A Report On Gynomastia- Essay, Research Paper

A Report on Gynomastia-

Definition

Gynecomastia is a common disease of the male breast

where there is a benign glandular enlargement of that breast

at some time in the male s life. It usually consists of the

appearance of a flat pad of glandular tissue beneath a

nipple which becomes tender at the same time. The

development may be unilateral or bilateral. There is rarely

a continued growth of the breast tissue; ordinarily the

process is of brief duration and stops short of the

production of permanent enlargement of the breast.

Causes

A great number of patients who suffer from this

disease have a disturbance in the proper ratio of androgen

and estrogen levels. The normal ratio of the two hormones

in plasma is approximately 100:1. The etiology of

gynecomastia in patients with a known documented cause

appears to be related to increased estrogen stimulation,

decreased testosterone levels, or some alteration of the

estrogens and androgen so that the androgen-estrogen ratio

is decreased (Williams 373). From this information it was

discovered that there is also a lower ratio of weaker

adrenal androgens (delta 4-androstenedione and

dehydroepiandrosterone) found in youths with this disease.

It was once believed that there was an imbalance in the

ratios of testosterone to estrogen or estradiol, but this is

now know to be untrue.

There are three areas the can be attributed to the

cause of gynecomastia: physiologic, pathologic and

pharmacologic. Enlargement of the male breast can be a

normal physiologic phenomenon at certain stages of life or

the result of several pathologic states. (Isselbacher, 2037)

In the case of physiologic gynecomastia the disease

can occur in a newborn baby, at puberty or at any time in a

man s life. In the newborn, transient enlargement of the

breast is due to the action of maternal and/or placental

estrogens. The enlargement usually disappears within a few

weeks. Adolescent gynecomastia is common during puberty

with the onset at the median age of 14. It is often

asymmetrical and frequently tender. It regresses so that by

the age of 20 only a small number of men have palpable

vestiges of gynecomastia in one or both the breasts.

Gynecomastia of aging also occurs in otherwise healthy men.

Forty percent or more of aged men have gynecomastia. One

explanation is the increase in age in the conversion of

androgens to estrogens in extra-

glandular tissues. Drug therapy and abnormal liver

functioning can also be causes of gynecomastia in older men.

When the disease is pathologic the patient can have

increased estrogen secretions, increased conversion of

androgens to estrogens or decreased androgen activity due to

a failure in protein receptors. Increased estrogen

secretions are found in such diseases and disorders as

Hermaphroditism, Kleinfelter s syndrome, congenital adrenal

hyperlasia, and adrenal carcinoma or testicular tumors. In

the second case some examples are adrenal carcinoma, liver

disorders, malnutrition and thyroidtoxicosis. Decreased

androgen activity can be found in complete testicular

feminization, incomplete testicular feminization and

Reifenstein s syndrome.

Many drugs can cause gynecomastia by several

mechanisms. The drugs can either act directly as estrogens

or cause and increase in plasma estrogen levels. Boys and

young men are particularly sensitive to estrogen, and can

develop gynecomastia after the use of dermal ointments

containing estrogen or after the ingestion of milk or meat

from estrogen-treated animals. (Isselbacher, 2038) Some

examples of drugs that may have cause gynecomastia include

Cannabinoids (methane and marijuana), Psychotropics

(pheno-thiazine, butyrophenone and reserpine),

Antihypertensives (reserpine, alpha-methyldopa and

spironolactone), Cardiac (digitalis), Gastrointestinal

(cimetidine, metoclopramide and domperidone),

Antituburculous (isoniazid), Cytoxic (cyclophospha-mide,

mustine, vincristine and mitotane) and Hormonal (sex

steroids, gonadotropins and antiandrogens). Use of these

drugs, however, will rarely cause gynecomastia. In some

instances, the feminization is due to effects of drugs on

liver functions.

