Male reproductive gland hypofunction

　　One, Hypothalamic-pituitary disease

　　1, Hypothalamic-pituitary tumors, inflammation, trauma, surgery, granulomas, and other factors affect the production and release of GnRH, resulting in insufficient secretion of pituitary gonadotropins, thus affecting testicular development, decreased androgen production, and spermatogenic defects. This leads to soft and shrunken testicles in men, atrophy of the reproductive organs, impotence, decreased libido, infertility, and may be accompanied by other manifestations of hypothalamic syndrome or anterior pituitary dysfunction.

　　2, Hypogonadotropic hypogonadism (Kallmann syndrome), also known as anosmia-eunuchoid syndrome: This condition is congenital, with a karyotype of 46XY, and the etiology may be autosomal dominant, recessive, or X-linked inheritance. Due to incomplete formation of the olfactory bulb during embryonic development, it can cause hypothalamic GnRH secretion deficiency, leading to hypogonadism, decreased testosterone secretion, and spermatogenic disorders of the testes. It is manifested by anosmia, poor development of secondary sexual characteristics, and a state similar to eunuchoidism.

　　3, Patients with simple LH deficiency have the characteristics of eunuchoidism, accompanied by gynecomastia, serum LH and testosterone are low, FSH can be normal, the seminiferous tubules can produce sperm and have fertility, and HCG can induce testicular maturation.

　　4, Pure FSH deficiency is rare, interstitial cells can normally secrete testosterone, male sexual characteristics are normal, and infertility is caused by FSH deficiency affecting spermatogenesis.

　　5, Hypotonia-intellectual disability-low sexual development-obesity syndrome (Prader-Willi syndrome) has an unknown etiology and may be an autosomal recessive inheritance. Birth is accompanied by hypotonia, drowsiness, disappearance of suckling and swallowing reflexes, and difficulty in feeding. After several months, the muscle tone improves, and polyphagia and obesity appear. Intellectual development disorders, gonadal development defects, poor development of secondary sexual characteristics, and may have cryptorchidism, gynecomastia, mild diabetes, short mandible, epicanthus, ear malformation, and other congenital abnormalities.

　　6. Hypogonadism-pigmented retinopathy-polysyndactyly syndrome (Laurence-Moon-Biedl syndrome) is an autosomal recessive genetic disorder. Due to congenital defects in the hypothalamus-pituitary gland, it causes insufficient secretion of gonadotropins, secondary hypofunction of the testes, intellectual disability, delayed growth and development, absence of secondary sexual characteristics at puberty, no development of penis and testes, and obesity. Pigmented retinopathy causes weakened vision or blindness. There are polydactyly or syndactyly deformities.

　　7. Alstrams syndrome is caused by an autosomal recessive gene, a rare disease with many similarities to the Laurence-Moon-Biedl syndrome, such as retinal pigmentary degeneration, obesity, and hypogonadism, but this syndrome does not have intellectual disability and polydactyly (polydactyly).

　　8. Obesity and hypogonadism syndrome (Froehlich syndrome) can be caused by any cause (such as craniopharyngioma) that leads to damage to the hypothalamus-pituitary gland. The characteristics are rapid onset of obesity, drowsiness, polyphagia, delayed skeletal development, possible male breast development or diabetes insipidus, poor development of external genitalia and secondary sexual characteristics, and low levels of LH and FSH in the blood.

　　9. Cushing's syndrome is characterized by the secretion of large amounts of cortisol and androgens by the adrenal cortex, which feedback inhibits the pituitary gland from releasing gonadotropins, resulting in decreased testosterone secretion and reduced gonadal function.

