Showing posts with label Autoimmune. Show all posts
Showing posts with label Autoimmune. Show all posts

Aortic Dissection

Aortic Dissection
Introductions in Aortic Dissection

The aorta is the large blood vessel that comes out of the heart and carries blood throughout the body. Aorta at aortic valve stems on the way out of the left heart chambers. He climbed inside the chest to the arc (arch) where the branching of blood vessels to provide blood flow to the hands and head. He then began to fall through the chest into the abdomen, where it divides into two iliac arteries that provide blood flow to the legs. Together with the decline, more small arteries branch off to supply blood to the stomach, intestine, large intestine (colon), kidneys, and spinal cord (spinal cord).
The aorta has a thick wall, with three layers of muscle that allow blood vessels to withstand the high pressures generated when the heart pumps blood to the body. The three layers are the tunica intima, tunica media and tunica adventitia. Intima is the layer in contact with blood, the media is the middle, and the adventitia is the outermost layer.

In aortic dissection, small tears occur in the tunica intima (inner lining of the aortic wall in contact with blood). Blood can enter this tear and cause peeling of the coating layer of the intima media, in effect splitting the muscle layers of the aortic wall and forming a false channel, or lumen. This channel may be short or may extend throughout the length of the aorta. A torn distal (farther along the path from the aorta rather than the initial tear) in the intima layer can let the blood back into the true lumen of the aorta.

In some cases dissection will pass through all three layers of the aortic wall and lead to cracking (divisions) that immediately. In most other cases of blood filled between the layers of the wall.

Where there have been different classifications according to history, Stanford is the most common classification used to classify dissection.

* Type A dissections involving the aorta and arch (arch) are rising.
* Type B aortic dissections involve the fall.

A patient can have a combination of both.

Some patients may experience an aortic dissection without pain, and he may discovered incidentally on imaging studies conducted for other purposes.
Causes of Aortic Dissection

Is not certain why the initial tear occurs in the intima layer of the aortic wall. Aortic dissection tends to occur most commonly in men aged between 50 and 70 years.

High Blood Pressure: Most cases (more than 70%) associated with high blood pressure (hypertension). The aorta must withstand the pressure changes are significant with each heartbeat, and it is possible that over time with hypertension, the weakening of the intima area will occur.

Disease-related illnesses:

* Bicuspid aortic valve (aortic valve abnormalities from congenital)
* Marfan's syndrome
* Ehlers-Danlos syndrome
* Turner Syndrome
* Syphilis
* Use of Cocaine

Pregnancy: Pregnancy is also associated risk factors, especially in the third trimester and early post-partum period.

Trauma: blunt injury is known to cause aortic dissection, often seen after car accidents where the patient's chest hit the steering wheel.

What are the complications of Operation: Aortic dissection can be a complication of medical operations including heart bypass surgery (coronary artery bypass grafting) and repair-aortic and mitral valve repair. It can also be a complication of cardiac catheterization.
Signs and Symptoms of Aortic Dissection

* Pain is the most common symptom of aortic dissection and is often described as tearing or ripping. The pain usually starts suddenly and centered in the chest, spreads directly into the upper back.
* There may be nausea, sweating, shortness of breath, and weakness associated.
* Patients may faint (syncope)
* Other symptoms may be related to the location of the dissection in the aorta and whether it affects some of artery-clogging ateri are branched and their blood supply. For example, if any arteries that supply blood to the brain is involved, there may be signs of a stroke, or if the dissection affects the anterior spinal artery and blood supply to the spinal cord, the patient may present with paraplegia.
* Coronary arteries that supply blood to the heart begins at the origin of the aorta to the aortic valve (aortic valve). If the involved coronary arteries, aortic dissection may caused heart attack (myocardial infarction).
* Patients may present with congestive heart failure with a collection of fluid in the lungs. If aortic dissection involving the aortic valve and cause it to fail, blood flows back into the heart with each heartbeat and cause the blood to flow back into the lungs.
* There may be abdominal pain or side (side of the body between ribs and hips) are significant.
* The pain of aortic dissection can be confused with that of a heart attack, but can sometimes be distinguished because of the sudden appear and a normal electrocardiogram.
* Patients may also have feelings of impending doom.
Diagnosing Aortic Dissection

Clinicians should suspect an aortic dissection as one of the causes being considered for chest pain, as well as for heart attack and pulmonary embolism.

If the patient has vital signs are unstable, poor breathing, abnormal pulse, low blood pressure, and or a reduced level of consciousness, ABCs of resuscitation (Airway, Breathing, Circulation) need to be addressed when the evaluation of patients continues.
Patient history

History is one of the first steps are important in decisions about diagnosis.

Physical examination may reveal the potential complications of aortic aneurysm to allow physicians to consider this as a potential diagnosis. Once again, the symptoms that were presented will depend on the location of dissection and what organs are involved. The symptoms, depending on the location of the dissection, may include:

* Differences in blood pressure between arms
* The delay between the pulse of the hands and feet
* Listen to the fluid in the lungs and to murmur (murmur) new heart may help assess the aortic valve (aortic valve).
* The symptoms of a new stroke
* Paraplegia

Initial tests for chest pain, electrocardiogram, and chest x-ray is usually done. Unless the dissection involves the coronary arteries, electrocardiogram are usually normal. X-ray chest may show an abnormal form in the aorta and the widened mediastinum (the room where the heart, aorta, vena cava, trachea, and esophagus sits inside the chest cavity).

A diagnostic test of choice is computerized tomography aortic angiogram of the chest and abdomen to look at the aorta (this test requires an injection of contrast dye).

