hypogonadism | pathology | Britannica.com

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

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

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

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

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

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Andropause – Wikipedia, the free encyclopedia

Andropause also known as male menopause[1] is said to be the result of a gradual drop in testosterone, which is an androgen. The medical community is currently debating whether or not men really do go through a well-defined menopause.[1] The condition "andropause" is currently not recognized by the World Health Organization. When andropause occurs, it is considered to be a deficiency state in which the hormone testosterone goes below the normal range for an aging male.[2][verification needed]

Andropause is caused by the reduction of hormones testosterone and dehydroepiandrosterone in middle-aged men. Testosterone assists the male body in building protein and it is crucial for normal sexual drive and stamina. Testosterone also contributes to several metabolic functions including bone formation, and liver function. Andropause is also associated with a decrease in Leydig cells.[3] A steady decline in testosterone levels with age (in both men and women) is well documented.[4]

External factors that can[5] cause testosterone levels to fall include certain forms of medication, poor diet, excessive alcohol consumption, illness, lack of sleep, lack of sex, stress, or surgery. It can also be a symptom of neuroendocrine dysfunction after a mild traumatic brain injury.[6]

Andropause is preceded by a condition called Hypogonadotropic hypogonadism.[7] A downturn in the circulation of testosterone can cause the hypothalamus and pituitary gland to trigger a release of brain hormones that stimulate the testicles to ramp up production of testosterone.[8]

Although, as men age, despite low testosterone the levels of gonadotropin-releasing hormone (GnRH) and luteinizing hormone (LH) will not rise. The luteinizing hormone, gonadotropic releasing hormone, and testosterone all are dropping below what is considered normal. Low GnRH, low LH, low testosterone indicate the syndrome of hypogonadotropic hypogonadism, and it is a downward trend that takes men closer to andropause. This phenomenon typically begins in the early forties.

Eventually, testosterone levels drop to such low levels, the hypothalamus and pituitary kick in and produce high levels of GnRH and LH to compensate. This triggers the production of testosterone, which will generally work for a while, but then will fall again. That's when men enter andropause. They have a low testosterone and a high LH and GnRH, whereas before they had a low testosterone as well as low LH and GnRH.

This shift in hormonal patterns occurs in all men at some point. The female version, a similar hormonal shift that occurs in women happens in a more narrow age grouping, from early forties to late fifties.[9]

Testosterone levels decline gradually with age. Unlike females going through menopause, the decline in testosterone in men is gradual, and there is variation among individuals.[10] Upon reaching 80 years of age, the rate of testosterone secretion has decreased about 50% for men.[10]

The American Association of Clinical Endocrinologists defines hypogonadism as a testosterone level that is below the lower limit of normal for young adult control subjects[11]

Researchers conclude there is no black-and-white cutoff for "low" or "suboptimal" testosterone. Different symptoms show up at different testosterone thresholds: Muscle mass and strength do not decline until testosterone drops quite low (significantly below normal levels) whereas libido may dampen with relatively small decreases in the hormone.[12] According to Joel Finkelstein, associate director of the Bone Density Center at Massachusetts General Hospital in Boston, mens functioning is not impaired solely by a loss of testosterone, but by a loss of estrogen as well.[11]

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Andropause - Wikipedia, the free encyclopedia

Hormone replacement therapy (menopause) – Wikipedia, the …

Hormone replacement therapy (HRT) in menopause is medical treatment in surgically menopausal, perimenopausal and postmenopausal women. Its goal is to mitigate discomfort caused by diminished circulating estrogen and progesterone hormones in menopause. Combination HRT is often recommended as it decreases the amount of endometrial hyperplasia and cancer associated with unopposed estrogen therapy.[1][2] The main hormones involved are estrogen, progesterone and progestin. Some recent therapies include the use of androgens as well.[3]

The 2002 Women's Health Initiative of the National Institutes of Health found disparate results for all cause mortality with hormone replacement, finding it to be lower when HRT was begun earlier, between age 50-59, but higher when begun after age 60. In older patients, there was an increased incidence of breast cancer, heart attacks and stroke, although a reduced incidence of colorectal cancer and bone fracture.[4] Some of the WHI findings were again found in a larger national study done in the UK, known as The Million Women Study. As a result of these findings, the number of women taking hormone treatment dropped precipitously.[5] The Women's Health Initiative recommended that women with non-surgical menopause take the lowest feasible dose of HRT for the shortest possible time to minimize associated risks.[4]

The current indications for use from the U.S. Food and Drug Administration include short-term treatment of menopausal symptoms, such as vasomotor hot flashes or urogenital atrophy, and prevention of osteoporosis.[6] In 2012, the United States Preventive Task Force concluded that the harmful effects of combined estrogen and progestin are likely to exceed the chronic disease prevention benefits in most women.[7][8] A consensus expert opinion published by the The Endocrine Society stated that when taken during perimenopause, or the initial years of menopause, hormonal therapy carries significantly fewer risks than previously published, and reduces all cause mortality in most patient scenarios.[9] The American Association of Clinical Endocrinology also released a position statement in 2009 that approved of HRT in appropriate clinical scenarios.

There have been a number of large scale cross sectional and cohort studies on the effects of hormone replacement in menopause, the largest being in the United States, the United Kingdom and China. Demographically, the vast majority of data available is in post-menopausal American women with concurrent pre-existing conditions, and with a mean age of over 60 years.[10]

In 2002 the Women's Health Initiative (WHI) was published. That study looked at the effects of hormonal replacement therapy in post-menopausal women. Both age groups had a slightly higher incidence of breast cancer, and both heart attack and stroke were increased in older patients, although not in younger participants. Progesterone is the major anabolic hormone for breast tissue, and accordingly breast cancer was not increased in patients who were on estrogen therapy alone after hysterectomy. Treatment with unopposed estrogen (the supplementation of endogenous estrogens without a progestogen) is contraindicated if the uterus is still present, due its proliferative effect on the endometrium. The WHI also found a reduced incidence of colorectal cancer when estrogen and progesterone were used together, and most importantly, a reduced incidence of bone fractures. Ultimately, the study found disparate results for all cause mortality with hormone replacement, finding it to be lower when HRT was begun during ages 5059, but higher when begun after age 60.[4] Some findings of the WHI were reconfirmed in a larger national study done in the UK, known as The Million Women Study. Coverage of the WHI findings led to a reduction in the number of post-menopausal women on hormone replacement therapy.[11] The authors of the study recommended that women with non-surgical menopause take the lowest feasible dose of HRT, and for the shortest possible time, to minimize risk.[4]

These recommendations have not held up with further data analysis, however. Subsequent findings released by the WHI showed that all cause mortality was not dramatically different between the groups receiving conjugated equine estrogen (CEE), those receiving estrogen and progesterone, and those not on HRT at all. Specifically, the relative risk for all-cause mortality was 1.04 (confidence interval 0.881.22) in the CEE-alone trial and 1.00 (CI, 0.831.19) in the estrogen plus progesterone trial.[12] Further, in analysis pooling data from both trials, post menopausal HRT was associated with a significant reduction in mortality (RR, 0.70; CI, 0.510.96) among women ages 50 to 59. This would represent five fewer deaths per 1000 women per 5 years of therapy.