　　10. Congenital adrenal hyperplasia refers to the congenital deficiency of an enzyme in the synthesis of adrenal cortical steroid hormones, leading to a decrease in cortisol synthesis. Due to weakened feedback inhibition, the pituitary gland secretes more ACTH, causing hyperplasia of the adrenal cortex. The synthesis of testosterone from cholesterol requires the participation of five enzymes, including cholesterol carbon chain enzyme (20,22-carbon chain cleavage enzyme), 3β-hydroxysteroid dehydrogenase, and 17-hydroxylase, which are present both in the adrenal glands and in the testicular tissues. Defects in these enzymes lead to disorders in the synthesis of glucocorticoids and mineralocorticoids in the adrenal glands, and disorders in the synthesis of testosterone in the testes. In the early stages of male embryonic development, severe defects in testosterone synthesis can affect the masculinization differentiation of the fetus, leading to blind-end vagina, hypospadias, cryptorchidism, but without uterus and fallopian tubes. Defects in cholesterol carbon chain enzyme prevent cholesterol from being converted to pregnenolone, causing disorders in the synthesis of cortisol, aldosterone, and sex hormones. Large amounts of cholesterol deposition lead to lipoid adrenal cortical hyperplasia. Clinically, it shows adrenal cortical insufficiency, male pseudohermaphroditism, and patients often lose their ability to copulate early. Deficiency of 3β-hydroxysteroid dehydrogenase leads to chronic adrenal cortical insufficiency, increased ACTH, adrenal cortical hyperplasia; incomplete differentiation and development of male reproductive organs, with hypospadias, cryptorchidism, breast development, and increased 17-ketosteroids in urine. Deficiency of 17-hydroxylase leads to reduced cortisol secretion, increased ACTH, increased 11-deoxycorticosterone, male external genitalia being female-type or pseudohermaphroditic, and the vas deferens may have varying degrees of development. Elevated pregnenolone in the blood helps with diagnosis.

　　11. Hyperprolactinemia PRL can inhibit the secretion of LH and FSH, reducing the secretion of testosterone and spermatogenic function of seminiferous tubules. May be accompanied by gynecomastia and galactorrhea.

　　12. Familial cerebellar ataxia is a familial disease, characterized by infantilism, small external genitalia, small and soft testes, sparse axillary hair, female-type pubic hair, high pitch, tall stature in a eunuchoid shape. Patients have low intelligence, even dementia, and slowly appear cerebellar ataxia. May be accompanied by neurosensory hearing loss, optic nerve atrophy.

　　13. Hemochromatosis is an autosomal recessive inheritance. Due to excessive iron absorption by the intestinal mucosa and iron storage disorder of reticuloendothelial cells, excessive iron deposits in the hypothalamus and pituitary gland, decreased secretion of gonadotropins, decreased gonadal function, testicular atrophy, and gynecomastia.

　　2. Abnormal testicular function

　　1. Abnormal development and structure of the testis

　　(1) Congenital incomplete testicular development syndrome (Klinefelter syndrome): It is a common genetic disease of sex chromosome aneuploidy, see Klinefelter syndrome for details.

　　(2) 46,XX male syndrome: The sex chromosome of this syndrome is XX, without Y chromosome, and H-Y antigen can be detected in serum, indicating that there is a small amount of Y embedded in X or autosomes, which cannot be found in in vitro culture. The phenotype is male, with an incidence rate of 1:20,000 to 24,000 in male infants. Patients lack all female internal reproductive organs and have male sexual psychological characteristics. Clinical manifestations are similar to Klinefelter syndrome: small and hard testes (usually less than 2 cm), frequent gynecomastia, normal or slightly smaller penis size than normal adults, usually with azoospermia and hyalinization of seminiferous tubules. Serum testosterone levels are low, estradiol levels are high, and gonadotropin levels are high. Clinically, this type is similar to XXY/XY mosaicism. Short stature, mild intellectual disability, and personality changes are rare, and the incidence of hypospadias is increased.

　　(3) Male Turner syndrome: Autosomal dominant inheritance, karyotype 46,XY, with typical clinical manifestations of Turner syndrome: short stature, webbed neck, radial clubfoot, congenital heart disease, and male phenotype. Often cryptorchidism, testicular atrophy, poor development of seminiferous tubules, infantilism, decreased serum testosterone, and increased serum gonadotropin levels. A few patients have normal testes and can reproduce.