Signs and Symptoms

There are very few signs and symptoms that are

associated with the this disease. Signs may appear at any

time in a male s life, although the most common time of

onset is during puberty. At the first indication of the

disease the patient will feel pain and tender-

ness in the breast area due to the rapid development of the

breast. The breasts grow because of the enlargement of the

glandular tissue. The concentric arrangement of the

connective tissue around the ducts is a characteristic

feature of the active phase of gynecomastia. (Delany, 67)

The enlargement of the breast is usually bilateral but some

cases have unilateral enlargement. In the case of

unilateral enlargement, Induration, fixation, or bloody

discharge should raise the possibility of

carcinoma. (Wyngaarden, 1450) Carcinoma is a cancerous

growth of the epithelial tissues.

It may be hard to distinguish true breast tissue

from masses of adipose tissue without true enlargement

(lipomastia). In such cases, a real case of gynecomastia

can be distinguished by mammography or by sonography.

Early gynocomastia is characterized by

proliferation of both the fibrobalstic stroma and the duct

system, which elongates, buds, and duplicates. As the

disease progresses, fibrosis and hyalinization are

associated with the regression of epithelial proliferation.

Eventually the number of ducts decreases, resolution occurs

by reduction in size of epithelial content leaving temporary

hyaline bands behind. (Isselbacher, 2037)

Diagnosis

A satisfactory diagnosis can be made in only half or

less of patients referred for gynecomastia. This is a

result of insufficient diagnostic techniques, causes that

are still undefined and/or difficult to diagnose, or in some

instances, gynecomastia may be normal rather than due to a

pathologic state. This disease should only be worked up

only if there is a negative drug history, if the breast is

tender (indicating rapid growth), or if the breast mass is

larger than 4 cm in diameter. A decision to perform an

endocrine evaluation depends on the clinical context. An

example would be gynecomastia associated with signs of under

androgenization.

Obesity can often be confused with gynecomastia. To

prevent this, the doctor can palpate the breast to see if

there is a lack of glandular elements that would indicate

only obesity.

Once the signs become evident, the doctor needs to

assess the patient with a number of test to give a proper

diagnosis since many other diseases and disorders are

commonly involved. This can be done with a physical

examination. The head and neck area may show signs of a

pituitary tumor or goiter which is found in Graves disease.

The skin and abdomen may reveal signs of liver failure and

the testes should be examined for asymmetric enlargement in

Klinefelter s syndrome. The doctor may consider liver

function tests of a karyotype if Kleinfelter s is suspected.

Other diseases related to gynecomastia include: testicular

tumors, hypo and hyperthyroidism, Cushing s disease,

cirrhosis, spinal cord lesions, Hodgkin s disease, enzymatic

defects in androgen synthesis and androgen resistance

syndromes, and many others.

The evaluation of patients with gynecomastia should

include a careful drug history, measurement and examination

of the testes, evaluation of liver function and endocrine

evaluation to include measurement of serum androstenedione

or 24-h urinary 17-keto-steriods, plasma estradiol and hCG,

and plasma luteinizing hormone (LH) and testoster-

one. If LH is high and testosterone is low, the diagnosis

is usually testicular failure. If LH and testosterone are

both low, the diagnosis is usually increased estrogen

production. If they are both high, the diagnosis is either

an androgen-resistance state or a gonadotropin -secreting

tumor. In true gynecomastia these tests would prove to be

unnecessary because the symptoms would regress.

Treatment

When the primary cause can be identified and

corrected, breast enlargement usually diminishes until it

usually disappears. For example, androgen replacement

therapy may produce dramatic improvement in men with

testicular insufficiency. However, if the gynecomastia is

of long duration (and fibrosis has replaced the original

ductal hyperplasia), correction of the primary defect may

not be followed by resolution. (Isselbacher, 2038) In this

case, surgery would be the only effective treatment.

Candidates for surgery include those with several

psychologic and/or cosmetic problems, continued growth, or a

suspected malignancy.