A robust Bayesian meta-analysis from 19 randomized clinical trials reported similar data with a RR of mortality of 0.73 (CI, 0.520.96) in women younger than age 60.[13] However, MHT had minimal effect among those between 60 and 69 years of age (RR, 1.05; CI, 0.871.26) and was associated with a borderline significant increase in mortality in those between 70 to 79 years of age (RR, 1.14; CI, 0.94 1.37; P for trend < 0.06).[14] Similarly, in the HERS trial, with participants having a mean age of 66.7 yr, MHT did not reduce in total mortality (RR, 1.08; CI, 0.84 1.38).[15] A 2003 meta-analysis of 30 randomized trials of menopausal HRT in relation to mortality showed that it was associated with a nearly 40% reduction in mortality in trials in which participants had a mean age of less than 60 yr or were within 10 yr of menopause onset but was unrelated to mortality in the other trials.[16] The findings in the younger age groups were similar to those in the observational Nurses' Health Study (RR for mortality, 0.63; CI, 0.56 0.70).[9][17]

The beneficial potential of HRT was bolstered in a consensus expert opinion published by the The Endocrine Society, which stated that when taken during perimenopause, or the initial years of menopause, hormonal therapy carries significantly fewer risks than previously published, and reduces all cause mortality in most patient scenarios.[9] The American Association of Clinical Endocrinology released a position statement in 2009 that approved of HRT in the appropriate clinical scenario.

Proprietary mixtures of progestins and conjugated equine estrogens are a commonly prescribed form of HRT. As the most common and longest-prescribed type of estrogen used in HRT, most studies of HRT involve CEE. More recently developed forms of drug delivery include suppositories, subdermal implants, skin patches and gels. They have more local effect, lower doses, fewer side effects and constant rather than cyclical serum hormone levels.[18]

The data published by the WHI suggested supplemental estrogen increased risk of venous emboli and breast cancer but was protective against osteoporosis and colorectal cancer, while the impact on cardiovascular disease was mixed.[19] These results were later confirmed in trials from the United Kingdom, but not in more recent studies from France and China. Genetic polymorphism appears to be associated with inter-individual variability in metabolic response to HRT in postmenopausal women.[20][21]

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CDC – Arthritis – Basics – Definition – Rheumatoid Arthritis

Rheumatoid arthritis (RA) causes premature mortality, disability and compromised quality of life in the industrialized and developing world (1). Rheumatoid arthritis is a systemic inflammatory disease which manifests itself in multiple joints of the body. The inflammatory process primarily affects the lining of the joints (synovial membrane), but can also affect other organs. The inflamed synovium leads to erosions of the cartilage and bone and sometimes joint deformity. Pain, swelling, and redness are common joint manifestations. Although the causes are unknown, RA is believed to be the result of a faulty immune response. RA can begin at any age and is associated with fatigue and prolonged stiffness after rest. There is no cure for RA, but new effective drugs are increasingly available to treat the disease and prevent deformed joints. In addition to medications and surgery, good self-management, including exercise, are known to reduce pain and disability.

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The etiology, or cause, of RA is unknown. Many cases are believed to result from an interaction between genetic factors and environmental exposures.

Socio-demographics: The incidence of RA is typically two to three times higher in women than men. The onset of RA, in both women and men, is highest among those in their sixties(2)

Genetics: There is longstanding evidence that specific HLA class II genotypes are associated with increased risk. Most attention has been given to the DR4 and DRB1 molecules of the major histocompatability complex HLA class II genes. The strongest associations have been found between RA and the DRB1*0401 and DRB1*0404 alleles (12). More recent investigations indicate that of the more than 30 genes studied, the strongest candidate gene is PTPN22, a gene that has been linked to several autoimmune conditions(12).

Modifiable: Several modifiable risk factors have been studied in association with RA including reproductive hormonal exposures, tobacco use, dietary factors, and microbial exposures.

Smoking Among these risk factors, the strongest and most consistent evidence is for an association between smoking and RA. A history of smoking is associated with a modest to moderate (1.3 to 2.4 times) increased risk of RA onset (2). This relationship between smoking and RA is strongest among people who are ACPA-positive (anti-citrullinated protein/peptide antibodies), a marker of auto-immune activity (12).

Reproductive and breastfeeding history Hormones related to reproduction have been studied extensively as potential risk factors for RA:

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CDC - Arthritis - Basics - Definition - Rheumatoid Arthritis

Butyric Acid: An Ancient Controller of Metabolism …

An Interesting Finding

Susceptible strains of rodents fed high-fat diets overeat, gain fat and become profoundly insulin resistant. Dr. Jianping Ye's group recently published a paper showing that the harmful metabolic effects of a high-fat diet (lard and soybean oil) on mice can be prevented, and even reversed, using a short-chain saturated fatty acid called butyric acid (hereafter, butyrate). Here's a graph of the percent body fat over time of the two groups:

The butyrate-fed mice remained lean and avoided metabolic problems. Butyrate increased their energy expenditure by increasing body heat production and modestly increasing physical activity. It also massively increased the function of their mitochondria, the tiny power plants of the cell.

Butyrate lowered their blood cholesterol by approximately 25 percent, and their triglycerides by nearly 50 percent. It lowered their fasting insulin by nearly 50 percent, and increased their insulin sensitivity by nearly 300 percent*. The investigators concluded:

I found this study thought-provoking, so I looked into butyrate further.

Butyrate Suppresses Inflammation in the Gut and Other Tissues

In most animals, the highest concentration of butyrate is found in the gut. That's because it's produced by intestinal bacteria from carbohydrate that the host cannot digest, such as cellulose and pectin. Indigestible carbohydrate is the main form of dietary fiber.

It turns out, butyrate has been around in the mammalian gut for so long that the lining of our large intestine has evolved to use it as its primary source of energy. It does more than just feed the bowel, however. It also has potent anti-inflammatory and anti-cancer effects. So much so, that investigators are using oral butyrate supplements and butyrate enemas to treat inflammatory bowel diseases such as Crohn's and ulcerative colitis. Some investigators are also suggesting that inflammatory bowel disorders may be caused or exacerbated by a deficiency of butyrate in the first place.

Butyrate, and other short-chain fatty acids produced by gut bacteria**, has a remarkable effect on intestinal permeability. In tissue culture and live rats, short-chain fatty acids cause a large and rapid decrease in intestinal permeability. Butyrate, or dietary fiber, prevents the loss of intestinal permeability in rat models of ulcerative colitis. This shows that short-chain fatty acids, including butyrate, play an important role in the maintenance of gut barrier integrity. Impaired gut barrier integrity is associated with many diseases, including fatty liver, heart failure and autoimmune diseases (thanks to Pedro Bastos for this information-- I'll be covering the topic in more detail later).

Butyrate's role doesn't end in the gut. It's absorbed into the circulation, and may exert effects on the rest of the body as well. In human blood immune cells, butyrate is potently anti-inflammatory***.

