Underactive Thyroid and Heart Failure a Bad Combination: Study

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WEDNESDAY, May 22 (HealthDay News) -- People with heart failure are more likely to experience poorer health from having a thyroid gland that is even mildly underactive, according to a new study.

And among black patients, the researchers found an increased risk of death linked to the condition, which is known as hypothyroidism.

"This study is the first to show that African-Americans who have hypothyroidism face a greater risk of death than patients of other racial and ethnic groups," Dr. Connie Rhee, of Brigham and Women's Hospital in Boston, said in a news release from the Endocrine Society. "This elevated risk exists despite the fact that hypothyroidism is less common in the African-American population compared to other groups."

"More research is needed to confirm these findings and to determine the underlying reasons why hypothyroidism has a differential impact on people of different races and ethnicities," Rhee said.

Hypothyroidism occurs when the thyroid doesn't produce enough hormones. The researchers noted that people with mild forms of the condition have thyroid function at the low end of the normal range.

In conducting the study, Rhee and her colleagues analyzed information on about 750 patients with hypothyroidism, including nearly 700 people with a mild form of the condition.

Although it's unclear why hypothyroidism has a different effect on people of various races and ethnicities, the study authors said doctors should not take a blanket approach to assessing people's risk for the condition and determining whether they require treatment.

"Our data suggest that mild hypothyroidism may, in fact, be harmful in specific populations, including people with heart failure," Rhee said in the news release. "A one-size-fits-all approach may not be appropriate for assessing risk and determining whether treatment is required for [mild] hypothyroidism."

More than 9.5 million people in the United States have hypothyroidism, the study authors said.

The study is scheduled for publication in the June issue of the Journal of Clinical Endocrinology & Metabolism.

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Underactive Thyroid and Heart Failure a Bad Combination: Study

Thyroid disease

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In conjunction with World Thyroid Day (May 25), we take a look at thyroid problems that may occur during pregnancy, and how this affects the developing foetus.

THYROID diseases may be broadly divided into two categories:

Hormonal problems, which may be due to an excess of thyroid hormone production (hyperthyroidism) or the opposite, which is insufficient thyroid hormone production (hypothyroidism).

An enlarged thyroid gland (goitre) or nodules in the gland, which may be cancerous or non-cancerous.

Generally, only hormonal problems affect pregnancy. Optimal levels of thyroid hormone are essential to health from foetal life to adulthood. This review will therefore concentrate only on hyperthyroidism and hypothyroidism.

Problems with conception

Both hyperthyroidism and hypothyroidism affect the levels of female hormones, leading to menstrual problems and infertility. In addition, women with hypothyroidism may have raised prolactin levels (the hormone which promotes breast milk production, so high levels simulate breastfeeding), further diminishing fertility.

Diagnosing hypothyroidism in pregnancy is a problem because it is usually silent. The women at risk would be those with a family history of thyroid disease. However since anyone can develop hypothyroidism, and since it may be harmful to the pregnancy and foetus, all pregnant women and those intending to be pregnant should ideally be screened.

However, this is not universally accepted. In the US, this is the norm, but not in the UK. Other countries go a step further and screen all women over a certain age whether or not they intend to have a child.

The reason for this controversy is because studies have not proven conclusively that population wide screening at the expense of the government will lead to an improvement in pregnancy and foetal outcomes. But if cost is not a problem, I would suggest that pregnant women or those contemplating pregnancy request for a simple blood test to screen for hypothyroidism.

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Thyroid disease

Animal thyroid extract as effective as T4 in treating hypothyroidism

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Public release date: 17-Jun-2013 [ | E-mail | Share ]

Contact: Aaron Lohr alohr@endocrine.org 240-482-1380 The Endocrine Society

San Francisco, CA Desiccated thyroid extract (DTE), derived from crushed preparations of animal thyroid glands, is a safe and effective alternative to standard T4 therapy in hypothyroid patients, a new study finds. The results will be presented Monday at The Endocrine Society's 95th Annual Meeting in San Francisco.

In adults, untreated hypothyroidism leads to poor mental and physical performance. It also can cause high blood cholesterol levels that can lead to heart disease. The condition is treated with Levothyroxine, a synthetic (laboratory-made) form of T4 that is identical to the T4 the thyroid naturally makes. Before the advent of synthetic thyroxine, patients with hypothyroidism were treated with DTE, which contains both T4 and the active thyroid hormone T3. Many patients claim they do not feel as well on T4 alone without the additional T3 hormone.

