Gynecomastia

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[edit] Gynecomastia

Geoffrey A. Modest


Male gynecomastia is remarkably common, occurring in about one half of adolescent males and one third to one half of postpubertal males. The occurrence of postpubertal gynecomastia increases with age and body mass index. In general, the development of gynecomastia is related to the ratio of estrogens to androgens and is typically found in the following settings: increased estrogen (e.g., from tumors); increased aromatization of androgens—either testicular testosterone or adrenal androstenedione—in fat, muscle, and liver cells (e.g., from hyperthyroidism, obesity, liver disease); increased sex hormone binding globulin, which binds testosterone more avidly than estrogen and causes a relatively higher free estrogen level (e.g., from liver disease, hyperthyroidism); or decreased androgens (e.g., from aging, liver disease, hypogonadism). Although high prolactin levels are most typically associated with galactorrhea, there is also an associated suppression of testosterone, which can also cause gynecomastia. Different medications can lead to gynecomastia through any of the above mechanisms (see D.) It is important to note that all of the causes of bilateral gynecomastia can initially present with unilateral or markedly asymmetrical gynecomastia. Also, because of the high prevalence of gynecomastia, it may well coexist with other medical conditions without a causal relationship.

In general, approximately 25% of patients presenting to a physician for gynecomastia have idiopathic gynecomastia, 25% have persistence of pubertal gynecomastia, 10% to 20% are secondary to drugs, 8% to cirrhosis or malnutrition, 8% to hypogonadism, 3% to testicular tumors, 2% to secondary hypogonadism, 1.5% to hyperthyroidism, and 1% to renal disease.[1]


[edit] Image:B0323008283500273_g00000a.jpg History.

Important historical clues can help elucidate both the etiology and appropriate workup of gynecomastia. The history should focus on medication/drug use (see D), symptoms of associated medical problems (liver or renal disease, hyperthyroidism, underlying malignancy, Cushing's disease, human immunodeficiency virus [HIV] infection), history of testicular problems (trauma, torsion, cryptorchidism, mumps orchitis, radiation), and symptoms of hypogonadism (decreased libido, erectile dysfunction, or infertility), as well as specific characteristics of the gynecomastia (acute vs. chronic, and whether or not it is painful or rapidly increasing in size). Painful, rapidly expanding gynecomastia is more likely to be pathologic.


[edit] Image:B0323008283500273_g00000b.jpg Physical Examination.

Gynecomastia (true glandular tissue) needs to be differentiated from pseudogynecomastia (adipose tissue), which can usually be reliably done through the physical examination. True glandular tissue feels rubbery and is subareolar when grasped between the thumb and index finger. If there is a question, compare this tissue with tissue in the axillary fold. When necessary, mammography can be used to differentiate gynecomastia from pseudogynecomastia. Most studies have defined gynecomastia as more than 2 cm of glandular tissue. Gynecomastia of greater than 5 cm is more likely to be pathologic. In addition to performing a standard physical examination, it is important to do a detailed breast examination (noting position, texture, and mobility of the breast tissue, as well as the presence of skin changes or discharge), and a detailed testicular examination, noting size (testes less than 3 cm suggest hypogonadism), and consistency (a nodule could represent an estrogen-secreting tumor). Also, it is useful to assess the patient for concurrent feminization, specifically for female hair pattern, small testes, and a eunuchoid body habitus. An abnormal physical finding (e.g., testicular mass, feminization) can lead directly to the appropriate branch on the algorithm.


[edit] Image:B0323008283500273_g00000c.jpg Male Breast Cancer.

Male breast cancer, which constitutes less than 1% of all male cancers and less than 1% of all breast cancers, usually presents as unilateral, eccentric breast tissue enlargement that is firm, irregular, and fixed to the underlying tissue. This enlargement may be accompanied by axillary adenopathy, nipple discharge, and skin dimpling. Mammography is often helpful, although as with suspicious lesions in females, biopsy is often necessary even with a negative mammogram. Other conditions can cause eccentric, asymmetric breast tissue, including lipomas, neurofibromas, and dermoid cysts.


[edit] Image:B0323008283500273_g00000d.jpg Medications.

