Elsevier

Mayo Clinic Proceedings

Volume 84, Issue 11, November 2009, Pages 1010-1015
Mayo Clinic Proceedings

CONCISE REVIEW FOR CLINICIANS
Gynecomastia: Pathophysiology, Evaluation, and Management

https://doi.org/10.4065/84.11.1010Get rights and content

Gynecomastia, defined as benign proliferation of male breast glandular tissue, is usually caused by increased estrogen activity, decreased testosterone activity, or the use of numerous medications. Although a fairly common presentation in the primary care setting and mostly of benign etiology, it can cause patients considerable anxiety. The initial step is to rule out pseudogynecomastia by careful history taking and physical examination. A stepwise approach that includes imaging and laboratory testing to exclude neoplasms and endocrinopathies may facilitate cost-effective diagnosis. If results of all studies are normal, idiopathic gynecomastia is diagnosed. The evidence in this area is mainly of observational nature and lower quality.

Section snippets

PATHOPHYSIOLOGY

The imbalance between estrogen action relative to androgen action at the breast tissue level appears to be the main etiology of gynecomastia.6 Elevated serum estrogen levels may be a result of estrogen-secreting neoplasms or their precursors (eg, Leydig or Sertoli cell tumors, human chorionic gonadotropin [hCG]—producing tumors, and adrenocortical tumors) but more commonly are caused by increased extragonadal conversion of androgens to estrogens by tissue aromatase (as occurs in obesity).

CLINICAL MANIFESTATIONS AND DIAGNOSIS

Careful history taking and physical examination (the relevant elements of which are presented in Table 1) often reveal that patients actually are presenting with pseudogynecomastia, which means accumulation of subareolar fat without real proliferation of glandular tissue. Examination of these patients reveals diffuse breast enlargement without a subareolar palpable nodule. These patients do not need additional work-up and only require reassurance. Gynecomastia is usually bilateral,3, 9 but

MANAGEMENT AND PROGNOSIS

Overall, gynecomastia is a benign condition and is usually self-limited. Over time, fibrotic tissue replaces symptomatic proliferation of glandular tissue and tenderness resolves. If the appropriate work-up does not reveal considerable underlying pathology, reassurance and periodic follow-up are recommended. Although evidence is lacking to support a recommendation for follow-up intervals, 6 months seems reasonable. Causative medications should be withdrawn or the underlying causative medical

CONCLUSION

The evaluation of gynecomastias can be complex. A step-wise approach that starts with careful history taking and physical examination may obviate the need for extensive work-up. Subsequent selective imaging and laboratory testing help exclude possible neoplasms and endocrinopathies. The etiology is usually benign.

CME Questions About Gynecomastia

  • 1.

    Which one of the following statements best describes a typical presentation of gynecomastia?

    • a.

      Unilateral peripheral mass

    • b.

      Painless bilateral hard and fixed masses

    • c.

      A mass associated with nipple discharge

    • d.

      Bilateral painful masses in an anxious adolescent

    • e.

      Bilateral masses with minimal axillary lymphadenopathy

  • 2.

    Which one of the following statements best describes the recommendations for gynecomastia evaluation?

    • a.

      Diagnostic work-up for gynecomastia is recommended if initial history and

REFERENCES (22)

  • GD Braunstein

    Aromatase and gynecomastia

    Endocr Relat Cancer

    (1999)
  • Cited by (181)

    • Management of Gynecomastia and Male Benign Diseases

      2022, Surgical Clinics of North America
      Citation Excerpt :

      Histologically, male and female breasts are different. In men, the breast usually consists of subcutaneous fat with few ducts and stroma, whereas in women, it mostly composed of ducts and glandular tissue surrounded of stroma.2,52 Simple breast cysts occur due to the obstruction of a terminal duct from lobular hyperplasia of the epithelium or ductal extrusion into the stroma with consequent inflammation, forming an epithelium-lined fluid-filled round structure.50,54

    View all citing articles on Scopus
    View full text