*GYNECOMASTIA          See gynecomastia2007.pdf                               Causes  |  Diff-Dx  |  Lab  |  Rx  

A benign glandular enlargement of the male breast that is generally bilateral (may be asymmetric, or rarely, unilateral)
Gynecomastia is affected by increased estrogen/androgen ratio.

Types of Gynecomastia:

Marshall & Tanner Stages of breast enlargement/ development
[Adapted from Marshall WA, Tanner JM. Variations in pattern of pubertal changes in girls. Arch Dis Child 1969: 44:2291-303.]
Stage 1:  Preadolescent; only papillae are elevated.
Stage 2:  Breast bud and papilla are elevated and a small mount is present; areola diameter is enlarged.
Stage 3:  Further enlargement of breast mound; increased palpable glandular tissue.
Stage 4: Areola and papilla are elevated to form a second mound above the level of the rest of the breast.
Stage 5: Adult mature breast; recession of areola to the mound of breast tissue, rounding of the breast mound,
             and projection of only the papilla are evident.


Physiologic cause - transient in neonatal boys, at puberty, aging; and idiopathic cause. 

Pathological causes:
1. Decreased production or action of testosterone

2. Increased estrogen production

3. Drug-induced gynecomastia :

  1. Inhibitors of testosterone synthesis +/or actions:
    ketoconazole, metrodazole, alkylating agents, cisplatin, spironolactone(Aldactone), cimetidine(Tagament), metoclopramide, flutamide, etomidate
  2. Estrogens, DES, Birth control pill, digoxin, phytoestrogens
  3. Drugs that enhance endogenous estrogen secretion as: Gonadotropins, clomiphene
  4. Unknown mechanism:  heroin, marijuana, sedatives as diazepam, amphetamine, busulphan, cytotoxic drugs,  INH, BP meds as: methyldopa, ACE inhibitors, Ca-blockers; tricyclic antidepressant, ethionamide, ?Flexeril, etc. primary hyperparathyroidism; Amphotericin B toxicity

4. Idiopathic pathologic gynecomastia
In all published series half or more of subjects evaluated for gynecomastia do not have an underlying endocrinopathy that is diagnosable at autopsy or by careful endocrine work-up. If one adds those instances in all large series in which the designated cause is tenuous, the idiopathic category accounts for approximately three fourths of cases.



An elevated estrogen level indicates the need for testicular ultrasonography and adrenal CT or MRI.
Estradiol, however, is so potent that significant gynecomastia can develop without elevation of the plasma estradiol level. Progressive gynecomastia without a known explanation (e.g., puberty, cirrhosis, hyperthyroidism) should therefore be evaluated by imaging of the adrenals and testes.

The combination of recent gynecomastia with elevated estrogen and hCG titers should prompt a search for a primary tumor. Although the finding of hCG in the plasma of normal people has thickened the plot, high hCG titers and dynamic studies can be used to identify a tumor as the probable cause.


Dambro: Griffith's 5-Minute Clinical Consult, 1999 ed.- Timothy L. Black
Scientific American Medicine 10-1999