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Endocarditis – Wikipedia, the free encyclopedia

Endocarditis is an inflammation of the inner layer of the heart, the endocardium. It usually involves the heart valves. Other structures that may be involved include the interventricular septum, the chordae tendineae, the mural endocardium, or the surfaces of intracardiac devices. Endocarditis is characterized by lesions, known as vegetations, which is a mass of platelets, fibrin, microcolonies of microorganisms, and scant inammatory cells.[1] In the subacute form of infective endocarditis, the vegetation may also include a center of granulomatous tissue, which may fibrose or calcify.[2]

There are several ways to classify endocarditis. The simplest classification is based on cause: either infective or non-infective, depending on whether a microorganism is the source of the inflammation or not. Regardless, the diagnosis of endocarditis is based on clinical features, investigations such as an echocardiogram, and blood cultures demonstrating the presence of endocarditis-causing microorganisms. Signs and symptoms include: fever, chills, sweating, malaise, weakness, anorexia, weight loss, splenomegaly, flu like feeling, cardiac murmur, heart failure, patechia of anterior trunk, Janeway's lesions, etc.

Since the valves of the heart do not receive any dedicated blood supply, defensive immune mechanisms (such as white blood cells) cannot directly reach the valves via the bloodstream. If an organism (such as bacteria) attaches to a valve surface and forms a vegetation, the host immune response is blunted. The lack of blood supply to the valves also has implications on treatment, since drugs also have difficulty reaching the infected valve.

Normally, blood flows smoothly past these valves. If they have been damaged (from rheumatic fever, for example) the risk of bacteria attachment is increased.[2]

Rheumatic fever is common worldwide and responsible for many cases of damaged heart valves. Chronic rheumatic heart disease is characterized by repeated inflammation with fibrinous resolution. The cardinal anatomic changes of the valve include leaflet thickening, commissural fusion, and shortening and thickening of the tendinous cords.[3] The recurrence of rheumatic fever is relatively common in the absence of maintenance of low dose antibiotics, especially during the first three to five years after the first episode. Heart complications may be long-term and severe, particularly if valves are involved. While rheumatic fever since the advent of routine penicillin administration for Strep throat has become less common in developed countries, in the older generation and in much of the less-developed world, valvular disease (including mitral valve prolapse, reinfection in the form of valvular endocarditis, and valve rupture) from undertreated rheumatic fever continues to be a problem.[4]

In an Indian hospital between 2004 and 2005, 4 of 24 endocarditis patients failed to demonstrate classic vegetation. All had rheumatic heart disease and presented with prolonged fever. All had severe eccentric mitral regurgitation. (One had severe aortic regurgitation also.) One had flail posterior mitral leaflet.[5]

Nonbacterial thrombotic endocarditis (NBTE), also called marantic endocarditis is most commonly found on previously undamaged valves.[2] As opposed to infective endocarditis, the vegetations in NBTE are small, sterile, and tend to aggregate along the edges of the valve or the cusps.[2] Also unlike infective endocarditis, NBTE does not cause an inflammation response from the body.[2] NBTE usually occurs during a hypercoagulable state such as system wide bacterial infection, or pregnancy, though it is also sometimes seen in patients with venous catheters.[2] NBTE may also occur in patients with cancers, particularly mucinous adenocarcinoma[2] where Trousseau syndrome can be encountered. Typically NBTE does not cause many problems on its own, but parts of the vegetations may break off and embolize to the heart or brain, or they may serve as a focus where bacteria can lodge, thus causing infective endocarditis.[2]

Another form of sterile endocarditis, is termed Libman-Sacks endocarditis; this form occurs more often in patients with lupus erythematosus and is thought to be due to the deposition of immune complexes.[2] Like NBTE, Libman-Sacks endocarditis involves small vegetations, while infective endocarditis is composed of large vegetations.[2] These immune complexes precipitate an inflammation reaction, which helps to differentiate it from NBTE. Also unlike NBTE, Libman-Sacks endocarditis does not seem to have a preferred location of deposition and may form on the undersurfaces of the valves or even on the endocardium.[2]

Examination of suspected infective endocarditis includes a detailed examination of the patient, complete history taking, and especially careful cardiac auscultation, various blood tests, ECG, cardiac ultrasound (echocardiography). In the overall analysis of blood revealed the typical signs of inflammation (increased erythrocyte sedimentation rate, leukocytosis). It is also necessary to sow twice venous blood in order to identify the specific pathogen (this requires two samples of blood). Negative blood cultures, however, does not exclude the diagnosis of infective endocarditis. The decisive role played by echocardiography in the diagnosis (through the anterior chest wall or transesophageal), with which you can reliably establish the presence of microbial vegetation, the degree of valvular and violations of the pumping function of the heart.[6]

Endocarditis at DMOZ

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Endocarditis - Wikipedia, the free encyclopedia

Multiple Sclerosis: MedlinePlus – National Library of Medicine

Multiple sclerosis (MS) is a nervous system disease that affects your brain and spinal cord. It damages the myelin sheath, the material that surrounds and protects your nerve cells. This damage slows down or blocks messages between your brain and your body, leading to the symptoms of MS. They can include

No one knows what causes MS. It may be an autoimmune disease, which happens when your immune system attacks healthy cells in your body by mistake. Multiple sclerosis affects women more than men. It often begins between the ages of 20 and 40. Usually, the disease is mild, but some people lose the ability to write, speak, or walk.

There is no single test for MS. Doctors use a medical history, physical exam, neurological exam, MRI, and other tests to diagnose it. There is no cure for MS, but medicines may slow it down and help control symptoms. Physical and occupational therapy may also help.

NIH: National Institute of Neurological Disorders and Stroke

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Multiple Sclerosis: MedlinePlus - National Library of Medicine

Multiple sclerosis – Wikipedia, the free encyclopedia

Multiple sclerosis (MS), also known as disseminated sclerosis or encephalomyelitis disseminata, is an inflammatory disease in which the insulating covers of nerve cells in the brain and spinal cord are damaged. This damage disrupts the ability of parts of the nervous system to communicate, resulting in a wide range of signs and symptoms,[1][2] including physical, mental,[2] and sometimes psychiatric problems.[3] MS takes several forms, with new symptoms either occurring in isolated attacks (relapsing forms) or building up over time (progressive forms).[4] Between attacks, symptoms may disappear completely; however, permanent neurological problems often occur, especially as the disease advances.[4]

While the cause is not clear, the underlying mechanism is thought to be either destruction by the immune system or failure of the myelin-producing cells.[5] Proposed causes for this include genetics and environmental factors such as infections.[2][6] MS is usually diagnosed based on the presenting signs and symptoms and the results of supporting medical tests.

There is no known cure for multiple sclerosis. Treatments attempt to improve function after an attack and prevent new attacks.[2] Medications used to treat MS while modestly effective can have adverse effects and be poorly tolerated. Many people pursue alternative treatments, despite a lack of evidence. The long-term outcome is difficult to predict, with good outcomes more often seen in women, those who develop the disease early in life, those with a relapsing course, and those who initially experienced few attacks.[7]Life expectancy is on average 5 to 10 years lower than that of an unaffected population.[1]

Multiple sclerosis is the most common autoimmune disorder affecting the central nervous system.[8] As of 2008, between 2 and 2.5 million people are affected globally with rates varying widely in different regions of the world and among different populations.[9] In 2013, 20,000 people died from MS, up from 12,000 in 1990.[10] The disease usually begins between the ages of 20 and 50 and is twice as common in women as in men.[11] The name multiple sclerosis refers to scars (scleraebetter known as plaques or lesions) in particular in the white matter of the brain and spinal cord.[12] MS was first described in 1868 by Jean-Martin Charcot.[12] A number of new treatments and diagnostic methods are under development.

