Gynecomastia is a disorder of the endocrine system in which the increase in breast size in male breast tissue does not occur. Psychological pressure can occur.
The development of gynecomastia is usually associated with benign pubertal changes. However, 75% of cases of puberty gynecomastia heal within two years after onset without treatment. In rare cases, gynecomastia has been known to occur in association with certain disease states. Pathological causes of gynecomastia vary and may include Klinefelter syndrome, certain cancers, endocrine disorders, metabolic dysfunction, various drugs, or may occur due to a natural decline in testosterone production. Disorders of the endocrine system that cause an estrogen/androgen ratio increase are considered responsible for the development of gynecomastia. This can happen even if estrogen and androgen levels are equally appropriate, but the ratio is modified. The diagnosis is based on signs and symptoms.
Conservative gynecomastia management is often appropriate, as this condition generally goes away by itself. Gynecomastia medical treatment that has lasted for more than two years is often ineffective. Drugs such as aromatase inhibitors have been found to be effective in cases of rare gynecomastia from disorders such as excess aromatase syndrome or Peutz-Jeghers syndrome, but excessive tissue removal surgery is usually necessary.
Gynecomastia is common. Physiological ginekomek develops up to 70% in adolescent boys. Newborns and adolescent males often experience temporary gynecomastia due to the influence of maternal hormones and hormonal changes during puberty, respectively.
Video Gynecomastia
Signs and symptoms
The classic feature of gynecomastia is male breast enlargement with subcutaneous soft, compressible, and cellular tissue that is palpated beneath the nipple areola in contrast to the softer fat tissue. This enlargement can occur on one side or both. Skin scratches and nipple retractions are not typical of gynecomastia. Milk extraction from the nipple is also not a typical finding, but can be seen in gynecomic individuals with prolactin secreting tumors. An increase in the diameter of the areola and asymmetry of chest tissue is another sign of gynecomastia.
Men with gynecomastia may seem anxious or stressed because of concerns about the possibility of developing breast cancer.
Maps Gynecomastia
Cause
Gynecomastia is thought to be caused by the ratio of estrogens turned to androgens mediated by increased estrogen production, decreased androgen production, or a combination of these two factors. Estrogen acts as a growth hormone to increase the size of male breast tissue. The cause of gynecomastia is unknown in about 25% of cases. Drugs are estimated to cause 10-25% of cases of gynecomastia.
Certain health problems in men such as liver disease, kidney failure, or low testosterone can cause breast growth in men. Drugs and liver disease are the most common causes in adults. Other drugs such as methadone, antagonists aldosterone (spironolactone and epelerenone), HIV drugs, cancer chemotherapy, hormone treatment for prostate cancer, ulcer and ulcers, calcium channel blockers, antifungal drugs such as ketoconazole, antibiotics such as metronidazole, tricyclic antidepressants such as amitriptyline, herbs such as lavender, tea tree oil, and dong quai are also known to cause gynecomastia. Phenothrin, an insecticide, has antiandrogen activity, and has been associated with gynecomastia.
Physiological
Many newborns of both sexes show breast development at birth or in the first weeks of life. During pregnancy, the placenta alters the androgenic hormones of dehydroepiandrosterone (DHEA) and DHEA sulfate to estrogen estrogen estrone and estradiol, respectively; once these estrogens are produced by the placenta, they are transferred to the baby's circulation, thus causing a temporary gynecomastia in the infant. In some babies neonatal milk (also known as "witch milk") can be secreted. The temporary gynecomastia seen in newborns usually disappears after two or three weeks.
Gynecomastia in adolescents usually begins between the ages of 10 and 12 and usually disappears after 18 months.
Decreased levels of testosterone and increased levels of subcutaneous fat tissue seen as part of the normal aging process can cause gynecomastia in older men. This is also known as senile gynecomastia. Increased fat tissue in this man causes an increase in androgenic hormone conversion such as testosterone to estrogen.
