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Hypogonadism | Conditions & Treatments | UCSF Medical Center

Hypogonadism is a condition that causes decreased function of the gonads, which are the testis in males and the ovaries in females, and the production of hormones that play a role in sexual development during puberty. You may be born with the condition or it can develop later in life from injury or infection. Some types of hypogonadism can be treated with hormone replacement therapy.

There are two forms of the condition primary hypogonadism resulting from problems of the testis or ovary and central hypogonadism caused by problems with the pituitary or hypothalamic glands. Central hypogonadism leads to decreased levels of luteinizing hormone (LH) and follicle stimulating hormones (FSH), released by the pituitary gland.

The condition may have genetic, menopausal autoimmune and viral causes or may develop after cancer treatments such as radiation and chemotherapy.

Fasting, weight loss, eating disorders such as anorexia nervosa, and bulimia, and stressful conditions can cause the condition.

In children before puberty, hypogonadism causes no symptoms. In adolescents, it can delay or prevent exual development.

Adult women with the condition may stop menstruating or develop infertility, loss of libido, vaginal dryness and hot flashes. Prolonged periods of hypogonadism can cause osteoporosis.

Men with the condition may experience loss of libido, erectile dysfunction and infertility.

To diagnose hypogonadism, tests may be performed to check hormone levels estogren in females and testosterone in males. In addition, levels of luteinizing hormone (LH) and follicle stimulating hormones (FSH) will be tested. LH and FSH are pituitary hormones that are stimulated by the gonads.

Other tests may measure thyroid hormones, sperm count and prolactin, a hormone released by the pituitary gland that stimulates breast development and milk production Tests also may be performed to test for anemia and possible genetic causes of symptoms.

For women, your doctor may request a sonogram of your ovaries.

If pituitary disease is suspected, a magnetic resonance imaging (MRI) scan or computed tomography (CT) scan may be performed to examine the the pituitary gland.

Hormone replacement therapy has proven to be effective treatment for hypogonadism in men and pre-menopausal women.

Estrogen may be administered in the form of a patch or pill. Testosterone can be given by a patch, a product soaked in by the gums, a gel or by injection.

For women who have not had their uterus removed, a combination of estrogen and progesterone is often recommended to decrease the chance of developing endometrial cancer. Low-dose testosterone may be added for women with hypogonadism who have a low sex drive.

Other hormones may be prescribed to restore fertility in men and women.

Reviewed by health care specialists at UCSF Medical Center.

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Hypogonadism | Conditions & Treatments | UCSF Medical Center

Male Hypogonadism | Uroweb

3.1.Epidemiology

Definition: male hypogonadism is a clinical syndrome caused by androgen deficiency which may adversely affect multiple organ functions and quality of life (QoL) [1].

Androgen deficiency increases slightly with age also in healthy men [2,3]. In middle-aged men, the incidence of biochemical hypogonadism varies from 2.1-12.8% [4]. The incidence of low testosterone and symptoms of hypogonadism in men aged 40-79 varies form 2.1-5.7% [3,4]. Hypogonadism is more prevalent in older men, in men with obesity, those with co-morbidities, and in men with a poor health status.

Androgens, which are produced by the testis and by the adrenal glands, play a pivotal role in male reproductive and sexual function. Androgens are crucial for the development of male reproductive organs, such as the epididymis, vas deferens, seminal vesicle, prostate and penis. In addition, androgens are needed for puberty, male fertility, male sexual function, muscle formation, body composition, bone mineralisation, fat metabolism, and cognitive functions [5].

Male sexual development starts between the 7th and 12th week of gestation. The undifferentiated gonads develop into a foetal testis through expression of multiple genes located on the short arm of the Y chromosome, including the sex-determining region of the Y chromosome (SRY gene complex) and the SOX gene on chromosome 17 [6]. The foetal testis produces three hormones: testosterone, insulin-like peptide 3 (INSL3) and anti-Mllerian hormone (AMH). Testosterone is needed for the stabilisation of the Wolffian ducts, resulting in formation of the epididymis, vas deferens and seminal vesicle. AMH activity results in regression of the Mllerian ducts (Figure 1). INSL3 and AMH regulate testicular descent.

Under the influence of intratesticular testosterone, the number of gonocytes per tubule increases threefold during the foetal period [7]. In addition, testosterone is needed for development of the prostate, penis and scrotum. However, in these organs testosterone is converted into the more potent metabolite 5a-dihydrotestosterone (DHT) by the enzyme 5a-reductase. Testosterone and DHT are required for penile growth, both activating the androgen receptor [8].

Intratesticular testosterone is needed to maintain the spermatogenic process and to inhibit germ cell apoptosis [9]. The seminiferous tubules of the testes are exposed to concentrations of testosterone 25-100 times greater than circulating levels. Suppression of gonadotropins (e.g. through excessive testosterone abuse) results in a reduced number of spermatozoa in the ejaculate and hypospermatogenesis [10]. Complete inhibition of intratesticular testosterone results in full cessation of meiosis up to the level of round spermatids [11,12]. Testosterone does not appear to act directly on the germ cells, but functions through the Sertoli cells by expression of the androgen receptor (AR) and influencing the seminiferous tubular microenvironment [11]. Testosterone can also be metabolised into oestradiol by aromatase, present in fat tissue, the prostate, the testes and bone. Oestradiol is also essential for bone mineralisation in men [13]. The production of testosterone is controlled in the foetus by placental choriongonadotropin (hCG) and after birth by luteinising hormone (LH) from the pituitary gland. Immediately after birth, serum testosterone levels reach adult concentrations over several months (mini puberty). Thereafter and until puberty, testosterone levels are low, thus preventing male virilisation. Puberty starts with the production of gonadotropins, initiated by gonadotropin-releasing hormone (GnRH) secretion from the hypothalamus and results in testosterone production, male sexual characteristics and spermatogenesis [14]. Figure 1 shows the development of the male reproductive system.

Testosterone exerts its action through the AR, located in the cytoplasm and nucleus of target cells. During the foetal period, testosterone increases the number of ARs by increasing the number of cells with the AR and by increasing the number of ARs in each individual cell [8,13]. The AR gene is located on the X chromosome (Xq 11-12): defects and mutations in the AR gene can result in male sexual maldevelopment, which may cause testicular feminisation or low virilisation (i.e. disorder of sexual development (DSD)). Less severe mutations in the AR gene may cause mild forms of androgen resistance and male infertility [15]. In exon 1 of the gene, the transactivation domain consists of a trinucleotide tract (cytosine-adenine-guanine (CAG) repeats)) of variable length. Androgen sensitivity may be influenced by the length of the CAG repeats in exon 1 of the AR gene [15]. The AR CAG repeat length is inversely correlated with serum total and bioavailable testosterone and oestradiol in men. Shorter repeats have been associated with an increased risk for prostate disease, and longer repeats with reduced androgen action in several tissues [16]. CAG repeat number may influence androgenic phenotypical effects, even in case of normal testosterone levels [17].

Summary of evidence

Testosterone is essential for normal male development.

Figure 1: Development of the male reproductive system

FSH=follicle-stimulating hormone; LH=luteinising hormone; SRY=sex determining region of the Y chromosome; INSL3=insulin-like peptide 3.

Hypogonadism results from testicular failure, or is due to the disruption of one or several levels of the hypothalamic-pituitary-gonadal axis (Figure 2).

Male hypogonadism can be classified in accordance with disturbances at the level of:

Primary testicular failure is the most frequent cause of hypogonadism and results in low testosterone levels, impairment of spermatogenesis and elevated gonadotropins. The most important clinical forms of primary hypogonadism are Klinefelter syndrome and testicular tumours.