"While thyroid experts recommend T4 alone for treatment of hypothyroidism, until now there have not been any randomized double-blind studies to compare the clinical effectiveness of synthetic T4 with DTE," said Thanh Hoang, of the Naval Medical Center in Portsmouth, Virginia. "We found that DTE is a safe and effective alternative to the standard T4 therapy. Furthermore, DTE caused modest weight loss compared to T4 alone."

In this study, researchers investigated the effectiveness of DTE compared to Levothyroxine (L-T4) in 70 hypothyroid patients. Patients were randomized to either DTE or L-T4 for 16 weeks and then crossed-over for the same duration. Study subjects underwent biochemical and neurocognitive tests along with measurements of symptoms and mental health at baseline and at the end of each treatment period.

DTE therapy did not result in a significant improvement in quality of life, but did cause modest weight loss and nearly half of the study patients expressed preference for DTE over L-T4.

"Providers may now have an additional option for the treatment of hypothyroidism in patients who are not satisfied with standard T4 therapy," said Hoang. "DTE could be considered for hypothyroid patients who still have symptoms despite normal thyroid blood tests while on T4 therapy."

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Animal thyroid extract as effective as T4 in treating hypothyroidism

Sofia Vergara talks about thyroid cancer diagnosis, living with hypothyroidism

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The vivacious star of Modern Family, Sofia Vergara, opened up about being diagnosed with cancer 10 years ago and how she adjusted her lifestyle to deal with hypothyroidism.

Vergara sat down with The Huffington Post to talk about the scary diagnosis she received back in 2000.

I was 28 years old, my son was really young so it was really scary, you know, when they tell you the word cancer. Of course it brought me down to earth to realize the important things.

Vergara went through radiation treatments and had her thyroid removed to get rid of the cancer, but now she lives with hypothyroidism a condition in which the thyroid gland fails to release the hormones needed to regulate vital body functions.

This forced the actress to be more diligent about her health. Vergara must take a pill every day to replace those necessary hormones. She also goes for a check-up every 3-6 months for blood tests.

Vergara said, I started taking more care of my body, to be more healthyI believe its all about taking control of it [hypothyroidism].

In April, Vergara also talked with FOX News about her involvement with the awareness campaign, Follow the Script.

Vergara told her personal story of how, at the time she was diagnosed, information about the thyroid and hypothyroidism wasnt as readily available as it is today.

Follow the Script provides overwhelmed patients with a wealth of knowledge, tips, and procedures to handle hypothyroidism. It also provides a place for people to connect and share their stories.

Vergara said about her proactive lifestyle, You realize that no matter how much beauty, money, success you have if you dont have health, you have nothing, because you cant do anything.

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Sofia Vergara talks about thyroid cancer diagnosis, living with hypothyroidism

IPE Kicks Off Phase-2 Clinical Trial for New Hypothyroid Drug

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Kingsport, Tennessee (PRWEB) June 12, 2013

Intellectual Property Executives (IPE) announced today that it is now recruiting participants for the second phase of clinical trials for its new T3 drug to treat hypothyroidism, BCT303. BCT303 successfully completed Phase-1 in August 2012 at Georgetown University Hospital.

BCT303, classified as a 505(b)(2) drug, is a formulation improvement to the active ingredient Liothyronine Sodium, which is already approved by the Food and Drug Administration (FDA). BCT303 utilizes IPEs patent-pending platform technology for sustained effects and improved stability.

IPE utilized the same platform technology to formulate its T4 drug candidate, BCT304, and its Reverse-T3 drug candidate, BCT305, both of which are ready for IND submission. It has also identified additional 505(b)(2) applications, including treatments for pain-relief and anti-inflammation.

The purpose of this Phase-2 study is to test the efficacy of BCT303, a new thyroid hormone preparation. The thyroid gland produces two thyroid hormones: mostly T4 and a smaller amount of T3. Thyroid hormone therapy for hypothyroidism or thyroid cancer is generally provided using levothyroxine, which is a synthetic form of T4. T4 is converted into the active hormone T3 in the circulation. Therefore, some researchers believe that T3 levels in T4-treated patients may be slightly lower than in individuals whose own thyroid gland is functioning normally. Symptoms of hypothyroidism have been suggested to occur because of this possible T3 deficiency, although this is controversial.