When the human body lacks sufficient nutrition, testosterone levels drop, while the adrenal glands continue to produce estrogen, causing hormonal imbalances. Gynecomastia can also occur after normal nutrition is restarted (this is known as refeeding gynecomastia).
A small proportion of cases of gynecomastia in males can be seen with rare congenital abnormalities such as spinal and bulbar muscle atrophy and extremely rare aromatase excess syndrome.
Non-physiological
Approximately 10-25% of cases are estimated to come from the use of drugs. This is known as nonphysiological gynecomastia. Drugs known to cause gynecomastia include ketoconazole, cimetidine, gonadotropin-releasing hormone, human growth hormone, human chorionic gonadotropin, 5 -reductase inhibitors such as finasteride and dutasteride, estrogen as used in transgender women and men with prostate cancer, and antiandrogens such as bicalutamide, flutamide, and spironolactone. Drugs that may be associated with gynecomastia include calcium channel blockers such as verapamil, amlodipine, and nifedipine; risperidone, olanzapine, anabolic steroids, alcohols, opioids, efavirenz, alkylating agents, and omeprazole. Certain components of personal care products such as lavender or tea tree oil and certain supplements such as dong quai and Tribulus terrestris have been linked to gynecomastia.
Chronic illness
People with kidney failure are often malnourished, which can contribute to the development of gynecomastia. Dialysis can reduce malnutrition in renal failure. In addition, many patients with renal failure experience hormonal imbalance due to suppression of testosterone production and testicular damage from high levels of urea, also known as uremia-related hypogonadism.
In individuals with liver failure or cirrhosis, the ability of the liver to precisely metabolize hormones such as estrogen may be impaired. In addition, those with alcoholic liver disease are at increased risk of developing gynecomastia; ethanol can directly interfere with the synthesis of testosterone and the presence of phytoestrogens in alcohol can also contribute to a higher estrogen ratio to testosterone. Conditions that can cause malabsorption such as cystic fibrosis or ulcerative colitis can also produce gynecomastia.
Tumor
Testicular tumors such as Leydig cell tumors or Sertoli cell tumors (as in Peutz-Jeghers syndrome) or hCG secreting coriocarcinomas can cause gynecomastia. Other tumors such as adrenal tumors, pituitary gland tumors (such as prolactinoma), or lung cancer, may produce hormones that alter the balance of male-female hormones and cause gynecomastia.
Individuals with prostate cancer treated with androgen deprivation therapy may develop gynecomastia.
Pathophysiology
The cause of general gynecomastia remains uncertain, but is thought to be caused by an imbalance between estrogen and androgen action in breast tissue. Breast superiority can occur due to breast tissue enlargement of the breast, adipose chest (fat) and skin, and usually a combination. As in women, estrogen stimulates breast tissue growth in men. In addition to directly stimulating the growth of male breast tissue, estrogen indirectly decreases the secretion of testosterone by suppressing the secretion of luteinizing hormone, resulting in decreased testicular testicular secretion. Furthermore, estrogen can increase protein levels of globulin binding-globulin (SHBG) protein, which binds free testosterone (active form) leading to decreased testosterone action in male breast tissue.
Primary hypogonadism (indicating intrinsic problems with testes in males) leads to decreased testosterone synthesis and increased conversion of testosterone to estradiol that potentially leads to gynicastic appearance. Klinefelter syndrome is an example of a disorder that causes hypogonadism and gynecomastia, and has a higher risk of developing breast cancer in men (20-50 times higher than uninterrupted men). Central hypogonadism (indicating a problem with the brain) leads to a decrease in the production and release of luteinizing hormone (LH, a stimulatory signal for endogenous steroid hormone synthesis) leading to a decrease in testosterone and estradiol production in the testes.