A person with MS can have almost any neurological symptom or sign; with autonomic, visual, motor, and sensory problems being the most common.[1] The specific symptoms are determined by the locations of the lesions within the nervous system, and may include loss of sensitivity or changes in sensation such as tingling, pins and needles or numbness, muscle weakness, very pronounced reflexes, muscle spasms, or difficulty in moving; difficulties with coordination and balance (ataxia); problems with speech or swallowing, visual problems (nystagmus, optic neuritis or double vision), feeling tired, acute or chronic pain, and bladder and bowel difficulties, among others.[1] Difficulties thinking and emotional problems such as depression or unstable mood are also common.[1]Uhthoff's phenomenon, a worsening of symptoms due to exposure to higher than usual temperatures, and Lhermitte's sign, an electrical sensation that runs down the back when bending the neck, are particularly characteristic of MS.[1] The main measure of disability and severity is the expanded disability status scale (EDSS), with other measures such as the multiple sclerosis functional composite being increasingly used in research.[13][14][15]

The condition begins in 85% of cases as a clinically isolated syndrome over a number of days with 45% having motor or sensory problems, 20% having optic neuritis, and 10% having symptoms related to brainstem dysfunction, while the remaining 25% have more than one of the previous difficulties.[16] The course of symptoms occurs in two main patterns initially: either as episodes of sudden worsening that last a few days to months (called relapses, exacerbations, bouts, attacks, or flare-ups) followed by improvement (85% of cases) or as a gradual worsening over time without periods of recovery (10-15% of cases).[11] A combination of these two patterns may also occur[4] or people may start in a relapsing and remitting course that then becomes progressive later on.[11] Relapses are usually not predictable, occurring without warning.[1] Exacerbations rarely occur more frequently than twice per year.[1] Some relapses, however, are preceded by common triggers and they occur more frequently during spring and summer.[17] Similarly, viral infections such as the common cold, influenza, or gastroenteritis increase their risk.[1]Stress may also trigger an attack.[18] Women with MS who become pregnant experience fewer relapses; however, during the first months after delivery the risk increases.[1] Overall, pregnancy does not seem to influence long-term disability.[1] Many events have not been found to affect relapse rates including vaccination, breast feeding,[1] physical trauma,[19] and Uhthoff's phenomenon.[17]

The cause of MS is unknown; however, it is believed to occur as a result of some combination of genetic and environmental factors such as infectious agents.[1] Theories try to combine the data into likely explanations, but none has proved definitive. While there are a number of environmental risk factors and although some are partly modifiable, further research is needed to determine whether their elimination can prevent MS.[20]

MS is more common in people who live farther from the equator, although exceptions exist.[1][21] These exceptions include ethnic groups that are at low risk far from the equator such as the Samis, Amerindians, Canadian Hutterites, New Zealand Mori,[22] and Canada's Inuit,[11] as well as groups that have a relatively high risk close to the equator such as Sardinians,[11] inland Sicilians,[23]Palestinians and Parsis.[22] The cause of this geographical pattern is not clear.[11] While the north-south gradient of incidence is decreasing,[21] as of 2010 it is still present.[11]

MS is more common in regions with northern European populations[1] and the geographic variation may simply reflect the global distribution of these high-risk populations.[11] Decreased sunlight exposure resulting in decreased vitamin D production has also been put forward as an explanation.[24][25][26] A relationship between season of birth and MS lends support to this idea, with fewer people born in the northern hemisphere in November as compared to May being affected later in life.[27] Environmental factors may play a role during childhood, with several studies finding that people who move to a different region of the world before the age of 15 acquire the new region's risk to MS. If migration takes place after age 15, however, the person retains the risk of his home country.[1][20] There is some evidence that the effect of moving may still apply to people older than 15.[1]

MS is not considered a hereditary disease; however, a number of genetic variations have been shown to increase the risk.[28] The probability is higher in relatives of an affected person, with a greater risk among those more closely related.[2] In identical twins both are affected about 30% of the time, while around 5% for non-identical twins and 2.5% of siblings are affected with a lower percentage of half-siblings.[1][2][29] If both parents are affected the risk in their children is 10 times that of the general population.[11] MS is also more c
ommon in some ethnic groups than others.[30]

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Multiple sclerosis - Wikipedia, the free encyclopedia

Autism spectrum – Wikipedia, the free encyclopedia

The autism spectrum or autistic spectrum describes a range of conditions classified as neurodevelopmental disorders in the fifth revision of the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders 5th edition (DSM-5). The DSM-5, published in 2013, redefined the autism spectrum to encompass the previous (DSM-IV-TR) diagnoses of autism, Asperger syndrome, pervasive developmental disorder not otherwise specified (PDD-NOS), and childhood disintegrative disorder.[1] These disorders are characterized by social deficits and communication difficulties, stereotyped or repetitive behaviors and interests, sensory issues, and in some cases, cognitive delays.

A revision to autism spectrum disorder (ASD) was proposed in the Diagnostic and Statistical Manual of Mental Disorders version 5 (DSM-5), released May 2013.[2] The new diagnosis encompasses previous diagnoses of autistic disorder, Asperger's disorder, childhood disintegrative disorder, and PDD-NOS. Rather than categorizing these diagnoses, the DSM-5 will adopt a dimensional approach to diagnosing disorders that fall underneath the autism spectrum umbrella. It is thought that individuals with ASDs are best represented as a single diagnostic category because they demonstrate similar types of symptoms and are better differentiated by clinical specifiers (i.e., dimensions of severity) and associated features (i.e., known genetic disorders, epilepsy and intellectual disability). An additional change to the DSM includes collapsing social and communication deficits into one domain. Thus, an individual with an ASD diagnosis will be described in terms of severity of social communication symptoms, severity of fixated or restricted behaviors or interests and associated features. The restriction of onset age has also been loosened from 3 years of age to "early developmental period", with a note that symptoms may manifest later when demands exceed capabilities.

Autism forms the core of the autism spectrum disorders. Asperger syndrome is closest to autism in signs and likely causes;[3] unlike autism, people with Asperger syndrome have no significant delay in language development.[4] PDD-NOS is diagnosed when the criteria are not met for a more specific disorder. Some sources also include Rett syndrome and childhood disintegrative disorder, which share several signs with autism but may have unrelated causes; other sources differentiate them from ASD, but group all of the above conditions into the pervasive developmental disorders.[3][5]

Autism, Asperger syndrome, and PDD-NOS are sometimes called the autistic disorders instead of ASD,[6] whereas autism itself is often called autistic disorder, childhood autism, or infantile autism.[7] Although the older term pervasive developmental disorder and the newer term autism spectrum disorder largely or entirely overlap,[5] the former was intended to describe a specific set of diagnostic labels, whereas the latter refers to a postulated spectrum disorder linking various conditions.[8] ASD, in turn, is a subset of the broader autism phenotype (BAP), which describes individuals who may not have ASD but do have autistic-like traits, such as avoiding eye contact.[7]

Under the DSM-5, autism is characterized by persistent deficits in social communication and interaction across multiple contexts, as well as restricted, repetitive patterns of behavior, interests, or activities. These deficits are present in early childhood, and lead to clinically significant functional impairment.[9] There is also a unique form of autism called autistic savantism, where a child can display outstanding skills in music, art, and numbers with no practice.[10]

