What Is Gynecomastia?

GYN can occur at any age, mostly 12 to 17 years. In recent years, with the improvement of people's living standards and the change in living patterns, the incidence and consultation rate of the disease have increased significantly. The reported incidence varies from 30% to 70%, and the incidence varies by age. The literature reports that the rate of autopsy of GYN is 40% to 55% [1] . Rohrich reported that the incidence of GYN in male groups was 32% to 65% [2] , and Zhang Qing [3] reported that the incidence of GYN in newborns was about 50%, the incidence of GYN in adolescence was about 39%, and the incidence of senile GYN The rate is above 40%. [4-6]

Liu Min (Attending physician) Department of Endocrinology, PLA General Hospital
Mother Yiming (Chief physician) Department of Endocrinology, PLA General Hospital
Gynecomastia (GYN) is a clinical condition of abnormal development of male breast tissue and abnormal hyperplasia of connective tissue in the breast caused by the imbalance of estrogen and androgen caused by physiological or pathological factors. GYN is the most common male breast disease, accounting for about 80% to 90% of male breast diseases. The clinical manifestations are usually painless, progressive enlargement of the breast on one or both sides, or tenderness in the area under the areola. 50% of GYN is physiological, most common in neonate and adolescence. At this time, GYN is usually transient and usually benign, but if it occurs before adolescence, youth and middle age are considered abnormal, it needs to be used. Further examination excludes the possibility of breast cancer or other new organisms.
Western Medicine Name
Gynecomastia
English name
gynecomastia, GYN
Affiliated Department
Internal Medicine-Endocrinology
Main cause
Hormonal imbalance
Contagious
Non-contagious

Gynecomastia epidemiology

GYN can occur at any age, mostly 12 to 17 years. In recent years, with the improvement of people's living standards and the change in living patterns, the incidence and consultation rate of the disease have increased significantly. The reported incidence varies from 30% to 70%, and the incidence varies by age. The literature reports that the rate of autopsy of GYN is 40% to 55% [1] . Rohrich reported that the incidence of GYN in male groups was 32% to 65% [2] , and Zhang Qing [3] reported that the incidence of GYN in newborns was about 50%, the incidence of GYN in adolescence was about 39%, and the incidence of senile GYN The rate is above 40%. [4-6]

Pathogenesis of gynecomastia

At present, it is believed that GYN is mainly caused by disorders of sex hormone levels in the blood circulation. There are basically two cases of disorders of sex hormone levels: one is increased estrogen, and the other is increased estrogen / androgen ratio. On the one hand, increased estrogen can promote the growth and development of male breasts. On the other hand, the increase of the estrogen / androgen ratio can also stimulate the synthesis of sex hormone binding protein (SHBG). SHBG has a greater affinity for androgens than estrogen, so The biologically active free estrogen / androgen ratio in the blood increases, which triggers breast hyperplasia [3] . In addition, some people believe that the occurrence of GYN is also related to the local estrogen / androgen ratio of the breast and the response of the breast to hormones. In some cases, the local aromatase activity of the breast is enhanced, causing more androgens to be converted into estrogen, and local excess estrogen causes GYN. Sometimes, although the levels of sex hormones in the blood circulation are normal, the response of the breast tissue to hormones has changed, such as: androgen receptor (AR) is not sensitive to testosterone or estrogen receptor (ER) is increased sensitivity to estradiol, androgen The effect is weakened, and the estrogen effect is relatively enhanced, causing breast hyperplasia. For example, Xu Peiyao et al. [7] reported that the serum estradiol and testosterone levels of patients with GYN were not significantly different from those of the control group, and the AR binding capacity was significantly lower than that of the control group. It is believed that the biological effects of testosterone cannot be exerted normally because of the reduction of AR Caused.
Recently, there are new discoveries about the mechanism of GYN. Pensler et al. [8] studied 34 cases of adolescent GYN patients with Klinefelter syndrome, whose breast ER and progesterone receptor (PR) expression increased, suggesting that the occurrence of GYN is related to the expression of local breast hormone receptors. Qin Jun et al. [9] applied immunohistochemical methods to detect the expression of heat shock protein 70 (HSP70) in breast tissue of 25 GYN patients, and found that the positive rate of HSP70 was 72%, which was similar to that in breast cancer tissue, suggesting that GYN Occurrence is closely related to cell proliferation. Zhao Guofa et al. [10] considered that GYN is actually a kind of chronic inflammatory response (non-infectious) caused by target organs (breast tissue) under the stimulation of estrogen or other factors. The prednisolone acetate suspension Local injection closed therapy can achieve better treatment results.