Individuals who have cirrhosis or chronic liver disease may develop gynecomastia for several reasons. Chirrhotic tends to increase androgenic secretion of the hormone androstenedione of the adrenal gland, increasing the conversion of these hormones into different types of estrogens, and increasing SHBG levels, leading to a decrease in blood-free testosterone levels. Approximately 10-40% of individuals with Graves' disease (a common form of hyperthyroidism) have gynecomastia. Increased conversion of testosterone to estrogen by increased aromatase activity, elevated SHBG levels and increased testosterone and estradiol production by the testes as elevated LH levels cause gynecomastia. Proper treatment of hyperthyroidism may lead to gynecomastia resolution.
Drugs are known to cause gynecomastia through several different mechanisms. These mechanisms include increasing estrogen levels, mimicking estrogen, lowering testosterone or other androgens, blocking androgen receptors, increasing prolactin levels, or by unidentified means. High levels of prolactin in the blood (which may occur as a result of a particular tumor or as a side effect of certain drugs) have been linked to gynecomastia. High levels of prolactin in the blood can inhibit the release of hormones that release gonadotropins and therefore cause central hypogonadism. Receptors for prolactin and other hormones include growth factors such as insulin 1, growth factors such as insulin 2, luteinizing hormone, progesterone, and human chorionic gonadotropin have been found in male breast tissue, but the effects of these hormones on the development of gynecomastia are not understood.
Diagnosis
To diagnose gynecomastia, a thorough history and physical examination are obtained by the physician. Important aspects of physical examination include evaluation of male breast tissue by palpation to evaluate breast cancer and pseudogynecomastia (enlargement of male breast tissue solely due to excess fat tissue), evaluation of penile size and development, evaluation of testicular development and assessment of mass that increases suspicion for testicular cancer, and the proper development of secondary sex characteristics such as the number and distribution of pubic hair and armpits. Gynecomastia usually presents with bilateral involvement of breast tissue but can occur unilaterally as well.
A review of any illegal drugs or ingredients a person may reveal causes the gynecomastia. Recommended laboratory tests to find the basic causes of gynecomastia include tests for aspartate transaminase and alanine transaminase to rule out liver disease, serum creatinine to determine if there is kidney damage, and thyroid-stimulating hormone levels to evaluate hyperthyroidism. Additional tests that may be considered are testicular, adrenal, or other tumors such as 17-ketosteroid urine, beta beta human chorionic gonadotropin, or serum dehydroepiandrosterone. Serum (free and total) testosterone levels, estradiol, LH, and follicle stimulating hormone can also be evaluated to determine whether hypogonadism can be a cause of gynecomastia.
Differential diagnosis
Other causes of male breast enlargement such as mastitis, breast cancer, pseudogynecomastia, lipoma, sebaceous cyst, dermoid cyst, hematoma, metastasis, ductal eccentasia, fat necrosis, or hamartoma are usually excluded before making the diagnosis. Another condition that may be confused with gynecomastia is pectoralis muscle enlargement.
Imaging
Mammography is the method of choice for radiological examination of male breast tissue in the diagnosis of gynecomastia when breast cancer is suspected on physical examination. However, because breast cancer is a rare cause of breast tissue enlargement in men, mammography is rarely needed. If mammography is performed and does not reveal findings that suggest breast cancer, further imaging is usually unnecessary. If a tumor of the adrenal gland or testicle is considered responsible for gynecomastia, ultrasound examination of this structure may be performed.
Histology
The initial histologic features expected to be seen in examination of gynecomic tissue achieved by fine needle aspiration biopsy include: proliferation and elongation of the ducts, increased connective tissue, increased inflammation and swelling surrounding the duct, and increased fibroblasts in connective tissue. Chronic gynecomastia may show different histologic features such as increased connective tissue fibrosis, increased ductal dose, less inflammation than in the acute stage of gynecomastia, increased subareolar fat, and hyalinization of the stroma. When surgery is done, the gland is routinely sent to the laboratory to confirm the presence of gynecomastia and to examine the tumor under a microscope. The utility of pathological examination of breast tissue removed from male teen gynecomastia patients has recently been questioned because of the scarcity of breast cancer in this population.
