eMedicine Specialties > Endocrinology > Gonads

Gynecomastia

Mark R Allee, MD, Associate Professor, Department of Medicine, University of Oklahoma Health Sciences Center
Mary Zoe Baker, MD, Professor, Department of Medicine, Section of Endocrinology, Metabolism and Hypertension, University of Oklahoma; Medical Director, University of Oklahoma Physicians, Medicine Specialty Clinic, General Medicine Clinic and Medicine Residents' Clinic

Updated: Sep 23, 2009

Introduction

Background

Gynecomastia is a benign enlargement of the male breast resulting from a proliferation of the glandular component of the breast. Gynecomastia is defined clinically by the presence of a rubbery or firm mass extending concentrically from the nipples. The condition known as pseudogynecomastia, or lipomastia, is characterized by fat deposition without glandular proliferation. Although gynecomastia is usually bilateral, it can be unilateral.

Pathophysiology

Gynecomastia results from an altered estrogen-androgen balance, in favor of estrogen, or from increased breast sensitivity to a normal circulating estrogen level.¹ The imbalance is between the stimulatory effect of estrogen and the inhibitory effect of androgen. Estrogens induce ductal epithelial hyperplasia, ductal elongation and branching, proliferation of the periductal fibroblasts, and an increase in vascularity. The histologic picture is similar in male and female breast tissue after exposure to estrogen.²

Estrogen production in males results mainly from the peripheral conversion of androgens (testosterone and androstenedione) — through the action of the enzyme aromatase, mainly in muscle, skin, and adipose tissue — to estradiol and estrone.

The normal production ratio of testosterone to estrogen is approximately 100:1. The normal ratio of testosterone to estrogen in the circulation is approximately 300:1.

Frequency

United States

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. One estimate is that 60-90% of infants have transient gynecomastia due to the high estrogen state of pregnancy. 

The next peak of occurrence is during puberty,^3,4 with a prevalence ranging from 4-69%. Some reports have shown a transient increase in estradiol concentration at the onset of puberty in boys who develop gynecomastia. Pubertal gynecomastia usually has an onset in boys aged 10-12 years. It generally regresses within 18 months, and persistence is uncommon in men older than 17 years. 

The third peak occurs in older men, with a prevalence of 24-65%. Gynecomastia in adults is often multifactorial. Increased aromatization of testosterone to estradiol 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 etiologies in males seeking medical attention for gynecomastia:

• Persistent pubertal gynecomastia – 25%
• Drugs – 10-25%
• No detectable abnormality – 25%
• Cirrhosis or malnutrition – 8%
• Primary hypogonadism – 8%
• Testicular tumors – 3%
• Secondary hypogonadism – 2%
• Hyperthyroidism - 1.5%
• Chronic renal insufficiency – 1%

Clinical

History

A thorough history is essential to evaluate the causes of gynecomastia.

• Note the age of onset and the duration.
• Ask about recent changes in the size of the nipples and the presence of pain or discharge from the nipples.
• Inquire if the patient has any history of mumps, trauma to the testicles, alcohol use, or drug use (eg, prescription medications, over-the-counter medications, recreational drugs).
• Note any family history of gynecomastia.
• Evaluate the patient's history for sexual dysfunction, infertility, or hypogonadism (impotence, decreased libido and strength).

Physical

• Perform a thorough examination of the breasts, noting their size and consistency. Also determine the presence of any nipple discharge or axillary lymphadenopathy.
• Differentiate between true gynecomastia and pseudogynecomastia. These 2 entities may be distinguished by having the patient lie on his back with his hands behind his head. The examiner then places a thumb on each side of the breast, and slowly brings the thumbs together. In true gynecomastia, a ridge of glandular tissue will be felt that is symmetrical to the nipple-areolar complex. With pseudogynecomastia, the fingers won't meet until they reach the nipple.
• Gynecomastia can be detected when the size of the glandular tissue exceeds 0.5 cm in diameter.
• Examine the testicles, noting their size and consistency. Carefully look for the presence of nodules or asymmetry.
• Note signs of feminization, including typical body hair distribution and eunuchoid habitus.
• Check for any stigmata of chronic liver disease, thyroid disease, or renal disease.

