Male Hypogonadism

Hypogonadism is defined as a problem associated with symptoms or findings testosterone deficiency as well as a deficit in the production of sperm, or both. This may be due to a fault in the testes (primary hypogonadism) or at the level of the hypothalamic-pituitary axis (secondary hypogonadism). Both can be congenital or acquired as a result of aging, disease, drugs or other factors. In addition, a number of congenital enzyme deficiencies leading to different levels of androgen in the target organ. The diagnosis is confirmed by determination of hormone levels. Treatment depends on the cause, but typically includes gonadotropin releasing hormone, gonadotropin or testosterone replacement therapy initiated.

Hypogonadism is defined as a problem associated with symptoms or findings testosterone deficiency as well as a deficit in the production of sperm, or both. This may be due to a fault in the testes (primary hypogonadism) or at the level of the hypothalamic-pituitary axis (secondary hypogonadism). Both can be congenital or acquired as a result of aging, disease, drugs or other factors. In addition, a number of congenital enzyme deficiencies leading to different levels of androgen in the target organ. The diagnosis is confirmed by determination of hormone levels. Treatment depends on the cause, but typically includes gonadotropin releasing hormone, gonadotropin or testosterone replacement therapy initiated.

(Male hypogonadism in children.) Hypogonadism is defined as a problem associated with symptoms or findings testosterone deficiency as well as a deficit in the production of sperm, or both. This may be due to a fault in the testes (primary hypogonadism) or at the level of the hypothalamic-pituitary axis (secondary hypogonadism). Both can be congenital or acquired as a result of aging, disease, drugs or other factors. In addition, a number of congenital enzyme deficiencies leading to different levels of androgen in the target organ. The diagnosis is confirmed by determination of hormone levels. Treatment depends on the cause, but typically includes gonadotropin releasing hormone, gonadotropin or testosterone replacement therapy initiated. The primary etiology hypogonadism arises respond by inability of the testes, on follicle stimulating hormone (FSH) and luteinizing hormone (LH). Since the primary hypogonadism affects the production of testosterone, the testosterone can not inhibit the production of FSH and LH. The most common cause of a primary hypogonadism is Klinefelter’s syndrome. It includes a dysgenesis of the seminiferous tubules, hypoplasia of the testis, epididymis and scrotum, and a 47, XXY karyotype (Klinefelter syndrome (47, XXY)). In secondary hypogonadism is a disorder of the hypothalamus to produce the Gonadropin-releasing hormone (GnRH) or not producing enough pituitary FSH and LH. In secondary hypogonadism, the testosterone levels are low, the FSH and LH levels are low or falsely normal. Each of acute systemic illness may temporarily cause a secondary hypogonadism. Some syndromes with hypogonadism both primary and secondary causes (Mixed hypogonadism). In causes of hypogonadism some common causes of hypogonadism are listed. Some forms of hypogonadism (z. B. cryptorchidism, some systemic diseases) affect more than the Spermatozoenproduktion testosterone levels. Causes of hypogonadism type Congenital causes Acquired causes primary (testicular) Klinefelter syndrome anorchia (bilateral) cryptorchidism Myotonic dystrophy Enzymatic defects in testosterone synthesis Leydig cell aplasia Noonan syndrome chemotherapy or radiotherapy infection of the testicles (z. B. mumps, Echo virus, flavivirus ) High doses of anti-androgens (eg. as cimetidine, spironolactone, ketoconazole, flutamide, cyproterone acetate) Secondary (hypothalamic-pituitary) Idiopathis cher hypogonadism Kallmann syndrome Prader-Willi syndrome Dandy-Walker malformation insulated luteinizing hormone deficiency Each acute systemic disease hypopituitarism (tumor, infarction, infiltrative disease, infection, trauma, radiation) hyperprolactinemia iron overload (hemochromatosis) Certain medications (eg. B. estrogens, psychotropics, metoclopramide, opioids, leuprolide, goserelin, triptorelin, newer androgen biosynthesis inhibitors for prostate cancer) Cushing’s syndrome cirrhosis Morbid obesity Idiopathic Mixed -. Skin aging alcoholism Systemic diseases (e.g. uremia, hepatic failure, AIDS, sickle cell anemia ) drugs (ethanol, corticosteroids) * In approximate order of frequency. Symptoms and complaints The age at onset of testosterone deficit determines the clinical presentation: congenital, beginning in childhood, adult onset. Congenital hypogonadism can occur in the 1st, 2nd or 3rd trimester of pregnancy. Congenital hypogonadism in the first quarter resulting in inadequate