The main reasons for primary testicular failure are summarised in Table 1.

Central defects of the hypothalamus or pituitary cause secondary testicular failure. Identifying secondary hypogonadism is of clinical importance, as it can be a consequence of pituitary pathology (including prolactinomas) and can cause infertility, which can be restored by hormonal stimulation in most patients with secondary hypogonadism.

The most relevant forms of secondary hypogonadism are:

These disorders are characterised by disturbed hypothalamic secretion or action of gonadatropin-releasing hormone (GnRH), as a pathophysiology common to the diseases, resulting in impairment of pituitary LH and FSH secretion. An additional inborn error of migration and homing of GnRH-secreting neurons results in Kallmann syndrome [23,24]. The most important symptom is the constitutional delay of puberty: it is the most common cause of delayed puberty (pubertas tarda) [25]. Other rare forms of secondary hypogonadism are listed in Table 2.

Combined primary and secondary testicular failure results in low testosterone levels and variable gonadotropin levels. Gonadotropin levels depend predominantly on primary or secondary failure. What has been labelled as late-onset hypogonadism and age-related hypogonadism is comprised of three types of hypogonadism and formally secondary hypogonadism is the most prevalent [26,27]. It should however be stated that low testosterone and low gonadotropin levels do not exclude a compromised gonadal response to LH stimulation as has been demonstrated in obesity, corticosteroid induced hypogonadism etc.

These forms are primarily rare defects and will not be further discussed in detail in these guidelines. There are AR defects with complete, partial and minimal androgen insensitivity syndrome; Reifenstein syndrome; bulbospinal muscular atrophy (Kennedy disease); as well as 5a-reductase deficiency (for a review, see Nieschlag et al. 2010) [28].

The classification of hypogonadism has therapeutic implications. In patients with secondary hypogonadism, hormonal stimulation with human chorionic gonadotropin (hCG) and FSH or alternatively pulsatile GnRH treatment can restore fertility in most cases [29,30]. Detailed evaluation may for example detect pituitary tumours, systemic disease, or testicular tumours. Combined forms of primary and secondary hypogonadism can be observed in ageing, mostly obese men, with a concomitant age-related decline in testosterone levels resulting from defects in testicular as well as hypothalamic-pituitary function.

Table 1: Most common forms of primary hypogonadism

Disease

Causes of deficiency

Maldescended or ectopic testes

Failure of testicular descent, maldevelopment of the testis

Testicular cancer

Testicular maldevelopment

Orchitis

Viral or unspecific orchitis

Acquired anorchia

Trauma, tumour, torsion, inflammation, iatrogenic, surgical removal

Secondary testicular dysfunction

Medication, drugs, toxins, systemic diseases

(Idiopathic) testicular atrophy

Male infertility (idiopathic or specific causes)

Congenital anorchia (bilateral in 1 in 20,000 males,

unilateral 4 times as often)

Intrauterine torsion is the most probable cause

Klinefelter syndrome 47,XXX

Sex-chromosomal non-disjunction in germ cells

46,XY disorders of sexual development (DSD)

(formerly male pseudohermaphroditism)

Disturbed testosterone synthesis due to enzymatic defects of steroid biosynthesis (17,20- lyase defect, 17-hydroxysteroid dehydrogenase defect)

Gonadal dysgenesis (synonym streak gonads)

XY gonadal dysgenesis can be caused by mutations in different genes

46,XX male syndrome (prevalence of 1 in 10,000-20,000)

Males with presence of genetic information from the Y chromosome after translocation of a DNA segment of the Y to the X chromosome during paternal meiosis

Noonan syndrome (prevalence of 1 in 1,000 to 1 in 5,000)

Short stature, congenital heart diseases, cryptorchidism

Inactivating LH receptor mutations, Leydig cell hypoplasia (prevalence of 1 in 1,000,000 to 1 in 20,000)

Leydig cells are unable to develop due to the mutation [31]

Table 2: Most common forms of secondary hypogonadism

Disease

Causes of deficiency

Hyperprolactinemia

Prolactin-secreting pituitary adenomas (prolactinomas) or drug-induced

Isolated hypogonadotropic hypogonadism (IHH) (formerly termed idiopathic hypogonadotrophic hypogonadism, IHH)

Specific (or unknown) mutations affecting GnRH synthesis or action

Kallmann syndrome (hypogonadotropic hypogonadism with anosmia, prevalence 1 in 10,000)

GnRH deficiency and anosmia, genetically determined

Secondary GnRH deficiency

Medication, drugs, toxins, systemic diseases.

Hypopituitarism

Radiotherapy, trauma, infections, haemochromatosis and vascular insufficiency or congenital

Pituitary adenomas

Hormone-secreting adenomas; hormone-inactive pituitary adenomas; metastases tothe pituitary or pituitary stalk

Prader-Willi syndrome (PWS) (formerly Prader-Labhart-Willi syndrome, prevalence 1 in 10,000 individuals)

Congenital disturbance of GnRH secretion

Congenital adrenal hypoplasia with hypogonadotropic hypogonadism (prevalence 1 in 12,500 individuals)

X-chromosomal recessive disease, in the majority of patients caused by mutations in the DAX1 gene

Pasqualini syndrome

Isolated LH deficiency

Recommendation

LE

GR

Differentiate the two forms of hypogonadism (primary and secondary) (LH levels), as this has implications for patient evaluation and treatment and makes it possible to identify patients with associated health problems and infertility.

1b

B

Figure 2: The hypothalamic-pituitary-testes axis

FSH=follicle-stimulating hormone; GnRH=Gonadotropin-releasing hormone; LH=luteinising hormone.

Hypogonadism is diagnosed on the basis of persistent signs and symptoms related to androgen deficiency and assessment of consistently low testosterone levels (on at least two occasions) with a reliable method [4,32-35].

Low levels of circulating androgens may be associated with signs and symptoms (Table 3) [4,36,37]

Table 3: Clinical symptoms and signs suggestive for androgen deficiency

Delayed puberty

Small testes

Male-factor infertility

Decreased body hair

Gynaecomastia

Decrease in lean body mass and muscle strength

Visceral obesity

Decrease in bone mineral density (osteoporosis) with low trauma fractures

Reduced sexual desire and sexual activity

Erectile dysfunction

Fewer and diminished nocturnal erections

Hot flushes

Changes in mood, fatigue and anger

Sleep disturbances

Metabolic syndrome

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Male Hypogonadism | Uroweb

Hypogonadism | University of Maryland Medical Center

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Hypogonadism occurs when the body's sex glands produce little or no hormones. In men, these glands (gonads) are the testes. In women, these glands are the ovaries.

Gonadal deficiency

The cause of hypogonadism can be primary or central. In primary hypogonadism, the ovaries or testes themselves do not function properly. Causes of primary hypogonadism include:

The most common genetic disorders that cause primary hypogonadism are

If you already have other autoimmune disorders you may be at higher risk of autoimmune damage to the gonads. These can include disorders that affect the liver and adrenal and thyroid glands as well as type 1 diabetes.

In central hypogonadism, the centers in the brain that control the gonads (hypothalamus and pituitary) do not function properly. Causes of central hypogonadism include:

A genetic cause of central hypogonadism is Kallmann syndrome. Many people with this condition also have a decreased sense of smell.

Girls who have hypogonadism will not begin menstruating. Hypogonadism can affect their breast development and height. If hypogonadism occurs after puberty, symptoms in women include:

In boys, hypogonadism affects muscle, beard, genital and voice development. It also leads to growth problems. In men the symptoms are:

If a pituitary or other brain tumor is present (central hypogonadism), there may be:

The most common tumors affecting the pituitary are craniopharyngioma in children and prolactinoma adenomas in adults.