Causes

Gynecomastia can be physiologic or pathologic; the characteristics of these forms are as follows:

• Physiologic gynecomastia is seen in newborn infants, pubescent adolescents,^3,4 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 estrogen, or by drug use; however, gynecomastia can also be idiopathic¹ :
  • Conditions that result in primary or secondary hypogonadism and cause decreased testosterone production and/or action include the following:
    • Klinefelter syndrome
    • Congenital anorchia
    • Testicular trauma
    • Testicular torsion
    • Viral orchitis
    • Kallmann syndrome - A form of hypogonadotropic hypogonadism, Kallmann syndrome is usually associated with varying degrees of abnormality in olfactory perception. This results from the defective migration of gonadotropin-releasing hormone–secreting cells (which comigrate with the cells of the olfactory epithelium) during embryogenesis.
    • Pituitary tumors
    • Malignancies that increase the serum human chorionic gonadotropin (hCG) (eg, large cell lung cancer, gastric carcinoma, renal cell carcinoma, hepatoma)¹
    • Renal failure¹
    • Hyperthyroidism
    • Malnutrition
    • Androgen insensitivity syndrome
    • Five-alpha-reductase deficiency syndrome
  • Increased estrogen 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)^5,6 :
    • Estrogens or drugs with estrogenlike activity, such as diethylstilbestrol, digitalis, and phytoestrogens, as well as estrogen-contaminated food and estrogen-containing cosmetics
    • Drugs that enhance estrogen synthesis, such as gonadotropins, 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, and heroin
• In pseudogynecomastia, a condition that occurs in obese men, there is only fat deposition, found in the subareolar area. This is not pathologic or physiologic. Patients with pseudogynecomastia will typically have bilateral deposition of fat, and over time, these deposits will not change in shape or size. A careful history may reveal that the lesions have remained unchanged over a span of several years. If mammography demonstrates no evidence of malignancy, a treatment option would be observation alone.

Differential Diagnoses

Breast Cancer
Dermoid Cyst
Hypogonadism
Lymphangioma

Other Problems to Be Considered

Hematoma
Lipoma
Male sexual dysfunction
Neurofibroma

Workup

Laboratory Studies

• 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.
• Free or total testosterone, luteinizing hormone (LH), estradiol, and dehydroepiandrosterone sulfate levels are used to evaluate a patient with possible feminization syndrome.
• Obtain thyroid-stimulating hormone (TSH) and free thyroxine levels if hyperthyroidism is suspected.

Imaging Studies

• Order a mammogram if 1 or more features of breast cancer are apparent upon clinical examination.⁷ This can be followed by fine-needle aspiration or breast biopsy, as the case merits.^8,9
• Obtain a testicular ultrasonogram if the serum estradiol level is elevated and the clinical examination findings suggest the possibility of a testicular neoplasm.

Other Tests

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

Histologic Findings

Characteristic findings include proliferation of ductules and stroma (consisting of connective-tissue elements such as fibroblasts, collagen, and myofibroblasts) and occasional acini. Gynecomastia of short duration consists of a prominent ductular component with loose stroma. Long-standing gynecomastia consists of dense stroma with few ductules.

Treatment

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.
• Identifying and managing an underlying primary disorder often alleviates breast enlargement.
• If hypogonadism (primary or secondary) is the cause of gynecomastia, parenteral or transdermal testosterone replacement therapy is instituted. However, testosterone does have the potential to exacerbate gynecomastia through the aromatization of the exogenous hormone into estradiol.
• For patients with idiopathic gynecomastia or with residual gynecomastia after treatment of the primary cause, medical or surgical treatment may be considered.
• Clomiphene,¹⁰ 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 estrogen antagonist, is effective for recent-onset and tender gynecomastia when used in doses of 10-20 mg twice a day.¹¹ 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.¹²
• Other drugs used less frequently include danazol and testolactone¹³ :
  
  
  • 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 200 mg twice 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.
  • Testolactone, a peripheral aromatase inhibitor, has been used with varying success rates in doses of 150 mg 3 times per day for 6 months. Nausea, vomiting, edema, and worsening of hypertension have been reported with its use.