　　(4) Decreased seminiferous tubule function in adults: Causes include orchitis, cryptorchidism, radiation damage, uremia, alcoholism, antitumor drugs, etc., which may have no clear etiology. In mild cases, the biopsy of the testis shows a decrease in the number of germ cells in all stages. In severe cases, spermatogenic development stops at the spermatogonial or primary spermatocyte stage. In severe cases, there may be no germ cells at all, only morphologically intact Sertoli cells. The most severe cases may show fibrosis and hyaline change of the seminiferous tubules. Clinical manifestations include infertility, mild to moderate testicular atrophy, normal Leydig cell testosterone secretion function, good development of secondary sexual characteristics, no breast development. Semen examination shows oligospermia or azoospermia, normal blood testosterone or LH concentration. Baseline blood FSH is normal or elevated, and FSH is excessively elevated after GnRH stimulation.

　　(5) Immature Leydig cell development: Impaired testosterone secretion by fetal Leydig cells, leading to male pseudohermaphroditism. There are testicles but spermatogenic dysfunction. Genital malformation, with a female phenotype, the penis resembles a clitoris, with a blind-ended vagina, but without a uterus or fallopian tubes, and primary amenorrhea is discovered during puberty. Sparse pubic and armpit hair. Patients have elevated FSH and LH baseline levels, a significant gonadotropin response to GnRH stimulation, significantly low blood testosterone levels, and no increase in testosterone after HCG stimulation.

　　(6) Eunuchoidism: Caused by complete atrophy of the testicles due to infection, trauma, vascular embolism, or testicular torsion during the embryonic period, with a male phenotype. Males do not develop secondary sexual characteristics during puberty, and the external genitalia remain infantile, without testicles. If androgen therapy is not given early, the appearance of a eunuchoid figure will occur. If there are residual or ectopic Leydig cells that secrete androgens, moderate secondary sexual characteristics may appear. Blood testosterone levels are low, gonadotropin levels are significantly elevated, and testosterone does not increase after HCG stimulation.

　　(7) Cryptorchidism: Can be unilateral or bilateral, most common in the inguinal region. Due to the higher temperature inside the abdomen than inside the scrotum, the spermatogenic function of cryptorchidism is suppressed and it is prone to cancer. Cryptorchidism usually has no symptoms, and testicles may not be palpable on one or both sides, without signs of androgen deficiency, often accompanied by infertility. Unlike eunuchs, the testosterone levels of cryptorchid patients increase significantly after HCG stimulation.

　　(8)萎缩性肌强直病: An adult-onset disease, characterized by rigid atrophy and weakness of the facial, neck, hand, and lower limb muscles, ptosis of the upper eyelid, compensatory contraction of the frontal muscles, leading to increased forehead lines. 80% are accompanied by primary testicular hypofunction, with significantly elevated serum FSH. It is a familial disease with autosomal dominant inheritance.

　　(9) Hypogonadism in adults: Also known as male menopause syndrome. After the age of 50, men gradually show a decline in sexual function, with possible changes in personality and mood. Blood testosterone levels gradually decrease, gonadotropin levels rise, and sperm count decreases or is absent.

　　(10) Immotile cilia syndrome: An autosomal recessive genetic defect characterized by respiratory and sperm cilia dysfunction. Such as Kartagener's syndrome, which manifests as a triad of visceral inversion, chronic paranasal sinusitis, and bronchiectasis. Infertility due to sperm cilia dysfunction.

　　2. Acquired testicular abnormalities

　　1) Testicular infection: It can be divided into non-specific, viral, fungal, spirochetal, parasitic, and other types. The most common is viral orchitis caused by mumps virus. The clinical manifestations include swelling and pain in the affected testis, edema of the scrotal skin, fluid in the tunica vaginalis, and often accompanied by chills, high fever, and abdominal pain. After the disease, the testes can show varying degrees of atrophy. Some patients can cause infertility.

