Archive for the ‘Hypogonadism’ Category

Male hypogonadism is a deficiency of testosterone in men. About 5 percent to 6 percent of men experience male hypogonadism, and the condition becomes more common as a man ages.

Hypogonadism may be congenital or may be acquired as the result of aging, disease, drugs or other factors. Symptoms include low sperm count, decreased libido, erectile dysfunction, fatigue, sleep disturbances and depression.

In primary hypogonadism, the testes fail to make testosterone because of infection or injury to the testes. Common causes of testicular dysfunction include cancer treatment, excessive alcohol consumption, Klinefelter syndrome, mumps orchitis and autoimmune disorders.

In secondary hypogonadism, which is more common, the hypothalamus or the pituitary gland fails to produce enough hormones. These hormones are needed to trigger the testes to produce testosterone. Secondary hypogonadism can be caused by Kallmann syndrome, pituitary or hypothalamic tumors or disorders, obesity, diabetes and Prader-Willi syndrome.

Following a complete medical history and physical, tests will be done to measure the man's testosterone level. Because testosterone levels naturally fall off during the day, a testosterone blood test is done between 7:00 am and 10:00 am.

If the test shows a low testosterone level, additional tests may be ordered to check for a pituitary gland disorder. A blood test to check serum follicle-stimulating hormone (FSH), luteinizing hormone (LH) and prolactin levels can help determine the cause. If needed, specialized testing may be performed in the Endocrine Diagnostic Unit, based at Froedtert Hospital.

Other tests may be used to measure sperm count, check for testicle or gland tumors, or identify a genetic (congenital) cause.

For men with primary hypogonadism, treatment typically involves lifelong testosterone replacement therapy. Options for replacement therapy include:

Too much testosterone can place a man at a higher risk for blood clots. As with any hormonal therapy, its important to monitor patients as treatment progresses. Men receiving hormone replacement therapy are seen for blood tests and a prostate exam at one, three and six months after beginning treatment. They continue to be seen every six months.

Secondary hypogonadism is treated by addressing the root cause - a disorder with the hypothalamus or pituitary gland.

Treatment may also be needed for conditions related to hypogonadism, including:

Infertility related to secondary hypogonadism may respond to hormonal replacement therapy. Infertility related to primary hypogonadism, however, does not respond to hormonal therapy. In these cases, a man and his partner can be referred to the Reproductive Medicine Center for help conceiving a child.

Link:
Testosterone Deficiency, Hypogonadism | Froedtert Hospital ...

Early symptoms of low testosterone in men include low libido (sex drive). As levels become very low, sexual dysfunction (also called "erectile dysfunction (ED)" or "impotence") often develops. Other signs and symptoms of low testosterone may include depression, fatigue, osteoporosis, loss of muscle mass, an increase in abdominal fat, development of breast tissue (gynecomastia) and infertility.

Symptoms of low testosterone in women may include low libido (sex drive), sexual dysfunction, fatigue, loss of muscle mass, an increase in body fat and bone loss.

Pituitary Symptoms

There are many causes of low testosterone. These can be differentiated with hormone testing. Pituitary dysfunction is one cause of low testosterone and can result from compression of the pituitary gland by a large pituitary tumor. In addition, excess hormone secretion by a pituitary tumor can cause low testosterone either directly or indirectly. For example, elevated prolactin, cortisol or GH levels can cause low testosterone. Testosterone levels normalize with treatment of the tumor in some, but not all, cases. There are other causes of low testosterone that are not related to pituitary tumors. These include anabolic steroid use (for body building or athletic enhancement), obesity, depression, and testicular failure.

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The complications of low testosterone in men include infertility, sexual dysfunction, osteoporosis, loss of muscle mass, depression and fatigue.

Research Studies

You're likely to start by seeing your family doctor or a general practitioner. However, in some cases when you call to set up an appointment, you may be referred immediately to an endocrinologist, a doctor who specializes in endocrine (hormonal) disorders.

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Appointments

Testosterone levels can be measured directly. An endocrinologist can test for causes of low testosterone, including elevated prolactin levels. Sometimes other blood tests are indicated to make the diagnosis or determine the cause, including free testosterone, sex hormone binding globulin, leutinizing hormone (LH) or evaluation for Cushing's disease or acromegaly.

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If the underlying cause of the low testosterone can be determined and corrected, testosterone levels often rise to normal levels. Medical treatment to lower prolactin levels from a prolactinoma often results in normalization of testosterone level. In addition, resection of large nonfunctioning pituitary tumors that are causing low testosteorne by compressing the pituitary gland results in restoration of normal testosterone levels in approximately 50% of cases. Cure of acromegaly or Cushing's disease also often results in normalization of testosterone levels. In patients for whom the cause cannot be determined or addressed, testosterone replacement therapy can be prescribed by an endocrinologist with expertise in this area. There are a number of different preparations available, including gels, creams, patches, and injections. Your endocrinologist can discuss the pros and cons of the different options with you. S/he will also check lab results to make sure it is safe to prescribe the medication and that your testosterone levels on the medication are appropriate. If bone density does not improve when testosterone has been normalized, additional medications may be necessary.

There are no FDA-approved testosterone preparations for women, who make 10 to 20 times less testosterone than men and therefore need much lower replacement doses than men.

Appointments

Research is ongoing in the Neuroendocrine Unit on the effects of low testosterone and testosterone treatment in both men and women.

Research Studies

Originally posted here:
Hypogonadism and Hypogonadism Resources - What is ...

Morbidity for men and women with hypogonadism includes infertility and an increased risk of osteoporosis; there is no increase in mortality.

Hypogonadotropic hypogonadism (see the image below) is one of several types of hypogonadism.