Surgical Care

• Reduction mammoplasty is considered for patients with macromastia or long-standing gynecomastia or in persons in whom medical therapy has failed.¹ It is also considered for cosmetic reasons (and for accompanying psychosocial reasons).^{14,15,16,17,18}
• 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.
• A Chinese study indicated that endoscopic subcutaneous mastectomy, without skin excision, could be an effective treatment for gynecomastia.¹⁹ In a report on the procedure's use in 65 patients (125 breasts) with gynecomastia, grade IIB or III, the authors stated that only a few operative complications occurred, including 2 cases of partial nipple necrosis and 1 case of subcutaneous hydrops. They also reported that postsurgical chest contour was satisfactory in all patients, and that no recurrences were seen during the 3- to 36-month follow-up period.

Medication

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Steroid hormones

These agents are used to inhibit the effects of estrogen.^{1,10,11,12,13,20}

Testosterone (Androderm, Andropository)

Predominant male sex hormone used for replacement therapy in male hypogonadism.

Dosing

Adult

200-300 mg (testosterone enanthate) IM q2-4wk
4-6 mg (scrotal patch) transdermally qd
5 mg (nonscrotal skin patch) transdermally qd

Pediatric

10-25 mg testosterone propionate 2-3 times/wk

Interactions

May increase cyclosporine levels and cause toxicity; may increase PT and risk of bleeding in patients receiving oral anticoagulants

Contraindications

Documented hypersensitivity, breast cancer, prostate cancer, severe cardiac dysfunction, hepatic or renal disease

Precautions

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Prostate hypertrophy or cancer; oligospermia (with prolonged use or excessive dosage); may accelerate bone maturation

Clomiphene (Clomid, Milophene, Serophene)

Stimulates release of pituitary gonadotropins.

Dosing

Adult

50-100 mg PO qd; not to exceed 6 mo

Pediatric

Not established

Interactions

Danazol may reduce response

Contraindications

Documented hypersensitivity, liver disease, abnormal uterine bleeding, uncontrolled thyroid or adrenal dysfunction, pituitary tumor and risk of hemorrhage into tumor

Precautions

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Perform ophthalmic evaluation if patient develops visual symptoms

Tamoxifen (Nolvadex)

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

Dosing

Adult

10-20 mg PO bid

Pediatric

Not established

Interactions

May 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

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in leukopenia, thrombocytopenia, and hyperlipidemia; decreased visual acuity, corneal changes, and retinopathy may occur with >1 y of use; may induce ovulation

Danazol (Danocrine)

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

Dosing

Adult

200 mg PO bid for 3 mo

Pediatric

Not established

Interactions

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

Contraindications

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

Precautions

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Increased risk of bleeding in hemophilic patients; risk of fluid retention, especially with overt CHF or renal failure; caution in seizure disorders

Testolactone (Teslac)

Synthetic peripheral aromatase inhibitor that blocks production of estradiol and estrone from testosterone and androstenedione.

Dosing

Adult

150 mg PO tid for up to 6 mo

Pediatric

Not established

Interactions

May alter PT in patients taking oral anticoagulants

Contraindications

Documented hypersensitivity, males with breast cancer

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor liver function; edema may develop in patients with CHF or liver or renal insufficiency; may worsen hypertension; may exacerbate epilepsy and migraine; monitor INR closely in patients taking warfarin (possibly adjust dose)

Follow-up

Complications

• Men with Klinefelter syndrome have a 10- to 20-fold increased risk for breast cancer.
• Other than the associated risk of breast cancer, gynecomastia does not cause any long-term complications.

Prognosis

• 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.