As an alternative, for people who can not undergo computerized tomography, transesophageal echocardiography is an alternative. A cardiologist include an ultrasound probe through the mouth into the esophagus and can identify potential problems with the heart, heart valves, and aorta.

Magnetic resonance imaging (MRI) can also be used, but the technique is not easily available to patients who are unstable.

Treatment Aortic Dissection

ABCs of resuscitation is always priority (overlooked).

In the emergency department, intravenous lines are placed, monitors for heart rate and rhythm will be attached, and supplemental oxygen provided. Treatments and diagnostic tests usually occur at the same time until the final diagnosis is made.

These drugs are used early directed to a decrease in blood pressure to prevent further tearing or damage to the aorta. Beta blocker medications [for example, esmolol (Brevibloc), labetalol (Normodyne, Trandate), metoprolol (Lopressor, Toprol XL)] reduces the action of adrenaline on the heart and blood vessels. Nitroglycerin dilate blood vessels to reduce blood pressure. Specific drug combinations will depend on the patient's purposes.

Finally, type A aortic dissections of the aorta which rose require surgery as the treatment of choice. The damaged area of ​​the aorta is replaced with artificial grafts. If the aortic valve has been tampered with, it also may require replacement or repair.

Medical management (rather than surgery) is preferred to type B dissection of the aorta are down, but again, every patient needs to be assessed individually in specific treatment recommended. Medications prescribed to control high blood pressure aggressively to prevent further dissection and aortic injuries.
The prognosis for Aortic Dissection

For aortic rupture, in which all three layers of the aorta is interrupted, the mortality rate is served until 80% of patients. Fifty percent of these patients die before reaching a hospital.

For type A aortic dissection, mortality rates remain high, with up to a mortality rate of 30% after surgery.

Type B aortic dissections, were treated medically, had an early mortality of 10%. This compares to the death of 30% when treated surgically.

Overall, for both types of aortic dissection, ten-year survival rate is more than 60%.
Prevent Aortic Dissection

As with any disease that involves the blood vessels, prevention is the key. Controlling high blood pressure, diabetes, cholesterol, and avoiding smoking reduces the risk of all vascular diseases. Because 70% of patients with aortic dissection have hypertension. Controlling high blood pressure, risk factors, may reduce the risk of this disease.

Any chest pain should not be ignored, and medical treatment should be immediately assessed by activating the system of emergency medical services and call 911.

Because the causes of chest pain may be unknown, giving baby aspirin to patients is appropriate, such as providing nitroglycerin (if the patient has been prescribed this drug for chest pain).

Hepatitis - Autoimmune

Hepatitis

Liver Function

The heart is the "engine room" of the body. It plays an important role in digestion, he made hundreds of components (eg, most blood proteins) are essential for life, he is the major site of energy production and worked as a storehouse of energy, and he helped in spending toxic compounds from the blood .

The human heart consists of two main segments or lobes: a large right lobe and smaller left lobe. He held against the diaphragm under the rib cage on the right side of the abdomen. In adults, it weighs about 2-3 lbs (1.0-1.5 kg) and maintains its size at a relatively constant proportion to body weight, increases or decreases in size when we add or lose weight. This represents a huge excess capacity on what is actually needed to sustain life, and we can actually manage quite well with only approximately 20-30% of our hearts that function normally. He is a very powerful organ. When damaged, and if the damage can be stopped, or when partially removed surgically, it is the only organ that has the ability to regenerate itself fully into the exact right size.

The liver helps digestion by producing bile, a liquid is brown-orange that is a mixture of cholesterol, various proteins and are called bile salts - which is a detergent-detergent is very strong. The color is caused by the presence of bilirubin, which is a waste product formed from hemoglobin (the main oxygen-carrying protein in red blood cells) when cells described crimson blood. Bile issued via the bile ducts and is stored in the gallbladder, from which he was expelled into the duodenum (the first part of the intestines) when necessary. Fatty foods entering the duodenum from the stomach is made more digestible by emulsification by bile salts. Bilirubin and product descriptions are the pigments that give color to normal stools their brown. Is also the pigment that makes skin turning yellow in those jaundiced. This is because, when the liver is damaged, bile often can not be removed properly and bilirubin tends to accumulate in the blood.
The definition of Auto-Immune Hepatitis

That is, it is a disease where the body "rejecting" his own heart. Body's immune system is normally designed to fight infection. When we are infected by, say, a virus, cell-specific white blood cells attack the infecting organism and eliminating direct or produce proteins known as antibodies that specifically recognize and help destroy the organism. Quite often, infections accompanied by some (usually fairly minor) damage "that happened" on the tissues of healthy, by white blood cells themselves or through the production of antibodies (known as auto-antibodies) against the tissues own body. The same thing can occur when the tissues damaged by chemical compounds (such as some types of drugs). With other words, we are all in a state of "autoimmunity", but in most people there are mechanisms that turn off (or control) autoimmune reactions by our immune systems against our own tissues. In people with AIH, it seems that they are born with (or developing) defects in this control system so that they can not turn off the autoimmune attack against their own care. Similar defects appear present in people with autoimmune diseases of other organs, such as autoimmune thyroid disease, myasthenia gravis (which affects the nerves and muscles), rheumatoid arthritis (which affects the joints), and some forms of diabetes.