　　2) Trauma: The testes are easily damaged by external violence. The disappearance of spermatogonia in the seminiferous tubules can lead to infertility. If there is a hematoma, the destruction of blood supply can also lead to testicular atrophy.

　　3) Radiation injury: Primordial germ cells are very sensitive to radiation damage. If damaged, it can lead to oligospermia or azoospermia.

　　4) Drugs: Spironolactone and ketoconazole can inhibit testosterone synthesis. Spironolactone and cimetidine compete with androgens for cytoplasmic receptor protein, interfering with the action of testosterone in target cells. Taking methadone and digitalis can increase plasma estradiol and decrease testosterone. Long-term alcoholism can lead to a decrease in plasma testosterone. Antitumor and chemotherapy drugs, pesticides, dibromochloropropane, cadmium and lead, can all inhibit sperm production, leading to infertility.

　　5) Autoimmune: Schmidt syndrome exists with anti-testicular basement membrane antibodies. If the blood-testis barrier is destroyed, seminal fluid as an antigen can cause an autoimmune reaction, producing anti-sperm antibodies. Male prostatitis or epididymitis, especially when infected with Escherichia coli, can produce anti-sperm antibodies. After the vas deferens is blocked or cut, sperm granuloma can form. Sperm is broken down and absorbed within the sperm granuloma to form an antigen, resulting in the production of anti-sperm antibodies. Currently, two types of anti-sperm antibodies can be detected, namely sperm agglutination antibodies and sperm immobilization antibodies. Anti-sperm antibodies can reduce sperm motility and cause sperm autoagglutination or non-coagulation. In addition, anti-sperm antibodies can induce autoimmune orchitis, causing antigen-antibody complexes to deposit on the reproductive cells of the testes, affecting the normal production of sperm.

　　4. Testicular abnormalities associated with systemic diseases: Chronic liver disease, renal insufficiency, severe malnutrition, metabolic disorders, diabetes, and other systemic diseases can lead to decreased testicular function and infertility.

　　III. Patients with defects in androgen synthesis or its action

　　The karyotype is 46,XY, and the gonads are testes. Due to insufficient androgens, the development of the embryonic sexual organs does not complete male differentiation, resulting in male pseudohermaphroditism. According to the etiology, it can be divided into three categories roughly:

　　1. Defects in androgen synthesis involve five different enzymes in the testosterone production pathway. Deficiency in any of these enzymes can lead to difficulties in testosterone synthesis, resulting in male pseudohermaphroditism. Among them, cholesterol carbon chain enzyme (20,22 carbon chain cleavage enzyme), 3β-hydroxysteroid dehydrogenase, and 17-hydroxylase are present in the testes and adrenal glands. Deficiency in any of these three can not only cause male pseudohermaphroditism but also congenital adrenal cortical hyperplasia; the other two enzymes (17,20 carbon chain cleavage enzyme, and 17β-hydroxysteroid dehydrogenase) are only present in the testes. Deficiency in these can only lead to male pseudohermaphroditism.

　　2. Incomplete regression of the paramesonephric duct is also a rare autosomal recessive or X-linked recessive genetic disease. In the fetal period, the Sertoli cells secrete insufficient paramesonephric duct inhibitory factor (MIF) or have binding disorders with the receptor. This causes some male patients with 46,XY to retain part of the female reproductive tract (fallopian tubes, uterus, upper third of the vagina). Since both MIF and the substance for testicular descent are secreted by Sertoli cells, incomplete regression of the paramesonephric duct can be accompanied by ipsilateral cryptorchidism, incomplete testicular development, and can also be accompanied by mixed gonadal dysgenesis with a high incidence of cancer.