Studies of T3, added to or substituted for T4 in traditional levothyroxine regimens, have generally not shown any benefit of T3. However, it is still possible that no benefit is seen because of the short duration of action or "half-life" of T3. This short-life makes it necessary to dose T3 twice or three times daily. Despite multiple daily doses of T3, T3 levels during its therapy tend to be troubled by peaks and troughs. These peaks can be associated with symptoms of excessive thyroid hormone levels.

This study will look at TSH and thyroid hormone levels following a daily dose of a new preparation of T3 that may have longer duration of action than liothyronine. This preparation of T3 is called Thyromax or BCT303. The investigators believe that steady levels of T3 will be seen after taking Thyromax. The investigators believe that in patients with hypothyroidism use of Thyromax in the correct dose will produce normal TSH levels, without producing symptoms of too much thyroid hormone. The goal of future studies is to test whether Thyromax may be a potential treatment for hypothyroidism, by comparing it with traditional levothyroxine therapy.

Visit http://ipeamerica.com/bct303-clinical-trials to learn more about the Phase-2 clinical trial.

ABOUT IPE:

Intellectual Property Executives (IPE) is a pharmaceutical technology discovery and development corporation located in Kingsport, Tennessee, USA. For more info on IPEs portfolio of patented technology and pipeline of drug candidates, go to http://www.ipeamerica.com.

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IPE Kicks Off Phase-2 Clinical Trial for New Hypothyroid Drug

Mild hypothyroidism raises mortality risk among heart failure patients

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Public release date: 22-May-2013 [ | E-mail | Share ]

Contact: Jenni Glenn Gingery jgingery@endo-society.org 301-941-0240 The Endocrine Society

Chevy Chase, MDPatients with underlying heart failure are more likely to experience adverse outcomes from mild hypothyroidism, according to a recent study accepted for publication in The Endocrine Society's Journal of Clinical Endocrinology & Metabolism (JCEM).

Hypothyroidism occurs when an underactive thyroid does not produce enough hormones. More than 9.5 million people nationwide have hypothyroidism. People who have thyroid function at the low end of the normal range have subclinical hypothyroidism, also called mild hypothyroidism.

"Our data suggest that mild hypothyroidism may, in fact, be harmful in specific populations, including people with heart failure," said Connie Rhee, MD, MSc, of Brigham and Women's Hospital in Boston. "A 'one-size-fits-all' approach may not be appropriate for assessing risk and determining whether treatment is required for subclinical hypothyroidism."

The retrospective cohort study used data from 14,130 participants in the Third National Health and Nutrition Examination Survey. Using laboratory data, researchers identified 749 participants with hypothyroidism, including 691 with the subclinical form.

Researchers found the condition can have varying impacts on diverse racial and ethnic groups.

"This study is the first to show that African-Americans who have hypothyroidism face a greater risk of death than patients of other racial and ethnic groups," Rhee said. "This elevated risk exists despite the fact that hypothyroidism is less common in the African-American population compared to other groups. More research is needed to confirm these findings and to determine the underlying reasons why hypothyroidism has a differential impact on people of different race and ethnicity."

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Other researchers working on the study include: G. Curhan, MD, ScM; E. Alexander, MD; I. Bhan, MD, MPH; and S. Brunelli, MD, MSCE of Harvard Medical School.

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Mild hypothyroidism raises mortality risk among heart failure patients

New Data Highlight Use of Tirosint® (levothyroxine sodium) Capsules in Patients with T4 Malabsorption Due to Gastric …

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CRANFORD, N.J., June 20, 2013 /PRNewswire/ --Akrimax Pharmaceuticals, LLC, a privately-held, innovative specialty pharmaceutical company, today announced data that show a lower dose of Tirosint (levothyroxine sodium) capsules is required as compared with standard T4 tablets for hypothyroidism patients with impaired gastric acid secretion to reach their target thyroid-stimulating hormone (TSH) levels.