Classification of gynecomastia

GYN can be divided into three types: physiological, pathological and idiopathic.

GYN Gynecomastia Physiological GYN

Including neonatal, adolescent and senile GYN.
1. GYN in the neonatal period: its incidence is 60% to 90%, which is manifested by an increase in breast nodules at birth, which is caused by the estrogen of the mother or placenta entering the fetal circulation and acting on the breast tissue. It usually subsides within 1 to 3 weeks and occasionally lasts for months or even years. If the duration is too long, be alert for endocrine and hereditary diseases.
2. Adolescent GYN: Transient breast enlargement can occur in adolescence in men, with an incidence rate of about 30% to 60%. It usually starts at the age of 10-12, peaks at the age of 13-14, and lasts for a few months. The length is 2 years, and most of them can return to normal within 1 year. GYN of less than 5% of adolescent men is persistent [1] . Most boys have asymmetric breast hyperplasia on both sides, which is larger on one side than the other. The timing of breast hyperplasia on both sides can also be inconsistent, with pain and no swelling. The exact cause of puberty GYN is not clear. At present, it is believed that the secretion of adolescent sex hormones is strong. The anterior pituitary gonadotropin stimulates the production of testosterone and estrogen. The testes synthesize a large amount of estrogen before secreting a large amount of testosterone, which causes estrogen in serum Increased / androgen ratio results in transient male breast development and proliferation [11] . The study found that the plasma estradiol concentration had reached adult levels before the boy's plasma testosterone reached adult levels, resulting in an increased estrogen / androgen ratio. And boys with mammary hyperplasia had higher average plasma estradiol levels. In addition, the role of aromatase in the mammary glands during puberty is enhanced, and local estrogen formation increases, resulting in adolescent breast hyperplasia. Other studies have suggested that it may be due to increased sensitivity of breast tissue to physiological levels of free estrogen [12] .
3. GYN in old age: GYN in old age is most common between 50 and 80 years old [13] . Older men are mostly accompanied by varying degrees of testicular function decline, and metabolism of estrogen and androgens has changed, including decreased plasma total testosterone levels, decreased free plasma testosterone levels, and increased SHBG levels. In addition, the increase in fat content in the body tissues of the elderly increases the aromatase effect in peripheral tissues. The above changes are sufficient to increase the estrogen / androgen ratio in plasma and breast tissues, and cause breast tissues to proliferate. It increases with age [14] . But for the elderly, we must first rule out the possibility of organic diseases, such as estrogen-producing tumors, cardiovascular disease, liver disease, kidney disease, or taking multiple drugs, these conditions may also cause breast hyperplasia.

