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- 73

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, 2 2007

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, 1 2007

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, 27 2007

- 68

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, 18 2007

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, 13 2007

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, 2 2007

- 55

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, 30 2007

- 54

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, 29 2007

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, 27 2007

52 -

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, 22 2007

- 47


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, 21 2007

- 43

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, 21 2007

- 42

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, 20 2007

- 41

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, 19 2007

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, 18 2007

- 38

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, 18 2007

37 -

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, 17 2007

34 - med article - Obesity-Testosterone

Reuters Health

Wednesday, March 14, 2007

NEW YORK (Reuters Health) - Gaining too much weight can accelerate the decline in testosterone levels that accompanies aging, a new study shows.

"Although hormone declines appear to be an integral aspect of the aging process, rapid declines need not be dismissed as inevitable," the researchers conclude.

Men's testosterone levels fall as they get older, which may contribute to health problems such as diabetes, loss of bone and muscle mass, and sexual dysfunction, Dr. Thomas G. Travison of New England Research Institutes in Watertown, Massachusetts and colleagues note in a report in The Journal of Clinical Endocrinology and Metabolism.

To better understand how much of the decline in testosterone over time is due to aging and how much might be related to health and lifestyle changes, the researchers looked at data for 1,667 men 40 to 70 years old followed from 1987-1989 to 2002-2004. They were able to gather data for the entire time period on 35 percent, or 584, of the men.

Sharper declines in testosterone occurred among men who developed a chronic illness during the course of the study, those who lost a spouse, those who began taking six or more medications, and those who quit smoking, the researchers found.

And adding 4 to 5 points to one's body mass index (BMI) -- a tool used to determine how fat or thin a person is -- resulted in a drop in testosterone levels similar to that seen over 10 years of aging.

On average, the men experienced a 14.5 percent drop in total testosterone levels for every decade of life and a 27 percent reduction in free testosterone, but when the researchers looked at a subset of men who were completely healthy throughout the course of the study, declines in total and free testosterone were 10.5 percent and 22.8 percent, respectively. This suggests, the researchers say, that a "substantial proportion" of testosterone decline is due to changes in health.

"These results suggest the possibility that age-related hormone decline may be decelerated through the management of health and lifestyle factors," they conclude.

SOURCE: The Journal of Clinical Endocrinology and Metabolism, February 2007.


, 16 2007

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, 16 2007

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, 12 2006

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, 4 2006

30 -

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, 30 2006

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, 27 2006

28 - med articles - Parathyroids

The sole purpose of the parathyroid glands is to control calcium within the blood in a very tight range between 8.5 and 10.2. In doing so, parathyroids also control how much calcium is in the bones, and therefore, how strong and dense the bones are. Although the parathyroid glands are located next to (and sometimes inside) the thyroid gland, they have no related function. The thyroid gland regulates the body's metabolism and has no effect on calcium levels while parathyroid glands regulate calcium levels and have no effect on metabolism.Calcium is the element that allows the normal conduction of electrical currents along nerves--its how our nervous system works and how one nerve 'talks' to the next. Our entire brain works by fluxes of calcium into and out of the nerve cells.Calcium is also the primary element which causes muscles to contract.

Knowing these two major functions of calcium helps explain why people can get a tingling sensation in their fingers or cramps in the muscles of their hands when calcium levels dropbelow normal. A sudden drop in the calcium level (like after a successful parathyroid operation where the patient doesn't take their calcium pills for the first few days after the surgery) can cause patients to feel "foggy", "weird" or "confused like my brain isn't working correctly". The brain DEMANDS a normal steady-state calcium level, so any change in the amount of calcium can cause the brain to feel un-loved and the patient to feel bad. Likewise, too much parathyroid hormone causes too high a calcium level--and this can make a person feel run down, cause them to sleep poorly, make them more irritable than usual, and even cause a decrease in memory. In fact, the most common symptoms for patients with parathyroid disease are related to the brain, and include depression and lack of energy! Even though one fourth of patients with this disease will state that they feel just fine, after an operation more than 85 percent of these patients will claim to "feel much better"! Some say its like "someone turned the lights on". REMEMBER: Even though you may think you have no symptoms from your calcium level being too high, nearly everybody feels better after the operation. Go to the page onSymptoms of Hyperparathyroidism to lean more.

NORMAL PARATHYROID ACTIVITY

Although the four parathyroid glands are quite small, they have a very rich blood supply. This suits them well since they are required to monitor the calcium level in the blood 24 hours a day. As the blood filters through the parathyroid glands, they detect the amount of calcium present in the blood and react by making more or less parathyroid hormone (PTH). When the calcium level in the blood is too low, the cells of the parathyroids sense it and make more parathyroid hormone. Once the parathyroid hormone is released into the blood, it circulates to act in a number of places to increase the amount of calcium in the blood (like removing calcium from bones). When the calcium level in the blood is too high, the cells of the parathyroids make less parathyroid hormone (or stop making it altogether), thereby allowing calcium levels to decrease. This feed-back mechanism runs constantly, thereby maintaining calcium (and parathyroid hormone) in a very narrow "normal" range. In a normal person with normal parathyroid glands, their parathyroid glands will turn on and off dozens of times per day...in an attempt to keep the calcium level in the normal range so our brain and muscles function properly.

HOW DOES PARATHYROID HORMONE INCREASE BLOOD CALCIUM ?

Like all endocrine glands, parathyroids make a hormone (a small protein capable of causing distant cells in the body to react in a specific manner). Parathyroid hormone (PTH) has a very powerful influence on the cells of the bones which causes them to release their calcium into the bloodstream. Calcium is the main structural component of bones which give them their rigidity--, the principle purpose of the bones is to provide a storage system for calcium--so our brain will never be without calcium. Under the presence of parathyroid hormone, bones will give up their calcium in an attempt to increase the blood level of calcium. Under normal conditions, this process is very highly tuned and the amount of calcium in our bones remains at a normal high level. Under the presence of too much parathyroid hormone, however, the bones will continue to release their calcium into the blood at a rate which is too high resulting in bones which have too little calcium. This condition is called osteopenia and osteoporosis and is illustrated in the bone segment on the top which has larger "pores" and less bone mass. When bones are exposed to high levels of parathyroid hormone for several years they become brittle and much more prone to fractures. Another way in which the parathyroid hormone acts to increase blood levels of calcium is through its influence on the intestines. Under the presence of parathyroid hormone the lining of the intestine becomes more efficient at absorbing calcium normally found in our diet.


, 27 2006

27 -

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http://www.mednet.gr/greek/soc/ede/diab76.htm


, 23 2006

26 - med articles - Self Injury

Many people with eating disorders also engage in the act of self-injury. Just like

the eating disorders are used to help the individual cope,

the act of injuring oneself is also used to help cope with, block out,

and release built up feelings and emotions.

Self-injury is probably the most widely misunderstood

forms of self harm and there are many myths

associated with it, which can make it difficult for people to

reach out and ask for help.

Self-injury (self-harm, self-mutilation)

can be defined as the attempt to deliberately cause

harm to one's own body and the injury is usually

severe enough to cause tissue damage.

This is not a conscious attempt at suicide,

though some people may see it that way.

It has been reported that many people who self-injure

have a history of sexual or physical abuse,

but that is not always the case.

Some may come from broken homes, alcoholic homes,

have emotionally absent parents, etc.

There are many factors that could cause someone

to self-injure as a way to cope.

There are three types of self-injury. The rarest and most

extreme form is Major self-mutilation.

This form usually results in permanent disfigurement, i.e.

castration or limb amputation.

Another form is Stereo typic self-mutilation which usually

consists of head banging, eyeball pressing and biting.

The third and most common form is Superficial

self-mutilation which usually involves cutting, burning,

hair-pulling, bone breaking, hitting, interference

with wound healing and basically any method used to harm oneself.

Most people who self-injure tend to be perfectionists,

are unable to handle intense feelings,

are unable to express their emotions verbally, have dislike for

themselves and their bodies, and can experience severe mood swings.

They may turn to self-injury as a way to express their feelings

and emotions, or as a way to punish themselves.