Why only some tissues affected, eg the liver in AIH, and not the others? This is because the control mechanism is very complex. It seems that he has several components, some of which have the effect of "dampening down" the public on the immune system and others that control the reactions separately against each of the different tissues in the body. Fatherly develop an autoimmune disease that affects only (or mainly) a single organ, it is possible that parts of the common controls are not working properly and that there is additional damage on one of the parts that control the reactions to each network separately .

The Different Types of Autoimmune Hepatitis

Until a few years ago, investigators who conduct research on diseases classify AIH according to the different types of auto antibodies are found in the blood of patients. Patients with antinuclear (ANA) or smooth muscle (SMA) auto antibodies, or both, is said to have type 1 AIH and those who do not have it but have so-called liver-kidney microsomal antibodies (LKM1) said the type of disease empunyai 2. Approximately 95% of people with AIH, which covers all the age limit of men and women, have type 1. atients type 2 consists of a small group of (usually) young women with severe disease. Later, recognized that some patients do not have any of these three antibodies, but reserve the other auto antibodies are found. It is classified as having AIH type 3 and other subdivisions-subdivis recommended by other auto-antibodies were found. Experience and further research has shown that the severity of the disease is more linked to the age when he developed (see section four) than on the type of auto antibodies and that, at least from a clinical view, there is little difference between different types or subtypes . All types respond to standard treatment (see section to eight) in most cases and there is not much difference in the long-term outcome. Nevertheless, the terms type 1 and type 2 is still commonly used because it is felt that the mechanisms of liver damage may be different on the two types of these - although the response to treatment and outcomes were similar.
Who's More Influenced, Men Or Women-Women?

Like most autoimmune diseases, it mainly affects women (only approximately 20% of people with AIH are male). He can develop at any age but the great majority of people with AIH develop the disease between the ages between 50 and 70 years (often around menopause in women). He tends to be more severe in people who are younger. People who are older generally have milder forms are often more easily controlled with treatment (see the section he was treated).

How Many Known From This Disease?

Quite a lot actually - at least with regard to the signs and symptoms and how to diagnose and treat. It is known that people with AIH seems to have a genetic predisposition to the disease and that there might be something, like a viral infection of the liver (which may not be detected), which is required to trigger an autoimmune reaction in the first place (which may explain why most people do not has an illness from birth, although they were born with defects). However, the exact nature of the defects, or how to correct them permanently, or what actually caused the liver damage, is still unknown.

Is He Or Rare Diseases Common, Very Rare Disease Found?

He seems quite rare, but we really do not know how common it is. Rough approximations suggest that probably somewhere between 6.000 and 10.000 people are affected in the UK. However, it is now known that many people may have no symptoms for long periods and it is possible that many of who have mild disease may never in diagnosis as having AIH. In some countries where other diseases of the liver (such as chronic viral hepatitis) is very common, these conditions may be hiding AIH and he may not be found.
Types of Problems That Can Go Wrong With This Disease Type

The vast majority of people with AIH respond well to treatment and felt pretty good most of the time. The main issues complained of by some people are feeling a bit tired from time to time. Also, for reasons that are not understood, in some people the illness continues to cirrhosis despite apparently adequate control with treatment. Cirrhosis is a term used to describe the deposition of scar tissue in the liver (whatever the cause). This may present problems of its own, the main one is the increasing pressure on the blood vessels leading to the liver (portal hypertension) which, in turn, may lead to the development of varicose veins (varices) in the stomach and around the lower end of the esophagus , which may be bloody. On the other hand, it is known that people can have cirrhosis for 20 or 30 years without developing problems like that, so they may never arise. Other problems that can develop may be caused by medications used to control the disease, but in most cases is not serious Adala. Approximately 50% of people find that they gain weight when they first start taking steroids. In approximately 20% of this, excessive weight gain causes an increase in blood pressure (which may require treatment). Steroids can also lead to the development of diabetes or osteoporosis (thinning bones) but, again, at low enough doses that are usually required to maintain remission, these complications are relatively rare. Approximately 10% of people can not tolerate azathioprine, because they develop a rash, or stomach-gastric she disturb them, or it affects the white blood cells they are. In these cases, doses slightly higher than steroids may be needed to maintain remission.

How?

AIH is a chronic liver diseases is very little that can be very effectively treated with medication therapy only in the great majority of cases. Corticosteroids (usually prednisone or prednisolone) is the standard treatment. Azathioprine is often also used, because this has the effect of allowing additional doses lower than steroids to be used, but approximately 10% of people can not tolerate azathioprine for a variety of causes. Initially, high doses of steroids are required for several weeks or months to get the disease under control as soon as possible. Subsequently, and especially if azathioprine tolerated, the dose of steroids can often be reduced to levels low enough. Three recent studies (in the U.S., Sweden and Germany) have indicated that, for most people with AIH whose disease well controlled, life expectancy did not differ significantly from the rest of the population. The important thing is to take the tablets exactly as in recipes by a doctor.

Medications Work And How They Help

Two major drugs, corticosteroids and azathioprine, reduce autoimmune reactions. In a sense, they act as the drugs' anti-rejection "and indeed they are also used (among other medications) to prevent rejection after transplantation. The drugs' anti-rejection "of other, newer shows promise for people who do not respond to standard treatments.
I Will Release Of Medications? Why?

This will depend partly on how severe your disease substantially and how well (how quickly) it responds to treatment. As noted above, the vast majority of people respond quickly enough and they began to control the disease within a few months on treatment, but it seems to take at least a year, sometimes several years, to get it under control completely (meaning fully entered remission). After that, it is possible to stop treatment, but the available evidence indicates that only approximately 20-30% of people can remain free of drugs for long periods. There is always the possibility that the disease may return (relapse), even years after stopping treatment. However, if he returns, he can usually be controlled with standard care anymore.