GYN Gynecomastia pathological GYN

1. Increased estrogen levels: Testicular tumors: Some testicular tumors (such as choriocarcinoma, teratoma, and a few seminoma) can produce chorionic gonadotropin (HCG), which can make testicular residual tissue synthesize testosterone and estrogen. Diol increased. At the same time, due to the increased aromatase concentration in cancer tissue, too much androgen can be converted into estrogen. Testicular tumors increase estrogen production and feedback inhibits gonadotropin secretion, resulting in a secondary decrease in androgen secretion. Increased estrogen secretion also has an effect on testosterone synthetase, further reducing testosterone synthesis, resulting in a significant imbalance of the estrogen / androgen ratio and the appearance of hyperplasia of the breast. Adrenal tumors: Some adrenal cancers can produce a large amount of estrogen or its precursors-androstenedione, and these precursors can be converted into estradiol by aromatase in the surrounding tissues. At the same time, pituitary gonadotropin secretion is inhibited by feedback, testosterone secretion decreases, resulting in an increase in estrogen / androgen ratio. Cirrhosis and alcoholism: Estrogen degradation is weakened when liver function is reduced, and the aromatization of androgens is enhanced, which results in relatively increased estrogen. Others: Testicular secretion of estrogen increases in patients with true hermaphroditism and congenital adrenal hyperplasia. Some rare genetic mutations and autosomal dominant genetic disease aromatase activity can increase, leading to a relative or absolute increase in estrogen production.
2. Androgen secretion is too low: primary or secondary testicular dysfunction, such as: Klinefelter syndrome, testicular dysfunction, orchitis, etc., testicular function declines, androgen secretion decreases; at the same time, gonadotropin feedback increases , Stimulate Leydig cells to secrete testosterone, some of which are converted into estrogen in the periphery; gonadotropins can also enhance the aromatase activity of Leydig cells, and increase the testosterone production of estrogen. Causes GYN.
3. Androgen receptor insensitivity: Although testosterone feminization patients have normal levels of sex hormones in the blood circulation, because the androgen receptor is not sensitive to testosterone, an estrogen / androgen effect ratio imbalance is formed in the breast, and the androgen effect is weakened. The relatively enhanced estrogen effect leads to breast hyperplasia.
4. Karyotype abnormalities: Some male breast development is due to clonal karyotype abnormalities, such as: 12p deletion, 9, 17, 19, and 20 chromosome monomers, and some patients have benign or malignant tumors of the breast [15] .
5. Other diseases: Hyperthyroidism: About 10% of male patients with hyperthyroidism have mammary gland development, but the cause is unknown. It may be due to the increase of thyroid hormone in the patient, which increases the plasma SHBG concentration and increases testosterone, which leads to free estrogen / male It is caused by an increase in the proportion of hormones and can disappear after treatment with antihyperthyroidism drugs [16] . In addition, hyperthyroidism can reduce Leydig cell function and increase the estrogen / androgen ratio. hypothyroidism: hypothyroidism with GYN may be related to excessive secretion of prolactin (PRL) and insufficient estrogen [17] . Chronic renal failure: The accumulation of toxic substances can inhibit testicular function, reduce testosterone levels, and increase pituitary gonadotropin and PRL levels. Malnutrition: It can cause the decline of androgen synthesis and the inhibition of pituitary gonadotropin synthesis and secretion. When the nutrition improves, this inhibitory effect disappears.
6. Drugs: In addition to estrogen and its analogs, chorionic gonadotropin, androgen antagonists, etc., which cause breast hyperplasia, the following drugs have also been reported to cause breast hyperplasia: cimetidine, spironolactone, androgens, isotonic Hydrazine, reserpine, busulfan (Malilan), calcium antagonists, ACE inhibitors, phenytoin, tricyclic antidepressants, penicillamine, diazepam (diazepam), cannabis, heroin, etc. These drugs can be It leads to an increase in estrogen / androgen ratio, but the specific mechanism of action is not clear.

GYN Gynecomastia idiopathic GYN

About half or more of men with mammary hyperplasia have no clear cause, and various hormone tests are normal, called idiopathic GYN, but it should be noted that some of these patients may have had short-term feminization factors. These factors no longer existed at the visit. They may have been exposed to small amounts of estrogen or anti-androgens in the work and living environment or have had mild endocrine dysfunction. Zhang Zhangqing et al [6] thought that the disease may be related to environmental pollution. Some of the environmental pollutants are estrogen-like compounds, such as organochlorine pesticides, dioxin compounds, etc., which can enter the human body to produce sex hormone-like effects. .
The etiology classification of GYN is shown in Table 1. In patients with GYN caused by various reasons, plasma PRL levels are usually normal, so PRL does not play a direct role in the occurrence of this disease. The majority of male patients with pituitary PRL tumors do not develop hyperplasia of mammary glands. A small number of patients with hyperplasia of mammary glands often result from the pressure stimulation of pituitary tumors or high PRL levels, which directly affect the secretion of gonadotropins, and secondary testicular hypofunction. Some patients with hyperplasia of mammary glands may have slightly elevated PRL levels, but this is a consequence of hyperestrogenemia.
Table 1 Etiology classification of male breast development
Physiological
Kallmann syndrome
Neonatal breast development
Hermaphroditism
Adolescent breast development
Hereditary testosterone deficiency
Senile breast development
Primary testicular dysfunction (acquired)
Pathological
Orchitis, after orchiectomy, or other lesions
Elevated serum estrogen
Secondary or triple testicular hypofunction
Increased aromatization
3.AR defects
Sertoli cell proliferation or cancer
4. Breast tissues are allergic to estrogen
Sex cord tumor
Medicinal
Germ cell tumor
1. Estrogen or its analog
Leydig cell proliferation or cancer
Estradiol, birth control pills, digitalis, etc.
Hermaphroditism
2. Drugs that promote estrogen synthesis
HyperHCGemia (velvet, lung, liver, kidney, etc.)
3. Gonadotropin, clomiphene, etc.
Drugs that inhibit testosterone synthesis or action
Obesity, hyperthyroidism
Busulfan, ethionamide, calcium channel blockers
Liver Disease
Tricyclic antidepressants, methyldopa, penicillamine,
Eat after starving
Testicular feminization
Isoniazid, heroin, etc.
4. Idiopathic
Estrogen is released from SHBG (spironolactone, etc.)
other
Hyper PRLemia (Pituitary PRL tumor, idiopathic hyper PRLemia, etc.)
HIV infection
Chronic systemic disease
2. Decreased testosterone synthesis
Chest wall trauma or spinal cord injury
Primary testicular hypofunction (congenital)
GH treatment
Klinefelter syndrome
Psychological stress