You may be wondering why someone would intentionally

harm themselves. Self-injury can help someone

relieve intense feelings such as anger, sadness,

loneliness, shame, guilt and emotional pain.

Many people who cut themselves, do this in an attempt

to try and release all the emotions they are feeling internally.

Others may feel so numb, that seeing their own

blood when they cut themselves, helps them to feel

alive because they usually feel so dead inside.

Some people find that dealing with physical pain

is easier than dealing with emotional pain.

Self-injury is also used as a way to punish oneself.

If they were abused, they may feel ashamed,

guilty and blame themselves for the abuse,

which in turn causes them to feel the need to punish

themselves by inflicting pain to their bodies.

Some people have such hatred for themselves

and their bodies that they will carve demeaning

names on their bodies as a way to remind themselves

of how terrible they are. Whatever form of self-injury is used,

the person is usually left with a peaceful and calm feeling

afterwards. Since those feelings are only temporary,

the person will probably continue to self-injure

until they deal with the underlying issues

and finds healthier ways to cope.

Many people who self-injure keep it a secret because they feel like they are crazy,

insane and evil. They fear if they tell anyone,

they might be locked away forever. The truth is,

people who intentionally harm themselves are in fact very normal

and sane people, who are in a lot of emotional pain.

They self-injure as a way to cope, because they were probably

never taught how to deal with intense feelings and emotions

in healthy ways. Unfortunately, when people hear about this form

of self-harm, they do tend to place labels on these people

as being psychotic and crazy, which is why so many people

do not come forward and ask for help.

Until society dispels all the myths surrounding self-injury

and start to educate themselves on this subject,

sufferers will continue to keep quiet and this form of abuse

will continue to be a secret for a long time to come.

http://www.mirror-mirror.org/selfinj.htm


, 21 2006

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, 4 2006

The Carney Complex

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Background:Primary tumors of the heart are rare in all age groups. However, they are still important to consider in differential diagnoses of valvular disease, congestive heart failure, and arrhythmia. Although myxomas are the most common cardiac tumors in adults, they are relatively rare in infants and children. While myxomas are usually sporadic, several autosomal dominant familial conditions that combine lentiginosis and cardiac myxomas have been described. Previously termed syndromes, such as LAMB (lentigines, atrial myxomas, mucocutaneous myxomas, and blue nevi) syndrome and NAME (nevi, atrial myxoma, myxoid neurofibroma, and ephelides) syndrome, now are grouped under the broader category of Carney complex, an autosomal dominant syndrome that accounts for 7% of all cardiac myxomas. Carney complex findings include cardiac myxomas, cutaneous myxomas, spotty pigmentation of the skin, endocrinopathy, and both endocrine and nonendocrine tumors.

Pathophysiology:Carney complex is inherited as an autosomal dominant trait with variable penetrance. Cardiac myxomas are thought to arise from primitive subendocardial mesenchymal multipotent precursor cells. However, these cells have not been specifically identified yet. The systemic symptoms (eg, fever, arthralgia, elevated sedimentation rate, lupuslike rashes) that accompany some myxomas may be due to the production of the proinflammatory cytokine interleukin-6 by the myxoma.

Cardiac myxomas occurring as part of Carney complex may recur at sites distant from the resection. These tumors may grow in diameter by as much as 1.8 cm/y. Initial genetic analyses suggested that a gene defect may map to arm 2p. More recent linkage analysis in several families affected by the Carney complex has also mapped a disease locus to band 17q2. Mutations in the PRKAR1A gene encoding the R1a regulatory subunit of protein kinase A have been shown to cause Carney complex.

In an analysis of 51 unrelated patients with Carney complex, 65% of the patients were shown to have mutations in the PRKAR1A gene. PRKAR1A may act as a tumor suppressor gene by regulating PKA activity, which in turn can suppress or stimulate the cell growth and differentiation. Furthermore, a variant form of Carney complex associated with distal arthrogryposis has been recently identified. Analysis of a large family with cardiac myxomas and other typical findings of Carney complex, as well as trismus-pseudocamptodactyly, revealed a missense mutation in the MYH8 gene that encodes perinatal myosin heavy chain. Further studies of the families with similar phenotypes revealed that this missense mutation was a common founder mutation. These findings suggest a role of protein kinase A and perinatal myosin heavy chain in cardiac tumorigenesis.

Cardiac involvement

Cardiac myxomas in the Carney complex often are multiple, can occur in any cardiac chamber, and have a predilection to recur at distant intracardiac and extracardiac sites after initial surgical resection. Although they usually are benign, cardiac myxomas are associated with significant cardiac morbidity due to stroke from tumor embolization and heart failure from intracardiac valvular obstruction.

Extracardiac involvement

In addition to cardiac myxomas, individuals with Carney complex exhibit spotty pigmentation of the skin, particularly on the face, trunk, lips, and sclera. Pigmentation also may affect the mucosal surfaces of the oral or genital regions. Extracardiac myxomas may also occur in the breast, testis, thyroid, brain, or adrenal gland. Nonmyxomatous tumors, such as pituitary adenoma, psammomatous melanotic schwannoma, and Sertoli cell tumors of the testis, also may be observed. Impaired fertility has been observed in males with Carney complex. Patients can also exhibit a spectrum of endocrine overactivity, including Cushing syndrome secondary to primary pigmented nodular adrenocortical hyperplasia. Thyroid and pituitary dysfunction may also be observed.

Frequency:

  • In the US:Cardiac myxomas are the most common primary cardiac tumor in the general population and occur with a frequency of 7 cases per 10,000 individuals. Myxomas occurring as part of Carney complex account for 7% of all cardiac myxomas.

Mortality/Morbidity:Morbidity and mortality from stroke and heart failure arise from cardiac involvement, and individuals with recurrent intracardiac myxomas may require additional cardiac surgery to resect such myxomas. Other extracardiac tumors may produce morbidity by local extension. Endocrine dysfunction also often is symptomatic but may be subclinical.

Sex:Sporadic myxomas occur with a greater frequency among middle-aged women. Myxomas that occur as part of the Carney complex affect both sexes with equal frequency.

Age:Although sporadic myxomas generally affect middle-aged adults (incidence higher in females than in males), myxomas arising in the setting of Carney complex may arise in persons of any age and either sex.

http://www.emedicine.com/MED/topic2941.htm


, 4 2006

24 - med articles - Addison's Disease

Addison's disease is an endocrine or hormonal disorder that occurs in all age groups and afflicts men and women equally. The disease is characterized by weight loss, muscle weakness, fatigue, low blood pressure, and sometimes darkening of the skin in both exposed and nonexposed parts of the body.

Addison's disease occurs when the adrenal glands do not produce enough of the hormone cortisol and, in some cases, the hormone aldosterone. The disease is also called adrenal insufficiency, or hypocortisolism.

Cortisol

Cortisol is normally produced by the adrenal glands, located just above the kidneys. It belongs to a class of hormones called glucocorticoids, which affect almost every organ and tissue in the body. Scientists think that cortisol has possibly hundreds of effects in the body. Cortisol's most important job is to help the body respond to stress. Among its other vital tasks, cortisol

  • helps maintain blood pressure and cardiovascular function
  • helps slow the immune system's inflammatory response
  • helps balance the effects of insulin in breaking down sugar for energy
  • helps regulate the metabolism of proteins, carbohydrates, and fats
  • helps maintain proper arousal and sense of well-being

Because cortisol is so vital to health, the amount of cortisol produced by the adrenals is precisely balanced. Like many other hormones, cortisol is regulated by the brain's hypothalamus and the pituitary gland, a bean-sized organ at the base of the brain. First, the hypothalamus sends "releasing hormones" to the pituitary gland. The pituitary responds by secreting hormones that regulate growth and thyroid and adrenal function, and sex hormones such as estrogen and testosterone. One of the pituitary's main functions is to secrete ACTH (adrenocorticotropin), a hormone that stimulates the adrenal glands. When the adrenals receive the pituitary's signal in the form of ACTH, they respond by producing cortisol. Completing the cycle, cortisol then signals the pituitary to lower secretion of ACTH.