What Can I  And Can not Do If I Have AIH

If your disease well controlled on treatment, there is actually little that you can not do. However, you should generally avoid alcohol. One glass of wine or half pint of beer at special events may not harm you, but this should really "sometimes" (meaning no more than once per month). On the other hand, if AIH you are not fully controlled, you can do anything you want to do but you should avoid alcohol completely. Your doctor is the best person to advise you on this.

Will Transplantation Necessary?

This will depend on whether your disease responds quite satisfactorily to treatment. As mentioned above, the vast majority of people with AIH respond well and therefore did not require transplantation. A small number of people who may need a transplant are those with severe disease who do not respond quickly enough on treatment and some of that with a prolonged illness that has continued to the point where not enough heart left to defend life or who have developed complication- serious complications.

Figures Survival Of Transplant

Because of improvements in operating improvement (and the drugs used to prevent rejection) over the last 5-10 years, the survival figures are usually taken into account for only 5 years (since the doctors still do not have enough experience with the development These new developments through periods longer). Also, because so few people with AIH who require liver transplants, the experience is still quite limited. The good news is that, between the centers of the world where most liver transplants for AIH is done, now 5-year survival is approximately 80-90%.
If the transplant is needed, Will Return illness?

Unfortunately, yes he can return. However, the drugs used to prevent rejection can also help control the AIH and usually only when these drugs are reduced to low doses or discontinued with the disease again. However, if he returns, he can often be controlled with standard therapy again.

Why go back?

Probably because the transplant does not cure the basic genetic defects associated with the control of autoimmune reactions.

Opportunities Return of Disease

This is really unknown, because the numbers of people with AIH who need transplants are so small and still no adequate long-term experience to make these calculations.

What Happens After Transplant, What Next?

It depends on how well the transplant goes. However, most people who are transplanted for AIH is running well and running nearly normal lives - even on a range of sometimes competing in the Transplant Olympics!

Medications Required To Stop Rejection

Previously, the main drugs used are steroids, azathioprine and cyclosporine, in various combinations. However, in the years recently tacrolimus are being increasingly used to great effect and other drugs, newer such as mycophenolate also gives promising results.
If I Have AIH, Can I Have Children?

If you are a male, should be no problem. If you are a woman, it would depend on how well you controlled the disease and complications of what (if any) which has been developed by you. Your doctor is the best person to advise you on this. If your disease is active, you may find that you can not become pregnant because of active disease that can affect ovulation. Studies recently have shown that women younger with AIH whose disease in remission often enough to become pregnant. Most do not have major problems during their pregnancies and have healthy babies are normal. However, for reasons that are not understood, some women relapse (relapse) during their pregnancies and others relapse within a few months after birth, even if they had continued throughout their normal drug treatment. Therefore, it is important to have check-ups are very regularly during pregnancy and after birth, and to recognize that an increase in your medication may be necessary at some stage. The available evidence suggests that, at doses normally used to maintain AIH in remission, steroids and azathioprine do not seem to affect the baby.

Can AIH Inherited?

Everything about our bodies is controlled by our genes, which we inherited from the parents, our parents and ancestors, their ancestors. But the functions of our genes can be influenced by external factors and changes throughout life - which is why we do not enjoy the "eternal youth". Furthermore, we all have defects of one kind or another in our genes. Whether these defects affect our lives depend on what they are. In many incidents the damage is not important or are there other genes that can compensate them. As discussed above, it seems likely that some defects in the control of the immune system is required for developing AIH, and that it is genetic in nature and may be inherited. So, it seems is a genetic predisposition to the development of AIH. However, AIH is not hereditary in the usual sense. It seems he is more "accidents of nature", where a number of different genes that tend to have the disease come together on a single individual. There are very few reports of AIH occurring in more than one family member, so now this knowledge suggests that it is highly unlikely that it can be lowered to one child.

Definition of Liver Biopsy

This is a diagnostic procedure used to obtain small amounts of liver tissue, which can be examined under the microscope to help identify the cause or stage of liver disease.

Dangers Of Liver Biopsy

Bleeding is a major risk of liver biopsy, from the side where the needle into the liver, although this occurs in less than 1% of patients. Fortunately, the risk of death from liver biopsy is very low, cover from 0.1% to 0.01%.

Definis Cirrhosis

Liver has a remarkable capacity to repair themselves when damaged. But when the cause of the damage persists, however, as in chronic hepatitis, the process of repair may not be able to be in line with the continuous cell death. As a consequence, reticulin framework in place that holds hepatocytes collapse on itself and eventually begin to stick together, forming scar tissue. This process is known as fibrosis. If fibrosisnya severe, the tissue that is formed can begin to interfere with the roads that cross the normal blood through the liver. Some liver cells may then be starved of oxygen and nutrients, and this can lead to further cell death and formation of more scar tissue - a kind of process that perpetuates itself that can be developed in common with anything that causes damage to the place first. When fibrosis becomes severe, he was known as cirrhosis - a term derived from the Greek word kirros, which means orange or Tawny, which really describes the appearance of liver cirrhosis caused by a reduction in the amount of blood flowing through it and the accumulation of pigments bile in it.

What causes Cirrhosis

Often it is estimated that cirrhosis caused by excessive alcohol consumption. This is not true. In fact, cirrhosis can be caused by any process that continuously damage the liver. Although heavy drinking is a major cause in Europe or North America, is responsible for only about 60% of cases of cirrhosis in these countries. In areas of the world where viral hepatitis and various other microbe infections of the liver is very common, the vast majority of cases of cirrhosis caused by chronic infections with these agents. Other important causes include autoimmune liver diseases and a variety of genetic diseases that affect the liver.