Patient Education

• Reassure patients with physiological gynecomastia regarding the benign nature of their condition, and inform them that most cases spontaneously resolve.
• Counsel patients regarding the various treatment modalities available, and highlight the risks, adverse effects, success rates, and benefits of each modality.
• For excellent patient education resources, visit eMedicine's Men's Health Center.

Miscellaneous

Medicolegal Pitfalls

• Failure to recognize signs or symptoms of breast cancer⁷

References

1. Glass AR. Gynecomastia. Endocrinol Metab Clin North Am. Dec 1994;23(4):825-37. [Medline].

2. Braunstein GD. Gynecomastia. N Engl J Med. Feb 18 1993;328(7):490-5. [Medline].

3. Mahoney CP. Adolescent gynecomastia. Differential diagnosis and management. Pediatr Clin North Am. Dec 1990;37(6):1389-404. [Medline].

4. Mauras N. Treatment of adolescents with gynecomastia. J Pediatr. Apr 2005;146(4):576; author reply 576-7. [Medline].

5. Thompson DF, Carter JR. Drug-induced gynecomastia. Pharmacotherapy. Jan-Feb 1993;13(1):37-45. [Medline].

6. Eckman A, Dobs A. Drug-induced gynecomastia. Expert Opin Drug Saf. Nov 2008;7(6):691-702. [Medline].

7. Mathew J, Perkins GH, Stephens T, et al. Primary breast cancer in men: clinical, imaging, and pathologic findings in 57 patients. AJR Am J Roentgenol. Dec 2008;191(6):1631-9. [Medline].

8. Volpe CM, Raffetto JD, Collure DW, et al. Unilateral male breast masses: cancer risk and their evaluation and management. Am Surg. Mar 1999;65(3):250-3. [Medline].

9. MacIntosh RF, Merrimen JL, Barnes PJ. Application of the probabilistic approach to reporting breast fine needle aspiration in males. Acta Cytol. Sep-Oct 2008;52(5):530-4. [Medline].

10. Plourde PV, Kulin HE, Santner SJ. Clomiphene in the treatment of adolescent gynecomastia. Clinical and endocrine studies. Am J Dis Child. Nov 1983;137(11):1080-2. [Medline].

11. Bedognetti D, Rubagotti A, Conti G, et al. An open, randomised, multicentre, phase 3 trial comparing the efficacy of two tamoxifen schedules in preventing gynaecomastia induced by bicalutamide monotherapy in prostate cancer patients. Eur Urol. May 19 2009;[Medline].

12. Boccardo F, Rubagotti A, Battaglia M, et al. Evaluation of tamoxifen and anastrozole in the prevention of gynecomastia and breast pain induced by bicalutamide monotherapy of prostate cancer. J Clin Oncol. Feb 1 2005;23(4):808-15. [Medline].

13. Jones DJ, Holt SD, Surtees P, et al. A comparison of danazol and placebo in the treatment of adult idiopathic gynaecomastia: results of a prospective study in 55 patients. Ann R Coll Surg Engl. Sep 1990;72(5):296-8. [Medline]. [Full Text].

14. Colombo-Benkmann M, Buse B, Stern J, et al. Indications for and results of surgical therapy for male gynecomastia. Am J Surg. Jul 1999;178(1):60-3. [Medline].

15. Davanco RA, Sabino Neto M, Garcia EB, et al. Quality of life in the surgical treatment of gynecomastia. Aesthetic Plast Surg. Oct 25 2008;[Medline].

16. Ridha H, Colville RJ, Vesely MJ. How happy are patients with their gynaecomastia reduction surgery?. J Plast Reconstr Aesthet Surg. Aug 28 2008;[Medline].

17. Benito-Ruiz J, Raigosa M, Manzano M, et al. Assessment of a suction-assisted cartilage shaver plus liposuction for the treatment of gynecomastia. Aesthet Surg J. Jul-Aug 2009;29(4):302-9. [Medline].

18. Hammond DC. Surgical correction of gynecomastia. Plast Reconstr Surg. Jul 2009;124(1 Suppl):61e-68e. [Medline].

19. Fan L, Yang X, Zhang Y, et al. Endoscopic subcutaneous mastectomy for the treatment of gynecomastia: a report of 65 cases. Surg Laparosc Endosc Percutan Tech. Jun 2009;19(3):e85-90. [Medline].