Aldosterone

Aldosterone belongs to a class of hormones called mineralocorticoids, also produced by the adrenal glands. It helps maintain blood pressure and water and salt balance in the body by helping the kidney retain sodium and excrete potassium. When aldosterone production falls too low, the kidneys are not able to regulate salt and water balance, causing blood volume and blood pressure to drop.

Causes

Failure to produce adequate levels of cortisol can occur for different reasons. The problem may be due to a disorder of the adrenal glands themselves (primary adrenal insufficiency) or to inadequate secretion of ACTH by the pituitary gland (secondary adrenal insufficiency).

Primary Adrenal Insufficiency

Addison's disease affects about 1 in 100,000 people. Most cases are caused by the gradual destruction of the adrenal cortex, the outer layer of the adrenal glands, by the body's own immune system. About 70 percent of reported cases of Addison's disease are caused by autoimmune disorders, in which the immune system makes antibodies that attack the body's own tissues or organs and slowly destroy them. Adrenal insufficiency occurs when at least 90 percent of the adrenal cortex has been destroyed. As a result, often both glucocorticoid (cortisol) and mineralocorticoid (aldostertone) hormones are lacking. Sometimes only the adrenal gland is affected, as in idiopathic adrenal insufficiency; sometimes other glands also are affected, as in the polyendocrine deficiency syndrome.

Polyendocrine Deficiency Syndrome

The polyendocrine deficiency syndrome is classified into two separate forms, referred to as type I and type II.

Type I occurs in children, and adrenal insufficiency may be accompanied by

  • underactive parathyroid glands
  • slow sexual development
  • pernicious anemia
  • chronic candida infections
  • chronic active hepatitis
  • hair loss (in very rare cases)

Type II, often called Schmidt's syndrome, usually afflicts young adults. Features of type II may include

  • an underactive thyroid gland
  • slow sexual development
  • diabetes
  • vitiligo
  • loss of pigment on areas of the skin

Scientists think that the polyendocrine deficiency syndrome is inherited because frequently more than one family member tends to have one or more endocrine deficiencies.

Tuberculosis

Tuberculosis (TB), an infection which can destroy the adrenal glands, accounts for about 20 percent of cases of primary adrenal insufficiency in developed countries. When adrenal insufficiency was first identified by Dr. Thomas Addison in 1849, TB was found at autopsy in 70 to 90 percent of cases. As the treatment for TB improved, however, the incidence of adrenal insufficiency due to TB of the adrenal glands has greatly decreased.

Other Causes

Less common causes of primary adrenal insufficiency are

  • chronic infection, mainly fungal infections
  • cancer cells spreading from other parts of the body to the adrenal glands
  • amyloidosis
  • surgical removal of the adrenal glands

Secondary Adrenal Insufficiency

This form of adrenal insufficiency is much more common than primary adrenal insufficiency and can be traced to a lack of ACTH. Without ACTH to stimulate the adrenals, the adrenal glands' production of cortisol drops, but not aldosterone. A temporary form of secondary adrenal insufficiency may occur when a person who has been receiving a glucocorticoid hormone such as prednisone for a long time abruptly stops or interrupts taking the medication. Glucocorticoid hormones, which are often used to treat inflammatory illnesses like rheumatoid arthritis, asthma, or ulcerative colitis, block the release of both corticotropin-releasing hormone (CRH) and ACTH. Normally, CRH instructs the pituitary gland to release ACTH. If CRH levels drop, the pituitary is not stimulated to release ACTH, and the adrenals then fail to secrete sufficient levels of cortisol.

Another cause of secondary adrenal insufficiency is the surgical removal of benign, or noncancerous, ACTH-producing tumors of the pituitary gland (Cushing's disease). In this case, the source of ACTH is suddenly removed, and replacement hormone must be taken until normal ACTH and cortisol production resumes.

Less commonly, adrenal insufficiency occurs when the pituitary gland either decreases in size or stops producing ACTH. These events can result from

  • tumors or infections of the area
  • loss of blood flow to the pituitary
  • radiation for the treatment of pituitary tumors
  • surgical removal of parts of the hypothalamus
  • surgical removal of the pituitary gland

Symptoms

The symptoms of adrenal insufficiency usually begin gradually. Characteristics of the disease are

  • chronic, worsening fatigue
  • muscle weakness
  • loss of appetite
  • weight loss

About 50 percent of the time, one will notice

  • nausea
  • vomiting
  • diarrhea

Other symptoms include

  • low blood pressure that falls further when standing, causing dizziness or fainting
  • skin changes in Addison's disease, with areas of hyperpigmentation, or dark tanning, covering exposed and nonexposed parts of the body; this darkening of the skin is most visible on scars; skin folds; pressure points such as the elbows, knees, knuckles, and toes; lips; and mucous membranes

Addison's disease can cause irritability and depression. Because of salt loss, a craving for salty foods also is common. Hypoglycemia, or low blood glucose, is more severe in children than in adults. In women, menstrual periods may become irregular or stop.

Because the symptoms progress slowly, they are usually ignored until a stressful event like an illness or an accident causes them to become worse. This is called an addisonian crisis, or acute adrenal insufficiency. In most cases, symptoms are severe enough that patients seek medical treatment before a crisis occurs. However, in about 25 percent of patients, symptoms first appear during an addisonian crisis.

Symptoms of an addisonian crisis include

  • sudden penetrating pain in the lower back, abdomen, or legs
  • severe vomiting and diarrhea
  • dehydration
  • low blood pressure
  • loss of consciousness

Left untreated, an addisonian crisis can be fatal.

Diagnosis

In its early stages, adrenal insufficiency can be difficult to diagnose. A review of a patient's medical history based on the symptoms, especially the dark tanning of the skin, will lead a doctor to suspect Addison's disease.

A diagnosis of Addison's disease is made by laboratory tests. The aim of these tests is first to determine whether levels of cortisol are insufficient and then to establish the cause. X-ray exams of the adrenal and pituitary glands also are useful in helping to establish the cause.

ACTH Stimulation Test

This is the most specific test for diagnosing Addison's disease. In this test, blood cortisol, urine cortisol, or both are measured before and after a synthetic form of ACTH is given by injection. In the so-called short, or rapid, ACTH test, measurement of cortisol in blood is repeated 30 to 60 minutes after an intravenous ACTH injection. The normal response after an injection of ACTH is a rise in blood and urine cortisol levels. Patients with either form of adrenal insufficiency respond poorly or do not respond at all.

CRH Stimulation Test

When the response to the short ACTH test is abnormal, a "long" CRH stimulation test is required to determine the cause of adrenal insufficiency. In this test, synthetic CRH is injected intravenously and blood cortisol is measured before and 30, 60, 90, and 120 minutes after the injection. Patients with primary adrenal insufficiency have high ACTHs but do not produce cortisol. Patients with secondary adrenal insufficiency have deficient cortisol responses but absent or delayed ACTH responses. Absent ACTH response points to the pituitary as the cause; a delayed ACTH response points to the hypothalamus as the cause.

In patients suspected of having an addisonian crisis, the doctor must begin treatment with injections of salt, fluids, and glucocorticoid hormones immediately. Although a reliable diagnosis is not possible while the patient is being treated for the crisis, measurement of blood ACTH and cortisol during the crisis and before glucocorticoids are given is enough to make the diagnosis. Once the crisis is controlled and medication has been stopped, the doctor will delay further testing for up to 1 month to obtain an accurate diagnosis.

Other Tests

Once a diagnosis of primary adrenal insufficiency has been made, x-ray exams of the abdomen may be taken to see if the adrenals have any signs of calcium deposits. Calcium deposits may indicate TB. A tuberculin skin test also may be used.

If secondary adrenal insufficiency is the cause, doctors may use different imaging tools to reveal the size and shape of the pituitary gland. The most common is the CT scan, which produces a series of x-ray pictures giving a cross-sectional image of a body part. The function of the pituitary and its ability to produce other hormones also are tested.