Cirrhosis Can Cured?

Once cirrhosis is essentially upheld the process can not be reversed. Healing is the only one liver transplant, but this may not always be possible or appropriate. However, the severity can often be reduced by removing or treating the underlying cause of cirrhosis. For example, individuals with cirrhosis caused by excessive alcohol consumption often experienced a dramatic improvement when they stop drinking alcohol.

Is there Treatment for Cirrhosis?

There is no treatment for cirrhosis itself, but complications arise in advanced stages can often be treated successfully, with the prolongation of life that can be considered. If portal hypertension develops, it is sometimes possible to treat with medications to reduce blood pressure. Other drugs, known as diuretics, often used to reduce fluid accumulation in patients with ascites or other forms of edema. If this does not work, surgery may be needed to reduce the ascites or liver transplantation may be needed. Gastric varices or esophageal can be injected with a compound known as a sclerosant to close this road and stop the bleeding. This is similar to the treatment of varicose veins on the legs, but this must be done by endoscopy. Development of a more recently involves the use of the endoscope to place small rubber bands around varices to end the local blood supply.

If there is severe bleeding, which can be inflated baloon may be lowered into the esophagus to apply the pressure as an emergency measure to stop bleeding to endoscopic injection or varices can be performed. In some cases, may need to consider surgery, known as a shunt procedure (or TIPS), to divert blood from the portal vein into other vessels that can handle pressure.

Symptoms

* Fatigue - symptoms-the most common are those with AIH will be facing.
* Liver is enlarged.
* Jaundice.
* Itching.
* Skin rash.
* Joint pain.
* Stomach discomfort.
* Fluid in the abdomen (ascites).
* Mental confusion.
* Amenorrhea.

People in advanced stages of disease likely to have symptoms such as fluid in the abdomen (ascites) or mental confusion. Women may stop having menstrual periods. Symptoms of autoimmune hepatitis range from mild to severe. Because severe viral hepatitis or hepatitis caused by drugs - for example, certain antibiotics - has the same symptoms, tests may be needed for proper diagnosis. Your doctor should also review and rule out all of your medicine before diagnosing autoimmune hepatitis.

Scleroderma

Scleroderma

The definition of Scleroderma

Scleroderma is an autoimmune disease of connective tissue. Autoimmune diseases are diseases that occur when the body's tissues are attacked by its own immune system. Scleroderma is characterized by the formation of scar tissue (fibrosis) in the skin and organs. This leads to thickness and firmness of involved areas. Scleroderma, when he scattered or widely spread throughout the body, also referred to as systemic sclerosis.

The cause of scleroderma is unknown. Researchers have found some evidence that genes are important factors, but the environment also seems to play a role. The result is activation of the immune system, causing injury to the tissues that results in injury similar to scar tissue formation. The fact that genes seem to cause a tendency to develop scleroderma at least mean that inheritance plays a part role. It is not unusual to find other autoimmune diseases in families of scleroderma patients. Some evidence for a possible role played by genes in the lead on the development of scleroderma comes from the study of Choctaw Native Americans who are a group with a reported incidence of the disease the most high. The disease is more common in women than in men.

Classification of Scleroderma

Scleroderma can be classified in terms of degree and location of involved skin. Therefore, scleroderma has been categorized into two major groups, diffuse (spread) and limited (limited).

Diffuse form of scleroderma (systemic sclerosis) involves symmetric thickening of the skin of the foot-kai and the hands, face and torso (chest, back, abdomen, or pelvis-pelvic) pliers can be quickly developed / evolved to hardening after an early inflammatory phase. Organ disease can occur early and are serious. Organs affected include the esophagus (esophageal), intestines, lungs with scarring (fibrosis), heart, and kidneys. High blood pressure can be a troublesome side effect.
Limited form of scleroderma tends to be limited to the skin of the fingers and face. Changes in skin and other features of the disease tends to occur more slowly than the diffuse form. Because a characteristic clinical pattern can occur in patients with limited forms of scleroderma, this form has taken another name which is composed of the beginning of the first letters of the common components. Thus, this form is also called the CREST variant of scleroderma. This name indicates the following characteristics:

C. .. calcinosis refers to the formation of tiny deposits of calcium in the skin. This is seen as whitish areas are hard on the superficial skin, generally covering the elbow-elbow, knees, or fingers. Solid deposits can be tender, can menkadi infected, and can fall off spontaneously or require surgical removal. This is the least common of the features of the CREST scleroderma variant.

R. .. Raynaud's phenomenon refers to the seizure of vessels are small arteries that mensupali blood to the fingers, toes, nose, tongue, or ears. These areas became blue, white, then red after exposure to extremes of cold, or even sometimes with extremes of heat or emotional disturbance.

E. .. Esophagus disease in scleroderma is characterized by the functioning of the muscles of the lower two-thirds of the esophagus that bad. This can lead to esophageal suau abnormally wide which allows stomach acid to flow back into the esophagus to cause heartburn (a burning sensation dihulu liver), inflammation, and scarring potential. This can eventually lead to difficulty in passing food from the mouth through the esophagus into the stomach. The symptoms of heartburn are treated aggressively in patients with scleroderma in order to prevent injury to the esophagus.