male sexual differentiation. A complete lack of testosterone leads to the formation normal appearing female external genitalia. A partial testosterone deficiency leads to changes that can range from a zwitter similar external genitals to hypospadias. If, in the second or third trimester to a testosterone deficiency, leading to micro-phallus and cryptorchidism. A testosterone deficiency beginning in childhood (Male hypogonadism in children), has little consequences and usually remains undetected until the delayed puberty. Untreated hypogonadism affects the development of secondary sexual characteristics. In adulthood, patients have underdeveloped muscles, a high voice, a small scrotum, decreased penile and testicular growth and a sparse pubic and underarm hair. The male body hair is missing. It can gynecomastia and eunuchoid body proportions develop (arm span> height 5 cm and distance pubic / Ground> distance pubic bone / crown by> 5 cm), which are caused by a delayed epiphyseal closure and prolonged length growth. Onset of testosterone deficiency with onset in adulthood has different manifestations, depending on the extent and duration of the deficit. Typical are decreased libido, erectile dysfunction, loss of cognitive skills such as spatial perception, sleep, Vasomotoreninstabilität (in acute serious male hypogonadism) and mood swings such as depression or angry outbursts. Decrease in muscle mass, increased abdominal circumference, testicular atrophy, osteoporosis, gynecomastia and sparse body hair develop normally until months to years. A testosterone deficiency can According to the current state of knowledge reduce the risk for coronary artery occlusion diagnostic tests, starting with FSH, LH and testosterone levels to a congenital or Kindheitshypogonadismus is often thought in developmental disorders or delayed puberty. A late-onset hypogonadism is suspected in the corresponding symptoms and signs, but is often overlooked because the clinical findings are atypical and unspecific. On Klinefelter’s syndrome should be considered with very small testes in adolescent males with delayed puberty, young men with hypogonadism and all adult men. Hypogonadism must be confirmed by appropriate laboratory findings (Laboratory evaluation of male hypogonadism.). Diagnosis of primary and secondary hypogonadism increases in FSH and LH levels rather suggest a primary hypogonadism as decreased testosterone levels. FSH and LH levels facilitate the determination of whether hypogonadism is primary or secondary. High gonadotropin levels, even at low or normal testosterone levels speak for a primary hypogonadism, during gonadotropin levels that are low or measured on testosterone levels lower than expected, leaving a secondary hypogonadism suspect. On the other hand, the low testosterone and gonadotropin levels can be caused by a constitutional delay of puberty in short stature boys with delayed puberty. An increase in serum FSH with normal testosterone and LH levels often occur when spermatogenesis is disturbed at normal testosterone production. The cause of hypogonadism is often clinically evident. Primary hypogonadism requires no further investigation, although some clinicians to definitive diagnosis for. As a Klinefelter’s syndrome carry karyotyping. Total serum testosterone (and if possible, free testosterone) and serum FSH and LH serum levels are measured simultaneously. The normal range for total testosterone is 300-1000 ng / dL (10.5 to 35 nmol / l). The testosterone levels should be measured in the morning (before 10 Uhrmorgens) to confirm hypogonadism. Because the sex-hormone binding globulin (SHBG) increases in age, the total is testosterone levels after the age of 50, a less sensitive parameter for confirming a hypogonadism. Although free testosterone reflects the functional testosterone levels more precisely, this provision requires an equilibrium dialysis, which is technically difficult and not available everywhere. Although some tests commercially available including analog free testosterone assays are trying to determine the free testosterone levels, but the results are often wrong (especially with type 2 diabetes, obesity and hypothyroidism) that affect SHBG levels. Free testosterone levels can be determined based on SHBG, albumin and testosterone levels; Calculators available online. See the Free and Bioavailable Testosterone Calculator. Because of the pulsating secretion of FSH and LH, these hormones are sometimes referred to as a pooled sample of 3 venipuncture measured in 20-minute intervals, but these pooled samples rarely provide additional clinically important information in comparison to a single blood sample. Typically, the FSH and LH levels are 5 mI.E./ml and adulthood 5-15 mI.E./ml before puberty ?. A semen analysis should be performed for all men who