Treatment

Treatment of Addison's disease involves replacing, or substituting, the hormones that the adrenal glands are not making. Cortisol is replaced orally with hydrocortisone tablets, a synthetic glucocorticoid, taken once or twice a day. If aldosterone is also deficient, it is replaced with oral doses of a mineralocorticoid called fludrocortisone acetate (Florinef), which is taken once a day. Patients receiving aldosterone replacement therapy are usually advised by a doctor to increase their salt intake. Because patients with secondary adrenal insufficiency normally maintain aldosterone production, they do not require aldosterone replacement therapy. The doses of each of these medications are adjusted to meet the needs of individual patients.

During an addisonian crisis, low blood pressure, low blood glucose, and high levels of potassium can be life threatening. Standard therapy involves intravenous injections of hydrocortisone, saline (salt water), and dextrose (sugar). This treatment usually brings rapid improvement. When the patient can take fluids and medications by mouth, the amount of hydrocortisone is decreased until a maintenance dose is achieved. If aldosterone is deficient, maintenance therapy also includes oral doses of fludrocortisone acetate.

Special Problems


Surgery

Patients with chronic adrenal insufficiency who need surgery with general anesthesia are treated with injections of hydrocortisone and saline. Injections begin on the evening before surgery and continue until the patient is fully awake and able to take medication by mouth. The dosage is adjusted until the maintenance dosage given before surgery is reached.

Pregnancy

Women with primary adrenal insufficiency who become pregnant are treated with standard replacement therapy. If nausea and vomiting in early pregnancy interfere with oral medication, injections of the hormone may be necessary. During delivery, treatment is similar to that of patients needing surgery; following delivery, the dose is gradually tapered and the usual maintenance doses of hydrocortisone and fludrocortisone acetate by mouth are reached by about 10 days after childbirth.

Patient Education

A person who has adrenal insufficiency should always carry identification stating his or her condition in case of an emergency. The card should alert emergency personnel about the need to inject 100 mg of cortisol if its bearer is found severely injured or unable to answer questions. The card should also include the doctor's name and telephone number and the name and telephone number of the nearest relative to be notified. When traveling, a needle, syringe, and an injectable form of cortisol should be carried for emergencies. A person with Addison's disease also should know how to increase medication during periods of stress or mild upper respiratory infections. Immediate medical attention is needed when severe infections, vomiting, or diarrhea occur. These conditions can precipitate an addisonian crisis. A patient who is vomiting may require injections of hydrocortisone.

People with medical problems may wish to wear a descriptive warning bracelet or neck chain to alert emergency personnel. A number of companies manufacture medical identification products.

http://endocrine.niddk.nih.gov/pubs/addison/addison.htm


, 4 2006

23 - med articles - Cushing's Syndrome

Introduction

Cushing's syndrome is a hormonal disorder caused by prolonged exposure of the body's tissues to high levels of the hormone cortisol. Sometimes called "hypercortisolism," it is relatively rare and most commonly affects adults aged 20 to 50. An estimated 10 to 15 of every million people are affected each year.

What are the symptoms?

Symptoms vary, but most people have upper body obesity, rounded face, increased fat around the neck, and thinning arms and legs. Children tend to be obese with slowed growth rates.

Other symptoms appear in the skin, which becomes fragile and thin. It bruises easily and heals poorly. Purplish pink stretch marks may appear on the abdomen, thighs, buttocks, arms and breasts. The bones are weakened, and routine activities such as bending, lifting or rising from a chair may lead to backaches, rib and spinal column fractures.

Most people have severe fatigue, weak muscles, high blood pressure and high blood sugar. Irritability, anxiety and depression are common.

Women usually have excess hair growth on their faces, necks, chests, abdomens, and thighs. Their menstrual periods may become irregular or stop. Men have decreased fertility with diminished or absent desire for sex.

What causes Cushing's syndrome?

Cushing's syndrome occurs when the body's tissues are exposed to excessive levels of cortisol for long periods of time. Many people suffer the symptoms of Cushing's syndrome because they take glucocorticoid hormones such as prednisone for asthma, rheumatoid arthritis, lupus and other inflammatory diseases, or for immunosuppression after transplantation.

Others develop Cushing's syndrome because of overproduction of cortisol by the body. Normally, the production of cortisol follows a precise chain of events. First, the hypothalamus, a part of the brain which is about the size of a small sugar cube, sends corticotropin releasing hormone (CRH) to the pituitary gland. CRH causes the pituitary to secrete ACTH (adrenocorticotropin), a hormone that stimulates the adrenal glands. When the adrenals, which are located just above the kidneys, receive the ACTH, they respond by releasing cortisol into the bloodstream.

Cortisol performs vital tasks in the body. It helps maintain blood pressure and cardiovascular function, reduces the immune system's inflammatory response, balances the effects of insulin in breaking down sugar for energy, and regulates the metabolism of proteins, carbohydrates, and fats. One of cortisol's most important jobs is to help the body respond to stress. For this reason, women in their last 3 months of pregnancy and highly trained athletes normally have high levels of the hormone. People suffering from depression, alcoholism, malnutrition and panic disorders also have increased cortisol levels.

When the amount of cortisol in the blood is adequate, the hypothalamus and pituitary release less CRH and ACTH. This ensures that the amount of cortisol released by the adrenal glands is precisely balanced to meet the body's daily needs. However, if something goes wrong with the adrenals or their regulating switches in the pituitary gland or the hypothalamus, cortisol production can go awry.

Pituitary Adenomas
Pituitary adenomas cause most cases of Cushing's syndrome. They are benign, or non-cancerous, tumors of the pituitary gland which secrete increased amounts of ACTH. Most patients have a single adenoma. This form of the syndrome, known as "Cushing's disease," affects women five times more frequently than men.

Ectopic ACTH Syndrome
Some benign or malignant (cancerous) tumors that arise outside the pituitary can produce ACTH. This condition is known as ectopic ACTH syndrome. Lung tumors cause over 50 percent of these cases. Men are affected 3 times more frequently than women. The most common forms of ACTH-producing tumors are oat cell, or small cell lung cancer, which accounts for about 25 percent of all lung cancer cases, and carcinoid tumors. Other less common types of tumors that can produce ACTH are thymomas, pancreatic islet cell tumors, and medullary carcinomas of the thyroid.

Adrenal Tumors
Sometimes, an abnormality of the adrenal glands, most often an adrenal tumor, causes Cushing's syndrome. The average age of onset is about 40 years. Most of these cases involve non-cancerous tumors of adrenal tissue, called adrenal adenomas, which release excess cortisol into the blood.

Adrenocortical carcinomas, or adrenal cancers, are the least common cause of Cushing's syndrome. Cancer cells secrete excess levels of several adrenal cortical hormones, including cortisol and adrenal androgens. Adrenocortical carcinomas usually cause very high hormone levels and rapid development of symptoms.

Familial Cushing's Syndrome
Most cases of Cushing's syndrome are not inherited. Rarely, however, some individuals have special causes of Cushing's syndrome due to an inherited tendency to develop tumors of one or more endocrine glands. In Primary Pigmented Micronodular Adrenal Disease, children or young adults develop small cortisol-producing tumors of the adrenal glands. In Multiple Endocrine Neoplasia Type I (MEN I), hormone secreting tumors of the parathyroid glands, pancreas and pituitary occur. Cushing's syndrome in MEN I may be due to pituitary, ectopic or adrenal tumors.

How is Cushing's syndrome diagnosed?

Diagnosis is based on a review of the patient's medical history, physical examination and laboratory tests. Often x-ray exams of the adrenal or pituitary glands are useful for locating tumors. These tests help to determine if excess levels of cortisol are present and why.

24-Hour Urinary Free Cortisol Level
This is the most specific diagnostic test. The patient's urine is collected over a 24-hour period and tested for the amount of cortisol. Levels higher than 50100 micrograms a day for an adult suggest Cushing's syndrome. The normal upper limit varies in different laboratories, depending on which measurement technique is used.

Once Cushing's syndrome has been diagnosed, other tests are used to find the exact location of the abnormality that leads to excess cortisol production. The choice of test depends, in part, on the preference of the endocrinologist or the center where the test is performed.