Pathological changes in gynecomastia

The histopathology of GYN is different from that of female mammary glands. There is no milky glandular lobules, only hyperplasia of the milk ducts and cystic dilation, accompanied by hyperplasia of fibrous adipose tissue (Figure 1). GYN caused by different causes has the same histological changes. The early features were hyperplasia of the glandular duct system, glandular ducts became longer, new tube buds and branches appeared, and fibroblasts of the matrix proliferated. In the late stage (several years), epithelial proliferation and degradation, progressive fibrosis and hyalinization, reduction in the number of glandular ducts, and infiltration of monocytes. As the disease progresses to extensive stages of fibrosis and hyaline degeneration, it is difficult for the breast to completely resolve.
Histological changes in male breast development
Cohan [18] divided breast parenchyma and adipose tissue according to the degree of hyperplasia of breast tissue. Cohan [18] divided them into the following three types: Gland size: the enlarged breast is mainly parenchymal hyperplasia; Fatty type: enlarged breast Adipose tissue hyperplasia is the main type; Glandular fat type: hyperplasia of breast parenchyma and adipose tissue in enlarged breasts. Bannayan and Hajdu [5] classified breast hypertrophy into 3 types according to the degree of hyperplasia of the mammary ducts and ductal tissues of breasts: Mammary hyperplasia in males: the disease course is within 4 months, and is characterized by epithelial hyperplasia Obviously, the interstitial is a large number of fibroblasts, containing adipose tissue, and mild lymphocytic infiltration with capillary proliferation; fibrous or sclerotic male mammary gland hyperplasia: the course of the disease is more than 1 year, characterized by the disease mainly composed of collagen Fibrous structure, there are scattered dilated mammary ducts, with mild or moderate epithelial cell proliferation; intermediate male breast hyperplasia: the course of disease is between 5 to 12 months, and interstitial fibrosis has begun, which is between the above An intermediate stage between the two types. Most scholars believe that this type 3 reproduces the duration of breast hyperplasia and the evolution of male breast developmental diseases associated with its symptoms.

Clinical manifestations of gynecomastia

Mainly manifested as breast enlargement, but unilateral or bilateral, sometimes accompanied by enlarged nipples and areola. You may feel pain, discomfort or tenderness locally,
Gynecomastia (2 photos)
A small amount of white discharge was seen in a few patients when the nipple was squeezed (Figure 2). Examination of the breast is very important. The patient takes a supine position. The examiner places the thumb and index finger at the bottom of the breast and slowly closes it. Disc-shaped nodules can be touched or diffusely increased, the texture is relatively tough, and the rubber-like tissue is mostly 3 to 5 stages according to the Turner stage. Currently, there are two indexing standards for GYN [19] , see Table 2. The clinical method is used to determine the surgical method. Pathological GYN caused by organic diseases and clinical manifestations of primary diseases.
Table 2 Simon and Rohrich classification of gynecomastia
Simon classification
Rohrich classification
Type I mild breast enlargement
No excess skin
Class mild hypertrophy without sagging (<250g)
A gland dominates B fiber dominates
Class IIA Moderate breast enlargement
No excess skin
Moderate hypertrophy without sagging (250-500g)
A gland is dominant and B fiber is dominant
Type B Moderate breast enlargement
With excess skin
Type severe hypertrophy with slight sagging (> 500g)
Glands or fibers
Type III severe breast enlargement
With marked excess skin
Similar to sagging female breasts
Type severe hypertrophy with severe sagging
(Class II or III)
Glands or fibers