History

Considerations in the evaluation of males with hypogonadism include the following:

For postpubertal males, the rate of beard growth, libido and sexual function, muscle strength, and energy levels

Possible causes of acquired testicular failure (eg, mumps orchitis, trauma, radiation exposure of the head or testes, and chemotherapy)

Drugs that may interrupt testicular function: Including agents that interfere with testosterone synthesis, such as spironolactone, cyproterone, marijuana, heroin, and methadone

Considerations in the evaluation of females with hypogonadism include the following:

Signs associated with Turner syndrome (eg, lymphedema, cardiac or renal congenital anomalies, and short growth pattern)

Age of menarche

Physical examination

Considerations in the physical examination of males with hypogonadism include the following:

Evaluation of the testes: This is the most important feature of the physical examination; determine whether both testes are palpable, their position in the scrotum, and their consistency; testes size can be quantitated by comparison with testicular models (orchidometer), or their length and width may be measured

Examination of the genitalia for hypospadias

Examination of the scrotum to see if it is completely fused

Evaluation of the extent of virilization

Staging of puberty: Use the Tanner criteria for genitalia, pubic hair, and axillary hair

Examination for signs of Klinefelter syndrome (eg, tall stature, especially if the legs are disproportionately long, gynecomastia, small or soft testes, and a eunuchoid body habitus)

Considerations in the physical examination of females with hypogonadism include the following:

Examination of the genitalia is important

Determination of the extent of androgenization: May be adrenal or ovarian in origin and is demonstrated in pubic and axillary hair

Determination of the extent of estrogenization: As evidenced by breast development and maturation of the vaginal mucosa

Examination for signs of Turner syndrome (eg, short stature, webbing of the neck [such as pterygium colli], a highly arched palate, short fourth metacarpals, widely spaced nipples, or multiple pigmented nevi)

See Clinical Presentation for more detail.

The following studies may be indicated in males with hypogonadism:

Follicle-stimulating hormone (FSH) levels

Luteinizing hormone (LH) levels

Prolactin levels

Testosterone levels

Thyroid function

Seminal fluid examination

Karyotyping

Testicular biopsy

For males after puberty, the Guidelines of the Endocrine Society[2] require that the diagnosis of hypogonadism be based on symptoms and signs of hypogonadism plus the presence of a low testosterone level measured on at least 2 occasions.

The following studies may be indicated in females with hypogonadism:

Additional tests in the evaluation of patients with hypogonadism include the following:

Adrenocorticotropic hormone (ACTH) stimulation testing: In patients in whom a form of congenital adrenal hyperplasia is suspected, adrenal steroid synthesis is best evaluated by performing a cosyntropin (ACTH 1-24) stimulation test

Luteinizing-hormone releasing hormone (LHRH) stimulation testing: To distinguish between true hypogonadotropic hypogonadism and constitutional delay in growth and maturation

Testicular tissue testing: If the testes are not palpable and if it is not certain whether any testicular tissue is present, administering human chorionic gonadotropin (hCG) and measuring testosterone response may be helpful

See Workup for more detail.

Hormonal replacement

The simplest and most successful treatment for males and females with either hypergonadotropic or hypogonadotropic hypogonadism is replacement of sex steroids, but the therapy does not confer fertility or, in men, stimulate testicular growth.

When fertility is desired, an alternative therapy for men with hypogonadotropic hypogonadism is administration of pulsatile LHRH or injections of hCG and FSH. (In patients with hypergonadotropic hypogonadism, fertility is not possible.)

In a 6-year European study of men being treated for hypogonadism, long-term transdermal testosterone treatment did not increase prostate-specific antigen (PSA) levels or influence prostate cancer risk.[3, 4]

Investigators used data from a 5-year, open-label extension of a 1-year trial of a transdermal testosterone patch (Testopatch) in men with hypogonadism. Study subjects wore two 60 cm2 patches, each of which delivered 2.4 mg of testosterone per day. More than 90% of patients had PSA concentrations below 2 ng/mL during the 6-year study, and no prostate cancer was found in patients over the course of the trial.

See Treatment and Medication for more detail.

Read more:
Hypogonadism - Medscape Reference

By Irvin H. Hirsch, MD

NOTE: This is the Professional Version. CONSUMERS: Click here for the Consumer Version

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Hypogonadism is defined as testosterone deficiency with associated symptoms or signs, deficiency of spermatozoa production, or both. It may result from a disorder of the testes (primary hypogonadism) or of the hypothalamic-pituitary axis (secondary hypogonadism). Both may be congenital or acquired as the result of aging, disease, drugs, or other factors. Additionally, a number of congenital enzyme deficiencies cause varying degrees of target organ androgen resistance. Diagnosis is confirmed by hormone levels. Treatment varies with etiology but typically includes gonadotropin-releasing hormone, gonadotropin, or testosterone replacement.

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Male Hypogonadism - Genitourinary Disorders - Merck ...

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Hypogonadism: Introduction

Hypogonadism: Medical term for a defect of the reproductive system that results in lack of function of the gonads (ovaries or testes). More detailed information about the symptoms, causes, and treatments of Hypogonadism is available below.

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See full list of 99 causes of Hypogonadism

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Commonly undiagnosed diseases in related medical categories:

Misdiagnosed weight-related causes of infertility: A woman's weight status can affect her level of fertility. Although obesity or overweight can in themselves reduce fertility, there are...read more

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Visit our research pages for current research about Hypogonadism treatments.

The US based website ClinicalTrials.gov lists information on both federally and privately supported clinical trials using human volunteers.

Some of the clinical trials listed on ClinicalTrials.gov for Hypogonadism include:

See full list of 55 Clinical Trials for Hypogonadism

Types of Hypogonadism

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Condition resulting from or characterized by abnormally decreased functional activity of the gonads, with retardation of growth and sexual development. - (Source - Diseases Database)

Incompetence of the gonads (especially in the male with low testosterone); results in deficient development of secondary sex characteristics and (in prepubertal males) a body with long legs and a short trunk - (Source - WordNet 2.1)

Hypogonadism is listed as a "rare disease" by the Office of Rare Diseases (ORD) of the National Institutes of Health (NIH). This means that Hypogonadism, or a subtype of Hypogonadism, affects less than 200,000 people in the US population. Source - National Institutes of Health (NIH)

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Hypogonadism Symptoms, Diagnosis, Treatments and Causes ...

Hypogonadism: Introduction

Hypogonadism: medical term for a defect of the reproductive system that results in lack of function of the gonads (ovaries or testes). See detailed information below for a list of 129 causes of Hypogonadism, Symptom Checker, including diseases and drug side effect causes.

Review Causes of Hypogonadism: Causes | Symptom Checker

Listed below are some combinations of symptoms associated with Hypogonadism, as listed in our database. Visit the Symptom Checker, to add and remove symptoms and research your condition.