Dexamethasone Suppression Test
This test helps to distinguish patients with excess production of ACTH due to pituitary adenomas from those with ectopic ACTH-producing tumors. Patients are given dexamethasone, a synthetic glucocorticoid, by mouth every 6 hours for 4 days. For the first 2 days, low doses of dexamethasone are given, and for the last 2 days, higher doses are given. Twenty-four hour urine collections are made before dexamethasone is administered and on each day of the test. Since cortisol and other glucocorticoids signal the pituitary to lower secretion of ACTH, the normal response after taking dexamethasone is a drop in blood and urine cortisol levels. Different responses of cortisol to dexamethasone are obtained depending on whether the cause of Cushing's syndrome is a pituitary adenoma or an ectopic ACTH-producing tumor.

The dexamethasone suppression test can produce false-positive results in patients with depression, alcohol abuse, high estrogen levels, acute illness, and stress. Conversely, drugs such as phenytoin and phenobarbital may cause false-negative results in response to dexamethasone suppression. For this reason, patients are usually advised by their physicians to stop taking these drugs at least one week before the test.

CRH Stimulation Test
This test helps to distinguish between patients with pituitary adenomas and those with ectopic ACTH syndrome or cortisol-secreting adrenal tumors. Patients are given an injection of CRH, the corticotropin-releasing hormone which causes the pituitary to secrete ACTH. Patients with pituitary adenomas usually experience a rise in blood levels of ACTH and cortisol. This response is rarely seen in patients with ectopic ACTH syndrome and practically never in patients with cortisol-secreting adrenal tumors.

Direct Visualization of the Endocrine Glands (Radiologic Imaging)
Imaging tests reveal the size and shape of the pituitary and adrenal glands and help determine if a tumor is present. The most common are the CT (computerized tomography) scan and MRI (magnetic resonance imaging). A CT scan produces a series of x-ray pictures giving a cross-sectional image of a body part. MRI also produces images of the internal organs of the body but without exposing the patient to ionizing radiation.

Imaging procedures are used to find a tumor after a diagnosis has been established. Imaging is not used to make the diagnosis of Cushing's syndrome because benign tumors, sometimes called "incidentalomas," are commonly found in the pituitary and adrenal glands. These tumors do not produce hormones detrimental to health and are not removed unless blood tests show they are a cause of symptoms or they are unusually large. Conversely, pituitary tumors are not detected by imaging in almost 50 percent of patients who ultimately require pituitary surgery for Cushing's syndrome.

Petrosal Sinus Sampling
This test is not always required, but in many cases, it is the best way to separate pituitary from ectopic causes of Cushing's syndrome. Samples of blood are drawn from the petrosal sinuses, veins which drain the pituitary, by introducing catheters through a vein in the upper thigh/groin region, with local anesthesia and mild sedation. X-rays are used to confirm the correct position of the catheters. Often CRH, the hormone which causes the pituitary to secrete ACTH, is given during this test to improve diagnostic accuracy. Levels of ACTH in the petrosal sinuses are measured and compared with ACTH levels in a forearm vein. ACTH levels higher in the petrosal sinuses than in the forearm vein indicate the presence of a pituitary adenoma; similar levels suggest ectopic ACTH syndrome.

The Dexamethasone-CRH Test
Some individuals have high cortisol levels, but do not develop the progressive effects of Cushing's syndrome, such as muscle weakness, fractures and thinning of the skin. These individuals may have Pseudo Cushing's syndrome, which was originally described in people who were depressed or drank excess alcohol, but is now known to be more common. Pseudo Cushing's does not have the same long-term effects on health as Cushing's syndrome and does not require treatment directed at the endocrine glands. Although observation over months to years will distinguish Pseudo Cushing's from Cushing's, the dexamethasone-CRH test was developed to distinguish between the conditions rapidly, so that Cushing's patients can receive prompt treatment. This test combines the dexamethasone suppression and the CRH stimulation tests. Elevations of cortisol during this test suggest Cushing's syndrome.

Some patients may have sustained high cortisol levels without the effects of Cushing's syndrome. These high cortisol levels may be compensating for the body's resistance to cortisol's effects. This rare syndrome of cortisol resistance is a genetic condition that causes hypertension and chronic androgen excess.

Sometimes other conditions may be associated with many of the symptoms of Cushing's syndrome. These include polycystic ovarian syndrome, which may cause menstrual disturbances, weight gain from adolescence, excess hair growth and sometimes impaired insulin action and diabetes. Commonly, weight gain, high blood pressure and abnormal levels of cholesterol and triglycerides in the blood are associated with resistance to insulin action and diabetes; this has been described as the "Metabolic Syndrome-X." Patients with these disorders do not have abnormally elevated cortisol levels.

How is Cushing's syndrome treated?

Treatment depends on the specific reason for cortisol excess and may include surgery, radiation, chemotherapy or the use of cortisol-inhibiting drugs. If the cause is long-term use of glucocorticoid hormones to treat another disorder, the doctor will gradually reduce the dosage to the lowest dose adequate for control of that disorder. Once control is established, the daily dose of glucocorticoid hormones may be doubled and given on alternate days to lessen side effects.

Pituitary Adenomas
Several therapies are available to treat the ACTH-secreting pituitary adenomas of Cushing's disease. The most widely used treatment is surgical removal of the tumor, known as transsphenoidal adenomectomy. Using a special microscope and very fine instruments, the surgeon approaches the pituitary gland through a nostril or an opening made below the upper lip. Because this is an extremely delicate procedure, patients are often referred to centers specializing in this type of surgery. The success, or cure, rate of this procedure is over 80 percent when performed by a surgeon with extensive experience. If surgery fails, or only produces a temporary cure, surgery can be repeated, often with good results. After curative pituitary surgery, the production of ACTH drops two levels below normal. This is a natural, but temporary, drop in ACTH production, and patients are given a synthetic form of cortisol (such as hydrocortisone or prednisone). Most patients can stop this replacement therapy in less than a year.

For patients in whom transsphenoidal surgery has failed or who are not suitable candidates for surgery, radiotherapy is another possible treatment. Radiation to the pituitary gland is given over a 6-week period, with improvement occurring in 40 to 50 percent of adults and up to 80 percent of children. It may take several months or years before patients feel better from radiation treatment alone. However, the combination of radiation and the drug mitotane (Lysodren) can help speed recovery. Mitotane suppresses cortisol production and lowers plasma and urine hormone levels. Treatment with mitotane alone can be successful in 30 to 40 percent of patients. Other drugs used alone or in combination to control the production of excess cortisol are aminoglutethimide, metyrapone, trilostane and ketoconazole. Each has its own side effects that doctors consider when prescribing therapy for individual patients.

Ectopic ACTH Syndrome
To cure the overproduction of cortisol caused by ectopic ACTH syndrome, it is necessary to eliminate all of the cancerous tissue that is secreting ACTH. The choice of cancer treatmentsurgery, radiotherapy, chemotherapy, immunotherapy, or a combination of these treatmentsdepends on the type of cancer and how far it has spread. Since ACTH-secreting tumors (for example, small cell lung cancer) may be very small or widespread at the time of diagnosis, cortisol-inhibiting drugs, like mitotane, are an important part of treatment. In some cases, if pituitary surgery is not successful, surgical removal of the adrenal glands (bilateral adrenalectomy) may take the place of drug therapy.

Adrenal Tumors
Surgery is the mainstay of treatment for benign as well as cancerous tumors of the adrenal glands. In Primary Pigmented Micronodular Adrenal Disease and the familial Carney's complex, surgical removal of the adrenal glands is required.

What research is being done on Cushing's syndrome?

The National Institutes of Health (NIH) is the biomedical research component of the Federal Government. It is one of the health agencies of the Public Health Service, which is part of the U.S. Department of Health and Human Services. Several components of the NIH conduct and support research on Cushing's syndrome and other disorders of the endocrine system, including the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), the National Institute of Child Health and Human Development (NICHD), the National Institute of Neurological Disorders and Stroke (NINDS), and the National Cancer Institute (NCI).