　　3. Androgen insensitivity

　　(1) Testicular feminization syndrome: It belongs to male pseudohermaphroditism, and the disease is caused by target organ androgen receptor and post-receptor defects, which make the body insensitive to androgens. It is an X-linked recessive genetic disease, and this syndrome is divided into complete and incomplete types. ①Complete androgen insensitivity - testicular feminization, also known as complete male pseudohermaphroditism, with a karyotype of 46,XY. During embryonic development, there are developed testes in the peritoneal cavity or vulva. Due to the insensitivity of the mesonephric duct to androgens, it cannot further differentiate and develop into the vas deferens, seminal vesicle, prostate, and ejaculatory duct. The vulva cannot differentiate in the male direction, but the fetal testicular Sertoli cells can still secrete MIF, so the paramesonephric duct regresses and atrophies, with no fallopian tubes, uterus, or upper vagina. At birth, the external genitalia are completely female, with a shallow blind-ended vagina, and the testes can be felt in the inguinal or vulvar region of the child. During puberty, due to the insensitivity of the target organ to androgens, an increase in LH secretion causes an increase in testosterone. Testosterone is converted into estradiol, causing female secondary sexual characteristics, such as fully developed breasts, but with primary amenorrhea. A few patients have an enlarged clitoris and mild masculinization. After puberty, the patient's testes are prone to malignancy and should be removed. ②Incomplete androgen insensitivity, also known as incomplete male pseudohermaphroditism type I, Reifenstein syndrome, with a karyotype of 46,XY, and the cause is partial or post-receptor androgen receptor defects. The phenotype tends to be male, but the degree of masculinization varies greatly. Severe cases have明显两性畸形的外生殖器, with blind-ended vagina and perineal scrotal urethral cleft. Milder cases are manifested as underdeveloped male external genitalia, small penis, urethral cleft, and bifid scrotum. During puberty, the development of masculinization is poor, and there may be breast development, and most have no fertility. Testosterone, LH, and estradiol are all elevated.

　　(2) 5α-reductase deficiency: Also known as incomplete male pseudohermaphroditism type II, it is an autosomal recessive inheritance, with a karyotype of 46,XY. Due to the insufficient conversion of testosterone to dihydrotestosterone due to the lack of 5α-reductase, there is a developmental disorder of male external genitalia, manifested as a small penis, perineal urethral cleft, scrotum being bilobed. Patients have testes, epididymis, vas deferens, and seminal vesicles, but no uterus, fallopian tubes, or ovaries. During puberty, masculinization occurs without breast development. Sperm count is normal, plasma testosterone levels are normal or increased, dihydrotestosterone is decreased, and LH is increased.

　　The clinical manifestations of male reproductive gland hypofunction vary with the age of onset. For example, if androgen deficiency occurs at 2-3 months of gestation, it can cause pseudohermaphroditism. During the pubertal period, androgen deficiency is manifested as a lack of secondary sexual characteristics and eunuchoid body shape, the penis is of child-like size, the testicles are small, the scrotum is smooth without wrinkles, the pubic and axillary hair are sparse, the hair on the face, chest, abdomen, and back is lacking or extremely sparse, the voice is shrill, the muscles are not developed, and the physical strength is lower than normal. If adult males have androgen deficiency, it is manifested as a decrease in libido, impotence, poor physical strength, reduced sexual hair and beard, and infertility.

　　It mainly complicates with impotence (erectile dysfunction), premature ejaculation, and male infertility.

　　1. Impotence:It refers to the inability of the penis to achieve or maintain an erection during sexual activity, or the inability to complete normal sexual activity, or the inability to insert the penis into the vagina for sexual intercourse. Impotence, also known as 'failure to raise the yang', is the most common male sexual dysfunction disease. Occasionally, 1-2 times of sexual failure cannot be considered as impotence. Only when the failure rate of sexual intercourse exceeds 25% can it be diagnosed as impotence.