You may need to have tests to check:

Other tests may include:

Sometimes imaging tests are needed, such as a

You may need to take hormone-based medicines. Estrogen and progesterone are used for girls and women. The medicines comes come in the form of a pill or skin patch. Testosterone is used for boys and men. The medicine can be given as a skin patch, skin gel, a solution applied to the armpit, a patch applied to the upper gum, or by injection.

For women who have not had their uterus removed, combination treatment with estrogen and progesterone may decrease the chance of developing endometrial cancer. Women with hypogonadism who have low sex drive may also be prescribed low-dose testosterone.

In some women, injections or pills can be used to stimulate ovulation. Injections of pituitary hormone may be used to help men produce sperm. Other people may need surgery and radiation therapy.

Many forms of hypogonadism are treatable and have a good outlook.

In women, hypogonadism may cause

Some women with hypogonadism take estrogen therapy, especially those who have early menopause. But long-term used of hormone therapy can increase the risk of breast cancer, blood clots and heart disease. Women should talk with their health care provider about the risks and benefits of hormone replacement therapy with your doctor.

In men, hypogonadism results in loss of sex drive and may cause:

Men normally have lower testosterone as they age. However, the decline in hormone levels is not as dramatic as it is in women.

Talk to your health care provider if you notice:

Both men and women should call their provider if they have headaches or vision problems.

Maintain normal body weight and healthy eating habits may help in some cases. Other causes may not be preventable.

Ali O, Donohoue PA. Hypofunction of the testes. In: Kliegman RM, Stanton BF, St. Geme JW III , et al., eds. Nelson Textbook of Pediatrics. 19th ed. Philadelphia, PA: Elsevier Saunders; 2011:chap 577.

Bhasin S, Cunningham GR, Hayes FJ, et al. Testosterone therapy in adult men with androgen deficiency syndromes: An Endocrine Society Clinical Practice guideline. J Clin Endocrinol Metab. 2010;95:2536-59. PMID: 20525905 http://www.ncbi.nlm.nih.gov/pubmed/20525905

Kansra AR, Donohoue PA. Hypofunction of the ovaries. In: Kliegman RM, Stanton BF, St. Geme JW III, et al., eds. Nelson Textbook of Pediatrics. 19th ed. Philadelphia, PA: Elsevier Saunders; 2011:chap 580.

Swerdloff RS, Wang C. The testis and male sexual function. In: Goldman L, Schafer AI. Goldman's Cecil Medicine. 24th ed. Philadelphia, PA: Elsevier Saunders; 2012:chap 242.

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What Is Low Testosterone? – Male Hypogonadism Symptoms and …

The straightforward, quick answer is: testosterone is the most important male sex hormone. Its produced in the testes, and its what causes boys to go through puberty.

In men, testosterone is responsible for maintaining:

The amount of testosterone in a mans body changes throughout the day, and its usually highest in the morning. A normal range of testosterone is 300 ng/dL to 1,000 ng/dL.

Low Testosterone Symptoms If you have low testosterone levels, you may begin to notice the following signs and symptoms:

In some men, low testosterone may be serious and they may experience more severe symptoms, especially the longer their testosterone levels remain low.

Severe low testosterone may lead to signs and symptoms, including:

Low Testosterone Causes There are several causes of low testosterone, and your doctor will work with you to figure out whats causing your low levels.

Low testosterone is broken into 2 main types: primary hypogonadism and secondary hypogonadism.

Primary hypogonadism is also known as primary testicular failure, and it is caused by a problem in the testicles. These problems can include:

Secondary hypogonadism is caused by a problem with the pituitary or hypothalamus glands. Those are glands that give a signal to the testicles to make testosterone, so if something affects them, testosterone production can be affected. Conditions that can cause secondary hypogonadism include:

These are just some examples of what can cause male hypogonadism. Through the diagnosis process, which youll learn about in the next article, your doctor should be able to figure out why you have low testosterone levels.

Updated on: 01/29/15

Low Testosterone Diagnosis

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What Is Low Testosterone? - Male Hypogonadism Symptoms and ...

Association of hypogonadism with vitamin D status: the …

OBJECTIVE:

Interrelationships between hormones of the hypothalamic-pituitary-testicular (HPT) axis, hypogonadism, vitamin D and seasonality remain poorly defined. We investigated whether HPT axis hormones and hypogonadism are associated with serum levels of 25-hydroxyvitamin D (25(OH)D) in men.

Cross-sectional survey of 3369 community-dwelling men aged 40-79 years in eight European centres. Testosterone (T), oestradiol (E(2)) and dihydrotestosterone were measured by gas chromatography-mass spectrometry; LH, FSH, sex hormone binding globulin (SHBG), 25(OH)D and parathyroid hormone by immunoassay. Free T was calculated from total T, SHBG and albumin. Gonadal status was categorised as eugonadal (normal T/LH), secondary (low T, low/normal LH), primary (low T, elevated LH) and compensated (normal T, elevated LH) hypogonadism. Associations of HPT axis hormones with 25(OH)D were examined using linear regression and hypogonadism with vitamin D using multinomial logistic regression.

In univariate analyses, free T levels were lower (P=0.02) and E(2) and LH levels were higher (P<0.05) in men with vitamin D deficiency (25(OH)D <50nmol/l). 25(OH)D was positively associated with total and free T and negatively with E(2) and LH in age- and centre-adjusted linear regressions. After adjusting for health and lifestyle factors, no significant associations were observed between 25(OH)D and individual hormones of the HPT axis. However, vitamin D deficiency was significantly associated with compensated (relative risk ratio (RRR)=1.52, P=0.03) and secondary hypogonadism (RRR=1.16, P=0.05). Seasonal variation was only observed for 25(OH)D (P<0.001).

Secondary and compensated hypogonadism were associated with vitamin D deficiency and the clinical significance of this relationship warrants further investigation.

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Male hypogonadism Causes – Mayo Clinic

Male hypogonadism means the testicles don't produce enough of the male sex hormone testosterone. There are two basic types of hypogonadism:

Either type of hypogonadism may be caused by an inherited (congenital) trait or something that happens later in life (acquired), such as an injury or an infection. At times, primary and secondary hypogonadism can occur together.

Common causes of primary hypogonadism include:

In secondary hypogonadism, the testicles are normal but function improperly due to a problem with the pituitary or hypothalamus. A number of conditions can cause secondary hypogonadism, including:

Concurrent illness. The reproductive system can temporarily shut down due to the physical stress of an illness or surgery, as well as during significant emotional stress. This is a result of diminished signals from the hypothalamus and usually resolves with successful treatment of the underlying condition.

The rate at which testosterone declines varies greatly among men. As many as 30 percent of men older than 75 have a testosterone level that's below the normal range of testosterone in young men, according to the American Association of Clinical Endocrinologists. Whether treatment is necessary remains a matter of debate.

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Male hypogonadism Causes - Mayo Clinic

Male Hypogonadism – Cleveland Clinic

Definition and Prevalence

Male hypogonadism is defined as the failure of the testes to produce androgen, sperm, or both. Although the disorder is exceedingly common, its exact prevalence is uncertain.

Testosterone production declines with advancing age; 20% of men older than 60 years and 30% to 40% of men older than 80 years have serum testosterone levels that would be subnormal in their younger adult male counterparts. This apparent physiologic decline in circulating androgen levels is compounded in frequency by permanent disorders of the hypothalamic-pituitary-gonadal axis (see later). These include the transient deficiency states associated with acute stressful illnesses, such as surgery and myocardial infarction, and the more chronic deficiency states associated with wasting illnesses, such as cancer and acquired immunodeficiency syndrome.