NIH-supported scientists are conducting intensive research into the normal and abnormal function of the major endocrine glands and the many hormones of the endocrine system. Identification of the corticotropin releasing hormone (CRH), which instructs the pituitary gland to release ACTH, enabled researchers to develop the CRH stimulation test, which is increasingly being used to identify the cause of Cushing's syndrome.

Improved techniques for measuring ACTH permit distinction of ACTH-dependent forms of Cushing's syndrome from adrenal tumors. NIH studies have shown that petrosal sinus sampling is a very accurate test to diagnose the cause of Cushing's syndrome in those who have excess ACTH production. The recently described dexamethasone suppression-CRH test is able to differentiate most cases of Cushing's from Pseudo Cushing's.

As a result of this research, doctors are much better able to diagnose Cushing's syndrome and distinguish among the causes of this disorder. Since accurate diagnosis is still a problem for some patients, new tests are under study to further refine the diagnostic process.

Many studies are underway to understand the causes of formation of benign endocrine tumors, such as those which cause most cases of Cushing's syndrome. In a few pituitary adenomas, specific gene defects have been identified and may provide important clues to understanding tumor formation. Endocrine factors may also play a role. There is increasing evidence that tumor formation is a multi-step process. Understanding the basis of Cushing's syndrome will yield new approaches to therapy.

http://endocrine.niddk.nih.gov/pubs/cushings/cushings.htm


, 4 2006

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Occupational therapy for patients with problems in activities of daily living after stroke (Review), The Cochrane Database of Systematic Reviews2006, Issue 4.

American Occupational Therapy Association

Stroke Association


, 3 2006

21 - med articles - Basedow-Graves

Graves-Basedow disease

Graves-Basedow disease, also known simply as Graves disease, is a medical disorder that may manifest several different conditions, includinggoitre and hyperthyroidism (over-activity of thyroid hormone production), infiltrativeexophthalmos (protuberance of one or both eyes and associated problems) and infiltrative dermopathy (a skin condition usually of the lower extremities). This disorder is the most common cause of hyperthyroidism. It is known to be related to an antibody mediated type of auto-immunity, but the trigger for the reaction is unknown.

Incidence and epidemiology

Also known in the English-speaking world simply as Graves' disease, the disease occurs most frequently in women (8:1 compared to men). It occurs most often in middle age (most commonly in the third to fifth decades of life), but is not uncommon in adolescents, during pregnancy, at the time of menopause and in people over age 50. There is a marked family preponderance, which has led to speculation that there may be a genetic component. To date, no clear genetic defect has been found that would point at amonogenic cause.

Etiology

The cause of this disease are unknown, but it is generally felt that genetic and environmental factors contribute to its development.[1] With this being an autoimmune disease which appears suddenly, often quite late in life, a cross reaction by the body to a viral disease is one suspected cause (this is a similar mechanism to that postulated for some cases of type Idiabetes).

One possible candidate is infection with yersinia enterocolitica (a cousin of the plague bacteria), but whilst there is indirect evidence for the structural similarity between the bacteria and the human thyrotropin receptor, direct causative evidence is limited.[1] Yersinia seems not to be a major cause of this disease, although it may contribute to the development of thyroid autoimmunity arising for other reasons in genetically susceptible individuals.[2] It has also been suggested that yersinia enterocolitica infection is not thecause of auto-immune thyroid disease, but rather is only anassociated condition; with both having a shared inherited susceptibility.[3] More recently the role for yersinia enterocolitica has been disputed.[4]

Signs and symptoms

Graves-Basedow disease is a disorder characterized by a triad ofhyperthyroidism,goitre, andexophthalmos (bulging eyeballs).

Due to the many physiological actions of thyroid hormone, many symptoms and signs are linked to Graves' disease:

Graves disease can lead to extreme hyperthyroidism which is life-threatening. This is calledthyroid storm.

Because similarantibodies to those stimulating the thyroid may also react with the eye muscles, patients may develop an enlargement of the ocular muscles with resultant forward movement of the eyeball (proptosis, also called exopthalmos) and inflammation of the tissues around the eye. Enlargement of the eye muscles may result in difficulty with proper movement and coordination of the eyes, and cause double vision and an obvious disparity in the relative position of both eyes. Difficulty in closing the eyelids may lead to eye dryness and occasionally corneal ulceration.

The ocular manifestations of Graves-Basedow disease are more common in smokers and tend to worsen (or develop for the first time) following radioiodine treatment of the thyroid condition. Thus, they are not caused by hyperthyroidism per se; this common misperception may result from the fact that hyperthyroidism from other causes may cause eyelid retraction or eyelid lag (so-called hyperthyroid stare) which can be confused with the general appearance of proptosis/exopthalmos, despite the fact that the globes do not actually protrude in other causes of hyperthyroidism. Also, both conditions may exist at the same time in the hyperthyroid patient with Graves-Basedow disease.

Diagnosis

On the basis of the signs and symptoms,thyroid hormone (thyroxine or T4, triiodothyronine or T3) andthyroid-stimulating hormone (TSH) are determined in themedical laboratory. Free T4 and Free T3 is markedly elevated, while TSH is suppressed due tonegative feedback. An elevated protein-boundiodine level may be detected. A large goiter is sometimes seen onX-rays.

Thyroid-stimulating antibodies may be detectedserologically.

Pathophysiology

Grave's disease is an example of atype II hypersensitivity autoimmune disorder. Most features are due to the production ofautoantibodies that bind to the TSH receptor, which is present on the follicular cells of the thyroid (the cells that produce thryoid hormone). These antibodies activate the cells in the same fashion as TSH itself, leading to an elevated production of thyroid hormone.

The infiltrative opthalmopathy (thyroid eye disease) that is frequently encountered has been explained by the expression of the TSH receptor on retroorbital tissue.

The exact cause of antibody production is not known.Viral infection may trigger antibodies against itsepitopes, which cross-react with the human TSH receptor. There appears to be agenetic predisposition for Graves' disease, suggesting that some people are more prone than others to develop TSH receptor activating antibodies due to a genetic cause.HLA DR (especially DR3) appears to play a significant role.

Treatment

Medical treatment of Graves' disease includes antithyroid drugs, radioactiveiodine andthyroidectomy (surgical excision of the gland).

Treatment of the hyperthyroidism of Graves-Basedow disease may be with medications such as methimazole or propylthiouracil (PTU), which reduce the production ofthyroid hormone, or withradioactive iodine. Surgical removal of the thyroid is another option, but still requires preoperative treatment with methimazole or PTU. This is done to render the patient "euthyroid" (i.e. normothyroid) before the surgery since operating on a frankly hyperthyroid patient is dangerous. Therapy with radioactive iodine (I-131) is the most common treatment in the United States and in many other parts of the world. Thyroid blocking drugs and/or surgical thyroid removal is used more often than radioactive iodine as definitive treatment in Japan, perhaps because of general fear of radioactivity among many Japanese.

The development of radioactive iodine (I-131) in the early 1940s and its widespread adoption as treatment for Graves' Disease has led to a progressive reduction in the use of surgical thyroidectomy for this problem. In general, RAI therapy is effective, less expensive, and avoids the small but definite risks of surgery. Treatment with antithyroid medications must be given for six months to two years, in order to be effective. Even then, upon cessation of the drugs, the hyperthyroid state may recur. Side effects of the antithyroid medications include a potentially fatal reduction in the level of white blood cells.

Antithyroid drugs

The main antithyroid drugs aremethimazole (US),carbimazole (UK) andpropylthiouracil (PTU). These drugs block the binding of iodine and coupling of iodotyrosines. The most dangerous side-effect isagranulocytosis (1/250, more in PTU); this is an idiosyncratic reaction which does not stop on cessation of drug). Others includegranulocytopenia (dose dependent, which improves on cessation of the drug) andaplastic anemia. Patients on these medications should see a doctor if they develop sore throat or fever. The most common side effects are rash and peripheral neuritis. These drugs also cross theplacenta and are secreted in breast milk.