want an infertility treatment performed. In adolescents and adults can be obtained by masturbation after 2 days (n. D. Talk .: 5 days) of abstinence a semen sample to be an excellent indicator of the function of the seminiferous tubules. A normal semen sample (WHO standard) has a volume of> 1.5 ml. Ml with> 20 million sperm / ml (n. D. Talk .: The WHO> 15% normal), of which 50% morphologically normal and mobile (n. d. Ed .:> 25% rapidly or> 50% quickly and easily movable) are (sperm sperm disorders disorders). Laboratory evaluation of male hypogonadism. Fe = iron, FSH = follicle stimulating hormone, GnRH = gonadotropin-releasing hormone, LH = luteinizing hormone. Examination of the secondary hypogonadism Since any systemic disease can cause reduction of testosterone, FSH and LH levels, a temporary, a secondary hypogonadism 4 should be confirmed by a second examination weeks after disappearance of the systemic disease frühestesn. To confirm a secondary hypogonadism in young people, the GnRH stimulation test can be used. If the values ??of FSH and LH rise in response to i.v. GnRH is simply delayed puberty. the levels do not increase, it is likely to be a true hypogonadism. In order to clarify the cause of a detected secondary hypogonadism, and the serum prolactin level should (in order to perform screening of a pituitary adenoma), and the transferrin saturation are determined (by screening durchzuführen- a hemochromatosis Hereditary hemochromatosis). Sella target shot with MRI or CT, a macroadenoma the pituitary gland or other lesions in men, exclude the one or apply more of the following: age <60 years with no other obvious cause of hypogonadism Very low testosterone levels (<200 ng / dl) elevated prolactin symptoms associated with a pituitary tumor (z. B. headache, blurred vision) If evidence or signs of Cushing's syndrome before, a 24-h urine should be tested for free cortisol or dexamethasone suppression are performed (Cushing's syndrome ). If no abnormalities are observed, the diagnosis of idiopathic acquired secondary hypogonadism is detected. Therapy therapy testosterone replacement therapy with gonadotropin to restore fertility due to a secondary hypogonadism The treatment of the primary hypogonadism aims at the gentle and safe androgen. Although patients are not fertile with a primary hypogonadism also by endocrine therapy, patients may be fertile with a secondary hypogonadism often by a gonadotropin therapy. Testosterone formulations described herein, those that are available in the United States. Other formulations may be available in other countries. Testosterone replacement therapy (TRT) Since exogenous testosterone impaired spermatogenesis, should a TRT, if possible with secondary hypogonadism or when a persisting fertility is desired (unless there is irreversible primary testicular failure) can be avoided. Treatment of the secondary hypogonadism in males with Gonadotropinersatztherapie (Male hypogonadism: Treatment of infertility caused by hypogonadism) stimulates usually androgen and spermatogenesis. TRT can be used for men who have no signs of puberty almost 15 years old In secondary hypogonadism which was excluded This will get for 4-8 months, the long-acting testosterone enanthate 50 mg i.m. once a month. These low doses lead to compromise to a certain virilization without linear growth. Older adolescents with testosterone deficiency received the long-acting testosterone enanthate or testosterone cypionate at a dose that about 18-24 months every 1-2 weeks gradually i.m. from 50 to 100 to 200 mg is increased. Transcutaneous gel can also be used, although it is more expensive, could be transferred to others in intimate contact, and is more difficult to dose accurately. It makes sense to make a switch from Testosterongelanwendungen an adult dose in older adolescents when their i.m. Dosage has reached a level of 100-200 mg every 2 weeks. Adults with established testosterone deficiency may benefit from replacement therapy. The treatment slows the progression of osteoporosis, muscle loss, vasomotor instability, loss of libido, depression and sometimes an erectile dysfunction. The effects of testosterone on coronary artery disease are not well understood. TRT can improve coronary artery blood flow and reduce the risk of coronary heart disease; However, concerns have increased that TRT increases the risk for cardiovascular events. Among the options for replacement therapy testosterone gel includes 1% or 1.62% (5 to 10 g of gel per day to provide 5 to 10 mg of testosterone per day) Transdermal axillary solution (60 mg 1 time / day) A buccal lozenge ( 30 mg 2 times daily) Transdermal testosterone patch (4 mg 1 time / day) a new nasal formulation (a spray of 5.5 mg in each nostril 3 times daily (75 mg / pellet) was added) Subcutaneous testosterone implants than 4 to 6 units placed every 3 to 6 months i. m. Testosterone enanthate or cypionate (100 mg every 7 days or 200 mg every 10 to 14 days) T gel gives more consistent physiological blood levels than other forms of therapy, but the i.m. Transfer or patches are sometimes preferred because of their lower cost. Oral formulations are absorbed unpredictably. Possible adverse effects of testosterone and analog materials: erythrocytosis not (especially in men received ? 