　　2. Premature ejaculation:It refers to the sexual intercourse disorder that occurs when the male ejaculates prematurely before the female reaches an orgasm, and the sexual intercourse time is shorter than 2 minutes. This condition is found in about 30% of males, although the problem is small, it can lead to a low quality of sexual life and may cause other sexual dysfunctions such as impotence, with serious consequences, and should be paid attention to and treated early. It is generally believed that if a man can enter the vagina for sexual intercourse but ejaculates quickly without much movement, it is also defined as premature ejaculation.

　　3. Male infertility:It refers to infertility caused by male factors. Generally, if a couple has been living together for more than 2 years without taking any contraceptive measures and the woman has not become pregnant, it is called infertility. The incidence rate is about 10%, of which about 60% is due to female factors, about 40% is due to male factors alone, and about 10% are due to both. Male infertility can be divided into absolute infertility and relative infertility according to clinical manifestations.

　　The determination of serum gonadotropin levels can differentiate hypogonadism into primary and secondary types, with the former showing elevated baseline gonadotropin levels; the latter showing decreased levels. The LHRH stimulation test and clomiphene citrate test can determine the pituitary reserve capacity. Hypopituitarism results in a weak or delayed response, while hypogonadism shows an active response. The chorionic gonadotropin (HCG) stimulation test shows that the plasma testosterone level in normal males or children should at least double, and in cryptorchidism, the plasma testosterone level also increases after injection, while eunuchoidism does not show the above response. The development of secondary sexual characteristics, the location, size, texture of the testicles, and the plasma testosterone level, as well as routine semen examination, help establish the presence and degree of testicular dysfunction. Chromosome karyotype analysis and the detection of plasma dihydrotestosterone levels are helpful for further classification.

　　The key to the prevention and treatment of male hypogonadism is early detection, early diagnosis, and early treatment. For male hypogonadism caused by insufficient secretion of gonadotropins by the hypothalamus-pituitary axis, treatment with gonadotropins can help restore spermatogenic function and promote the development of secondary sexual characteristics. Cryptorchidism should be treated with HCG between the ages of 2 and 9 to stimulate the secretion of endogenous testosterone, which may correct cryptorchidism. In cases of intersex with ambiguous external genitalia, the choice of gender is very important, and the chosen gender should enable the patient to better adapt to social life and have better sexual development during puberty.

　　1. Blood and urine hormone measurements

　　1. Testosterone Measurement:90% of male blood testosterone comes from the testes, reflecting the function of the interstitial cells. The normal blood testosterone level in adult males is 10-35nmol/L (3-10mg/L, RIA method).

　　2. Dihydrotestosterone (DHT):The normal plasma level of dihydrotestosterone (DHT) in young adult males is about 10% of testosterone, approximately 2nmol/L (0.5mg/L) (RIA method).

　　3. 24-hour Urinary 17-ketosteroid Measurement:Urinary 17-ketosteroids mainly come from weak androgenic steroids or their metabolites from the adrenal glands, only 40% are metabolites of testosterone, and they cannot accurately reflect the functional state of the testes, so the results should be combined with clinical analysis.

　　4. Plasma LH Measurement:The normal value of LH in adult males is 5-10IU/L (RIA method). When measuring LH, testosterone should also be measured. If both levels are low at the same time, it indicates hypothalamic and pituitary diseases; if the plasma testosterone level is low and the LH level is high, it suggests primary testicular dysfunction.

　　5. Plasma FSH Measurement:The normal range of FSH in adult males is 5-20IU/L. If the hypothalamus-pituitary axis is normal and the spermatogenic epithelium is severely damaged, the FSH level will increase.

　　6. Chorionic Gonadotropin (HCG) Stimulation Test:The biological activity of HCG is similar to that of LH. The method is intramuscular injection of HCG 4000IU once a day for 4 days, and on the 5th day, blood is drawn to measure testosterone. The normal response is that the blood testosterone level increases exponentially from the normal value, and for those with a very low baseline value, the absolute increase should be calculated. In cases of primary gonadal dysfunction, there is no significant increase in blood testosterone after HCG stimulation; whereas in cases of interstitial cell dysfunction in the testes secondary to hypopituitarism, blood testosterone levels significantly increase.

