract, and extragonadal germ cell tumors
From peripheral conversion, which can be due to increased substrate or increased activity of aromatase as in chronic liver disease, malnutrition, hyperthyroidism, adrenal tumors, and familial gynecomastia

 Various drugs are implicated in gynecomastia and can be classified into the following categories (although drugs in the same class do not all cause gynecomastia to the same extent

Oestrogens or drugs with estrogen like activity, such as Digoxin, and phytoestrogens

Drugs that enhance oestrogen synthesis, such as  clomiphene, phenytoin, and exogenous testosterone

Drugs that inhibit testosterone synthesis or action, such as ketoconazole, metronidazole, alkylating agents, cisplatin, spironolactone, cimetidine, flutamide, finasteride, and etomidate

Drugs that act by unknown mechanisms, such as isonicotinic acid hydrazide, methyldopa, busulfan, tricyclic antidepressants, diazepam, penicillamine, omeprazole, phenothiazines, calcium channel blockers, angiotensin-converting enzyme (ACE) inhibitors,
alcohol, marijuana,  (Very Common)


Patients with physiologic gynecomastia do not require further evaluation.
Further evaluation is necessary in patients with the following:

Breast size greater than 5 cm (macromastia)
A lump that is tender, of recent onset, progressive, or of unknown duration
Signs of malignancy (eg, hard or fixed lymph nodes or positive lymph node findings)

A serum chemistry panel may be helpful in evaluating for renal or liver disease.
Obtain thyroid-stimulating hormone (TSH) and free thyroxine levels if hyperthyroidism is suspected.

Imaging Studies
mammogram or ultrasound if 1 or more features of breast cancer are apparent upon clinical examination.This can be followed by fine-needle aspiration or breast biopsy, as the case merits.

Other Tests

Asymptomatic and pubertal gynecomastia do not require further tests and should be reevaluated in 6 months.


Medical Care

Generally, no treatment is required for physiologic gynecomastia.
A major factor that should influence the initial choice of therapy is the duration of gynecomastia. It is unlikely that any medical therapy will result in significant regression in the late fibrotic stage (a duration of 12 mo or longer). As a result, medical therapies, if used, should be tried early in the condition's course.
Pubertal gynecomastia resolves spontaneously within several weeks to 3 years in approximately 90% of patients. Breasts greater than 4 cm in diameter may not completely regress.
For patients with idiopathic gynecomastia or with residual gynecomastia after treatment of the primary cause, medical or surgical treatment may be considered.
Clomiphene, an antiestrogen, can be administered on a trial basis at a dose of 50-100 mg per day for up to 6 months. Approximately 50% of patients achieve partial reduction in breast size, and approximately 20% of patients note complete resolution. Adverse effects, while rare, include visual problems, rash, and nausea.
Tamoxifen, an oestrogen antagonist, is effective for recent-onset and tender gynecomastia when used in doses of 20 mg a day.[14 ]Up to 80% of patients report partial to complete resolution. Tamoxifen is typically used for 3 months before referral to a surgeon. Nausea and epigastric discomfort are the main adverse effects. Thrombosis is rare
Other drugs used less frequently include danazol.

Danazol, a synthetic derivative of testosterone, inhibits pituitary secretion of LH and follicle-stimulating hormone (FSH), which decreases estrogen synthesis from the testicles. The dose used for gynecomastia is 100 mg  a day. Complete resolution of breast enlargement has been reported in 23% of cases. Adverse effects include weight gain, acne, muscle cramps, fluid retention, nausea, and abnormal liver function test results.

Surgical Care

Reduction mammoplasty is considered for patients with macromastia or long-standing gynecomastia or in persons in whom medical therapy has failed.It is also considered for cosmetic reasons (and for accompanying psychosocial reasons).
If surgery is necessary for patients with pseudogynecomastia, liposuction may be warranted.
More extensive plastic surgery may be required in patients with marked gynecomastia or who have developed excessive sagging of the breast tissue due to weight loss.
Complications of surgery include sloughing of tissue due to a compromised blood supply, contour irregularity, hematoma or seroma formation, and permanent numbness in the nipple-areolar area.


Tamoxifen (Nolvadex)

Competitively binds to estrogen receptor, producing a nuclear complex that decreases DNA synthesis and inhibits estrogen effects.



20 mg PO od

InteractionsMay exacerbate hepatotoxic effects of allopurinol; may increase cyclosporine serum levels; increases anticoagulant effects of warfarin; aminoglutethimide reduces serum concentration; cyclophosphamide, methotrexate, and 5-FU increase thrombotic risk


Synthetic steroid analog with strong antigonadotropic activity (inhibits LH and FSH) and weak androgenic action.



100 mg PO  for 3 mo


May increase risk of carbamazepine and cyclosporine toxicity; may increase PT in patients receiving oral anticoagulants; inhibits response to clomiphene


Documented hypersensitivity, seizure disorders, renal or hepatic insufficiency, lactation, conditions influenced by edema


Prognosis (outcome)

In approximately 90% of cases, pubertal gynecomastia resolves within a period of months to several years.
Gynecomastia that occurs secondary to an underlying, treatable cause (eg, drug-induced gynecomastia) usually responds to treatment or removal of the primary cause.
Macromastia seldom resolves completely and often requires surgery.



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