S. .. sclerodactyly refers to the thickening and tightening skin in place of fingers or toes. This can give them a vision of "shimmering" and a little swollen. Tightening can cause severe restriction of movement of the fingers and toes. These skin changes generally continue more slowly than that of patients with diffuse form of scleroderma.

T. .. Telangiectasias are areas of small red, often on the face, hands and mouth behind the lips. These areas blanch when they are pressed on top and represent a dilated capillaries.
Patients can have variations from CREST, for example, CRST, REST, ST, and so on. Patients may also have the disease "overlap" with characteristics of both CREST and the diffuse form of scleroderma. Some patients have overlap-overlap of scleroderma and connective tissue diseases, such as, systemic lupus erythematosus, and polymyositis. When the characteristics of scleroderma are present along with the characteristics of polymyositis and systemic lupus erythematosus, a condition referred to as mixed connective tissue disease or mixed connective tissue disease (MCTD).

Finally, these changes can be very localized scleroderma skin. Morphea scleroderma skin is localized in a field area of ​​the skin becomes hardened and slightly pigmented. Sometimes morphea can cause various injuries to the skin. Morphea not associated with disease elsewhere in the body. Linear scleroderma is scleroderma is typically located at a distance, often presented as an area of ​​hardened skin down the leg of a child. Linear scleroderma in children can slow the growth of bone from the affected limb. Sometimes linear scleroderma associated with an area of ​​"satellite" of a small area of ​​skin of localized scleroderma, such as the stomach.
 

Symptoms of Scleroderma
The symptoms of scleroderma depends on the type of scleroderma present and extent of involvement of external and internal to the individuals affected. Because scleroderma can affect the skin, esophagus, blood vessels, kidneys, lungs, blood pressure and intestines, the symptoms it causes can involve many areas of the body.
Scleroderma affects the skin to cause signs of inflammation are in place (local) or widespread (redness, swelling, tenderness, itching, and pain) that can lead to a tightening or hardening of the skin. These skin changes can be widespread, but is most common for them to affect the fingers, feet, face and neck. This can lead to a reduced restriction of movement of the fingers, toes, and jaw. Small areas of calcification or calcification (calcinosis), while not common, can sometimes be noted as a hard nodules at the ends of the bracket arms or fingers.
Scleroderma affecting the esophagus (esophageal) lead to heartburn. This is directly as a result of stomach acid flows back up into the esophagus. Sometimes this can lead to scarring of the esophagus with difficulty swallowing and / or localized pain in the center of the chest.

Blood vessels that can be affected including the arterioles, small arterioles of the ends of fingers, toes, and elsewhere. These vessels may have a tendency to kink when the areas exposed to cold, leading to the bluish, pallor, and redness of the fingers, toes, and sometimes the nose or ears are involved. These color changes are referred to as Raynaud's phenomenon. Raynaud's phenomenon can cause an insufficient oxygen supply to the ends of the fingers or toes are involved, causing small ulcers or skin is blackened (dead). Sometimes Raynaud's phenomenon is also associated with a tingling sensation (tingling). Other blood vessels that DAPT involved in scleroderma is small capillaries of the face, lips, mouth, or fingers. Capillaries are dilated to form small red spots that blanch, called telangiectasias.
Elevated blood pressure is potentially serious and can lead to kidney damage. Symptoms include headache, fatigue, and in severe cases, stroke.
Inflammation of the lungs in scleroderma can cause scarring, resulting in shortness of breath, especially with physical exertion. Rising pressure in the arteries of the lungs (pulmonary hypertension) can also cause shortness of breath and difficulty breathing memdapatkan a considerable activity.
Scleroderma affecting the large intestine (colon) most often causes constipation but can also lead to cramps and diarrhea. When this is the heavy / severe, can result in barriers defecation completely.