The treatment selected for this disease is related

to how the patient was affected by the disease. The

treatment for a person who contracted the disease through

certain drug use will be treated different from a person who

is affected from a related disease. If gynecomastia is

contracted through drug use, the patient will needs to

discontinue the medications that are associated with the

disease. The only exception is when there is a life

threatening illness involved, and there is no alternative

medication available.

For those suffering from gynecomastia, the doctor

may prescribe antiestrogens such as clomiphene citrate or

tamoxiten to eliminate tenderness of the breast. The

non-aromatizable androgen dihydrotesosterone also has been

reported to reduce gynecomastia by reducing testicular

secretion of estradiol, by decreasing peripheral conversion

of precursors to estradiol and by increasing circulating

levels of androgen. (Kohler, 295) In patient with painful

gynecomastia and who are not candidates for other therapy,

treat-ments with antiestrogens such as tamoxifen may be

used.

When other related diseases are the cause for the

onset of gynecomastia, treatment of these diseases will

often cure gynecomastia, too. The removal of a sex steroid

produc-ing tumor or treatment of thyroidtoxicosis are two

examples. Testosterone treatment of androgen deficiency

will also cause great improvement in this condition.

Prophylactic radiation of the breasts prior to the

institution of diethylstilbestrol therapy is effective in

preventing gynecomastia and has a low complication rate in

elderly men. (Isselbacher, 2039)

In most cases of true gynecomastia the signs and

symptoms should regress in about a year. However, in the

case of severe gynecomsatia where the breast has an increase

of fibrous tissue stroma the patient will require a surgical

reduction mammo-plasty. Once this has been done the tissue

is sent to a lab to be examined. The results should show

elongated circular ducts imbedded in cellular fibrous tissue

with a rubbery fatty quality. From these laboratory tests

it can be determined if there is any cribiform epithelial

hyperlasia or a case of carcinoma. Although the relative

risk of carcinoma of the breast is increased in men with

gynecomastia, it is rare nevertheless.

Statistical Data

Gynecomastia is found only in males, and the signs

can appear any time in a male s lifetime. It is the leading

breast disorder in males and it accounts for 60% of all

disorders of the male breast. About 85% of male breast

masses are due to gynecomastia. Forty percent of the cases

affect pubescent boys occurring most often between the ages

of 14 to 15.5. Approximately 40% of normal men and up to

70% of hospitalized men have palpable breast tissue. Active

gynecomastia in autopsy data is between 5 and 9%. More than

80% of their hospitalized patients with a body mass index of

25 kg/m2 or greater had gynocamastia. (Williams, 373) About

70% of pubertal males required no treatment. If the

threshold for judging that the breast is enlarged is set at

2.0cm in diameter, the incidence is 32-36% in normal aged

men 17-58 years. (Williams, 340) A bloody discharge is

present in about 60% of patients, while a milky discharge is

present in about 1% of patients.

Recent Research

In the Wilford Hall USAF Medical Center a set of

experiments were done to see if there is a connection

between 3B-HSD deficiency and gynecomastia. The researchers

tested a male who had developed right side gynecomastia at

the age of twenty-four. When a series of tests were run, no

other underlying conditions were evident. He was found only

to have a deficiency of 3B-HSD. The patient also had

abnormally high ratios of estradiol, estrogen and

aldosterone and other serums. This showed the presence of

adrenal sex steroid production on the right side of his

body.

This is not to say that all males patients with a

deficiency of 3B-HSD will develop gynecomastia. Other

patients with the same deficiency showed no signs, and still

others with normal 3B-HSD levels have also been found to

have reduced breast tissue. Researchers, however, do

believe that the deficiency of 3B-HSD later in life is quite

possibly a frequently unrecognized cause of new-onset

gynecomastia.

There are so many causes and factors that lead to

the disease gynecomastia that it is very difficult for

researchers to try to agree upon one main factor. So many

of the cases differ from one another, and, perhaps, no one

cause will ever be agreed upon as the leading factor of the

disease. As long as there is no other underlying disease or

disorder, gynecomastia is not a life threatening disease.

Experimentation with hormone therapy is the main research

being tested at this time.