Gynecomastia disease check

1. Examination of gonads and related hormones: luteinizing hormone (LH), follicle stimulating hormone (FSH), estradiol, testosterone, HCG, PRL (especially when there is a galactorrhea). Testicular or non-gonadal germ cell tumors or secreted ectopic HCG non-trophoblastic tumors have elevated HCG levels; increased LH concentrations with reduced testosterone levels during primary testicular hypofunction; secondary testes caused by abnormal hypothalamus or pituitary Testosterone and LH levels decrease during hypofunction. Testosterone or adrenal tumors secrete estrogen in plasma with elevated levels of estradiol and normal or suppressed LH levels.
Imaging examination of male breast development (3 photos)
2. Imaging examination: Breast ultrasound is the first choice. Its typical performance is a fan-shaped hypoechoic area centered on the nipple. It is clearly separated from surrounding tissues, with small lumens visible, thick glandular tissues, and sometimes strong stripe echoes. Converge toward the nipple without lymphadenopathy and poor blood flow (Figure 3). X-ray examination of breast molybdenum can also be performed. The typical manifestation is a round, nodular or patch-like uniform dense shadow under the areola. The diameter of the mass is mostly 2 to 4 cm, the edges are smooth, or there are burrs. Very few have The lobular changes, fine sand-like calcification is sometimes seen in or around the hyperplastic breast tissue, the blood vessel structure is clear, and the boundary with the surrounding tissue is clear. Generally, there is no inverted nipple and thickened skin tissue (Figure 4). For patients with elevated HCG, brain, chest, and abdominal MR I or CT and testicular B ultrasound are required to exclude tumors that secrete HCG. If the dehydroepiandrosterone sulfate is elevated, an ultrasound of the adrenal gland is required.
3. Chromosome examination: If the penis is shorter than 3 cm or the testis volume is less than 6 mL, a karyotype analysis is required to exclude Klinefelter syndrome. At the same time, karyotype detection can exclude GYN caused by abnormal karyotype.
4. Others: Check liver function, kidney function, and thyroid function if necessary to rule out whether these chronic diseases cause breast development.