See full list of 501 Symptom Checkers for Hypogonadism

Some of the possible treatments listed in sources for treatment of Hypogonadism may include:

Review further information on Hypogonadism Treatments.

Some of the comorbid or associated medical symptoms for Hypogonadism may include these symptoms:

See all associated comorbid symptoms for Hypogonadism

Research the causes of these more general types of symptom:

Research the causes of these symptoms that are similar to, or related to, the symptom Hypogonadism:

Read more about causes and Hypogonadism deaths.

Other medical conditions listed in the Disease Database as possible causes of Hypogonadism as a symptom include:

See full list of 129 causes of Hypogonadism - (Source - Diseases Database)

Condition resulting from or characterized by abnormally decreased functional activity of the gonads, with retardation of growth and sexual development. - (Source - Diseases Database)

Incompetence of the gonads (especially in the male with low testosterone); results in deficient development of secondary sex characteristics and (in prepubertal males) a body with long legs and a short trunk - (Source - WordNet 2.1)

Condition resulting from or characterized by abnormally decreased functional activity of the gonads, with retardation of growth and sexual development. - (Source - CRISP)

Hypogonadism is listed as a "rare disease" by the Office of Rare Diseases (ORD) of the National Institutes of Health (NIH). This means that Hypogonadism, or a subtype of Hypogonadism, affects less than 200,000 people in the US population. - (Source - National Institute of Health)

The list below shows some of the causes of Hypogonadism mentioned in various sources:

See full list of 129 causes of Hypogonadism

This information refers to the general prevalence and incidence of these diseases, not to how likely they are to be the actual cause of Hypogonadism. Of the 129 causes of Hypogonadism that we have listed, we have the following prevalence/incidence information:

See the analysis of the prevalence of 129 causes of Hypogonadism

The following list of conditions have 'Hypogonadism' or similar listed as a symptom in our database. This computer-generated list may be inaccurate or incomplete. Always seek prompt professional medical advice about the cause of any symptom.

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The following list of medical conditions have Hypogonadism or similar listed as a medical complication in our database. The distinction between a symptom and complication is not always clear, and conditions mentioning this symptom as a complication may also be relevant. This computer-generated list may be inaccurate or incomplete. Always seek prompt professional medical advice about the cause of any symptom.

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Gonadal failure - (Source - Diseases Database)

Medical Conditions associated with Hypogonadism:

Male reproductive symptoms (577 causes), Female reproductive symptoms (928 causes), Fertility symptoms (370 causes), Women's health symptoms (1177 causes), Men's health symptoms (291 causes), Pregnancy symptoms (699 causes), Sexual symptoms (1838 causes), Intercourse symptoms (258 causes)

Symptoms related to Hypogonadism:

3-M Syndrome, 46, XX Gonadal dysgenesis epibulbar dermoid, Acrocephalopolysyndactyly type 2, Alagille Syndrome (1 cause), Alopecia

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Originally posted here:
Hypogonadism - RightDiagnosis.com

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.

Read more from the original source:
Hypogonadotropic hypogonadism - Wikipedia, the free encyclopedia

Hypogonadism is a disorder where the testes in men and ovaries in women do not work properly. It can be very distressing. Thanks to the discovery and development of gender specific hormone treatments, men and women with hypogonadism can lead a normal life.

Hypogonadism is the clinical manifestation of the impaired function of the gonads, which in men are the testes and in women are the ovaries. Certain patients have hypogonadism from birth, while others may develop the condition later in their life. The disease has different features in males and in females, before and after the onset of puberty.

If onset is in pre-pubertal boys, signs and symptoms of lack of testicular function include a change of male hair distribution, including facial, chest, and axillary hair, poor development of skeletal muscles, and disturbance of bone growth resulting in abnormally long arms and legs. Blood levels of the male hormone testosterone are low. Also observed are missing laryngeal enlargement, failure of vocal chord thickening, and alterations in body fat distribution. When hypogonadism occurs in males after puberty, low concentration of testosterone in the blood causes lack of energy, weakness, lethargy and diminished sexual function, reduced bone mass and often anaemia.

In girls with hypogonadism before puberty, impaired ovarian function leads to failure of progression through puberty. The absence of periods (primary amenorrhoea) is the most common feature. Blood levels of estradiol are low. When hypogonadism occurs after puberty, irregular periods or absence of periods (secondary amenorrhea) is the usual concern. The patients develop ovarian suppression which manifests as infertility, decreased libido, breast atrophy, and osteoporosis.

Testis and ovary function are part of a hormonal loop which consists of two components in the brain (the hypothalamic region and the pituitary gland) and the gonads themselves. This hypothalamic-pituitary-gonadal axis acts like a waterfall. A hypothalamic generator releases luteinising hormone-releasing hormone (LHRH). In response to these LHRH pulses, the pituitary secretes follicle-stimulating hormone (FSH) and luteinising hormone (LH), which in turn stimulate testis and ovary. The increased blood levels of the gonadal hormones (androgens in men and estrogens in women) leads to lowered FSH and LH secretion at the pituitary level, completing the negative feedback loop.

Hypogonadism may occur if this hypothalamic-pituitary-gonadal axis is interrupted at any level. Primary or hypergonadotrophic hypogonadism results if the gonad does not produce the amount of sex hormone sufcient to suppress secretion of LH and FSH at normal levels. Hypogonadotrophic hypogonadism may result from hypothalamic LHRH deciency or from inability of the pituitary to secrete LH and FSH. Most commonly, hypogonadotrophic hypogonadism is observed after hypothalamic-pituitary injury from tumours, trauma, or radiation.

For male patients with primary hypogonadism, the most common cause is a genetic disorder known as Klinefelter syndrome, a chromosome abnormality which occurs in one case per approximately 1,000 live births. Primary hypogonadism is more common in boys than in girls because the incidence of Klinefelter syndrome is higher than the incidence of the equivalent condition for girls, Turner syndrome. Hypogonadotrophic hypogonadism in men occurs more rarely. It is estimated, though, that less than ve per cent of men with hypogonadotrophic hypogonadism are diagnosed and are receiving hormone replacement therapy (HRT); around a fth of men aged more than 50 years are believed to have androgen deciency.

For women with primary hypogonadism, the most common cause is a genetic disorder known as Turner syndrome, a chromosome abnormality which occurs with an incidence of one case per approximately 5,000 live births. The incidence of hypogonadotropic hypogonadism in females is equal to that in males.