50 years i.m. testosterone) Venous thromboembolism associated with erythrocytosis acne gynecomastia Low sperm count Very rare prostate enlargement or edema. Prostate obstructive symptoms are rare. Currently is not assumed that the amounts of testosterone that are given to achieve physiological levels, cause new prostate cancer or accelerate the growth of localized prostate cancer or spread and it is assumed that (TRT minimal effects on the levels of prostate specific antigen PSA) has in men with benign prostatic hyperplasia and prostate cancer in men with treated. According to package inserts TRT is contraindicated in men with prostate cancer and men who suffer from prostate cancer or are at high risk should be advised and careful digital rectal examinations and measurements of the PSAs are performed while taking TRT. A prostate biopsy may be necessary if the PSA increase after completion of the TRT continues. Men with hypogonadism is believed by those that they have prostate cancer should seek consultation with an expert. Orally administered preparations Birgen risks of hepatocellular dysfunction and hepatic adenomas. Men, the extra testosterone should be monitored regularly. HCT, PSA and testosterone levels should during the first year of TRT and half-yearly quarterly thereafter measured. Digital rectal examination should be offered at the same time. If the hematocrit ? 54%, the testosterone dose should be reduced. Significant increases in PSA levels prompt a prostate biopsy in men, where you otherwise diagnose prostate cancer and treat them accordingly würde.Therapie a hypogonadism caused by infertility infertility, which can have many causes other than hypogonadism, is discussed in detail in (infertility). An existing basis of primary hypogonadism, infertility does not respond to hormonal therapy. Men with a primary hypogonadism occasionally have some intratesticular sperm, may be used the various recovered by microsurgical techniques and for the fertilization of an egg by means of ART (Assisted reproductive techniques, for. Example, intracytoplasmic sperm injection). A secondary hypogonadism due infertility usually speaks at a Gonadotropinersatztherapie. The other symptoms of secondary hypogonadism respond to a sole testosterone replacement therapy. If the secondary hypogonadism caused by a Hypophysenkrankheit that Gonadotropinersatztherapie is usually successful. The therapy is initiated with LH and FSH replacement. LH-replacement is with human chorionic gonadotropin (hCG) initiated with dosages of 1500 I.U. s.c. 3 times / week. In the FSH-replacement therapy that is expensive, human menotropisches gonadotropin or human recombinant FSH is used, with doses of 150 IU 3 times / week. Doses may be adjusted based on the results of tests carried out on semen and serum levels of FSH, LH and testosterone. Once a sufficient number of sperm is reached, FSH and hCG may be stopped monotherapy be continued. Most men who have secondary hypogonadism due to a malfunction of the hypothalamus (z. B. idiopathic hypogonadism, Kallman's syndrome) become fertile with the treatment despite low sperm counts (z. B., <5,000,000 / ml). If LH and FSH treatments are ineffective, a vibrant GnRH replacement therapy may (every 2 h, s.c. by a programmable mini pump), even if it is less readily available, be more effective. Most men (80-90%) respond to these measures. Conclusion FSH and LH levels help to distinguish (low or inappropriately normal levels) between primary hypogonadism (high values) and secondary hypogonadism. Age-related symptoms of male hypogonadism include inadequate sexual differentiation (congenital), delayed puberty (onset in childhood) and various non-specific symptoms such as decreased libido, erectile dysfunction, cognitive decline, percentage decrease in lean body mass, insomnia and mood swings (onset in adulthood) , Free testosterone levels, which can be calculated and are sometimes measured reflect a gonadal sufficiency better than complete testosterone levels do so. The diagnosis can be systematically addressed using an algorithm. Testosterone replacement therapy can alleviate the symptoms of hypogonadism, but not restore fertility. A Gonadotropinersatztherapie can restore normally fertility in men with secondary hypogonadism.

Health Life Media Team

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