Male factor infertility is probably responsible for one third of the 10% to 15% of couples who are unable to conceive within 1 year of unprotected intercourse. Most of these male-associated cases result from diminished, absent, or faulty spermatogenesis. In addition to abnormal sperm production, other conditions, including obstructive ductal disease, epididymal hostility, immunologic disorders, and erectile or ejaculatory dysfunction should be considered. Finally, because combined female-male infertility is common, and fertility as well as psychological well-being are ultimate goals, both partners must be assessed from the outset.

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The physiologic regulation of the hypothalamic-pituitary-gonadal axis is shown in Figure 1. Circulating testosterone is largely protein-boundthe major protein is sex hormonebinding globulin (SHBG)with only 2% present as the biologically active or free fraction. Some clinicians believe that the bioavailable fraction, the fraction present in the supernatant after ammonium sulfate precipitation, representing testosterone loosely bound predominantly to serum albumin, is more meaningful. Hepatic SHBG production rises with aging and thyroid hormone excess and declines in hyperinsulinemic states (obesity and type 2 diabetes), so that free testosterone values may not always be concordant with total testosterone values. The biologic effects of testosterone may be mediated directly by testosterone or by its metabolites 5-dihydrotestosterone or estradiol (Fig. 2).

Male hypogonadism is caused by a primary (hypergonadotropic) testicular disorder or is secondary (hypo- or normogonadotropic) to hypothalamic-pituitary dysfunction, as illustrated in Figure 3. Combined disorders also occur. Examples of the major causes of male hypogonadism are shown in Boxes 1 and 2.

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Persistent failure of the testes to descend may be an early manifestation of testicular dysfunction. In addition, a normally formed but hypotrophic penis may provide a clue to an abnormality of the hypothalamic-pituitary-gonadal axis.

Delayed, arrested, or absent testicular growth and secondary sexual characteristic development are hallmarks of pubertal disorders. Skeletal proportions may be abnormal (eunuchoid) with more than a 5-cm difference between span and height and between pubis-floor and pubis-vertex dimensions.

Manifestations in adults are generally more subtle. Perhaps the minor contribution of adrenal androgens (or androgenic precursors) may substitute for testicular deficiency once the target tissues have been fully developed. Moreover, ingrained behavior patterns may be resistant to androgenic hormone deficiency. Certainly, prolactin excess, testosterone deficiency, or both in men may result in impaired libido and erectile dysfunction. The yield of finding hyperprolactinemia or testosterone deficiency, or both, in patients presenting with these symptoms is generally considered to be low, usually less than 5%. However, a large survey of patients with erectile dysfunction presenting to a Veterans Affairs center has suggested that the prevalence of these abnormalities is substantial: 18.7% of patients with low testosterone levels and 4.6% with elevated prolactin levels.1

The first manifestation of hypogonadism may be a consequence of a large space-occupying intrasellar or parasellar lesion manifested by headaches, bitemporal hemianopia, or extraocular muscle palsy. Galactorrhea as a manifestation of hyperprolactinemia is rare, but rarely sought. Unexplained osteoporosis or mild anemia sometimes is the clue to an underlying hypogonadal state. Some common clinical conditions associated with male hypogonadism are listed in Box 3. The subject of androgen deficiency and the aging man is dealt with in greater detail later in this chapter.

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Because of the well-known diurnal rhythm of serum testosterone, which appears to be lost with age (>60 years), with values 30% or so higher near 8 am versus the later day trough, a testosterone value should be determined first thing in the morning. Normal ranges vary among laboratories. Although the usually quoted range for young men is 300 to 1000ng/dL, the lower limit reported for the Cleveland Clinic is 220ng/dL. In general, values below 220 to 250ng/dL are clearly low in most laboratories; values between 250 and 350ng/dL should be considered borderline low. Because the acute effect of stressful illness may result in a transient lowering of testosterone levels, a confirmatory early morning specimen should be obtained. Measurement of free testosterone levels or bioavailable testosterone levels, determined adequately in select commercial laboratories, may provide additional information (see later, Pathophysiology). For example, free testosterone levels may be lower than expected from the total testosterone level as a result of aging and higher than expected in insulin-resistant individuals, such as in obesity. In addition, serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), and prolactin levels should be determined to help delineate the cause of the testosterone-deficient state.

If gonadotropin levels are not elevated, despite clearly subnormal testosterone values, anterior pituitary (thyroid-adrenal) function should be determined by measuring free thyroxine and thyroid-stimulating hormone levels, as well as an early morning cortisol level. A magnetic resonance imaging (MRI) scan of the brain and sella should be considered. An exception to this recommendation is the condition of morbid obesity, in which both total and free testosterone levels are typically low and gonadotropin values not elevated. Hyperprolactinemia, even of a small degree, may also warrant ordering MRI, because interference of hypothalamic-pituitary vascular flow by space-occupying, stalk-compressing lesions will lead to disruption of the tonic inhibitory influence of hypothalamic dopamine, and result in modest hyperprolactinemia (usually 20 to 50 ng/mL range).

A semen analysis should be performed when fertility is in question.

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Androgen replacement therapy is relatively straightforward; see Box 4 for testosterone preparations currently available in the United States. Typically, the depot esters are administered by the deep intramuscular route once every 2 weeks at a dose of 200mg in adults. A usual dosage for the transdermal or the buccal preparations results in the systemic absorption of 2.5 to 10mg daily. If the parenteral route is chosen, patients should and can be taught to self inject. The major disadvantage with the parenteral route is that testosterone levels exhibit a saw-toothed pattern, with high-normal or supranormal levels on days 2 to 4 and low-normal or borderline low trough values before the next injection. Mood, sense of well-being, and libido may vary accordingly in some patients.

Dosages may be adjusted by aiming for midnormal (400- 600ng/dL) testosterone levels after 1 week or at the low end (250-350ng/dL) just before the next injection is due at 2 weeks. Values are stable within a few days or weeks of the skin patch, gel, or newer buccal preparation. It must be ascertained that the preparation was actually used on the day the sample was drawn; again, a value in the midnormal range (400-600ng/dL) is the goal. Although comparable testosterone levels are reached by the patch and the gels, skin reactions at the application site are much more common with the patch. Also, the buccal preparation is difficult for patients to get used to. Alkylated oral androgens should be viewed as potentially hepatotoxic and should not be used. Useful criteria for selecting preparations for individual patients are summarized in Table 1.

+, ++, and +++ are semiquantitative assessments of effect.

2002 The Cleveland Clinic Foundation.

In addition to monitoring testosterone levels periodically, prostate screening and measurement of hemoglobin and hematocrit levels must also be performed at intervals when the patient is on therapy.2

Levels of prostate-specific antigen (PSA) should be checked at 3, 6, and 12 months. If the patient is truly hypogonadal to begin with, expect a significant rise at the 3-month assessment. Thereafter, the usual criteria apply regarding the possible presence of an underlying malignancy (>4ng/mL, or rate of increase >1.5ng/mL/2yr or >2ng/mL overall). These criteria continue to be revised by our urology colleagues, tending to become more stringent with time. For example, a PSA rise of more than 1ng/mL/year has been suggested as an early warning guide, and closer surveillance has been recommended, even at rates of 0.7 to 0.9ng/mL/year.2 A digital rectal examination should be performed at 3 to 6 months and at 1 year after therapy is initiated. A urologic consultation should be obtained if indicated.