　　Chapter 7: Clomiphene (Clomiphene) Test:100-200mg/d orally. Normal people show a doubling of LH and FSH after 6 days, while patients with pituitary or hypothalamic lesions show a significantly reduced response.

　　Chapter 8: LRH Stimulation Test:It can reflect the reserve of pituitary gonadotropin hormones. The method is intravenous injection of LRH 50μg, blood is taken at 0', 15', 30', 120' to measure LH and FSH. The normal male peak appears between 15' and 30', with an increase of about 2-5 times in LH and about 2 times in FSH. Patients with pituitary dysfunction show a weak response in this test, with no increase in LH and FSH; hypothalamic lesions show a delayed response. After intravenous infusion of LRH for 7-14 days, the pituitary response to LRH stimulation can return to normal. Primary testicular disease shows an overreaction in the secretion of LH and FSH, and if the lesion is limited to the seminiferous tubules, FSH may be abnormally elevated, but the LH response is normal.

　　Chapter 2: Chromosomal Gender Analysis

　　1. Sexual chromosomes:Lymphocytes from peripheral venous blood are used for chromosomal karyotype analysis by fluorescence banding method. The normal male karyotype is 46,XY, and the normal female karyotype is 46,XX. C-banding analysis can identify the presence or absence of the Y chromosome at the metaphase of mitosis, and G-banding analysis is conducive to discovering the types of chromosomal abnormalities.

　　2. Sexual chromatin:Also known as Barr body (Barr: body), it can be detected by smearing the oral mucosa. Female chromatin is positive, and male chromatin is negative.

　　Chapter 3: Semen Examination

　　The normal volume of seminal ejaculation in a male is 2-6ml, with a total sperm count exceeding 60 million, density greater than 20 million/ml, and normal vitality and morphology of sperm should reach more than 60%.

　　Chapter 4: Sperm Penetration Cervical Mucus Test

　　Sperm can penetrate cervical mucus, and fertility is present; otherwise, infertility is present.

　　Chapter 5: Anti-Sperm Antibodies and Anti-Sperm Plasma Antibodies

　　If positive, it indicates that these antibodies are present in the female reproductive tract, causing sperm agglutination or inhibiting sperm activity, leading to infertility.

　　Chapter 6: Testicular Biopsy

　　It can differentiate between seminal duct obstruction and spermatogenic dysfunction.

　　Chapter 7: Seminal Vesicle, Sperm Duct造影

　　It can understand the condition of obstructed seminal ducts.

　　Chapter 8: Histocompatibility Y Antigen (H-Y Antigen)

　　It is a gender identification marker that is more essential than sex chromosomes, exclusive to males, and does not exist in females. It is helpful in analyzing the etiology of hermaphroditism. The most common true hermaphroditism is 46,XX male, where no shifted Y chromosome fragments can be found in cytogenetics, but the expression of H-Y antigen indicates the presence of Y chromosome genes. Male pseudohermaphroditism has a normal male karyotype and bilateral testicular differentiation, with a positive H-Y antigen. Female pseudohermaphroditism has a normal female karyotype, with bilateral ovaries and a negative H-Y antigen.

　　Chapter 9: Other Auxiliary Diagnoses

　　X-ray bone age determination, pelvic ultrasound, CT, MRI for the exploration of reproductive glands and ducts, etc.

　　Smoking and drinking can cause harm to the testes, and it is best to quit smoking and drinking. In addition, high cholesterol foods can increase the risk of early onset of male menopause, so it is better to eat less. Antioxidants and unsaturated fatty acids in food can help men alleviate the discomfort symptoms of menopause.