Asperger syndrome was distinguished from autism in the DSM-IV by the lack of delay or deviance in early language development.[11] Additionally, individuals diagnosed with Asperger syndrome did not have significant cognitive delays.[12]PDD-NOS was considered "subthreshold autism" and "atypical autism" because it was often characterized by milder symptoms of autism or symptoms in only one domain (such as social difficulties).[13] In the DSM-5, both of these diagnoses have been subsumed into autism spectrum disorder.[9]

Although autism spectrum disorders are thought to follow two possible developmental courses, most parents report that symptom onset occurred within the first year of life.[14][15] One course of development follows a gradual course of onset in which parents report concerns in development over the first two years of life and diagnosis is made around 34 years of age. Some of the early signs of ASDs in this course include decreased looking at faces, failure to turn when name is called, failure to show interests by showing or pointing, and delayed pretend play.[16] A second course of development is characterized by normal or near-normal development followed by loss of skills or regression in the first 23 years. Regression may occur in a variety of domains, including communication, social, cognitive, and self-help skills; however, the most common regression is loss of language.[17][18] There continues to be a debate over the differential outcomes based on these two developmental courses. Some studies suggest that regression is associated with poorer outcomes and others report no differences between those with early gradual onset and those who experience a regression period.[19] Overall, the prognosis is poor for persons with classical (Kanner-type) autism with respect to academic achievement and poor to below-average for persons across the autism spectrum with respect to independent living abilities; in each case, a lack of early intervention exacerbates the odds against success.[19] However, many individuals show improvements as they grow older. The two best predictors of favorable outcome in autism are the absence of intellectual disability and the development of some communicative speech prior to five years of age.[medical citation needed] Overall, the literature stresses the importance of early intervention in achieving positive longitudinal outcomes.[20]

While a specific cause or specific causes of autism spectrum disorders has yet to be found, many risk factors have been identified in the research literature that may contribute to the development of an ASD. These risk factors include genetics, prenatal and perinatal factors, neuroanatomical abnormalities, and environmental factors. It is possible to identify general risk factors, but much more difficult to pinpoint specific factors. In the current state of knowledge, prediction can only be of a global nature and therefore requires the use of general markers.[21]

The results of family and twin studies suggest that genetic factors play a role in the etiology of autism and other pervasive developmental disorders.[22] Studies have consistently found that the prevalence of autism in siblings of autistic children is approximately 15 to 30 times greater than the rate in the general population.[23] In addition, research suggests that there is a much higher concordance rate among monozygotic twins compared to dizygotic twins.[24] It appears that there is no single gene that can account for autism. Instead, there seem to be multiple genes involved, each of which is a risk factor for part of the autism syndrome through various groups.[25][26][27]

A number of prenatal and perinatal complications have been reported as possible risk factors for autism. These risk factors include maternal gestational diabetes, maternal and paternal age over 30, bleeding after first trimester, use of prescription medication (e.g. valproate
) during pregnancy, and meconium in the amniotic fluid. While research is not conclusive on the relation of these factors to autism, each of these factors has been identified more frequently in autistic children compared to their non-autistic siblings and other normally developing youth.[30]

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Autism spectrum - Wikipedia, the free encyclopedia

Stem cell – Wikipedia, the free encyclopedia

Stem cells are undifferentiated biological cells that can differentiate into specialized cells and can divide (through mitosis) to produce more stem cells. They are found in multicellular organisms. In mammals, there are two broad types of stem cells: embryonic stem cells, which are isolated from the inner cell mass of blastocysts, and adult stem cells, which are found in various tissues. In adult organisms, stem cells and progenitor cells act as a repair system for the body, replenishing adult tissues. In a developing embryo, stem cells can differentiate into all the specialized cellsectoderm, endoderm and mesoderm (see induced pluripotent stem cells)but also maintain the normal turnover of regenerative organs, such as blood, skin, or intestinal tissues.

There are three known accessible sources of autologous adult stem cells in humans:

Stem cells can also be taken from umbilical cord blood just after birth. Of all stem cell types, autologous harvesting involves the least risk. By definition, autologous cells are obtained from one's own body, just as one may bank his or her own blood for elective surgical procedures.

Adult stem cells are frequently used in medical therapies, for example in bone marrow transplantation. Stem cells can now be artificially grown and transformed (differentiated) into specialized cell types with characteristics consistent with cells of various tissues such as muscles or nerves. Embryonic cell lines and autologous embryonic stem cells generated through Somatic-cell nuclear transfer or dedifferentiation have also been proposed as promising candidates for future therapies.[1] Research into stem cells grew out of findings by Ernest A. McCulloch and James E. Till at the University of Toronto in the 1960s.[2][3]

The classical definition of a stem cell requires that it possess two properties:

Two mechanisms exist to ensure that a stem cell population is maintained:

Potency specifies the differentiation potential (the potential to differentiate into different cell types) of the stem cell.[4]

In practice, stem cells are identified by whether they can regenerate tissue. For example, the defining test for bone marrow or hematopoietic stem cells (HSCs) is the ability to transplant the cells and save an individual without HSCs. This demonstrates that the cells can produce new blood cells over a long term. It should also be possible to isolate stem cells from the transplanted individual, which can themselves be transplanted into another individual without HSCs, demonstrating that the stem cell was able to self-renew.

Properties of stem cells can be illustrated in vitro, using methods such as clonogenic assays, in which single cells are assessed for their ability to differentiate and self-renew.[7][8] Stem cells can also be isolated by their possession of a distinctive set of cell surface markers. However, in vitro culture conditions can alter the behavior of cells, making it unclear whether the cells will behave in a similar manner in vivo. There is considerable debate as to whether some proposed adult cell populations are truly stem cells.

Embryonic stem (ES) cells are stem cells derived from the inner cell mass of a blastocyst, an early-stage embryo.[9] Human embryos reach the blastocyst stage 45 days post fertilization, at which time they consist of 50150 cells. ES cells are pluripotent and give rise during development to all derivatives of the three primary germ layers: ectoderm, endoderm and mesoderm. In other words, they can develop into each of the more than 200 cell types of the adult body when given sufficient and necessary stimulation for a specific cell type. They do not contribute to the extra-embryonic membranes or the placenta.

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Stem cell - Wikipedia, the free encyclopedia

The menopause – Netdoctor

Reviewed byDrJeniWorden, GP

The menopause, also called the change of life, is defined as the end of the last menstrual period.

In Western women, it occurs on average at 51 years, but there's a wide range extending from your 30s to 60s.

Going through the menopause before the age of 40 is known as premature menopause and between 41 and 45 as early menopause.

The menopause occurs when the ovaries no longer respond to the controlling hormones released by the pituitary gland of the brain.

As a result, the ovaries fail to release an egg each month and to produce the female sex hormones oestrogen and progesterone.

It is the fall in the levels of these hormones in the bloodstream that gives rise to the symptoms of menopause.

Research into the menopause is relatively recent. One hundred years ago, when life expectancy was shorter, most women did not live long after the menopause and so little was known about it.

Many women experience symptoms of the menopause and irregular periods for several years up to the menopause itself.