No increase in mortality exists in patients with hypogonadism. Morbidity for men and women includes infertility, anaemia and an increased risk of osteoporosis. There does not appear to be a racial pattern.

The action of gonadotrophin-releasing hormone (GnRH) from the hypothalamus on the pituitary, and the subsequent action of LH and FSH from the pituitary on the testes to stimulate testosterone and sperm production

In men, low blood levels of testosterone should be increased. HRT may be given as a bi-weekly intramuscular injection, as a patch form, or a gel preparation. In Europe, there exist a number of transdermal testosterone therapies, including gels containing one per cent testosterone or in the form of dermal patches containing the active compound. Several formulations are available, including a scrotal patch and several patches that may be applied at other sites. Patches are changed daily. Another treatment option is the prescription of tablets which dissolve in the mouth. Additionally, there are hormone implants. These cylindrical pellets are inserted under the skin in the abdomen, buttock or thigh. They are given once every three to six months. Oral preparations of testosterone are still available but rarely used.

In women, estrogen should be increased. To initiate pubertal development in girls, HRT can be given orally as conjugated estrogen or as a patch applied twice weekly. Transdermal application allows a very low starting dose of estrogen which is desired in young girls with bone ages below 12 years. Starting at higher doses may cause rapid closure of epiphyses and growth will be halted. Women taking estrogen also need to take progesterone replacement unless they have undergone a surgical removal of the uterus. Progesterone agents are added during the last 12 to 14 days of the menstrual cycle to transform the proliferative inner lining of the uterus (endometrium) into the secretory state.

Men and women with hypogonadism can lead a normal life with HRT.

To restore fertility, preparations called human chorionic gonadotrophin (hCG) or human menopausal gonadotrophin (hMG) are given as intramuscular injections to treat men and women, respectively. In men, they act on the testicles and encourage the production of sperm and testosterone. While on gonadotrophin injections, there is no need to take testosterone or estrogen replacement therapy.

At the end of 2003, a new androgen replacement depot received its rst approval in a European country for the treatment of hypogonadism in men. The slow releasing depot formulation means it can be administered by just four injections a year, which is a vast improvement over existing treatments for testosterone deciency, which require an average of 22 injections per year.

At the end of February 2004, it was found that the benets of HRT in males suffering from hypogonadism are maintained for more than a year. Using a one per cent once-daily testosterone gel, researchers reported signicant improvements in sexual function, mood, lean body mass and bone mineral density.

Research has shown a higher incidence of hypogonadotrophic hypogonadism with concomitant conditions such as diabetes and AIDS. According to latest results, some 30 per cent of men suffering from type 2 diabetes are affected, because of the improper functioning of the hypothalamic-pituitary axis. Research into new treatments for patients suffering from diseases such as diabetes and AIDS will therefore reduce the overall prevalence of hypogonadism.

Hypogonadism can be seen as an area in which the development of new medicines over the past twenty years has been very successful. With the improvements in outcome now achievable, the somewhat slower pace of new development can be taken as a sign of a job well done.

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EFPIA - Hypogonadism

INTRODUCTION

Hypogonadism in a male refers to a decrease in either of the two major functions of the testes: sperm production or testosterone production. These abnormalities can result from disease of the testes (primary hypogonadism) or disease of the pituitary or hypothalamus (secondary hypogonadism). The use of testosterone to treat hypogonadism in adult men, primary or secondary, is reviewed here. The clinical manifestations and diagnosis of male hypogonadism, induction of spermatogenesis in men with secondary hypogonadism, and induction of puberty with testosterone are discussed elsewhere. (See "Clinical features and diagnosis of male hypogonadism" and "Induction of fertility in men with secondary hypogonadism" and "Diagnosis and treatment of delayed puberty", section on 'Testosterone therapy'.)

MECHANISMS OF TESTOSTERONE ACTION

Testosterone has many different biologic effects, at least in part because it can act as three hormones. It can act directly by binding to the androgen receptor. It can also act in tissues that express the enzyme 5-alpha-reductase, via conversion to dihydrotestosterone, which binds more avidly to the androgen receptor than testosterone itself. Finally, it can act as an estrogen following conversion by aromatase to estradiol, which binds to the estrogen receptor.

Testosterone requires conversion to dihydrotestosterone for its action on the external genitalia (which include the prostate gland) and sexual hair. This mechanism provides the basis for the use of the 5-alpha-reductase inhibitor, finasteride, to treat benign enlargement of the prostate and male pattern baldness. (See "Treatment of androgenetic alopecia in men", section on 'Finasteride' and "Medical treatment of benign prostatic hyperplasia", section on '5-alpha-reductase inhibitors'.)

Testosterone requires conversion to estradiol for much of its action on bone. This effect is illustrated by the rare condition of aromatase deficiency in men, which results in failure of epiphyseal closure and severe osteoporosis. Treatment with estradiol corrects both. (See "Epidemiology and etiology of osteoporosis in men", section on 'Estrogen'.)

Testosterone also appears to require conversion to estradiol to stimulate normal sexual function and decrease body fat in men, as shown by an experiment in which men 20 to 50 years old were treated with a gonadotropin-releasing hormone (GnRH) agonist to suppress testosterone and estradiol secretion and then replaced with testosterone, with or without an aromatase inhibitor [1]. Addition of the aromatase inhibitor partially blocked testosterone from increasing libido and erectile function and from decreasing subcutaneous and intraabdominal fat.

Literature review current through: Apr 2016. | This topic last updated: Wed Apr 27 00:00:00 GMT 2016.

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Testosterone treatment of male hypogonadism - UpToDate

The hormone testosterone is responsible for numerous sex characteristics in men including the growth and development of the sex and reproductive organs. In addition to assisting with fat distribution, bone mass and deepening of the voice, testosterone also helps keep up energy levels, sex drive and fertility. As men age, their production of testosterone naturally begins to decline. However, some men may develop a testosterone deficiency during their life. This disorder is known as hypogonadism.

What Is It? Hypogonadism is one of the main causes of male infertility. It is estimated that 13 million men in the United States alone are affected by hypogonadism, yet less than 10% of these men actually seek treatment for the disorder. Hypogonadism occurs when there is disease or damage to the pituitary gland, testicles or hypothalamus. Any problems in these areas can lead to a deficient production of the gonadotropin hormone.