20. Gruntmanis U, Braunstein GD. Treatment of gynecomastia. Curr Opin Investig Drugs. May 2001;2(5):643-9. [Medline].

21. Braunstein GD, Glassman HA. Gynecomastia. Curr Ther Endocrinol Metab. 1997;6:401-4. [Medline].

22. Neuman JF. Evaluation and treatment of gynecomastia. Am Fam Physician. Apr 1997;55(5):1835-44, 1849-50. [Medline].

Keywords

gynecomastia, male breast, male breasts, gynecomastia surgery, male breast reduction, male breast cancer, gynecomastia treatment, gynecomastia cure, gynaecomastia, pseudogynecomastia, enlargement of the male breast, male breast surgery, male breast reduction surgery, breast lump, physiologic gynecomastia, pathologic gynecomastia, testicular neoplasm, lipomastia, macromastia, pubertal gynecomastia, florid gynecomastia, fibrous gynecomastia, feminization, granular glandular tissue, breast cancer, hypogonadism, Kallmann syndrome, Klinefelter syndrome, congenital anorchia, testicular trauma, testicular torsion, viralorchitis, pituitary tumor, hypopituitarism, renal failure, kidney failure, androgen insensitivity syndrome, 5-alpha-reductase deficiency syndrome, altered estrogen-androgen balance, mumps, sexual dysfunction, infertility, chronic liver disease, thyroid disease, renal disease, eunuchoid habitus, testicular tumors, extragonadal germ cell tumors, malnutrition, hyperthyroidism, adrenal tumors, familial gynecomastia

Contributor Information and Disclosures

Author

Mark R Allee, MD, Associate Professor, Department of Medicine, University of Oklahoma Health Sciences Center
Mark R Allee, MD is a member of the following medical societies: American College of Physicians
Disclosure: Nothing to disclose.

Coauthor(s)

Mary Zoe Baker, MD, Professor, Department of Medicine, Section of Endocrinology, Metabolism and Hypertension, University of Oklahoma; Medical Director, University of Oklahoma Physicians, Medicine Specialty Clinic, General Medicine Clinic and Medicine Residents' Clinic
Mary Zoe Baker, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, American Chemical Society, and American College of Physicians-American Society of Internal Medicine
Disclosure: Nothing to disclose.

Medical Editor

Barry J Goldstein, MD, PhD, Director, Division of Endocrinology, Diabetes and Metabolic Diseases, Professor, Department of Internal Medicine, Thomas Jefferson University
Barry J Goldstein, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American College of Clinical Endocrinologists, American College of Physicians-American Society of Internal Medicine, American Diabetes Association, and Endocrine Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Yoram Shenker, MD, Chief of Endocrinology Section, Veterans Affairs Medical Center of Madison; Interim Chief, Associate Professor, Department of Internal Medicine, Section of Endocrinology, Diabetes and Metabolism, University of Wisconsin at Madison
Yoram Shenker, MD is a member of the following medical societies: American Heart Association, Central Society for Clinical Research, and Endocrine Society
Disclosure: Nothing to disclose.

CME Editor

Mark Cooper, MBBS, PhD, FRACP, Head, Diabetes & Metabolism Division, Baker Heart Research Institute, Professor of Medicine, Monash University
Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD, Professor of Medicine, St Louis University School of Medicine
George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

Related eMedicine topics:
Breast Embryology
Breast Reduction, Liposuction Only
Disorders of the Breast
Gynecomastia [Plastic Surgery]
Klinefelter Syndrome
Prepubertal Testicular and Paratesticular Tumors

Clinical guidelines:
Practice advisory on liposuction. American Society of Plastic Surgeons - Medical Specialty Society. 2004 Apr. 13 pages. NGC:004125

Clinical trials:
Adaptation Among Adolescents and Adults With Klinefelter Syndrome

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