Diagnosing SclerodermaThe diagnosis of scleroderma syndrome is based on the discovery of the clinical characteristics of diseases. Almost all patients with scleroderma have blood tests which suggest autoimmunity, antinuclear antibodies (ANAs). A particular antibody, the anticentromere antibody, is found almost exclusively in the limited, or CREST, form of scleroderma. Anti-SCL 70 antibody (antitopoisomerase I antibody) is most Often seen in Patients with the diffuse form of scleroderma.
Other tests used to evaluate the presence or extent of any internal disease (in). This may include tests of upper and lower digestive tract to evaluate the intestines, chest x-rays, pulmonary function testing, and CAT scanning to examine the lungs, ECG and echocardiograms, and sometimes cardiac catheterization to evaluate the pressure in the arteries from the heart and lungs.Treating Scleroderma
Treatment of scleroderma is directed toward the individual characteristics that affect areas of the body are different.
Aggressive treatment of the elevation-elevation in blood pressure has become very important in preventing kidney failure. Blood pressure medications, such as captopril, are often used.
Recent data indicate that colchicine may be useful in reducing inflammation and tenderness that periodically accompanies the calcinosis nodules on the skin. Itching skin can be freed with lotion-lotion (emollients) such as Eucerin and Lubriderm.
Raynaud's phenomenon may require only mild heating and hand protection. Low-dose aspirin is often added to prevent small blood clots in the fingers, especially in patients with a history of ulceration, ulceration of the fingertips. Raynaud's phenomenon that is can be helped by medications that open the arteries, such as nifedipine (Procardia, Adalat) and nicardipine (Cardene), or with topical (topical) nitroglycerin applied to the fingers / legs are most affected (the most effective on the sides of the fingers / legs where the arteries are). Buffer is applied gentle finger can protect tender tissues. A group of medications that are typically used for depression, called serotonin reuptake inhibitors, like fluoxetine (Prozac), can sometimes improve the circulation of the fingers / legs are affected. Raynaud's phenomenon severe / severe to require surgical procedures, such as to interrupt the nerve-syraf of fingers which stimulates constriction of blood vessels (digital sympathectomy). Ulceration, ulceration of the fingers may require topical antibiotics (topical) or oral (mouth).
Irritation of the esophagus and heartburn can be relieved with omeprazole (Prilosec), esomeprazole (Nexium), or lansoprazole (Prevacid). Antacids may also be useful. Raising the head of the bed can reduce backflow of acid into the esophagus causing inflammation and heartburn. Avoiding caffeine and cigarette smoking also helps.
Constipation, cramps, and diarrhea is sometimes caused by bacteria that can be treated with tetracycline or erythromycin. These studies have recently shown that erythromycin can also be used. Fluid intake and fiber enhanced measures are generally good.
Dry, irritated skin and itching can be helped with emollients such as Lubriderm, Eucerin, or Bagbalm.
Telangiectasias, as on the face, can be treated with local laser therapy. Exposure to sunlight should be minimized because it can worsen telangiectasias.
Approximately 10% of patients with the CREST variant develop elevated pressures in the blood vessels to the lungs (pulmonary hypertension). Abnormally elevated blood pressure of the arteries that supply the lungs is often treated with calcium antagonist drugs, such as nifedipine, and blood-thinning drugs (anticoagulation). More severe pulmonary hypertension can be helped by intravenous infusion of prostacyclin (Iloprost) are continuous. A new drug is taken, bosentan (Tracleer), is now available to treat pulmonary hypertension severe / severe.
In addition, drugs used to suppress an active immune system that seems excessive spontaneously cause disease in the affected organs. Drugs that are used for this purpose include penicillamine, azathioprine, and methotrexate. Recent research has found that low-dose penicillamine  is as effective as high doses of penicillamine previously used, with less toxicity. Serious inflammation of the lungs (alveolitis) can require immune suppression with cyclophosphamide (Cytoxan) along with prednisone. Optimal treatment of scleroderma lung disease is an area of ​​active research. Stem cell transplantation (stem-cell transplantation) is being explored as a possible option.
No cure has been found that is universally effective for all patients with scleroderma. On an individual patient, the illness may be mild and require no treatments. In some, the disease is destroyed and without mercy.

Prognosis for Patients-Patients With Scleroderma
The prognosis of a patient is optimized with observations (monitor) the stringent requirements of the overall health status and treatment of complications, especially blood pressure is rising. Recent data indicate that the critical period of risk organs is generally within the first three years of skin involvement. This means that patients can be reassured her that the risk of complications that threaten their organs were significantly less after three years has symptoms kuliut.
More research is needed in all areas of scleroderma disease, from causes to treatments. Today scleroderma continues astonishing medical scientists. Researchers are evaluating the effectiveness of thalidomide for the treatment of scleroderma. These tests are more sensitive for detecting early lung disease of scleroderma are also being evaluated. Psoralen and ultraviolet light therapy (PUVA) is being studied as a possible treatment for scleroderma is limited.
Many researchers are investigating the roles of diverse cell messengers, called cytokines, in causing scleroderma. Researchers are also currently studying a hormone of pregnancy, called relaxin, for the treatment of scleroderma. Preliminary results suggest that it might ameliorate scleroderma. Relaxin normally loosen the ligaments of the pelvis and uterus to the birth of a child mature. How it might work in scleroderma is not clear.

Antinuclear Antibody Test (ANA)

Antinuclear Antibody Test  (ANA)

Definition of Antinuclear antibodies

We normally have the antibodies in the blood of us who reject / repel invaders into our body, such as microbes, viruses and bacteria. Antinuclear antibodies (ANAs) are antibodies that are not common, can be detected in the blood, which has the ability to bind to certain structures within the nucleus of cells. The nucleus is the core of the most deep within body cells and contain DNA, the primary genetic material. ANAs are found in patients whose immune system may tend to cause inflammation against their own body tissues. Antibodies directed against a person's own tissues are referred to as auto-antibodies. Tendency of the immune system to work against his own body is referred to as autoimmunity. ANAs indicate the possible presence of autoimmunity and provide, therefore, an indication for doctors to consider the possibility of autoimmune disease.

How ANA Designed And For What?

ANA test was designed by Dr. George Friou in 1957. The ANA test is performed using a blood sample. Antibodies in blood serum exposed to cells in the laboratory. Is then determined whether the antibodies are present or not that react to various parts of the nucleus of cells. Thus, the term anti-"nuclear" antibody. Fluorescence techniques are frequently used to actually detect antibodies in the cells, so ANA testing is sometimes referred to as fluorescent antinuclear antibody test (FANA). ANA test is a sensitive screening test used to detect autoimmune diseases.
The definition of Autoimmune Diseases

Autoimmune diseases are conditions in which there is a disorder of the immune system characterized by the abnormal production of antibodies (auto-antibodies) directed against the tissues of the body. Autoimmune diseases typically feature inflammation of various body tissues. ANAs are found in patients with a number of autoimmune diseases are different, such as systemic lupus erythematosus, Sjogren's syndrome, rheumatoid arthritis, polymyositis, scleroderma, Hashimoto's thyroiditis, juvenile diabetes mellitus, Addison disease, vitiligo, pernicious anemia, glomerulonephritis, and pulmonary fibrosis. ANAs can also be found in patients with conditions that are not considered as autoimmune diseases are classic, such as chronic infections and cancer.