Hemoglobin (Hb) and hematocrit (Hct) levels should be checked periodically. Incremental increases are to be expected, but an Hb level higher than 17.5g/dL, Hct higher than 55%, or both suggests overtreatment, occasionally abuse. Greater increments tend to occur more frequently with the intramuscular than with the transdermal preparations. If dosage adjustments do not solve the problem, look for another underlying cause.

Physicians Box 5). It should be noted that no long- term studies in large numbers of patients (neither young or old) have been performed, so potential risks and benefits need to be individualized.

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In genuinely hypogonadal men, testosterone administration can be expected to result in improvements in a variety of clinical areas (Box 6). Least predictable are the effects on sexual function, cognitive function, and muscle strength.

2002 The Cleveland Clinic Foundation.

Concerns regarding the use of testosterone have been noted in Box 5 and by Rhoden and Morgentaler.2 There is no evidence that the incidence of prostate cancer is increased by testosterone replacement. The underlying concern is that it might alter the course of an occult malignancy estimated to be present in more than 50% of men older than 50 years. On the other hand, no one would recommend prophylactic castration to prevent prostate cancer so that, in my view, testosterone replacement in the hypogonadal man should not be avoided. Although there are genuine concerns about worsening of benign prostatic hyperplasia, this may apply only to severe cases with large prostate volumes. Indeed, one study in older men has even suggested improvement in benign prostatic hyperplasia symptoms, although not statistically significant and by an unknown mechanism.3

The aging man represents a special case and has been the subject of a review.4 There is a well-known decline in testosterone production with aging in otherwise healthy men. This decline in mean values can be seen in free testosterone levels, beginning in the mid-40s (some clinicians suggest even earlier), as a consequence of increasing SHBG levels, mechanism unknown. Total testosterone levels decline on average beyond 70 years. The diurnal rhythm, seen in younger men, is lost beyond 60 years.5 Although testicular volume also declines in this age group, spermatogenesis may be well maintained into the 80s or even beyond. Gonadotropin levels tend to rise after 70 years, indicating that the testosterone deficiency is usually primary.6Figure 4 schematically presents these hormonal changes with age. Using the criterion of a low testosterone value, and remembering that there is considerable variability in commercially available tests regarding normal young adult ranges, it has been estimated that 7% of 40- to 60-year-olds, 22% of 60- to 80-year-olds, and 36% of 80- to 100-year-olds are hypogonadal.7

The ultimate issue as to whether these changes are normal and physiologic or should be considered pathologic, thus demanding therapy, remains unresolved. Indeed, it is a situation analogous to the ongoing dilemma of hormone replacement therapy for postmenopausal women, although in this group the hormonal deficiency state is usually more abrupt and symptomatic.

The scientific basis to help formulate guidelines for dealing with the issue of hormone replacement therapy in men was reviewed in a December 17, 2003, conference by the Institute of Medicines Committee on Testosterone and Aging (IMCTA).8 Many of the potential benefits of therapy (see Box 6) have been realized in small, well-controlled studies of older men. Moreover, none of the risks has been proven in a clinical trial. The IMCTA has not recommended a large-scale study to determine whether the risk for prostate cancer would be increased, because the costs of such a study were deemed to be too prohibitive.

In the meantime, practical guidelines for dealing with hypogonadism in older men have been suggested.9 I have found the recent overview in the Cleveland Clinic Mens Health Advisor newsletter to be useful for patients.10

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The American Association of Clinical Endocrinologists has published 2002 updated guidelines for the evaluation and treatment of hypogonadism in adult male patients.11 This review, geared particularly for endocrinologists, expands on some of the areas reviewed in this chapter and provides a more detailed look into aspects of male infertility.

The Endocrine Society has published clinical practice guidelines12 for testosterone replacement therapy. The major recommendations are summarized in Box 7.

Adapted from Bhasin S, Cunningham GR, Hayes FJ, etal: Testosterone therapy in adult men with androgen deficiency syndromes: An endocrine society clinical practice guideline. J Clin Endocrinol Metab 2006;91:1995-2010.

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Hypogonadism | Disorders | Knowledge Base

Hypogonadism can occur for a number of reasons. Certain men have hypogonadism since birth while others may develop this condition later in life. Two types of hypogonadism are:

Primary hypogonadism (testicular failure) - Low serum testosterone levels and gonadotropins (FSH, LH) above the normal range.

Hypogonadotropic hypogonadism - Idiopathic gonadotropin or LHRH deficiency or pituitary - hypothalamic injury from tumors, trauma, or radiation.

Characterized by low serum testosterone levels, but with gonadotropins in the normal or low range. Men develop testicular suppression with decreased libido, impotence, decreased ejaculate volume, loss of body and facial hair, weakness, fatigue and often anemia. On testing, blood levels of testosterone are low and should be replaced. In the United States, testosterone may begiven as a bi-weekly intramuscular injection, a patch form, or a gel preparation. In other countries, oral preparations of testosterone are available.

Women develop ovarian suppression with irregular periods or absence of periods (amenorrhea), infertility, decreased libido, decreased vaginal secretions, breast atrophy, and osteoporosis. Blood levels of estradiol are low. Estrogen should be replaced and can be given orally as Premarin or Estrace, or can be given as a patch applied twice weekly. Women taking estrogen also need to take progesterone replacement (unless they have undergone a hysterectomy). Annual pap smears and mammograms are mandatory.

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Hypergonadotropic hypogonadism – Wikipedia, the free …

Hypergonadotropic hypogonadism (HH), also known as primary or peripheral/gonadal hypogonadism, is a condition which is characterized by hypogonadism due to an impaired response of the gonads to the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), and in turn a lack of sex steroid production and elevated gonadotropin levels (as an attempt of compensation by the body). HH may present as either congenital or acquired, but the majority of cases are of the former nature.[1][2]

There are a multitude of different etiologies of HH. Congenital causes include the following:[1][3][4]

Acquired causes (due to damage to or dysfunction of the gonads) include gonadal torsion, vanishing/anorchia, orchitis, premature ovarian failure, ovarian resistance syndrome, trauma, surgery, autoimmunity, chemotherapy, radiation, infections (e.g., sexually-transmitted diseases), toxins (e.g., endocrine disruptors), and drugs (e.g., antiandrogens, opioids, alcohol).[1][3][4]

Examples of symptoms of hypogonadism include delayed, reduced, or absent puberty, low libido, and infertility.

Treatment of HH is usually with hormone replacement therapy, consisting of androgen and estrogen administration in males and females, respectively.[3]

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hypogonadism | pathology | Britannica.com

hypogonadism,in men, decreased testicular function that results in testosterone deficiency and infertility.

Hypogonadism is caused by hypothalamic, pituitary, and testicular diseases. Hypothalamic and pituitary diseases that may cause decreased testicular function include tumours and cysts of the hypothalamus, nonsecreting and prolactin-secreting pituitary tumours, trauma, hemochromatosis (excess iron storage), infections, and nonendocrine disorders, such as chronic illness and malnutrition. The primary testicular disorders that result in hypogonadism in postpubertal men include Klinefelter syndrome and related chromosomal disorders, although these disorders usually manifest at the time of puberty.

Other causes of hypogonadism in men include testicular inflammation (orchitis) caused by mumps; exposure to gonadal toxins, including alcohol, marijuana, and several anticancer drugs (e.g., cyclophosphamide, procarbazine, and platinum); and radiation with X-rays. Many of the disorders that cause delayed puberty are sufficiently mild that affected men do not seek care until well into adult life. This particularly applies to those disorders that decrease spermatogenesis and therefore fertility but spare Leydig cell function.