Radioiodine

This modality is suitable for most patients, although some prefer to use it mainly for older patients. Indications forradioiodine are: failed medical therapy or surgery and where medical or surgical therapy are contraindicated.

Contraindications to RAI arepregnancy (absolute), ophthalmopathy (relative- it can aggravate thyroid eye disease), solitarynodules. Disadvantages of this treatment are a high incidence ofhypothyroidism (up to 80%) requiring hormone suppletion. It acts slowly and has a relapse rate that depends on the dose administered.

Surgery

This modality is suitable for young patients and pregnant patients. Indications are: a large goitre (especially when compressing thetrachea), suspicious nodules or suspectedcancer (to pathologically examine the thyroid) and patients with opthalmopathy.

Both bilateral subtotal thyroidectomy and the Hartley-Dunhill procedure (hemithyroidectomy on 1 side and partial lobectomy on other side) are possible.

Advantages are: immediate cure and potential removal ofcarcinoma. Its risks are injury of therecurrent laryngeal nerve,hypoparathyroidism (due to removal of theparathyroid glands),hematoma (which can be life-threatening if it compresses thetrachea) andscarring.

Eye disease

  • For mild disease -artificial tears, steroid eyedrops, oral steroids (to reduce chemosis)
  • For moderate disease - lateraltarsorrhaphy
  • For severe disease - orbital decompression or retro-orbital radiation

If left untreated

If left untreated, more seriouscomplications could result, includingbirth defects in pregnancy, increased risk of amiscarriage, and in extreme cases, death. Graves-Basedow disease is often accompanied by an increase in heart rate, which may lead to further heart complications. If the eyes are proptotic (bulging) severely enough that the lids do not close completely at night, severe dryness will occur with a very high risk of a secondary corneal infection which could lead to blindness. Pressure on the optic nerve behind the globe can lead to visual field defects and vision loss as well.

http://www.answers.com/topic/graves-basedow-disease


, 3 2006

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Altered Brain Serotonin 5-HT1A Receptor Binding After Recovery From Anorexia Nervosa Measured by Positron Emission Tomography and [Carbonyl11C]WAY-100635 , Archives of General Psychiatry2005;62:1032-1041, 2005.

http://www.medlook.net/


, 3 2006

19 - med articles - Anorexia nervosa

Anorexia nervosa

Anorexia nervosa is the formal name given to a condition in which patients, mostly women, seek to continually lower their body weights. They believe they look better as they become more and more depleted and wasted. Anorexics have a distorted body image. They think they are too fat, no matter what their weight is, and always want to become thinner. Anorexia nervosa is the most medically serious and least understood of all the eating disorders. Patients with anorexia nervosa often develop secondary changes in their endocrine system, such as the absence of menstrual periods.

Psychologists studying this condition have speculated that patients with anorexia nervosa want to return to a pre-pubertal state as a way of dealing with intense anxiety related to sexual development. Biological investigators have focused on abnormalities in the endocrine system, such as excessive cortisol production, abnormal regulation of water balance, abnormal thyroid function, elevated resting metabolic rate, and exaggerated responses to leptin, as indications of the biological disturbance this condition causes.

Individuals with anorexia nervosa attempt to control their body weights through a number of different strategies, such as compulsive hyperactivity. For example, one patient would jog five hours per day, then come home, wash, and go on an exercycle for another hour. Her day was spent trying to burn off any and all calories that she consumed.

Other anorexics restrict food. They eat as few calories as possible and, as a result, are able to continuously drive their weight down. Anorexics, like bulimics, can become progressively desperate if they see their weight increasing. At those times, they are likely to start inducing vomiting (purging) or abusing laxatives, diuretics, or appetite suppressants. Intense depression, anxiety, and insomnia are common in patients with anorexia nervosa.

Because anorexia nervosa involves a significant degree of self-starvation, affected individuals deprive their bodies of essential nutrients that are necessary for maintaining normal brain function, which actually results in at least temporary shrinkage of the brain itself. The psychological symptoms of anorexia nervosa rarely diminish until an anorexic regains sufficient weight to maintain normal endocrine and neurochemical functions. Therefore, the treatment of anorexia nervosa is primarily focused on controlling the behaviors anorexics use to drive their weight down and establishing clear weight goals.

Although the majority of patients with mild anorexia nervosa can be managed on an outpatient basis, frequently hospitalization is required if the individual's weight begins to fall dramatically or if their electrolytes (salts in the blood) become disturbed by purging and laxative abuse. Following an episode of acute anorexia nervosa, approximately two-thirds of patients recover completely and one-third have periodic problems during their lifetimes. Those who have abandoned hope of being helped can now find definitive treatment.


http://www.weight.com/eatingmoods.asp?page=3


, 2 2006

18 - Med article - Hashimoto's Thyroiditis

What is Hashimoto's Thyroiditis?

Hashimoto's Thyroiditis is a type of autoimmune thyroid disease in which the immune system attacks and destroys the thyroid gland. The thyroid helps set the rate of metabolism, which is the rate at which the body uses energy. Hashimoto's stops the gland from making enough thyroid hormones for the body to work the way it should. It is the most common thyroid disease in the U.S.

What is an autoimmune disease?

An autoimmune disease occurs when the body's immune system becomes misdirected and attacks the organs, cells or tissues that it was designed to protect. About 75% of autoimmune diseases occur in women, most often during their childbearing years.

What are the symptoms of Hashimoto's Thyroiditis?

Some patients with Hashimoto's Thyroiditis may have no symptoms. However, the common symptoms are fatigue, depression, sensitivity to cold, weight gain, forgetfulness, muscle weakness, puffy face, dry skin and hair, constipation, muscle cramps, and increased menstrual flow. Some patients have major swelling of the thyroid gland in the front of the neck, called goiter.

Does this disease run in families?

There is some evidence that Hashimoto's Thyroiditis can have a hereditary link. If autoimmune diseases in general run in your family, you are at a higher risk of developing one yourself.

How can I know for sure if I have this disease?

Your doctor will perform a simple blood test that will be able to tell if your body has the right amount of thyroid hormones. This test measures the TSH (thyroid stimulating hormone) to find out if the levels are in the normal range. The range is set by your doctor and should be discussed with you. Work with your doctor to figure out what level is right for you. There are other available tests that your doctor may choose to do if need be, such as a blood test to measure the level of "active thyroid hormone" or Free T4 and a scan (picture) to look at the thyroid.

What is the treatment for this disease?

Hypothyroidism caused by Hashimoto's Thyroiditis is treated with thyroid hormone replacement. A small pill taken once a day should be able to keep the thyroid hormone levels normal. This medicine will, in most cases, need to be taken for the rest of the patient's life. When trying to figure out the amount of hormone you need, you may have to return to your doctor several times for blood tests to guide adjustments in the medicine dose. It is important that the dose be right for you. A yearly visit to your doctor will help keep your levels normal and help you stay healthy overall. Be aware of the symptoms. If you note any changes or the return of symptoms, return to your doctor to see if you need to have your medicine dosage adjusted.

What would happen without medication to regulate my thyroid function?

If left untreated, hyporthyroidism can cause further problems, including changes in menstrual cycles, prevention of ovulation, and an increased risk of miscarriage. Symptoms such as fatigue, depression and constipation, may progress and there can be other serious consequences, including heart failure. It is also important to know that too much thyroid replacement hormone can mimic the symptoms ofhyperthyroidism. This is a condition that happens when there is too much thyroid hormone. These symptoms include insomnia, irritability, weight loss without dieting, heat sensitivity, increased perspiration, thinning of your skin, fine or brittle hair, muscular weakness, eye changes, lighter menstrual flow, rapid heart beat and shaky hands.

What happens if I have this disease and I get pregnant?

It is important to get checked out by your doctor more often if you are pregnant. Inadequately treated thyroid problems can affect a growing baby, and the thyroid replacement needs of pregnant women often change. A doctor can help you figure out your changing medicine needs.

This FAQ was reviewed by Dr. David Cooper, Sinai Hospital of Baltimore, Division of Endocrinology.

