Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
Dr. Perlstein received his Medical Degree from the University of Cincinnati and then completed his internship and residency in pediatrics at The New York Hospital, Cornell medical Center in New York City. After serving an additional year as Chief Pediatric Resident, he worked as a private practitioner and then was appointed Director of Ambulatory Pediatrics at St. Barnabas Hospital in the Bronx.
Gynecomastia is enlargement of the gland tissue of the male breast. During
infancy, puberty, and in middle-aged to older men, gynecomastia can be common.
Gynecomastia must be distinguished from pseudogynecomastia, which refers to the
presence of fat deposits in the breast area of obese men. True gynecomastia
results from growth of the glandular, or breast tissue, which is present in very
small amounts in men.
What causes gynecomastia?
Gynecomastia results from an imbalance in hormone levels in which levels
of estrogen (female hormones)
are increased relative to levels of androgens (male hormones). Gynecomastia
that occurs in normally-growing infant and pubertal boys that
resolves on its own with time is known as physiologic gynecomastia.
All individuals, whether male or female, possess both female hormones (estrogens) and male hormones
(androgens). During puberty, levels of these hormones may fluctuate and rise at
different levels, resulting in a temporary state in which estrogen concentration
is relatively high. Studies regarding the prevalence of gynecomastia in
normal adolescents have yielded widely varying results, with prevalence
estimates as low as 4% and as high as 69% of adolescent boys. These differences
probably result from variations in what is perceived to be normal and the
different ages of boys examined in the studies.
Gynecomastia caused by transient changes in hormone levels with growth
usually disappears on its own within six months to two years. Occasionally,
gynecomastia that develops in puberty persists beyond two years and is referred to
as persistent pubertal gynecomastia.
A number of medical conditions may also result in gynecomastia:
Malnutrition and
re-feeding (recovery from malnutrition) have both been shown to create a
hormonal environment that may lead to gynecomastia. Similarly,
cirrhosis of the
liver alters normal hormone metabolism and may lead to
gynecomastia.
Disorders of the male sex organs (testes) can result in decreased
testosterone production and
relatively high estrogen levels, leading to gynecomastia. These disorders may be
genetic, such as Klinefelter's syndrome, or acquired due to
trauma,
infection, reduced blood flow,
or aging.
Testicular cancers
may also secrete hormones that cause gynecomastia.
Other conditions that are associated with an altered hormonal environment
in the body and may be associated with gynecomastia are
chronic renal failure and
hyperthyroidism. Rarely, cancers other than testicular tumors may produce
hormones that can cause gynecomastia.
Gynecomastia can also be a side effect of a number of medications. Examples
of drugs that can be associated with gynecomastia are listed below:
spironolactone
(Aldactone), a diuretic that has
anti-androgenic activity;
Calcium channel blockers used to treat
hypertension [such as
nifedipine (Procardia and others)];
ACE inhibitor drugs
for hypertension [captopril
(Capoten), enalapril (Vasotec)];
some antibiotics [for example, isoniazid,
ketoconazole (Nizoral,
Extina, Xolegel, Kuric), and
metronidazole (Flagyl)];
anti-ulcer drugs [such as ranitidine
(Zantac), cimetidine (Tagamet), and
omeprazole (Prilosec)];
highly active anti-retroviral therapy (HAART) for
HIV disease, which may cause fat
redistribution leading to pseudogynecomastia or, in some cases, true
gynecomastia;