Testosterone deficiency can occur at any stage of a mans life. Some males are born with the deficiency, making it a congenital abnormality, while others develop the disorder before the onset of puberty. Others still develop it later in life, during adulthood.

Due to the lack of testosterone, men affected by hypogonadism often have troubles producing sperm. The low levels of testosterone also result in an adult male having a low sex drive and erectile dysfunctions. All of these factors combine to make it difficult for a man to father a child.

What Causes Hypogonadism? There are two types of male hypogonadism: primary and secondary. Primary hypogonadism refers to a testosterone deficiency that stems from abnormal testicular function. Secondary hypogonadism is the result of problems with the pituitary gland or the hypothalamus, which controls the secretion of pituitary hormones. When messages from either of these sources become impaired, normal performance of the testicles is compromised.

There are numerous causes for primary hypogonadism such as undescended testicles, excess iron in the blood (known as hemochromatosis), an injury that causes damage to the testicles, mumps, and chemotherapy or radiation treatment. Klinefelters syndrome, which results in a male being born with an extra x chromosome, can lead to impaired testicular growth as well as problems in sperm production and is another cause of primary hypogonadism.

Secondary hypogonadism can be the result of pituitary disorders and inflammatory diseases that affect the pituitary gland. Also, Kallmans syndrome, which affects the proper development of the hypothalamus, ultimately leads to a testosterone deficiency. Additionally, certain medications, like those used to help heartburn or control moods, can affect the level of testosterone produced by the body.

Signs And Symptoms The effects of hypogonadism vary depending on when a man develops the disorder. In cases where hypogonadism is congenital, the gonads fail to produce enough testosterone for proper development of the external genitals and internal reproductive organs. This results in a child whose sex is ambiguous at birth.

When testosterone deficiency becomes present at the start of puberty, normal growth and development is impaired. Muscle mass does not increase as much and the male voice remains high. There is often a lack of facial body hair growth while the penis and testicles fail to mature. The arms and legs may grow to be out of proportion with trunk of the body. There may even be some development of breasts.

The onset of hypogonadism in adulthood can significantly change the physical appearance of men as well as hinder the normal reproductive functions and cause emotional changes that mirror the experience of menopausal women. Signs of hypogonadism in adult males include:

Getting Help If you display any of the symptoms of hypogonadism, make an appointment with your family physician. A blood test that measures testosterone levels can reveal whether or not there is a deficiency. Proper evaluation by an endocrinologist (a doctor that specializes in hormones) will be necessary, though, for a definitive diagnosis. Ask for a referral to an endocrinologist if your family physician does not automatically provide one.

There are different types of treatments available to help those with a testosterone deficiency. If you have primary hypogonadism, the most likely method of treatment will be testosterone replacement therapy (TRT). This will aid in increasing the production of testosterone. However, it may not help you recover your fertility. It may be necessary for you and your partner to employ assisted reproductive technology methods in order to conceive. Those men affected by secondary hypogonadism have a better chance of recovering their fertility through the use of TRT.

There are numerous ways in which TRT can be administered. The most popular method is a patch that can be worn on the scrotum or elsewhere on the body that will allow the body to receive a continuous supply of hormones. Aside from the patch, there are intramuscular injections that are given every two weeks, which men can do at home. A testosterone gel for hypogonadism is also available as is a mucoadhesive that dissolves into a more gel-like substance when you place it on your gum line. This allows the testosterone to be absorbed directly into the blood stream. There are also oral testosterone supplements available but these are rarely used nowadays due to the associated side effects.

Psychological counseling for both yourself and your partner is also a good idea to help you mutually deal with the emotional aspects of the problem. Additionally, you may want to seek a support group in your area where you can talk with other people who are also affected by the disorder.

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Hypogonadism Causes Infertility. Learn how to detect and ...

Definition (NCI) A disorder characterized by decreased function of the gonads. Clinical manifestations in both males and females include poor libido, infertility, and osteoporosis. Additional signs in males include erectile dysfunction, muscle atrophy, gynecomastia and increased abdominal fat. In females, additional signs include shrinking of the breasts and loss of, or failure to develop menstruation. Definition (CSP) condition resulting from or characterized by abnormally decreased functional activity of the gonads, with retardation of growth and sexual development. Definition (MSH) Condition resulting from deficient gonadal functions, such as GAMETOGENESIS and the production of GONADAL STEROID HORMONES. It is characterized by delay in GROWTH, germ cell maturation, and development of secondary sex characteristics. Hypogonadism can be due to a deficiency of GONADOTROPINS (hypogonadotropic hypogonadism) or due to primary gonadal failure (hypergonadotropic hypogonadism). Concepts Disease or Syndrome (T047) MSH D007006 SnomedCT 48130008 English Hypogonadism, Hypogonadotropism, hypogonadism (diagnosis), hypogonadism, Hypogonadism [Disease/Finding], hypogonadotropism, Hypogonadism (disorder), Hypogonadism, NOS Swedish Hypogonadism Japanese , , , , , , , , , , Czech hypogonadismus, Hypogonadismus Finnish Hypogonadismi Russian INFANTILIZM POLOVOI, INFANTILIZM PSIKHOSEKSUAL'NYI, GIPOGONADIZM, INFANTILIZM GENITAL'NYI, , , , Polish Hipogonadyzm, Infantylizm, Niedoczynno gonad Hungarian Hypogonadismus Norwegian Hypogonadisme Spanish hipogonadismo (trastorno), hipogonadismo, Hipogonadismo Dutch hypogonadisme, Gonadisme, hypo-, Hypogonadisme French Hypogonadisme German Hypogonadismus Italian Ipogonadismo Portuguese Hipogonadismo

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Hypogonadism - FPnotebook.com

The sex glands, also known as gonads, primarily consist of the testes in men and the ovaries in women. These glands produce sex hormones such as testosterone and estrogen. Sex hormones help control secondary sex characteristics, including breast development in women, testicular development in men, and pubic hair growth in both sexes. They also play a role in the menstrual cycle and sperm production.

Hypogonadism develops when the sex glands produce little or no sex hormones, resulting in reduced function of the testes in males and ovaries in females. The condition can be present at birth, but it may also develop after infection or injury.