The American Association of Clinical Endocrinologist (AACE) Guidelines for Clinical Practice for Evaluation and Treatment of Hypothyroidism call for physicians to treat hypothyroidism with oral levothyroxine replacement therapy. Careful dose titration and monitoring is necessary in order to maintain a euthyroid state, while avoiding adverse events due to overtreatment.1 TSH levels in patients receiving levothyroxine should be no more than 4.0 mU/L.2

Azeez Farooki, MD, Assistant Attending Physician, Endocrinology Service, Memorial Sloan-Kettering Cancer Center, said, "Dose titration can be cumbersome for patients with hypothyroidism who suffer from gastrointestinal disorders like H.pylori infection, lactose intolerance or celiac disease. These patients often require higher doses of T4 due to malabsorption issues. Such patients may endure frequent dose changing and lab tests, which is less than ideal. These data are encouraging because they suggest that, in many patients with malabsorptive disorders, Tirosint improves upon the absorption of traditional levothyroxine (T4) tablets."

The pilot study examined patients who had T4 malabsorption and were in T4 treatment for more than 5 years with the same brand of tablets. A total of 36 patients met the study criteria, and 30 (28 females / 2 males; median age=51 years; median T4 dose=2.05 mg/kg/day) completed the study. T4 treatment was switched from the usual tablets to a lower dose of the softgel T4 capsules (median T4 dose=1.77 mg/kg/day; p=0.0082). Thyroid function and TSH were measured before and after 3, 6, 12 and 18 months from the treatment switch.

A slight serum TSH increase was observed in some patients after 3 months of treatment, with no change in Free T4 (FT4) levels. After 6 months, however, despite the reduced dose of T4, mean TSH values were similar (1.82 vs. 1.86 mU/l) in about two out of three patients (responders n=21) and so remained until the end of the study. In all of the remaining patients (non-responders n=9), TSH levels were significantly higher than baseline values throughout the study. In 4 of them, additional intestinal disorders were detected. Mean levels of FT4 and FT3 were in the normal range and not significantly modified throughout the study.

These findings were recently presented during an oral session at ENDO 2013, the Endocrine Society's 95th Annual Meeting, in San Francisco, CA. The abstract is available on the ENDO web site: https://endo.confex.com/endo/2013endo/webprogram/Paper6139.html.

About Hypothyroidism

Hypothyroidism is an endocrine disorder with numerous causes resulting in a deficiency in thyroid hormone. About 2% of the U.S. population has pronounced hypothyroidism, and as much as 10% has subclinical (mild) hypothyroidism.3 Up to 13 million Americans have undiagnosed hypothyroidism.4 The condition is most common in women over 40 years of age and in the elderly of both sexes.3 The signs and symptoms of hypothyroidism are nonspecific and may include fatigue, cold intolerance, coarse hair, dry skin, weight gain, delayed return phase of reflexes, and constipation.1, 5 Laboratory tests (TSH, FT3 and FT4) are the most common way hypothyroidism is detected. Treatment with levothyroxine sodium oral tablets is the standard of care in hypothyroidism.

Studies in women taking levothyroxine sodium during pregnancy have not shown an increased risk of congenital abnormalities. Therefore, the possibility of fetal harm appears remote. Tirosint should not be discontinued during pregnancy and hypothyroidism diagnosed during pregnancy should be promptly treated.6

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Hypogonadism | Disorders | Knowledge Base

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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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If you are a nurse or medical professional, register for PNA CEU Membership and earn CEU credits to learn about the symptoms, diagnosis and treatment options for patients with pituitary disorders. Help PNA reduce the time it takes for patients to get an accurate diagnosis.

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Hypogonadism | Disorders | Knowledge Base

Compare 37 Hypogonadism, Male Medications | Drugs.com

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Compare 37 Hypogonadism, Male Medications | Drugs.com

Causes of secondary hypogonadism in males UpToDate

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INTRODUCTION

Hypogonadism in a male refers to a decrease in either or both of the two major functions of the testes: sperm production and/or testosterone production (see "Male reproductive physiology"). These abnormalities can result from disease of the testes (primary hypogonadism) or disease of the pituitary or hypothalamus (secondary hypogonadism). The distinction between these disorders is made by measurement of the serum concentrations of luteinizing hormone (LH) and follicle-stimulating hormone (FSH):

The patient has primary hypogonadism if his serum testosterone concentration and/or sperm count are low and/or his serum LH and FSH concentrations are high.

The patient has secondary hypogonadism if his serum testosterone concentration and/or the sperm count are low and/or his serum LH and FSH concentrations are inappropriately normal or low, which would be inappropriate if gonadotroph cell function were normal.