The clinical manifestations of hypogonadism in adult men include decreased libido, erectile dysfunction (inability to have or maintain an erection or to ejaculate), slowing of facial and pubic hair growth and thinning of hair in those regions, drying and thinning of the skin, weakness and loss of muscle mass, hot flashes, breast enlargement, infertility, small testes, and osteoporosis (bone thinning). The evaluation of men suspected to have hypogonadism should include measurements of serum testosterone, luteinizing hormone, follicle-stimulating hormone, and prolactin, in addition to the analysis of semen. Men with hypogonadism who have decreased or normal serum gonadotropin concentrations are said to have hypogonadotropic hypogonadism and may need to be evaluated for hypothalamic or pituitary disease with computerized axial tomography or magnetic resonance imaging (MRI) of the head. Men with hypogonadism who have increased serum gonadotropin concentrations are said to have hypergonadotropic hypogonadism, and their evaluation should be focused on the causes of testicular disease, including chromosomal disorders.

Men with hypogonadism caused by a hypothalamic disorder, pituitary disorder, or testicular disorder are treated with testosterone. Testosterone can be given by intramuscular injection or by patches or gels applied to the skin. Testosterone treatment reverses many of the symptoms and signs of hypogonadism but will not increase sperm count. Sperm count cannot be increased in men with testicular disease, although it is sometimes possible to increase sperm count in men with hypothalamic or pituitary disease by prolonged administration of gonadotropin-releasing hormone or gonadotropins. In men with testicular disease, viable sperm can sometimes be obtained by aspiration from the testes for in vitro fertilization.

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Low Testosterone in Men | Hypogonadism

In men 45 and older, most cases of hypogonadism or Low-T often go overlooked due to the fact that the symptoms may be more general in nature and slower in onset. Many men simply attribute their symptoms to aging and often dismiss them because they don't think that there is anything that they can do about them. This is largely because the symptoms of hypogonadism are nearly identical to those experienced by men going through andropause (the male menopause): low libido, fatigue, depression, memory loss, difficulty concentrating and irritability. The difference between andropause and hypogonadism is simple. Andropause is a natural part of a man's life where his hormones begin to decline right around the age of 35 and continue to decrease until they plateau in his late 60's. Hypogonadism is a condition where testosterone is not being produced due to a physical abnormality of the testes or brain. It can also be due to an outside factor such as stress, poor diet or pre-existing health conditions. Both Hypogonadism and andropause however can be treated and corrected under the care of experienced hormonal specialists.

There are two basic forms of hypogonadism found in men. Primary hypogonadism is also known as ?testicular failure? and stems from a complication in the testicles. Some common causes of primary hypogonadism are:

The other type of hypogonadism is called secondary hypogonadism, and it describes a condition where the testicles are normal on a physiological level, but still don't function properly due to a problem stemming from the pituitary gland or the hypothalamus. This creates a problem with the signal from the brain to the testicle. Although the testicles function well, they can't get the information from the brain that testosterone needs to be produced. Some common causes of secondary hypogonadism are:

The most effective ways to treat hypogonadism are to enhance the body's ability to make its own testosterone or to supplement the testosterone that your body would produce normally, using natural bioidentical testosterone replacement therapy. It is critical to combine bioidentical hormone therapy with appropriate diet, exercise, lifestyle and stress management. Although there are many different causes for the condition, hypogonadism always leads to hormonal imbalance and can lead to a wide range of symptoms and chronic health issues. Fortunately, under the proper care of a highly trained BodyLogicMD affiliated physician, the condition can be corrected.

Through comprehensive testing, your BodyLogicMD affiliated physician will determine your hormone levels to uncover potential hormone deficiencies. Based on cutting edge diagnostic technologies, BodyLogicMD affiliated physicians pinpoint the source of underlying hormonal imbalances and use all natural bioidentical hormone replacement therapy (BHRT) interlaced with customized nutrition and fitness regimens to help men find relief symptoms of hormonal imbalance. BodyLogicMD affiliated physicians have helped thousands of men get their edge back and overcome testosterone deficiencies such as andropause and hypogonadism.

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Low Testosterone in Men | Hypogonadism

Male hypogonadism: Symptoms and treatment

Abstract

Male hypogonadism is a condition in which the body does not produce enough of the testosterone hormone; the hormone that plays a key role in masculine growth and development during puberty. There is a clear need to increase the awareness of hypogonadism throughout the medical profession, especially in primary care physicians who are usually the first port of call for the patient. Hypogonadism can significantly reduce the quality of life and has resulted in the loss of livelihood and separation of couples, leading to divorce. It is also important for doctors to recognize that testosterone is not just a sex hormone. There is an important research being published to demonstrate that testosterone may have key actions on metabolism, on the vasculature, and on brain function, in addition to its well-known effects on bone and body composition. This article has been used as an introduction for the need to develop sensitive and reliable assays for sex hormones and for symptoms and treatment of hypogonadism.

Keywords: Male hypogonadism, pituitary, sex hormone, testosterone, testis

Hypogonadism is a medical term for decreased functional activity of the gonads. The gonads (ovaries or testes) produce hormones (testosterone, estradiol, antimullerian hormone, progesterone, inhibin B, activin) and gametes (eggs or sperm).[1] Male hypogonadism is characterized by a deficiency in testosterone a critical hormone for sexual, cognitive, and body function and development. Clinically low testosterone levels can lead to the absence of secondary sex characteristics, infertility, muscle wasting, and other abnormalities. Low testosterone levels may be due to testicular, hypothalamic, or pituitary abnormalities. In individuals who also present with clinical signs and symptoms, clinical guidelines recommend treatment with testosterone replacement therapy.

There are two basic types of hypogonadism that exist:

Primary: This type of hypogonadism also known as primary testicular failure originates from a problem in the testicles.

Secondary: This type of hypogonadism indicates a problem in the hypothalamus or the pituitary gland parts of the brain that signal the testicles to produce testosterone. The hypothalamus produces the gonadotropin releasing hormone, which signals the pituitary gland to make the follicle-stimulating hormone (FSH) and luteinizing hormone. The luteinizing hormone then signals the testes to produce testosterone. Either type of hypogonadism may be caused by an inherited (congenital) trait or something that happens later in life (acquired), such as an injury or an infection.

Common causes of primary hypogonadism include:

Klinefelter's Syndrome: This condition results from a congenital abnormality of the sex chromosomes, X and Y. A male normally has one X and one Y chromosome. In Klinefelter's syndrome, two or more X chromosomes are present in addition to one Y chromosome. The Y chromosome contains the genetic material that determines the sex of a child and the related development. The extra X chromosome that occurs in Klinefelter's syndrome causes abnormal development of the testicles, which in turn results in the underproduction of testosterone.

Before birth, the testicles develop inside the abdomen and normally move down into their permanent place in the scrotum. Sometimes, one or both of the testicles may not descend at birth. This condition often corrects itself within the first few years of life without treatment. If not corrected in early childhood, it may lead to malfunction of the testicles and reduced production of testosterone.

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Male hypogonadism: Symptoms and treatment

Male hypogonadism Symptoms – Mayo Clinic

Hypogonadism can begin during fetal development, before puberty or during adulthood. Signs and symptoms depend on when the condition develops.

If the body doesn't produce enough testosterone during fetal development, the result may be impaired growth of the external sex organs. Depending on when hypogonadism develops and how much testosterone is present, a child who is genetically male may be born with:

Male hypogonadism may delay puberty or cause incomplete or lack of normal development. It can cause:

In adult males, hypogonadism may alter certain masculine physical characteristics and impair normal reproductive function. Signs and symptoms may include:

Hypogonadism can also cause mental and emotional changes. As testosterone decreases, some men may experience symptoms similar to those of menopause in women. These may include:

See a doctor if you have any symptoms of male hypogonadism. Establishing the cause of hypogonadism is an important first step to getting appropriate treatment.

