What Causes Gynecomastia?

 

Gynecomastia, more frequently referred to as man boobs, is the most common reason for breast evaluation in males. This physiologic condition may be seen during infancy, puberty and during old age. In infants, transient gynecomastia occurs due to high estrogen levels. During adolescence, pubertal gynecomastia is also seen in boys from ten to twelve years due to the temporary elevation of estradiol concentration. This typically regresses within one and a half year. In the elderly, gynecomastia occurs due to the gradual decreased testosterone production and increase in the formation of estradiol from testosterone.

 

Obesity causes pseudogynecomastia, a non-clinical condition wherein fat deposits in the subareolar area of one’s breast. People with pseudogynecomastia often have bilateral fat deposits and these fat depots do not change in shape or size.


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Causes of Man-Boobs or Gynecomastia

 

Having Gynecomastia or man-boobs can be pathologic, physiologic, or idiopathic. Pathologic gynecomastia may be caused by (1) an increase in the production or action of estrogen, (2) a decrease in the production or action of testosterone, or (3) drug use.

 

Conditions that cause decreased testosterone, hypogonadism and gynecomastia include: testicular trauma, testicular torsion, viral orchitis, congenital anorchia, Klinefelter’s syndrome, Kallman syndrome, pituitary tumor, increased human chorionic gonadotropin (hCG), renal failure, hyperthyroidism, androgen insensitivity syndrome, 5-α-reductase deficiency syndrome, and malnutrition.

 

Elevated estrogen production and action may occur in two ways. At the testicular level, testicular tumors and ectopic hCG production happens as a result of lung carcinoma, renal carcinoma, gastric cancers, and extragonadal germ cell tumors. At the periphery, aromatase increases the conversion of testosterone to estradiol as seen in chronic liver disease, malnutrition, hyperthyroidism, adrenal tumor, and familial gynecomastia.

 

Drugs also give rise to this condition, but vary in the degree to which it causes gynecomastia. Some examples are:

 

• Drugs similar to estrogen such as diethylstilbestrol, digitalis, phytoestrogen, estrogen-containing cosmetics

 

• Drugs enhancing estrogen production such as gonadotropins, clomiphene, phenytoin, exogenous testosterone

 

• Drugs inhibiting testosterone production such as ketoconazole, metronidazole, cisplatin, spironolactone, cimetidine, flutamide, finasteride, etomidate, and alkylating agents

 

• Other drugs: heroin, angiotensin-converting enzyme (ACE) inhibitors, phenothiazine, isonicotinic acid hydrazide, calcium channel blockers, diazepam, omeprazole, tricyclic antidepressants, marijuana, busulfan, alcohol, methyldopa, penicillamine

 

Gynecomastia Treatment Options

 

Patients with physiologic gynecomastia do not need treatment. Pubertal gynecomastia spontaneously normalizes within three years. In hypogonadism, there is the need to institute testosterone replacement therapy. For idiopathic gynecomastia, surgical treatment may be needed.

 

Anti estrogen can also be administered for a trial period of six months but 20% do not completely resolve.  Side effects of this therapy include visual problems, rash, and nausea. Tamoxifen, an estrogen antagonist, may also be used for three months. Danazol and testolactone may also be used because it inhibits the pituitary gland from secreting leutinizing hormone (LH) and follicle-stimulating hormone (FSH). This mechanism decreases the production of estrogen in the testes. Side effects of Danazol include weight gain, acne, muscle cramps, fluid retention, nausea, and abnormal liver function.

 

For Testolactone, an aromatase inhibitor, side effects include nausea, vomiting, edema, worsened hypertension. Surgical care may also be employed for people with long-standing gynecomastia especially when medical therapy has failed. For cosmetic reasons and pseudogynecomastia, liposuction may be used along with plastic surgery to prevent excessive skin sagging.


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