This is called the climacteric, or 'perimenopause', and represents the gradual decline in the normal function of the ovaries.

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The menopause - Netdoctor

Menopause – Symptoms – NHS Choices

The menopause can cause a wide range of physical and psychological symptoms.

The first symptom is usually a change in the pattern of your monthly periods.

The start of the menopause is known as the perimenopausal stage, during which you may have light or heavy periods (menorrhagia).

The frequency of your periods may also be affected. You may have one every two or three weeks, or you may not have one for months at a time.

Other menopausal symptoms include:

It's difficult to predict how long the menopause will last because it affects each woman differently.

The severity of symptoms and the overallduration of the menopause will vary depending on a number of factors including genetics, lifestyle, diet, stress and overall health.

The perimenopause (the initial stage) may only last for a few months or for some women it may continue for as long as 10 years. The average duration of the perimenopause is around four years.The perimenopause ends when a woman has gone 12 months without having a period.

Vaginal symptoms, such as dryness, can sometimes persist and get worse with age.

If you experience the menopause suddenly, rather than gradually, your symptoms may be worse.

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Menopause - Symptoms - NHS Choices

Frequently asked HYPOPITUITARY questions….and their …

Home Frequently asked HYPOPITUITARY questions.and their answers

When not on any thyroid meds, you find yourself with a very low TSH lab (the TSH is a pituitary hormone), yet you have a low free T3, plus hypothyroid symptoms, you may have hypopituitarism.

Here are the most frequently asked questions concerning this condition, created by Chris, a hypopituitary patient who has worked with other hypopituitary patients for several years. Please note these are quick general answers so its recommended you do your own research to learn more. You can also join Chriss Hypopituitary Support Group on Yahoo. It is closed to posting, but you can join to access the great deal of information it contains, including over 500 links and 100 files.

1) What is hypopituitarism? 2) What are symptoms of hypopituitarism? 3) What causes hypopituitarism? 4) Is adrenal and/or thyroid treatment different if I am hypopituitary? 5) What labs will detect hypopituitarism? 6) If I cant afford all those labs, can you tell just from TSH? DHEA? 7) Can you detect hypopituitarism from saliva cortisol labs? 8 ) Im already on HC, can I test cortisol or ACTH levels? 9) Is there any test for hypopituitarism once Im already on HC? 10) If one pituitary hormone is low, does that mean all of them are? 11) My Dr or Insurance wont approve further tests what should I do? 12) Should I start treating the sex hormones right away? 13) Is hypopituitarism curable? 14) My doctor says my cortisol doubled during the ACTH stimulation test, so I am ok-is he right? 15) Could I have a pituitary tumor? Should I get an MRI? Is it gonna grow? Will I need an operation? 16) Are there shades of Gray on this? Does someone get sort-of hypo-pit, then then next guys labs even more so, then finally one sets off the buzzer and gets a definitive label of Hypo-Pit? 1) What is hypopituitarism? Hypopituitary is the pituitary gland functioning below where it needs to be, and one or more hormones can be involved. The pituitary is a pea sized gland located at the base of the brain and it runs the adrenals, thyroid, and sex hormones. It also produces growth hormone and stores oxytocin and vasopressin, both of which are made in the hypothalamus. If the pituitary doesnt put out enough TSH, thyroid hormone production can decrease. It the pituitary doesnt produce enough ACTH, cortisol (and DHEA) can decrease. 2) What are the symptoms of hypopituitarism? Because the pituitary may not be sending adequate levels of TSH and or ACTH, you could feel fatigue, weakness, have low blood pressure, feel colder than normal, have a decrease in your appetite, headaches, and depression. Symptoms of hypopit (concerning low TSH, low ACTH, low LH and FSH) are the same as if thyroid-adrenals-gonads are the cause. In most cases you cant tell by symptoms if you may be hypopituitary or not. If you arent getting enough ACTH, you could have symptoms of weight loss and nausea, plus the fatigue, low blood pressure, weakness, and depression. Because of a deficiency of TSH and LH, women could lose their periods, or have problems conceiving. Men could have a decreased libido, erectile dysfunction, and loss of facial hair. If hypopituitary occurs in childhood, the result can be a short stature. Thirst and increased need to urinate can occur is you have an ADH deficiency. (Note: a large body of hypothyroid patients have a low normal TSH without hypopituitarism. Why? Because the man-made TSH lab is often slow to reveal the hypothyroid state. Those with hypopituitarism will often have a TSH at 0.8 and lower for women, and 1.8 and lower for men, with accompanying hypo symptoms. See #5 and 6 below.)

3) What causes hypopituitarism? A common cause of hypopituitarism is head injury. Even a seemingly mild bump to the head can damage the pituitary. A Pituitary tumor can also cause hypopituitary, though perhaps less than 3 percent have this as a cause. Sheehans syndrome is another cause, which is any type of blood loss, and where the pituitary at least partially dies from the lack of blood. Blood loss from childbirth, or an injury can result in Sheehans syndrome. Other causes can be radiation, antibody attack, and environmental. In most cases, it can not be known for sure what the cause is.

4) Is adrenal and/or thyroid treatment different if I am hypopituitary? In treating the adrenals and thyroid caused by low ACTH (secondary AI) and low TSH (secondary hypothyroid), treatment is the same as it is for primary Adrenal Insufficiency and primary hypothyroid. Sex hormone treatment can be different with the use of HCG (almost identical to LH) in secondaries hypogonadism (low LH and FSH production in the pituitary which will cause low sex hormones in men and women), whereas primary hypogonadism involves the gonads being the cause of low sex hormones, LH and FSH will go up. The treatment for primary hypogonadism is the use of testosterone (in men, sometimes along with estrogen blocker) and estrogen, progesterone and even testosterone in women. Some men with primary hypogonadism also use HCG, but is rarely used in women.

5) What labs will detect hypopituitarism? -low TSH (below 1.8 for men, below 0.8 for women) -low ACTH (below 30 for am. Is possible to be secondary with ACTH as high as low 40s) -ACTH stimulation or ITT that doubles cortisol from a low base value. -ITT for GH stim -low GHRH -low TRH -low vasopressin (hypothalamic hormone which is stored in the pituitary) -low renin and low aldosterone -very low or below range prolactin-usually this test is inconclusive for determing if other low pituitary hormones could be present. -low oxytocin (rarely tested, is a hypothalamic hormone which isstored and released from the pituitary) -alpha MSH (rarely tested, is a byproduct of ACTH) 6) If I cant afford all those labs, can you tell just from TSH? DHEA? If not on any thyroid treatment, I go by the TSH: less than .8 for women, less than 1.8 for men for determining secondary hypothyroid. I use 1.3 and above for women and 2.2 and above for men to determine primary hypo. In between .8 and 1.3 for women and 1.8 and 2.2 for men is less certain to whether secondary or not. A serum TRH and TRH STIM can help if you fall in that grey area. DHEA, if in the lower half of the range usually, but not always, indicates possible secondary adrenal insufficiency. Serum ACTH and ACTH STIM are the best tests for determining if secondary. If one has already started steroid without proper testing, the next best test for determining secondary AI is the renin test.