There are two types of hypogonadism.Primary hypogonadismoriginates from a problem with the testes or the ovaries, causing the sex glands to produce fewer sex hormones.

Secondary hypogonadism, also known as hypogonadotropic hypogonadism, is caused by a problem with the pituitary gland or hypothalamus. The hypothalamus and pituitary gland are located in the brain and help regulate various body functions, including the production of sex hormones. Disorders affecting these parts of the brain can result in lowered function of the sex glands and insufficient amounts of sex hormones.

The complications of hypogonadism in newborns may include abnormal genitals. In pubescent boys, a lack of treatment can lead to impaired genital growth, the absence of body hair, and enlarged breasts.

The complications of hypogonadism in untreated adult males include:

The complications of hypogonadism in untreated females include:

Hypogonadism is usually treated with hormone replacement therapy (HRT). However, your course of treatment may differ depending on the exact cause of your condition. The symptoms of hypogonadism often improve significantly with the proper treatment.

In most cases, hypogonadism can be treated effectively with HRT. This treatment consists of taking medications containing the hormone that your body is lacking, such as testosterone, estrogen and progesterone, or pituitary hormones to replace the ones that the body no longer produces.

Adult males can be treated with testosterone replacement therapy if their condition is caused by testicular failure. This treatment can:

In young boys and adolescent males, low doses of testosterone over time can be used to replace naturally occurring testosterone during puberty. This also lowers the risk of negative side effects from taking hormones. Aside from stimulating puberty, testosterone replacement therapy for young males can:

Women who have a decreased sex drive may also benefit from low-dose testosterone.

Testosterone replacement therapy can be administered is several ways, including the following:

You or a healthcare provider can inject testosterone into a muscle, usually at two-week intervals.

You can rub a clear gel containing testosterone onto the skin of your shoulder, upper arm, or lower abdomen. After applying the gel, you must avoid bathing for several hours so your skin has time to absorb the testosterone properly. The gel can also be transferred to someone else through direct contact, so make sure you refrain from skin-to-skin contact until the gel has dried.

You can place a skin patch containing testosterone on your body at night. The patch should be switched to a different area of the body every few weeks. This helps to reduce the risk of having an adverse site reaction. You may want to consider rotating where you place the patch. You can place the patch on your:

You can take testosterone in a pill form. Over time, however, oral testosterone can cause cholesterol levels to rise and can increase your risk of heart and liver problems. For these reasons, it usually isnt considered for long-term use.

You can apply a small patch containing testosterone to your upper gum, above your front teeth. This is called a buccal patch. The patch softens and releases the hormone gradually. Its generally applied every 12 hours on alternating sides. The gum looks like a tablet, but you should never chew or swallow it.

You and your doctor can discuss which method would be best for you.

For females, treatment for hypogonadism mostly consists of increasing the amount of female sex hormones in the body. Increasing levels of estrogen and progesterone can help strengthen bones, improve cholesterol levels, and support sex drive.

If youre a premenopausal female, you can benefit from estrogen that comes in pill or patch form. Estrogen and progesterone are sometimes combined to lower the chances of developing endometrial cancer.

Pituitary hormones can help treat hypogonadism that was caused by a problem with the pituitary gland. In adults, pituitary hormone replacement administered in pill form can increase sperm production. In boys and adolescent males, it can help promote growth of the testicles.

If a tumor is found on the pituitary gland, it can be treated with surgery, medication, or radiation therapy.

Testosterone replacement tends to increase the risk of urinary problems. It may also increase the risk of edema, or water retention, in people who have heart, liver, or kidney problems. Testosterone therapy may even aggravate sleep apnea or interfere with male fertility.

When used for an extended period, oral testosterone can increase your risk of liver problems, heart disease, and high cholesterol.

Your doctor will monitor your blood counts and hormone levels during treatment, and they can make adjustments if necessary. This will help reduce the risks associated with HRT.

If youre a male, then your doctor will also perform prostate screening tests to check prostate-specific antigen levels for signs of serious medical conditions. These tests will need to be done every three, six, and 12 months while you receive HRT.

Hypogonadism can take an emotional toll, but there are things you can do to minimize stress, including:

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Treatment Options for Hypogonadism Healthline

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Morbidity for men and women with hypogonadism includes infertility and an increased risk of osteoporosis; there is no increase in mortality.

Hypogonadotropic hypogonadism (see the image below) is one of several types of hypogonadism.

History

Considerations in the evaluation of males with hypogonadism include the following:

Developmental anomalies associated with the genital system (eg, hypospadias, micropenis, and cryptorchidism)[1]

For postpubertal males, the rate of beard growth, libido and sexual function, muscle strength, and energy levels

Possible causes of acquired testicular failure (eg, mumps orchitis, trauma, radiation exposure of the head or testes, and chemotherapy)

Drugs that may interrupt testicular function: Including agents that interfere with testosterone synthesis, such as spironolactone, cyproterone, marijuana, heroin, and methadone

Considerations in the evaluation of females with hypogonadism include the following:

Signs associated with Turner syndrome (eg, lymphedema, cardiac or renal congenital anomalies, and short growth pattern)

Age of menarche

Physical examination

Considerations in the physical examination of males with hypogonadism include the following:

Evaluation of the testes: This is the most important feature of the physical examination; determine whether both testes are palpable, their position in the scrotum, and their consistency; testes size can be quantitated by comparison with testicular models (orchidometer), or their length and width may be measured

Examination of the genitalia for hypospadias

Examination of the scrotum to see if it is completely fused

Evaluation of the extent of virilization

Staging of puberty: Use the Tanner criteria for genitalia, pubic hair, and axillary hair

Examination for signs of Klinefelter syndrome (eg, tall stature, especially if the legs are disproportionately long, gynecomastia, small or soft testes, and a eunuchoid body habitus)

Considerations in the physical examination of females with hypogonadism include the following:

Examination of the genitalia is important

Determination of the extent of androgenization: May be adrenal or ovarian in origin and is demonstrated in pubic and axillary hair

Determination of the extent of estrogenization: As evidenced by breast development and maturation of the vaginal mucosa

Examination for signs of Turner syndrome (eg, short stature, webbing of the neck [such as pterygium colli], a highly arched palate, short fourth metacarpals, widely spaced nipples, or multiple pigmented nevi)

See Clinical Presentation for more detail.