A complete medication history is extremely important because many different medications can be associated with gynecomastia. Since gynecomastia is so common in older men, and since the use of medications for chronic diseases also increases with age, it is useful to formally assess men for gynecomastia before beginning any of the following medications, which have been associated with gynecomastia[2]: estrogens, antiandrogens (cyproterone, flutamide, finasteride, leuprolide), calcium channel blockers (especially verapamil, although also reported with nifedipine and diltiazem), cancer chemotherapy agents (especially alkylating agents), digitalis preparations, H2-receptor blockers (especially cimetidine, but also reported with much lower frequency with ranitidine), phenothiazines (mostly associated with hyperprolactinemia and galactorrhea, but case reports of gynecomastia), ketoconazole, reserpine, spironolactone, marijuana and other substances of abuse (alcohol, amphetamines, heroin, methadone), and a variety of medications with a few case reports, including angiotensin-converting enzyme (ACE) inhibitors (captopril, enalapril), amiodarone, auranofin, clomiphene, diazepam, etretinate, isoniazid, methyldopa, metoclopramide, metronidazole, omeprazole, penicillamine, phenytoin, sulindac, theophylline, and tricyclic antidepressants. Discontinuation of the potentially offending medication should lead to decreasing gynecomastia within 1 month, if that medication is the culprit.


[edit] Image:B0323008283500273_g00000e.jpg Underlying Medical Conditions.

Gynecomastia is found in men with renal failure, as well as in 50% of men on dialysis. Cirrhosis has been one of the classical settings for gynecomastia; however, one recent small study did confirm the anticipated hormonal changes in cirrhotic men, but without confirming an increased prevalence of gynecomastia.[3] Gynecomastia can occasionally be the presenting symptom of hyperthyroidism. Some, but not all, authorities consider laboratory screening for these conditions (e.g., renal, liver, and thyroid function tests) in all cases of postpubertal gynecomastia even in the absence of specific symptoms or signs. In addition, gynecomastia has been reported with HIV infection, Cushing's syndrome, and refeeding after starvation (e.g., prisoners of war). It has been postulated that gynecomastia associated with therapy for some cancer, tuberculosis, diabetes, or other chronic disorders may be related to regaining weight after the nutritional insult of these diseases.


[edit] Image:B0323008283500273_g00000f.jpg Further Endocrinologic Workup.

Further endocrinologic workup is appropriate (blood for free testosterone, human chorionic gonadotropin, luteinizing hormone, and estradiol) when investigation shows no systemic disease or potentially offending medication usage, especially if the patient is non-obese, or the gynecomastia is increasing and painful.


[edit] Image:B0323008283500273_g00000g.jpg Adolescents.

Adolescents typically have gynecomastia approximately 6 months after pubertal development (development of pubic hair, testicular enlargement). If gynecomastia occurs before puberty or later than 6 months after,

Image:B0323008283500273_g022001.jpg

further workup is appropriate. Pubertal gynecomastia often resolves spontaneously within 6 months, 75% regressing within 2 years and 90% within 3 years.


[edit] Image:B0323008283500273_g00000h.jpg High Human Chorionic Gonadotropin Levels.

High human chorionic gonadotropin (hCG) levels are found with testicular and extragonadal germ cell tumors, as well as non trophoblastic tumors of the lung, stomach, liver, or kidney.


[edit] Image:B0323008283500273_g00000i.jpg Adrenal Tumors.

Adrenal tumors that are capable of causing gynecomastia should be large enough to be visualized by computed tomography (CT) scan.


[edit] TREAT OR REFER

It is probably best to refer the patient to an endocrinologist for therapy when no underlying, correctable cause can be found. In patients with recent onset gynecomastia, some success has been reported with injectable dihydrotestosterone, danazol, clomiphene, tamoxifen, and testolactone (an aromatase inhibitor) and with surgery.


[edit] REFERENCES

  1. ↑ GD Braunstein: Gynecomastia. N Engl J Med 1993; 328:490 - 495.
  2. ↑ DF Thompson, JR Carter: Drug-induced gynecomastia. Pharmacotherapy 1993; 13 (1):37 - 45.
  3. ↑ J Cavanaugh, CB Niewoehner, FQ Nuttall: Gynecomastia and cirrhosis of the liver. Arch Intern Med 1990; 150:563 - 565.

[edit] ADDITIONAL READINGS

  • LJ DeGroot,et al.: Endocrinology ed 3. Philadelphia: WB Saunders; 1995:
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