Classification
The spectrum of gynecomastia severity has been categorized into the scoring system:
- Level I: Small magnification, no excess skin
- Level II: Medium magnification, no excess skin
- Level III: Medium enlargement, excess skin
- Level IV: Marks magnification, excess skin
Treatment
The case of mild gynecomastia in adolescence can be treated with advice on lifestyle habits such as proper diet and exercise with certainty. In more severe cases, medical treatments may be tried including surgical intervention.
Drugs
Gynecomastia's medical treatment is most effective when done within the first two years after the start of male breast enlargement. Selective estrogen receptor modulators (SERMs) such as tamoxifen, raloxifene, and clomifene may be useful in the treatment of gynecomastia but are not approved by the Food and Drug Administration for use in gynecomastia. Clomifene appears to be less effective than tamoxifen or raloxifene. Tamoxifen can be used for painful gynecomastia in adults. Aromatase inhibitors (AIs) such as anastrozole have been used off-label for cases of gynecomastia that occur during puberty but are less effective than SERMs. Several cases of gynecomastia caused by rare abnormalities of excess aromatase syndrome and Peutz-Jeghers syndrome have responded to treatment with AIs such as anastrozole. Andabans/anabolic steroids may be effective for gynecomastia. Testosterone itself may not be suitable for treating gynecomastia because it can become aromatose to estradiol, but androgen sulfonates such as topical androstanolone (dihydrotestosterone) may be beneficial.
Surgery
If chronic gynecomastia is treated, surgical removal of the glandular breast tissue is usually necessary. Surgical approaches to gynecomastics treatment include subcutaneous mastectomy, liposuction-assisted mastectomy, laser assisted liposuction, and laser-lipolysis without liposuction. Complications of a mastectomy may include hematoma, surgical wound infection, breast asymmetry, changes in breast sensation, neck or isola necrosis, seroma, visible or painful injuries, and contour defects.
More
Radiation and tamoxifen therapy has been shown to help prevent gynecomastia and developing breast pain in prostate cancer patients who will receive androgen deprivation therapy. The efficacy of this treatment is limited after gynecomastia has occurred and is therefore most effective when prophylaxis is used.
In the United States, many insurance companies refuse coverage for surgery for the treatment of gynecomastia or male breast reduction on the basis that it is a cosmetic procedure.
Prognosis
Gynecomastia is not physically harmful, but in some cases it can be an indicator of other more serious underlying conditions, such as testicular cancer. Glandular tissue usually grows under the influence of hormonal stimulation and is often soft or painful. In addition, gynecomastia often creates social and psychological difficulties such as low self-esteem or shame for the sufferer. Weight can change the condition in cases triggered by obesity, but losing weight will not reduce the components of the gland and patients can not target areas to lose weight. Massive weight loss can lead to sagging chest tissue known as chest ptosis.
Epidemiology
Gynecomastia is the most common benign disorder in male breast tissue. New cases of gynecomastia are common in three age populations: newborns, adolescents, and men older than 50 years. Newborn gynecomastia occurs in about 60-90 percent of boys and most cases resolve on their own. During adolescence, up to 70 percent of men are estimated to show signs of gynecomastia. Gynecomastia senile is thought to be present in 24-65 percent of men between fifty and eighty years of age.
The prevalence of gynecomastia in men may have increased in recent years, but epidemiologic disorders are not fully understood. The use of anabolic steroids and exposure to chemicals that mimic estrogen in cosmetic products, organochlorine pesticides, and industrial chemicals have been suggested as factors driving this improvement. According to the American Society of Plastic Surgeons, breast reduction surgery to improve gynecomastia is becoming increasingly common. In 2006, there were 14,000 procedures of this type performed in the United States alone.
Society and culture
Gynecomastia can cause psychological distress for those who experience the condition. Common slang terms or contempt for gynecomastia include man boobs or moobs . Support groups exist to help increase the self-esteem of affected people.
See also
- Bra man
- Male lactation
- Mammoplasia
References
Explanation notes
Quotes
External links
- Media related to Gynecomastia in Wikimedia Commons
Source of the article : Wikipedia
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