January 2006

http://www.4woman.gov/faq/hashimoto.htm


, 2 2006

17 - Medical Articles - Thyroid tests

The following are commonly used thyroid tests


alt
Measurement of Serum Thyroid Hormones: T4 by RIA.
T4 by RIA (radioimmunoassay) is the most used thyroid test of all. It is frequently referred to as a T7 which means that a resin T3 uptake (RT3u) has been done to correct for certain medications such as birth control pills, other hormones, seizure medication, cardiac drugs, or even aspirin that may alter the routine T4 test. The T4 reflects the amount of thyroxine in the blood. If the patient does not take any type of thyroid medication, this
test is usually a good measure of thyroid function.

altMeasurement of Serum Thyroid Hormones: T3 by RIA. As stated on our thyroid hormone production page, thyroxine (T4) represents 80% of the thyroid hormone produced by the normal gland and generally represents the overall function of the gland. The other 20% is triiodothyronine measured as T3 by RIA. Sometimes the diseased thyroid gland will start producing very high levels of T3 but still produce normal levels of T4. Therefore measurement of both hormones provides an even more accurate evaluation of thyroid function.

altThyroid Binding Globulin. Most of the thyroid hormones in the blood are attached to a protein called thyroid binding globulin (TBG). If there is an excess or deficiency of this protein it alters the T4 or T3 measurement but does not affect the action of the hormone. If a patient appears to have normal thyroid function, but an unexplained high or low T4, or T3, it may be due to an increase or decrease of TBG. Direct measurement of TBG can be done and will explain the abnormal value. Excess TBG or low levels of TBG are found in some families as an hereditary trait. It causes no problem except falsely elevating or lowering the T4 level. These people are frequently misdiagnosed as being hyperthyroid or hypothyroid, but they have no thyroid problem and need no treatment.

alt Measurement of Pituitary Production of TSH. Pituitary production of TSH is measured by a method referred to as IRMA (immunoradiometric assay). Normally, low levels (less than 5 units) of TSH are sufficient to keep the normal thyroid gland functioning properly. When the thyroid gland becomes inefficient such as in early hypothyroidism, the TSH becomes elevated even though the T4 and T3 may still be within the "normal" range. This rise in TSH represents the pituitary gland's response to a drop in circulating thyroid hormone; it is usually the first indication of thyroid gland failure. Since TSH is normally low when the thyroid gland is functioning properly, the failure of TSH to rise when circulating thyroid hormones are low is an indication of impaired pituitary function. The new "sensitive" TSH test will show very low levels of TSH when the thyroid is overactive (as a normal response of the pituitary to try to decrease thyroid stimulation). Interpretations of the TSH level depends upon the level of thyroid hormone; therefore, the TSH is usually used in combination with other thyroid tests such as the T4 RIA and T3 RIA.

altTRH Test. In normal people TSH secretion from the pituitary can be increased by giving a shot containing TSH Releasing Hormone (TRH...the hormone released by the hypothalamus which tells the pituitary to produce TSH). A baseline TSH of 5 or less usually goes up to 10-20 after giving an injection of TRH. Patients with too much thyroid hormone (thyroxine or triiodothyronine) will not show a rise in TSH when given TRH. This "TRH test" is presently the most sensitive test in detecting early hyperthyroidism. Patients who show too much response to TRH (TSH rises greater than 40) may be hypothyroid. This test is also used in cancer patients who are taking thyroid replacement to see if they are on sufficient medication. It is sometimes used to measure if the pituitary gland is functioning. The new "sensitive" TSH test (above) has eliminated the necessity of performing a TRH test in most clinical situations.

alt Iodine Uptake Scan. A means of measuring thyroid function is to measure how much iodine is taken up by the thyroid gland (RAI uptake). Remember, cells of the thyroid normally absorb iodine from our blood stream (obtained from foods we eat) and use it to make thyroid hormone (described on our
thyroid function page). Hypothyroid patients usually take up too little iodine and hyperthyroid patients take up too much iodine. The test is performed by giving a dose of radioactive iodine on an empty stomach. The iodine is concentrated in the thyroid gland or excreted in the urine over the next few hours. The amount of iodine that goes into the thyroid gland can be measured by a "Thyroid Uptake". Of course, patients who are taking thyroid medication will not take up as much iodine in their thyroid gland because their own thyroid gland is turned off and is not functioning. At other times the gland will concentrate iodine normally but will be unable to convert the iodine into thyroid hormone; therefore, interpretation of the iodine uptake is usually done in conjunction with blood tests.

altThyroid Scan. Taking a "picture" of how well the thyroid gland is functioning requires giving a radioisotope to the patient and letting the thyroid gland concentrate the isotope (just like the iodine uptake scan above). Therefore, it is usually done at the same time that the iodine uptake test is performed. Although other isotopes, such as technetium, will be concentrated by the thyroid gland; these isotopes will not measure iodine uptake which is what we really want to know because the production of thyroid hormone is dependent upon absorbing iodine. It has also been found that thyroid nodules that concentrate iodine are rarely cancerous; this is not true if the scan is done with technetium. Therefore, all scans are now done with radioactive iodine. Both of the scans above show normal sized thyroid glands, but the one on the left has a "HOT" nodule in the lower aspect of the right lobe, while the scan on the right has a "COLD" nodule in the lower aspect of the left lobe (outlined in red and yellow). Pregnant women should not have thyroid scans performed because the iodine can cause development troubles within the baby's thyroid gland.

  • Two types of thyroid scans are available. A camera scan is performed most commonly which uses a gamma camera operating in a fixed position viewing the entire thyroid gland at once. This type of scan takes only five to ten minutes. In the 1990's, a new scanner called a Computerized Rectilinear Thyroid (CRT) scanner was introduced. The CRT scanner utilizes computer technology to improve the clarity of thyroid scans and enhance thyroid nodules. It measures both thyroid function and thyroid size. A life-sized 1:1 color scan of the thyroid is obtained giving the size in square centimeters and the weight in grams. The precise size and activity of nodules in relation to the rest of the gland is also measured. CTS of the normal thyroid gland In addition to making thyroid diagnosis more accurate, the CRT scanner improves the results of thyroid biopsy. The accurate sizing of the thyroid gland aids in the follow-up of nodules to see if they are growing or getting smaller in size. Knowing the weight of the thyroid gland allows more accurate radioactive treatment in patients who have Graves' disease.

Thyroid Scans are used for the following reasons:

altIdentifying nodules and determining if they are "hot" or "cold".

altMeasuring the size of the goiter prior to treatment.

altFollow-up of thyroid cancer patients after surgery.

altLocating thyroid tissue outside the neck, i.e. base of the tongue or in the chest.



altThyroid Ultrasound. Thyroid ultrasound refers to the use of high frequency sound waves to obtain an image of the thyroid gland and identify nodules. It tells if a nodule is "solid" or a fluid-filled cyst, but it will not tell if a nodule is benign or malignant. Ultrasound allows accurate measurement of a nodule's size and can determine if a nodule is getting smaller or is growing larger during treatment. Ultrasound aids in performing thyroid needle biopsy by improving accuracy if the nodule cannot be felt easily on examination. Several more pages are dedicated to the
use of ultrasound in evaluating thyroid nodules.

altThyroid Antibodies. The body normally produces antibodies to foreign substances such as bacteria; however, some people are found to have antibodies against their own thyroid tissue. A condition known as
Hashimoto's Thyroiditis is associated with a high level of these thyroid antibodies in the blood. Whether the antibodies cause the disease or whether the disease causes the antibodies is not known; however, the finding of a high level of thyroid antibodies is strong evidence of this disease. Occasionally, low levels of thyroid antibodies are found with other types of thyroid disease. When Hashimoto's thyroiditis presents as a thyroid nodule rather than a diffuse goiter, the thyroid antibodies may not be present.

altThyroid Needle Biopsy. This has become the most reliable test to differentiate the "cold" nodule that is cancer from the "cold" nodule that is benign ("hot" nodules are rarely cancerous). It provides information that no other thyroid test will provide. While not perfect, it will provide definitive information in 75% of the nodules biopsied.


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, 2 2006

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, 31 2006

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