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Male hypogonadism Tests and diagnosis – Mayo Clinic

Your doctor will conduct a physical exam during which he or she will note whether your sexual development, such as your pubic hair, muscle mass and size of your testes, is consistent with your age. Your doctor may test your blood level of testosterone if you have any of the signs or symptoms of hypogonadism.

Early detection in boys can help prevent problems from delayed puberty. Early diagnosis and treatment in men offer better protection against osteoporosis and other related conditions.

Doctors base a diagnosis of hypogonadism on symptoms and results of blood tests that measure testosterone levels. Because testosterone levels vary and are generally highest in the morning, blood testing is usually done early in the day, near 8 a.m.

If tests confirm you have low testosterone, further testing can determine if a testicular disorder or a pituitary abnormality is the cause. Based on specific signs and symptoms, additional studies can pinpoint the cause. These studies may include:

Testosterone testing also plays an important role in managing hypogonadism. This helps your doctor determine the right dosage of medication, both initially and over time.

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Hypogonadotropic hypogonadism – Wikipedia, the free …

Hypogonadotropic hypogonadism (HH), also known as secondary or central hypogonadism, as well as gonadotropin-releasing hormone deficiency or gonadotropin deficiency (GD), is a condition which is characterized by hypogonadism due to an impaired secretion of gonadotropins, including follicle-stimulating hormone (FSH) and luteinizing hormone (LH), by the pituitary gland in the brain, and in turn decreased gonadotropin levels and a resultant lack of sex steroid production.[1]

The type of HH, based on its cause, may be classified as either primary or secondary. Primary HH, also called isolated HH, is responsible for only a small subset of cases of HH, and is characterized by an otherwise normal function and anatomy of the hypothalamus and anterior pituitary. It is caused by congenital syndromes such as Kallmann syndrome, CHARGE syndrome, and gonadotropin-releasing hormone (GnRH) insensitivity. Secondary HH, also known as acquired or syndromic HH, is far more common than primary HH, and is responsible for most cases of the condition. It has a multitude of different causes, including brain or pituitary tumors, pituitary apoplexy, head trauma, ingestion of certain drugs, and certain systemic diseases and syndromes.[1]

Primary and secondary HH can also be attributed to a genetic trait inherited from the biologic parents. For example, the male mutations of the GnRH coding gene could result in HH. Hormone replacement can be used to initiate puberty and continue if the gene mutation occurs in the gene coding for the hormone. Chromosomal mutations tend to affect the androgen production rather than the HPG axis.

Examples of symptoms of hypogonadism include delayed, reduced, or absent puberty, low libido, and infertility.

Treatment of HH may consist of administration of either a GnRH agonist or a gonadotropin formulation in the case of primary HH and treatment of the root cause (e.g., a tumor) of the symptoms in the case of secondary HH. Alternatively, hormone replacement therapy with androgens and estrogens in males and females, respectively, may be employed.

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Hypogonadotropic hypogonadism - Wikipedia, the free ...

Hypogonadism – Wikipedia, the free encyclopedia

Hypogonadism is a medical term which describes a diminished functional activity of the gonads the testes and ovaries in males and females, respectively that may result in diminished sex hormone biosynthesis. In layman's terms, it is sometimes called "interrupted stage 1 puberty". Low androgen (e.g., testosterone) levels are referred to as hypoandrogenism and low estrogen (e.g., estradiol) as hypoestrogenism, and may occur as symptoms of hypogonadism in both sexes, but are generally only diagnosed in males and females respectively. Other hormones produced by the gonads which may be decreased by hypogonadism include progesterone, DHEA, anti-Mllerian hormone, activin, and inhibin. Spermatogenesis and ovulation in males and females, respectively, may be impaired by hypogonadism, which, depending on the degree of severity, may result in partial or complete infertility.

Deficiency of sex hormones can result in defective primary or secondary sexual development, or withdrawal effects (e.g., premature menopause) in adults. Defective egg or sperm development results in infertility. The term hypogonadism is usually applied to permanent rather than transient or reversible defects, and usually implies deficiency of reproductive hormones, with or without fertility defects. The term is less commonly used for infertility without hormone deficiency. There are many possible types of hypogonadism and several ways to categorize them. Hypogonadism is also categorized by endocrinologists by the level of the reproductive system that is defective. Physicians measure gonadotropins (LH and FSH) to distinguish primary from secondary hypogonadism. In primary hypogonadism the LH and/or FSH are usually elevated, meaning the problem is in the testicles, whereas in secondary hypogonadism, both are normal or low, suggesting the problem is in the brain.

Hypogonadism can involve just hormone production or just fertility, but most commonly involves both.

Women with hypogonadism will not begin menstruating and it may affect their height and breast development. Onset in women after puberty causes cessation of menstruation, lowered libido, loss of body hair and hot flashes. In boys it causes impaired muscle and beard development and reduced height. In men it can cause reduced body hair and beard, enlarged breasts, loss of muscle, and sexual difficulties. A brain tumor (central hypogonadism) may involve headaches, impaired vision, milky discharge from the breast and symptoms caused by other hormone problems.[2]

The symptoms of hypogonadotrophic hypogonadism, a subtype of hypogonadism, include late, incomplete or lack of development at puberty, and sometimes short stature or the inability to smell; in females, a lack of breasts and menstrual periods, and in males a lack of sexual development, e.g., facial hair, penis and testes enlargement, deepening voice.

Low testosterone can be identified through a simple blood test performed by a laboratory, ordered by a physician. This test is typically ordered in the morning hours, when levels are highest, as levels can drop by as much as 13% during the day.[3]

Normal total testosterone levels range from 3001000ng/dL (nanograms per decilitre)[4]

Treatment is often prescribed for total testosterone levels below 350ng/dL.[5] If the serum total testosterone level is between 230 and 350ng/dL, repeating the measurement of total testosterone with sex hormone-binding globulin (SHBG) to calculate free testosterone or free testosterone by equilibrium dialysis may be helpful.

Treatment may be necessary even if the patient's total testosterone level is within the "normal" range. The standard range given is based off widely varying ages and, given that testosterone levels naturally decrease as humans age, age-group specific averages should be taken into consideration when discussing treatment between doctor and patient.[6] A twenty-seven-year-old male with a testosterone level of 380ng/dL would be in the "normal" range, but would likely have low testosterone to blame if he experiences some or many of the above symptoms. This score would put him in the bottom 5% of his age-group, but would be a more common score for a man who is 80+ years old.[6] Although, this doesn't automatically mean that a young man with 380ng/dL has the same amount of testosterone of an 80+ year old, since there is usually a big difference in SHBG levels in the bloodstream between young and elderly, resulting in a much higher free testosterone level in the young. In fact, some people with low SHBG and low-normal testosterone experience no symptoms of hypogonadism.

A downturn in the circulation of testosterone should cause the hypothalamus and pituitary gland to trigger a release of brain hormones that stimulate the testicles to ramp up production of testosterone. The specific brain hormones include gonadotropin releasing hormone (abbreviated GnRH), which is released by the hypothalamus, and luteinizing hormone (abbreviated LH), released by the pituitary. They act to control the production of testosterone in synchrony. This response system in the body is a negative feedback loop. When this loop is functioning at its best, the body gets enough testosterone to bind to receptors on the various organs that require it. In the bodies of men as they hit their thirties and forties, testosterone falls approximately 1 to 3 percent each year.[7]

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Hypogonadism - Wikipedia, the free encyclopedia

Prevalence, Diagnosis and Treatment of Hypogonadism in …

by Culley C. Carson III, MD

Hypogonadism is defined as deficient or absent male gonadal function that results in insufficient testosterone secretion. Hypogonadism may be primary due to testicular failure, or secondary due to hypothalamic-pituitary axis dysfunction, resulting in the production or release of insufficient testosterone to maintain testosterone-dependent functions and systems. Hypogonadism can also result from a combination of testicular failure and hypothalamic-pituitary axis dysfunction.