The following studies may be indicated in males with hypogonadism:

Follicle-stimulating hormone (FSH) levels

Luteinizing hormone (LH) levels

Prolactin levels

Testosterone levels

Thyroid function

Seminal fluid examination

Karyotyping

Testicular biopsy

For males after puberty, the Guidelines of the Endocrine Society[2] require that the diagnosis of hypogonadism be based on symptoms and signs of hypogonadism plus the presence of a low testosterone level measured on at least 2 occasions.

The following studies may be indicated in females with hypogonadism:

Additional tests in the evaluation of patients with hypogonadism include the following:

Adrenocorticotropic hormone (ACTH) stimulation testing: In patients in whom a form of congenital adrenal hyperplasia is suspected, adrenal steroid synthesis is best evaluated by performing a cosyntropin (ACTH 1-24) stimulation test

Luteinizing-hormone releasing hormone (LHRH) stimulation testing: To distinguish between true hypogonadotropic hypogonadism and constitutional delay in growth and maturation

Testicular tissue testing: If the testes are not palpable and if it is not certain whether any testicular tissue is present, administering human chorionic gonadotropin (hCG) and measuring testosterone response may be helpful

See Workup for more detail.

Hormonal replacement

The simplest and most successful treatment for males and females with either hypergonadotropic or hypogonadotropic hypogonadism is replacement of sex steroids, but the therapy does not confer fertility or, in men, stimulate testicular growth.

When fertility is desired, an alternative therapy for men with hypogonadotropic hypogonadism is administration of pulsatile LHRH or injections of hCG and FSH. (In patients with hypergonadotropic hypogonadism, fertility is not possible.)

In a 6-year European study of men being treated for hypogonadism, long-term transdermal testosterone treatment did not increase prostate-specific antigen (PSA) levels or influence prostate cancer risk.[3, 4]

Investigators used data from a 5-year, open-label extension of a 1-year trial of a transdermal testosterone patch (Testopatch) in men with hypogonadism. Study subjects wore two 60 cm2 patches, each of which delivered 2.4 mg of testosterone per day. More than 90% of patients had PSA concentrations below 2 ng/mL during the 6-year study, and no prostate cancer was found in patients over the course of the trial.

See Treatment and Medication for more detail.

Hypogonadism manifests differently in males and in females before and after the onset of puberty.[5] If onset is in prepubertal males and testosterone replacement is not instituted, the individual has features of eunuchoidism, which include sparse body hair, poor development of skeletal muscles, and delay in epiphyseal closure, resulting in long arms and legs. When hypogonadism occurs in postpubertal males, lack of energy and decreased sexual function are the usual concerns. In females with hypogonadism before puberty, failure to progress through puberty or primary amenorrhea is the most common presenting feature. When hypogonadism occurs in postpubertal females, secondary amenorrhea is the usual concern.

The gonad (ovary or testis) functions as part of the hypothalamic-pituitary-gonadal axis. A hypothalamic pulse generator resides in the arcuate nucleus, which releases luteinizing hormone (LH)-releasing hormone (LHRH), which is also termed gonadotropin-releasing hormone (GnRH), into the hypothalamic-pituitary portal system. Data suggest that a gene named KISS is important in the development of the LHRH-secreting cells.[6, 7]

In response to these pulses of LHRH, the anterior pituitary secretes follicle-stimulating hormone (FSH) and LH, which, in turn, stimulate gonadal activity. The increase in gonadal hormones results in lowered FSH and LH secretion at the pituitary level, completing the feedback loop. In the testes, LH stimulates Leydig cells to secrete testosterone, whereas FSH is necessary for tubular growth. In the ovaries, LH acts on theca and interstitial cells to produce progestins and androgens, and FSH acts on granulosa cells to stimulate aromatization of these precursor steroids to estrogen.

Hypogonadism may occur if the hypothalamic-pituitary-gonadal axis is interrupted at any level. Hypergonadotropic hypogonadism (primary hypogonadism) results if the gonad does not produce the amount of sex steroid sufficient to suppress secretion of LH and FSH at normal levels. Hypogonadotropic hypogonadism may result from failure of the hypothalamic LHRH pulse generator or from inability of the pituitary to respond with secretion of LH and FSH. Hypogonadotropic hypogonadism is most commonly observed as one aspect of multiple pituitary hormone deficiencies resulting from malformations (eg, septooptic dysplasia, other midline defects) or lesions of the pituitary that are acquired postnatally. In 1944, Kallmann and colleagues first described familial isolated gonadotropin deficiency. Recently, many other genetic causes for hypogonadotropic hypogonadism have been identified.

Normosmic hypogonadotropic hypogonadism, in which the sense of smell is not disrupted, has been associated with mutations in GNRH1, KISS1R, and GNRHR genes. Although their exact functions are unclear, the genes TAC3 and TACR3 have also been associated with normosmic hypogonadotropic hypogonadism. Kallmann syndrome (anosmic hypogonadotropic hypogonadism) has been associated with mutations in KAL1, FGFR1, FGF8, PROK2, and PROKR2 genes. The relationship with Kallmann syndrome is thought to be because these genes are all related to the development and migration of GnRH neurons. Mutations of an additional gene, CHD7, which has been associated with CHARGE syndrome, has also been found in patients with both normosmic or anosmic hypogonadotropic hypogonadism.

In women with hypergonadotropic hypogonadism (ie, gonadal failure), the most common cause of hypogonadism is Turner syndrome, which has an incidence of 1 case per 2,500-10,000 live births. In men with hypergonadotropic hypogonadism, the most common cause is Klinefelter syndrome, which has an incidence of 1 case per 500-1000 live births. Hypogonadotropic hypogonadism is more rare.

No racial predilection has been described.

Hypergonadotropic hypogonadism is more common in males than in females because the incidence of Klinefelter syndrome (the most common cause of primary hypogonadism in males) is higher than the incidence of Turner syndrome (the most common cause of hypogonadism in females). Incidence of hypogonadotropic hypogonadism is equal in males and females.

Hypogonadism may occur at any age; however, consequences differ according to the age at onset. If hypogonadism occurs prenatally (even if incomplete), sexual ambiguity may result. If hypogonadism occurs before puberty, puberty does not progress. If hypogonadism occurs after puberty, infertility and sexual dysfunction result.