Diagnosis of male breast growth

Glandular tissues> 0.5 cm are usually considered clinically as the diagnostic criteria for this disease. The diagnosis of GYN must first distinguish between true GYN and false GYN. Pseudo-GYN is an enlargement of the breast due to fat deposits rather than glandular hyperplasia. Patients with this condition are mostly obese and have no breast pain or tenderness. The identification of the two can be obtained by palpation of the breast. Patients with true GYN can touch the elastic or solid disc-shaped tissue, which extends around the nipple.
Molybdenum Target X-ray Imaging of Male Breast Development and Breast Cancer
, And fingers close together can feel resistance, while pseudo GYN fingers close together without resistance. If the examination is indistinguishable, a breast ultrasound can be performed, which can intuitively show the size, shape and internal echo of the breast, and can also visually show whether there is a lump in the breast, and the nature, location, size, shape, border and Blood flow signals, etc., are accurate and reliable in distinguishing true and false GYN, with an accuracy rate of almost 100% [20]. Second, it needs to be distinguished from breast cancer. GYN tissue is tough and elastic. Patients are mostly bilateral, with little nipple discharge. Men's breast cancer is more common in older men. It is usually a solitary mass in the unilateral breast. May occur areola skin adhesion and axillary lymph node enlargement, and more skin changes such as nipple discharge, depression or deviation. Localized ulcers or lymphadenopathy in the adjacent area are the manifestations of advanced breast cancer. If pure clinical examination fails to differentiate between GYN and breast cancer, a mammography X-ray examination should be performed (Figure 5). The sensitivity and specificity of identifying breast benign and malignant lesions can reach 90% [20] . X-ray examination of the breast cancer showed that the mass was mostly located in the upper quarter of the breast, showing eccentricity, unclear edges, and burr-like extension. The sensitivity and specificity of breast ultrasound in identifying benign and malignant breast lesions can reach over 90% [21] . Ultrasound shows that breast cancer masses often deviate from the areola, the border is unclear, and there is more attenuation at the rear. For patients with high suspicion of breast cancer, fine needle aspiration cytology and pathological examination should be performed as early as possible to confirm the diagnosis.
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After making a clinical diagnosis of GYN, the etiology should be determined by asking detailed medical history, physical examination, and related hormone tests. Tests for secondary sexual characteristics, testicular volume, body size, sex hormones, and gonadotropins can help diagnose primary or secondary testicular hypofunction. Corticotropin, cortisol, 17-hydroxyprogesterone, 17-ketosteroids, and 17-ketogenic steroid assays can assist the diagnosis of congenital adrenal hyperplasia. The measurement of HCG and sex hormones is helpful to judge the existence of tumors. When the level of HCG increases, it indicates the presence of testicular tumors, germ cell tumors or ectopic non-trophoblast tumors that secrete HCG. Testicular ultrasound, abdominal and chest CT should be further performed an examination. When plasma estradiol levels are accompanied by normal or decreased LH levels, testicular or adrenal tumors that secrete estrogen are considered. In addition, ask carefully for a history of liver, kidney, and hyperthyroidism and hypothyroidism, and perform liver and kidney function tests and thyroid function tests if necessary. Ask if they have taken sex steroid hormones and their precursors, anti-androgen drugs, anti-ulcer drugs such as: cimetidine, cancer chemotherapy drugs, especially alkylating agents, cardiovascular drugs such as spironolactone, psychotropic drugs and drugs of abuse Wait. If the above test results are normal, it can be diagnosed as idiopathic GYN. GYN diagnosis and differential diagnosis procedures can be performed with reference to FIG. 6.