Hypogonadism affects an estimated 4 to 5 million men in the United States, and although it may occur in men at any age, low testosterone levels are especially common in older males. More than 60% of men over age 65 have free testosterone levels below the normal values of men aged 30 to 35. Studies suggest that hypogonadism in adult men is often underdiagnosed and under treated. This may be because the symptoms are easily attributed to aging or other medical causes, or ignored by patients and physicians. In fact, only about 5% of hypogonadal men receive testosterone replacement. Some experts also believe that we need to reevaluate normal testosterone the levels and lower the diagnostic cutoff for hypogonadism. By doing so, many patients who we now consider to be low- normal would probably be considered candidates for androgen replacement.

Signs and Symptoms of Hypogonadism Low testosterone, or male hypogonadism, is associated with a number of signs and symptoms, most notably loss of libido and erectile dysfunction (ED). Other signs of low testosterone include depressive symptoms, a decrease in cognitive abilities, irritability and lethargy or loss of energy. Deficient endogenous testosterone also has negative effects on bone mass and is a significant risk factor for osteoporosis in men. Progressive decrease in muscle mass and muscle strength and testicular dysfunction, often resulting in impaired sperm production, are also associated with low testosterone levels.

A younger patient may have pure hypogonadism as a primary event, whereas an older man may have an age-related decline in testosterone production that is a part of his ED profile. However, because both ED and loss of libido are hallmarks of hypogonadism, any patient who presents with ED should have a basic hormone profile to determine if he has low testosterone. Treatments to normalize testosterone can not only improve libido, energy level and the potential to have normal erections, but can also improve the response to sildenafil, if that is deemed appropriate treatment.

Screening for Hypogonadism An inexpensive and reliable screening test for hypogonadism is a morning serum total testosterone level, which measures free testosterone plus protein-bound testosterone. A morning sample is recommended, because testosterone levels demonstrate a diurnal pattern in which the highest level is reached in the early morning hours. Morning testosterone values <300 ng/dL (10.4 nmol/L) suggest hypogonadism and should be confirmed by a second assay.

If a repeat assay confirms low testosterone, luteinizing hormone (LH) should be measured to determine whether the cause is primary or secondary. LH levels <2 ng/mL suggest a hypothalamic lesion (pituitary adenoma, trauma, etc), whereas LH levels >10 ng/mL indicate primary testicular failure. Levels within the normal range suggest an age-related, decreased hypothalamic response to declining testosterone levels. In addition, serum prolactin should also be measured to rule out the presence of a pituitary tumor.

At our institution we are also currently measuring dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEAS) levels. Some investigators believe that replacing DHEA in patients with low libidos and normal or borderline testosterone is an important component of treatment to restore sexual desire and performance. Although controlled clinical studies are needed to confirm this approach, there is growing evidence that DHEA may play an important role in the treatment of male sexual dysfunction.

ADAM Questionnaire In addition to laboratory tests and a careful physical examination, a brief screening instrument has also been developed to aid in the diagnosis of hypogonadism. Researchers at St. Louis University created the Androgen Deficiency in the Aging Male (ADAM) questionnaire, which has been shown to be a highly sensitive (88%) instrument but with low specificity (66%), largely due to questions that identify patients with depression. However, because many men with hypogonadism dont seek medical attention, instruments such as the ADAM questionnaire can be a useful way to screen for clinical symptoms of androgen deficiency. Once testosterone deficiency is confirmed, we then consider testosterone replacement therapy.

Goals of Treatment The goal of testosterone replacement therapy is to provide and maintain a normal level of testosterone, thereby restoring libido and improving erectile function; improving mood and providing a sense of well-being; decreasing fatigue; and improving lean body mass, strength and stamina. Also, because hypogonadism is the most common cause of osteoporosis in men, testosterone replacement may improve bone density to help prevent this disease and related complications.

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Prevalence, Diagnosis and Treatment of Hypogonadism in ...

Hypogonadism: Types, Causes, & Symptoms Healthline

What is Hypogonadism?

Hypogonadism occurs when your sex glands produce little or no sex hormones. The sex glands, also called gonads, are the testes in men and the ovaries in women. Sex hormones help control sex characteristics, such as breast and testicle development, and pubic hair growth. Sex hormones also play a role in menstrual cycles and sperm production.

Hypogonadism may also be called gonad deficiency. In males, it may be called low serum testosterone or andropause.

Most cases of this disorder can be successfully treated.

9 Warning Signs of Low Testosterone

There are two types of hypogonadism: primary and central hypogonadism.

Primary hypogonadism means that you do not have enough sex hormones in your body due to a problem in the gonads. The gonads are still receiving the message to produce hormones from the brain, but are not able to produce them.

In central hypogonadism, the problem lies in the brain. Here the hypothalamus and pituitary glandwhich control the gonadsare not working properly.

Causes of primary hypogonadism include:

Central hypogonadism may be caused by:

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Hypogonadism: Types, Causes, & Symptoms Healthline

What is Male Hypogonadism? Learn Hormone.org’s …

Male hypogonadismis defined as the underproduction of sperm or testosterone, or both, by the testes (also called testicles). Starting at puberty, the pituitary gland releases luteinizing hormone (LH), which stimulates the testicles to produce testosterone, the hormone responsible for male physical characteristics. In the testicles, follicle stimulating hormone (FSH) and LH also act together to stimulate the production of sperm.

Diagnosis of male hypogonadism begins with a medical history and physical examination. Many possible symptoms and signs may suggest low testosterone, orandrogen deficiency, in adult men:

Blood tests determine whether testosterone levels are in the normal range. This is generally 300 to 1,000 ng/dL (10.4 to 34.7 nmol/L), but the normal range may differ depending on the laboratory that conducts the test. To diagnose low testosterone, a man generally needs to have more than one early-morning blood test. If his blood testosterone is repeatedly low, then tests of pituitary gland function, such measuring LH and FSH levels, must also be done.

Male hypogonadism can beprimary(resulting from a problem with the testes) orsecondary(resulting from a problem with the pituitary gland or hypothalamus and their release of LH and FSH), or a mix.

Speaking more generally, low testosterone can be caused by:

Many older men have low testosterone levels and, in many cases, the cause isnt known.

Treatment with testosterone replacement therapy is recommended for men with consistently low testosterone levels and symptoms or signs of androgen deficiency. Men with one of the following should not be treated with testosterone replacement therapy:

The overall goal of testosterone hormone therapy is to increase testosterone levels from below the normal range to the middle of the normal range. Goals may vary from patient to patient but should include improving or maintaining the signs of masculinity (such as deep voice, beard growth, pubic hair), and improving sex drive and function,, mood and energy, muscle strength, and the amount of bone.

There are several ways to replace testosterone:

The way testosterone is given will depend on the patients preference and tolerance, and cost. The various types of testosterone therapy may have certain side effects. . Injections may be uncomfortable and linked to ups and downs in symptoms; patches may cause skin redness and rashes; gels may transfer testosterone to others who come into contact with the patients skin where the medication is applied; and buccal tablets may cause gum irritation.

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What is Male Hypogonadism? Learn Hormone.org's ...

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