No increase in mortality is observed in patients with hypogonadism. Morbidity for men and women includes infertility and an increased risk ofosteoporosis. In women, an increased risk of severe osteoporosis is noted. In men, hypogonadism causes decreased muscle strength and sexual dysfunction.

Men and women with hypogonadism can lead a normal life with hormone replacement.

Approximately 20-25% of females with Turner syndrome have some spontaneous puberty. Spontaneous estrogenization occurs more commonly in women with mosaic karyotypes and those karyotypes with an abnormal second X chromosome, such as 46,XXiq or 46,XXip. Reports exist of women with mosaic Turner syndrome becoming pregnant without in vitro fertilization.

For patient education resources, see theMen's Health CenterandWomen's Health Center, as well asImpotence/Erectile DysfunctionandAmenorrhea.

For both males and females with hypogonadism, determining whether evidence of a genital abnormality is present at birth or determining the timing and extent of puberty is important. In addition, because Kallmann syndrome (hypogonadotropic hypogonadism and anosmia [ie, lack of a sense of smell]) is a common cause of hypogonadotropic hypogonadism, inquiring about the sense of smell is important.

Physical findings may include the following:

The following causes of hypogonadism are noted:

Hypogonadotropic hypogonadism

See the image below.

Causes of hyogonadotropic hypogonadism include the following:

CNS disorders

Hypergonadotropic hypogonadism in males

Hypergonadotropic hypogonadism in females

Genetics of hypogonadotropic hypogonadism

To date, numerous genes have been identified as causes of hypogonadotropic hypogonadism. The genes include the following:

KALis located on the X chromosome, just below the pseudoautosomal region. An abnormality in this gene results in Kallmann syndrome, which is characterized by anosmia and hypogonadotropic hypogonadism.FGFR1, FGF8, PROK2,andPROKR2have also been associated with Kallmann syndrome. The relationship with Kallmann syndrome is thought to be due to the relation of these genes to the development and migration of gonadotropin-releasing hormone (GnRH) neurons.

TheDAX1gene is associated with X-linked adrenal hypoplasia congenita (hypogonadotropic hypogonadism and adrenal insufficiency).

GNRHRis the gene associated with the GnRH (LHRH) receptor.

GNRH1, KISS1R,andGNRHRgenes have been associated with normosmic (sense of smell is not disrupted) hypogonadotropic hypogonadism.

TAC3andTACR3mutations have also been associated with normosmic hypogonadotropic hypogonadism, although their exact functions are unclear.

CHD7mutation, which has been associated with CHARGE syndrome, has also been found in patients with both normosmic and anosmic hypogonadotropic hypogonadism.

PC1is the gene for prohormone convertase 1. Abnormality of this gene causes hypogonadotropic hypogonadism and defects in prohormone processing.

In addition, mutations in thePROP1gene have resulted in absence of several pituitary hormones, including growth hormone, thyroid-stimulating hormone, prolactin, and gonadotropins.PROP1encodes a protein expressed in the embryonic pituitary, which is necessary for function ofPOU1F1(formerlyPIT1), which codes for a pituitary transcription factor.

In addition, mutation of the geneHESX1has been associated with septooptic dysplasia, which may include poor development of the pituitary.

The following studies may be indicated in hypogonadism:

Pelvic ultrasonography may be helpful in females.

Adrenocorticotropic hormone (ACTH) stimulation testing: In patients in whom a form of congenital adrenal hyperplasia is suspected, adrenal steroid synthesis is best evaluated by performing a cosyntropin (ACTH 1-24) stimulation test. Baseline serum adrenocortical hormone levels are measured, then 0.25 mg of cosyntropin is intravenously injected, and serum hormone levels are remeasured after 60 minutes. Precursor product ratios are compared with those in age-matched control subjects to determine whether a steroidogenic defect is involved in sex hormone synthesis.

Luteinizing-hormone releasing hormone (LHRH) stimulation testing: To distinguish between true hypogonadotropic hypogonadism and constitutional delay in growth and maturation, performing a stimulation test with LHRH may be helpful.

LHRH is intravenously injected, and LH and FSH levels are determined at 15-minute intervals following LHRH administration.

A shortened version of the study has been used, in which LHRH is subcutaneously injected, and the specimen for LH and FSH levels is taken at 30-40 minutes.

Obtaining LHRH for testing over the past several years has been difficult. Some centers have substituted testing LH response to aqueous leuprolide.

Testicular tissue testing: If testes are not palpable and whether any testicular tissue is present is unclear, administering human chorionic gonadotropin (hCG) and measuring testosterone response may be helpful.

Bone age may be helpful in distinguishing hypogonadism from constitutional delay in growth and maturation. Timing of onset of puberty is related more to bone age than to chronologic age. Distinguishing hypogonadism from constitutional delay in growth and maturation is often difficult until the bone age is at a point adequate for pubertal development.

Occasionally, testicular biopsy findings are helpful, particularly if azoospermia or oligospermia is present.

In prepubertal patients with hypogonadism, treatment is directed at initiating pubertal development at the appropriate age. All such treatment is hormonal replacement therapy. Although the simplest and most successful treatment for both males and females with either hypergonadotropic or hypogonadotrophic hypogonadism is replacement of sex steroids, in hypogonadotropic hypogonadism, the therapy does not confer fertility or, in men, stimulate testicular growth.

An alternative for men with hypogonadotropic hypogonadism has been treatment with pulsatile LHRH or hCG, either of which can stimulate testicular growth. Because such treatment is more complex than testosterone replacement, and because treatment with testosterone does not interfere with later therapy to induce fertility, most male patients with hypogonadotropic hypogonadism prefer to initiate and maintain virilization with testosterone.

At a time when fertility is desired, it may be induced with either pulsatile luteinizing hormone-releasing hormone (LHRH) or (more commonly) with a schedule of injections of human chorionic gonadotropin (hCG) and follicle-stimulating hormone (FSH).

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Hypogonadism - Medscape

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

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

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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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Hypogonadism | University of Maryland Medical Center

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 ...

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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Association of hypogonadism with vitamin D status: the ...

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

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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Male Hypogonadism - Cleveland Clinic

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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Hypogonadism | Disorders | Knowledge Base

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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Hypergonadotropic hypogonadism - Wikipedia, the free ...

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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hypogonadism | pathology | Britannica.com

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