Secondary hypogonadism differs from primary hypogonadism in two characteristics:

Secondary hypogonadism is usually associated with similar decreases in sperm and testosterone production. This occurs because the reduction in LH secretion results in a decrease in testicular testosterone production and, therefore, in intratesticular testosterone, which is the principal hormonal stimulus to sperm production. In contrast, there is generally a greater fall in sperm production than in testosterone secretion in primary hypogonadism because the seminiferous tubules are damaged to a greater degree than the Leydig cells. Men with primary hypogonadism, therefore, might have normal serum testosterone and LH concentrations even when the number of ejaculated sperm is very low or zero and the FSH concentration is elevated.

Literature review current through: Aug 2015. | This topic last updated: Wed May 20 00:00:00 GMT 2015.

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Causes of secondary hypogonadism in males UpToDate

CRL for Endo Health’s Aveed

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The US Food and Drug Administration (:FDA) recently issued a complete response letter (CRL) for Endo Health Solutions (ENDP) new drug application on Aveed. The company is looking to get Aveed (a long-acting testosterone undecanoate injection) approved as a treatment for male hypogonadism.

The FDA declined to approve the new drug application for Aveed in the present form, as it is apprehensive about the risks and complications which may emanate after the injection of the drug. While issuing the CRL, the US regulatory body asked Endo to develop a medication guide. Specifically, the FDA asked Endo to ensure that the Risk Evaluation and Mitigation Strategy includes the guide in addition to Elements to Assure Safe Use to address the safety issue mentioned above.

However, the US regulatory body did not ask the company to conduct additional studies on Aveed. The requirement of additional trials would have pushed up its research and development costs. Endo intends to respond to the CRL by the end of the third quarter of 2013.

We note that the Aveed setback is not the first one for Endo this year. Last month, Endo suffered a blow with the FDA turning down its request to prevent the entry of generic versions of its painkiller, Opana ER. The decision by the FDA implies that the generic formulations of the original version of Opana ER will continue to be available in the market.

Endo expects the FDA decision to impact its 2013 guidance adversely. The company expects the adverse FDA ruling to reduce 2013 total net sales of Opana ER by up to $120 million. Moreover, Endos 2013 adjusted earnings per share outlook is expected to be hurt by approximately 55 cents following the FDA verdict.

While announcing its first-quarter 2013 results, Endo stated that it expects adjusted earnings per share for 2013 in the range of $4.40$4.70 per share and revenues of $2.80$2.95 billion. The Zacks Consensus Estimate for 2013 pegs earnings at $4.31 per share on revenues of $2.8 billion. Endo intends to throw more light on its 2013 guidance in the coming months.

Moreover, another painkiller at Endo, Lidoderm is expected to face generic competition later in the year from Actavis, Inc. (ACT). This will hamper sales of the drug significantly.

Endo currently carries a Zacks Rank #3 (Hold). Jazz Pharmaceuticals (JAZZ) and Santarus, Inc. (SNTS) appear to be more attractive with a Zacks Rank #1 (Strong Buy) each.

Read the Full Research Report on ACT

Read the Full Research Report on SNTS

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CRL for Endo Health's Aveed

Male hypogonadism Symptoms – Mayo Clinic

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

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

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

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

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

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

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Male hypogonadism Symptoms - Mayo Clinic

Male hypogonadism Tests and diagnosis – Mayo Clinic

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

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

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

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

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

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Male hypogonadism Tests and diagnosis - Mayo Clinic

Hypogonadism: Types, Causes, & Symptoms Healthline

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What is Hypogonadism?

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

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

Most cases of this disorder can be successfully treated.

9 Warning Signs of Low Testosterone

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

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

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

Causes of primary hypogonadism include:

Central hypogonadism may be caused by:

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Hypogonadism: Types, Causes, & Symptoms Healthline

hypogonadism | pathology | Britannica.com

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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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Hypogonadotropic hypogonadism – Wikipedia, the free …

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

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

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

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

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

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Hypogonadotropic hypogonadism - Wikipedia, the free ...

Hypogonadism – Wikipedia, the free encyclopedia

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

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

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

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

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

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

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

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

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

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

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Hypogonadism - Wikipedia, the free encyclopedia

Prevalence, Diagnosis and Treatment of Hypogonadism in …

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by Culley C. Carson III, MD

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

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

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

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

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

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

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

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

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

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