Gynecomastia Disease Treatment

GYN treatment should make a reasonable choice based on its etiology, length of medical history, presence or absence of accompanying symptoms, and breast size. The cause should be treated first. Under normal circumstances, most patients have obvious onset factors. For patients with exact onset factors, the symptoms of breast hyperplasia will disappear after removing the original disease. Those who are caused by drugs should stop taking the relevant drugs, and they can recover on their own. Most GYN can resolve on its own (the most common is adolescent transient GYN), so most do not require treatment, just patiently and carefully explain to the patient after clinical observation. However, those who are clinically associated with breast pain or tenderness and whose large breast development continues to affect the shape and beauty of the patient need to be given clinical intervention. GYN commonly used treatment methods are drug treatment and surgical treatment.
(1) Drug treatment
During the rapid proliferative phase of GYN (early onset), histologically, ductal epithelial proliferation, inflammatory cell infiltration, increased stromal fibroblasts, and increased blood vessel distribution are often associated with breast pain or tenderness clinically. Can alleviate symptoms. And can promote the regression of developing breasts. In addition, within 5 cm or limited to induration under the areola, drug treatment is feasible. There are several commonly used drugs:
Androgen preparation
Testosterone: good effect on patients with testicular hypofunction. Commonly used is testosterone enanthate, which can increase testosterone levels in the body without being converted into estradiol by aromatase. Generally, 200 mg is administered intramuscularly every 3 to 4 weeks. Some studies have reported that the breast gland shrinks 67% -78% after 3 months of treatment. Plasma dihydrotestosterone increases during the treatment, and levels of LH, FSH, testosterone, and estradiol are inhibited. It returns to normal after 2 months of treatment. ~ 15 months without recurrence. Dihydrotestosterone heptane salt: It directly acts on target cells, and is not affected by aromatase.
2. Tamoxifen (Tamoxifen)
It is an estrogen antagonist, which can bind to the ER of the target tissue and block the effect of estrogen. The usual dose is 20 mg orally daily. Some people report that the breast gland has shrunk significantly after taking the drug for one month, and the dose can be appropriately increased if the effect is not obvious. The literature reports that oral tamoxifen 20 mg daily for 3 consecutive months. 80% of men's breast development has partially subsided, and 60% of patients have completely subsided. Patients who are effective with tamoxifen have reduced breast pain or tenderness within one month. [22-23] .
3. Clomiphene (clomiphene)
As an anti-estrogen drug, it has a significant effect and can reduce breast development in middle-aged people, but it can also cause breast development itself with large side effects. 50 to 100 mg orally daily, about 70% of patients have different degrees of efficacy.
Aromatase inhibitor
Testosterone: It can block the conversion of testosterone into estradiol in the periphery. Some people took 450 mg daily, orally in divided doses, which had better efficacy and no adverse reactions were found. After taking the drug, androstenedione levels increased significantly, testosterone, dehydroepiandrosterone, and E0 increased slightly, the androstenedione / E0 ratio increased, and LH, PRL, and E2 levels did not change significantly. Anastrazole: A new type of aromatase inhibitor, which has been used to treat postmenopausal breast cancer patients. It has been clinically proven to be safe and effective in treating male breast development. This medicine inhibits tissue estrogen secretion, reduces estrogen production, and does not inhibit pituitary function. The dose is gradually increased from 1 mg to 10 mg daily. Side effects include flushing, thinning hair, and gastrointestinal reactions (anorexia, vomiting, diarrhea).
5. Danazol (danazo1)
It is an anti-chorionic gonadotropin drug with a dose of 200 mg 3 times a day for a period of 3 to 9 months. It is effective for both adult and adolescent breast hyperplasia, and can reduce the degree of pain and breast development, but there are edema, nausea, Seborrheic dermatitis, side effects such as weight gain.
(B) surgical treatment
If the drug treatment is ineffective over a period of time or the breast has been proliferated for many years and it becomes a very burdensome mental burden on the patient, or if a larger male breast develops or is suspected of being cancerous, surgically remove the hyperplastic breast glandular tissue. Indications include: men at the end of adolescence or those who still have breast development, breast diameter> 4 cm, drug treatment is not effective; severely affect aesthetics; suspected malignant changes.
The Simon classification and Rohrich classification provide important clinical evidence for the choice of GYN surgical methods. When choosing a surgical method before surgery, the surgeon must not only consider the cause of the patient's disease, the size of the breast, the tissue composition of the enlarged breast, and whether there is any excess. Skin and other conditions, but also take into account the patient's requirements for aesthetic appearance. The first surgeon to report a surgical treatment of male breast development was Paulus Aegineta. In 1933, Menvill first considered surgical treatment of male breast development based on plastic surgery principles. Modern breast plastic surgery can be roughly divided into three types, namely liposuction, open resection, and liposuction combined with open resection. The halo approach is generally used to remove the breast tissue under the areola. In recent years, the application of laparoscopic technology has improved the safety of surgery. Domestic Fan Linjun and others used laparoscopic technology to perform subcutaneous glandectomy on 65 patients with male breast development. They believe that total laparoscopic subcutaneous glandectomy has fewer complications and cosmetic effects. Well, it is the best surgical method for breast growth in most men. [24] However, after one side mastectomy, the other side of the breast can develop again. Therefore, pay attention to follow-up observation and timely detection. If the other side of the breast develops, drug treatment is effective, and it can be removed again when it cannot be resolved.
(C) other
In recent years, reports have shown that radiation therapy can be one of the treatment options for GYN. The most convincing is the randomized scandinavian trial, whose data shows that preventive radiation therapy can significantly reduce antiandrogens The incidence of GYN and breast pain [25] . However, more clinical evidence is lacking.
To sum up, there are two points to pay attention to in the treatment of GYN: 1. GYN, especially adolescent GYN, most patients can resolve on their own; 2. Drug therapy (including traditional Chinese medicine and traditional Chinese medicine) is often in the early stages of the disease and the most active period of glandular hyperplasia Effective, once the gland enlarges for more than a certain period of time (usually 12 months), the gland will undergo interstitial hyaline transformation, tissue fibrosis, and the reactivity to the drug will be severely reduced.

Gynecomastia expert opinion

GYN brings varying degrees of physical and mental damage to patients, so how to effectively treat them is a major problem facing clinicians. At present, surgery has become the main measure of treatment. Despite the continuous development of surgical theory and operation technology, surgeons often find that it is still difficult to choose the best surgical method for a confirmed patient. Therefore, it is imperative to explore a systemic treatment plan for male breast development that can take breast size, texture, skin excess, and skin elasticity into consideration.

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