　　For male hypogonadism caused by insufficient secretion of gonadotropins from the hypothalamus-pituitary, the use of gonadotropin therapy can help restore spermatogenic function and promote the development of secondary sexual characteristics. The preparations that can be used include:

　　1. Chorionic gonadotropin (HCG):It can stimulate the interstitial cells of the testes to produce testosterone.

　　2. Menopausal gonadotropin (HMG):Each vial contains 75 IU of FSH and LH, which has the function of promoting spermatogenesis and the secretion of androgens in the testes. It is necessary to take the medicine 2 to 3 times a week, at least for 3 months. To improve fertility, HCG 2000 IU can be tried first, injected intramuscularly three times a week, for a course of 12 weeks. After a rest period of 12 weeks, the treatment can be repeated to promote the secretion of testosterone by interstitial cells and to promote the development of male secondary sexual characteristics. Then, HMG can be added, 150 IU injected intramuscularly three times a week, and after 4 months of treatment, once the spermatogenic development is restored, HCG can usually be used alone for maintenance therapy, 500 to 1500 IU per dose, twice a week, and regular semen examinations should be conducted. The therapeutic effect of long-term single use of HCG may gradually diminish. In addition, LRH 100 μg per dose, once every other day, or LRH 25 to 200 ng/kg body weight can be injected using a pocket-sized injection pump every 2 hours, or nasal medication can be taken at regular intervals, with a course of 90 days. This can induce spermatogenesis and the production of testosterone in the testes. In addition, some people use clomiphene citrate for treatment, which is a weak estrogen that can competitively inhibit the feedback inhibition of estrogen on the hypothalamus, causing an increase in LRH secretion by the hypothalamus, stimulating the pituitary to release FSH and LH. The dose is 50 to 100 mg orally per day, for a course of 3 months. Vitamin E, Chinese medicine deer antler extract, and other treatments can also be tried. For patients with primary hypogonadism, androgen replacement therapy can promote the development of external genitalia, but there is no spermatogenesis, so there is no fertility. Oral methyltestosterone is harmful to the liver and should not be used. Other oral medications include 1α-methyl-5α-dihydrotestosterone (Mesterolone), 30 to 60 mg/d, which does not cause cholestasis jaundice. Intramuscular medications include testosterone propionate, a short-acting androgen, 25 to 50 mg per dose, twice or three times a week, but it has a strong local irritation and is not suitable for long-term use. For androgen deficiency, it is best to use long-acting testosterone undecanoate or testosterone decanoate 200 mg per dose, injected intramuscularly once every 1 to 2 weeks. After 2 to 3 years of use, complete male sexual characteristics can be achieved, and then the dose can be reduced to maintenance dose, 100 to 200 mg per dose, injected intramuscularly once every 2 to 3 weeks. The use of androgens in children can lead to premature closure of the epiphyses, affecting height, and should not be started before the age of 13.

　　Cryptorchidism is suitable for the use of HCG between 2 to 9 years old to stimulate the secretion of endogenous testosterone, which may correct cryptorchidism. For bilateral cryptorchidism, short-term HCG treatment can be performed, with intramuscular injection of 3000U every other day for a total of 3 times. For unilateral cryptorchidism, long-term HCG treatment should be given, with intramuscular injection of 500U three times a week for those under 5 years old, or 1500U twice a week, for a total of 6.5 weeks. For those over 5 years old, 1000U should be injected intramuscularly three times a week for a total of 6.5 weeks. It can also be combined with the use of LRH spray Crypfocur for nasal mucosal absorption. If hormone treatment fails, surgery should be performed to bring the testicles into the scrotum and fix them. Intra-abdominal cryptorchidism has a high risk of cancer, and if repositioning fails, it should be removed.

　　For individuals with hermaphroditism in the external genitalia, the choice of gender is very important, and the chosen gender should enable the patient to better adapt to social life and have better sexual development during puberty. After deciding on the gender, corrective surgery of the reproductive system and necessary hormone replacement therapy are required. For female caregivers, estrogen and progesterone cycle therapy should be adopted at appropriate times; for male caregivers, it is advisable to use androgen therapy for a long time at the beginning of puberty.