7) Can you detect hypopituitarism from saliva cortisol labs? No, because the test only shows what cortisol levels are, not what ACTH levels are doing. There is no saliva lab for ACTH as far as I know. 8 ) Im already on hydrocortisone (HC), can I test cortisol and or ACTH levels? No, once steroid is started, those tests are not reliable. In every case Ive seen where a doctor uses these tests for dosing a patients cortisol replacement, the patient was left undertreated. ACTH will go to pretty much zero in proper cortisol dosing.

9) Is there any test for hypopituitarism once started on HC? For detecting secondary (low ACTH) AI when proper testing hasnt been done (serum acth, DHEA-S, acth stimulation test), the renin test (with aldosterone) is the next best thing and is highly reliable if the test is done right (fast salt for 24 hours). Renin is low 99% of the time in secondaries.seehttp://www.ncbi.nlm.nih.gov/pubmed/518024

10) If one pituitary hormone is low, does that mean all of them are? In more than 99% of cases of hypopituitary, 2 to 3 pituitary hormones will be deficie
nt. Keep in mind interpreting tests is subjective. One doc like an osteopath (US) may see problems, an endocrinologist will probably will say your tests are ok. When all pituitary hormones are deficient to missing, this is called panhypopituitarism. True panhypopituitarism is fairly rare. Some definitions say not all pituitary hormones have to be deficient, but most. I go by the the strict definition all pituitary hormones being deficient or absent in the anterior pituitary. Ive seen one case of real panhypopituitarism.

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Frequently asked HYPOPITUITARY questions....and their ...

Hypothyroidism – In-Depth Report – NY Times Health

In-Depth From A.D.A.M. Background

The thyroid is a small, butterfly-shaped gland located in the front of the neck that produces hormones, notably thyroxine (T4) and triiodothyronine (T3), which stimulate vital processes in every part of the body. These thyroid hormones have a major impact on the following functions:

These hormones can also alter the actions of other hormones and drugs.

The thyroid gland, a part of the endocrine (hormone) system, plays a major role in regulating the body's metabolism.

Regulating thyroid function is a complex and important process that involves several factors, including iodide and four thyroid hormones. Any abnormality in this intricate system of hormone synthesis and production can have far-reaching consequences on health.

Iodide. An understanding of the multi-step thyroid hormone process begins with iodide, a salt that is extracted from the blood and trapped by the thyroid gland. Iodide is converted to iodine in the thyroid gland. (Eighty percent of the body's iodine supply is stored here.) Iodine is the material used to make the hormone thyroxine (T4).

Thyroid Hormones. Four hormones are critical in the regulation of thyroid function:

Hypothyroidism occurs when thyroxine (T4) levels drop so low that body processes begin to slow down. Hypothyroidism was first diagnosed in the late nineteenth century when doctors observed that surgical removal of the thyroid resulted in the swelling of the hands, face, feet, and tissues around the eyes. They named this syndrome myxedema and correctly concluded that it was the outcome of the absence of substances, thyroid hormones, normally produced by the thyroid gland. Hypothyroidism is usually progressive and irreversible. Treatment, however, is nearly always completely successful and allows a patient to live a fully normal life.

Hypothyroidism is separated into either overt or subclinical disease. That diagnosis is determined on the basis of the TSH laboratory blood tests. The normal range of TSH concentration falls between 0.45 - 4.5 mU/L.

Subclinical, or mild, hypothyroidism (mildly underactive thyroid), also called early-stage hypothyroidism, is a condition in which thyrotropin (TSH) levels have started to increase in response to an early decline in T4 levels in the thyroid. However, blood tests for T4 are still normal. The patient may have mild symptoms (usually slight fatigue) or none at all. Mildly underactive thyroid is very common (affecting about 10 million Americans) and is a topic of considerable debate among professionals because it is not clear how to manage this condition.

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Hypothyroidism - In-Depth Report - NY Times Health

Adult Hypothyroidism – Thyroid Disease Manager

The full-blown expression of hypothyroidism is known as myxedema. Adult myxedema escaped serious attention until Gull described it in 1874 1 . That it was a state resembling the familiar endemic cretinism, but coming on in adult life, was what chiefly impressed Gull. Ord 2 invented the term myxedema in 1873. The disorder arising from surgical removal of the thyroid gland (cachexia strumipriva) was described in 1882 by Reverdin 3 of Geneva and in 1883 by Kocher of Berne 4 . After Gulls description, myxedma aroused enormous interest, and in 1883 the Clinical Society of London appointed a committee to study the disease and report its findings 5 . The committees report, published in 1888, contains a significant portion of what is known today about the clinical and pathologic aspects of myxedema. It is referred to in the following discussion as the Report on Myxedema. The final conclusions of the 200-page volume are penetrating. They are as follows:

1. That myxedema is a well-defined disease.

2. That the disease affects women much more frequently than men, and that the subjects are for the most part of middle age.

3. That clinical and pathological observations, respectively, indicate in a decisive way that the one condition common to all cases is destructive change of the thyroid gland.

4. That the most common form of destructive change of the thyroid gland consists in the substitution of a delicate fibrous tissue for the proper glandular structure.

5. That the interstitial development of fibrous tissue is also observed very frequently in the skin, and, with much less frequency, in the viscera, the appearances presented by this tissue being suggestive of an irritative or inflammatory process.

6. That pathological observation, while showing cause for the changes in the skin observed during life, for the falling off the hair, and the loss of the teeth, for the increased bulk of body, as due to the excess of subcutaneous fat, affords no explanation of the affections of speech, movement, sensation, consciousness, and intellect, which form a large part of the symptoms of the disease.

7. That chemical examination of the comparatively few available cases fails to show the general existence of an excess of mucin in the tissues adequately corresponding to the amount recorded in the first observation, but that this discrepancy may be, in part, attributed to the fact that tumefaction of the integuments, although generally characteristic of myxedema, varies considerably throughout the course of the disease, and often disappears shortly before death.

8. That in experiments made upon animals, particularly on monkeys, symptoms resembling in a very close and remarkable way those of myxedema have followed complete removal of the thyroid gland, performed under antiseptic precautions, and with, as far as could be ascertained, no injury to the adjacent nerves or to the trachea.

9. That in such experimental cases a large excess of mucin has been found to be present in the skin, fibrous tissues, blood, and salivary glands; in particular the parotid gland, normally containing no mucin, has presented that substance in quantities corresponding to what would be ordinarily found in the submaxillary gland.

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Adult Hypothyroidism - Thyroid Disease Manager

Symptoms Of Andropause (Male Menopause) Renew Man

The Symptoms Of Andropause (Male Menopause) Include:

Click on any of the symptoms listed above to learn more about each one.

By your early 30s, the hormones that give you energy, boost your sex drive, and allow you to build lean muscle mass, begin to decline. For men, testosterone is the anti-aging hormone. Its what allows you to maintain muscle mass and strength. It also fuels your sex drive, and facilitates bone growth. It keeps your moods even, and enables you to focus and concentrate. It keeps men motivated, and fuels their desire to be productive and to succeed.

But as you age, testosterone levels begin to diminish. This is when men experience the symptoms of andropause. If youre experiencing any of the symptoms shown above, you may be andropausal.

Its important to remember that all men will experience andropause and the symptoms that come with it at some point in their lives. Its unavoidable. In fact, the U.S. Census Bureau estimates that 100% of men over age 50 will experience at least some symptoms of hormone imbalance. To see if youre likely to be experiencing the symptoms of andropause, depending upon your age, please see the chart below:

Percentage of Men Experiencing Andropause Symptoms Based On Age

Men age 30+: 10% Men age 35+: 25% Men age 40+: 50% Men age 45+: 75% Men age 50+: 100%

If youre experiencing any of the symptoms listed above, you should consider learning more about hormone therapy for men. Low testosterone and hormone imbalance are easily and safely corrected if done properly, and if done under the care of a qualified physician. With one of our physician-supervised, uniquely individualized hormone treatment programs, you can start to feel like a new man 2-6 weeks after hormones are restored to healthy levels.

If youd like to know just how male hormone therapy can help you overcome your andropause symptoms, please click here.

Or contact us with your questions. Call us at 800-859-7511, or request a consultation through our contact form.

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Symptoms Of Andropause (Male Menopause) Renew Man

Andropause – Male menopause – Symptoms – Causes …

Andropause is the male equivalent of female menopause. It is generally characterized by a decline in sexuality and energy due to the decreasing level of male hormones, such as testosterone.

We all know about the female menopause but how many of us have heard of andropause, considered by some as the male menopause?

Mid-life crisis is the euphemism of choice that is used to refer to the symptoms of a waning male. Today, it has been widely accepted by the scientific world that males encounter andropause- a term that refers to the paucity of vital male hormones. This, in turn, leads to an array of symptoms -from feeling blue to low libido.

Andropause refers to the biological changes that men in mid-life experience; some like to compare this state with the female menopause. These changes are not universal and males continue to reproduce well into their old age.

'Men do not quit playing because they grow old; they grow old because they quit playing.' - Oliver Wendell Holmes

Andropause was first described medically, in the 1940's, but was not accepted by the medical fraternity until recently. The term, andropause is not recognized by WHO and its ICD-10 medical classification.

Approximately, 25 million American males aged between 40 and 55 years are currently experiencing the symptoms of andropause.

During Andropause, the levels of the hormones testosterone and dehydroepiandrosterone are diminished. As a consequence of this drop, the individual may experience -loss of concentration, low energy levels, fatigue, change in attitude, depression, low libido, and mood swings. Even healthy males experience these symptoms. It is not clear if hereditary factors, enviornment or lifestyle are associated with andropause.

Research reveals that low testosterone levels also predisposes an individual to health problems, such as heart disease and osteoporosis.

Andropause was an under diagnosed and under treated health condition. Today there is a lot of improvement in understanding and managing this condition. Simple blood tests diagnose this disorder. Treatment is carried out through Hormone Replacement Therapy (HRT).

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Andropause - Male menopause - Symptoms - Causes ...

Andropause / Male Menopause – Treatment – Medindia

The treatment of choice for andropause includes Testosterone Replacement Therapy. Some experts feel that a holistic approach is the key to the management of andropause.

The treatment of choice for andropause includes Testosterone Replacement Therapy (TRT) for men with reduced levels of testosterone. Although this is still a controversial area it was found that many patients benefitted immensely from the treatment. Some of the benefits include:

Improvement in attitude Increase in self-confidence and self-esteem Increased energy levels Enhanced concentration, cognition Enhanced mood and sense of well being Enhanced libido and sexual performance Improvement in mood and sense of well-being Improved sleep Increase in physical fitness

Testosterone replacement is not a benign treatment and must be carried out according to the advise of the doctor. Men getting TRT should be regularly monitored for prostate cancer.

Other risks from the treatment include stroke, breast development, and impairment in sperm production and liver toxicity.

Testosterone treatment should be completely avoided in the case of breast cancer (in males) and Prostate cancer.

It must be carried out according to the advise of a doctor in case of the following conditions:

Liver /heart/blood vessel /kidney disease Edema Diabetes mellitus Enlarged prostate

In the presence of certain catalysts, the aromatase enzyme found in the human body converts testosterone into the female hormone estrogen. Grapes, fatty substances and alcohol act as these catalysts.

Vitamin C and Zinc are recommended for andropausal men.

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Andropause / Male Menopause - Treatment - Medindia

Eczema: Read About Treatment of Various Eczema Types

Eczema facts What is eczema?

Rather than a specific condition, eczema is a group of unrelated diseases that have a similar appearance. When it is new eczema, the affected skin appears red and elevated with small blisters (vesicles) containing a clear fluid. When the blisters break, the affected skin will weep and ooze. In older eczema, chronic eczema, the blisters are less prominent and the skin is thickened, elevated, and scaling. Eczema almost always is very itchy.

There are at least 11 different types of skin conditions that produce eczema. In order to develop a rational treatment plan, it is important to distinguish them. This is often not easy.

Medically Reviewed by a Doctor on 1/26/2015

Eczema - Treatment Question: What treatment has been effective for your eczema?

Eczema - Symptoms and Signs Question: What were your eczema symptoms and signs?

Eczema - Experience Question: Please describe your experience with eczema.

Eczema - Home Remedies Question: What home remedies have been effective for your eczema?

Eczema - Types Question: What type of eczema did you have, and what causes eczema?

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Eczema: Read About Treatment of Various Eczema Types

Eczema: Read About Symptoms, Treatment and Causes

Eczema (Atopic Dermatitis) Eczema Overview

The term eczema is derived from the Greek, meaning "to boil out." The name is particularly apt since to ancient medical practitioners it may have appeared that the skin was "boiling." Today the usage is rather imprecise since this term is frequently used to describe any sort of dermatitis (inflammatory skin condition). But not all dermatitis is eczematous. All eczematous dermatitis, whether due to a familial atopic dermatitis or an acquired allergic contact dermatitis, has a similar appearance. Acute lesions are composed of many small fluid-filled structures called vesicles that usually reside on red, swollen skin. When these vesicles break, clear or yellowish fluid leaks out, causing characteristic weeping and oozing. When the fluid dries, it produces a thin crust which may mimic impetigo. In older lesions, these vesicles may be harder to appreciate, but an examination of the tissue under the microscope will reveal their presence. Eczematous dermatitis has many causes. One of the most common is a condition called atopic dermatitis. Often those using the term eczema are referring to atopic dermatitis. Although atopy refers to a lifelong inherited (genetic) predisposition to inhalant allergies such as asthma and allergic rhinitis (hay fever), atopic dermatitis is not known at this time to be a pure allergic disease. Atopic patients are likely to have asthma, hay fever, and dermatitis. Atopy is a very common condition, and it affects all races and ages, including infants. About 1%-2% of adults have the skin rash, and it is even more common in children. Most affected individuals have their first episode before 5 years of age. For most, the dermatitis will improve with time. For an unlucky few, atopic dermatitis is a chronic, recurrent disorder.

Other eczematous dermatoses include, but are not limited to, allergic contact dermatitis (cell-mediated allergy to a common substance such as poison oak or nickel), irritant dermatitis (from excessive contact with a harsh chemical substance), fungal infections, scabies infestations, stasis dermatitis, very dry skin (asteatosis), pompholyx (dyshidrosis), nummular dermatitis, and seborrheic dermatitis. The differentiation among these conditions is often difficult and time consuming. In addition, it is not uncommon for atopic dermatitis to coexist with another eczematous dermatitis.

Medically Reviewed by a Doctor on 5/12/2015

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