What other conditions cause ANAs Produced

ANAs can be generated in patients with infections (viral or bacterial), lung diseases (primary pulmonary fibrosis, pulmonary hypertension), gastrointestinal diseases (ulcerative colitis, Crohn's disease, primary biliary cirrhosis, alcoholic liver disease), diseases hormone (Hashimoto's autoimmune thyroiditis, Grave's disease), diseases of the blood (idiopathic thrombocytopenic purpura, hemolytic anemia), cancers (melanoma, breast, lung, kidney, ovarian, etc.), diseases of the skin (psoriasis, pemphigus), as well as in the elderly and those with a history of rheumatic diseases of the family.

Can medications cause ANAs to be produced?

Many medications can sometimes stimulate the production of ANAs, including procainamide (Procan SR), hydralazine, and dilantin. ANAs are stimulated by the drugs referred to as drug-induced ANAs. This does not necessarily mean that the disease is present when these ANAs "induced". Sometimes diseases are associated with these ANAs, and they are referred to as diseases of drug-induced (drug-induced diseases).
ANAs are defined in certain patterns. What Is It?

ANAs present the "patterns" are different depending on the staining (staining) of cell nuclei in the laboratory: homogeneous or diffuse; speckled; nucleolar, and peripheral or rim. When these patterns are not specific to individual diseases, specific diseases can be more often associated with one pattern or another. These patterns can then sometimes give the doctor clues to find the types of diseases in evaluating a patient. For example, the nucleolar pattern is more commonly seen in the disease scleroderma. The speckled pattern seen in many conditions and in people who do not have any autoimmune disease.

Are ANAs always associated with illness?

No. ANAs can be found in approximately 5% of the normal population, usually at low titers (low levels). These people usually do not have the disease. Titers lower than 1:80 are less likely to be significant. ANA titers less than or equal to 1:40 are considered negative. Titers even higher are often not significant in patients older than 60 years. Finally, the ANA must be interpreted within the specific context of the symptoms and results of other tests of an individual patient. He may or may not be significant in a given individual.

Multiple Sclerosis (nerves of the central nervous system)


Multiple Sclerosis (nerves of the central nervous system)

Definition Multiple Sclerosis

Multiple sclerosis (MS) is a disease where the nerves of the central nervous system (brain and spinal cord or spinal cord) or degeneration worsens. Myelin, which provides a covering or insulation for nerves, improves delivery (conduction) of impulses along nerves and also is important to maintain the health of the nerves. In multiple sclerosis, inflammation causes the myelin eventually disappear. Consequently, the electrical impulses along nerves running slow, which is becoming more slowly. In addition, the nerves themselves become damaged. As more and more nerves are affected, a patient experiences a progressive interference with functions that are controlled by the nervous system such as vision, speech, walking, writing, and memories.

Approximately 350,000 people in the United States have multiple sclerosis. Typically, a patient diagnosed with multiple sclerosis between 20 and 50 years, but multiple sclerosis has been diagnosed in children and in the elderly. Multiple sclerosis is twice as likely to occur in Caucasians (white people) than in any other group. These women are two times more likely than men are affected by multiple sclerosis early in life.
Causes of Multiple Sclerosis

The cause of multiple sclerosis is still unknown. In the last 20 years, researchers have to concentrate (focus) on disorders of the immune system and genetics for explanations. The immune system is the body's defenses and is very organized and orderly. If triggered by an attacker (aggressor) or a foreign object, the immune system mounts a defense measures that identify and attack the invaders and then withdrew. This process is dependent on rapid communication among immune cells and the production of cells that can destroy the intruder. In multiple sclerosis, researchers suspect that a foreign agent such as a virus alters the immune system so that the immune system perceives myelin as an intruder and attacks. The attack by the immune system on the tissues that should protect the so-called autoimmunity, and multiple sclerosis is believed to be a disease of autoimmunity. Where some of the myelin may be repaired after illumination, some of the missing myelin and nerve endings are released from this cover (the demyelinated). Scarring also occurs, and the material deposited into the scarring and form plaques (plaques).
Multiple Sclerosis Reduced / inherited?
Although its role remains unclear, genetics may play a role in multiple sclerosis. European gipsies, Eskimo-Eskimo and African Bantu basically did not develop multiple sclerosis, where the native people Indians of North and South America, the Japanese and other Asian groups have a low incidence. The general population has less than one percent chance to ever get multiple sclerosis. The chance is increased in families where a relative degree one had the disease. So, a sister / brother, brother / sister, parent, or child of someone with multiple sclerosis from one to three percent chance of developing multiple sclerosis. In the same way, two identical twins have a chance of nearly 30% gain multiple sclerosis while the two are not identical twins have only a chance of 4% if one twin has the disease. These statistics suggest that genetic factors play a major role in multiple sclerosis. However, other data suggest that environmental factors also play an important role.

Types Of Multiple Sclerosis

There are clinical manifestations are different from multiple sclerosis. During an attack, a patient experiences a sudden deterioration in physical abilities normal which may range from mild to severe / severe. This attack, sometimes referred to as an exacerbation of multiple sclerosis, typically lasts more than 24 hours and generally more than a few weeks (rarely more than four weeks).

Approximately 65-80% of patients begin with Relapsing-Remitting (RR) MS, the most common type. In this type, patients experience a series of attacks followed by a loss of symptoms (remission) SCARA full or in part until another attack occurs (relapse). It may be weeks to decades between relapse-recurrence.

In Primary-Progressive (PP) MS, there is a gradual decline that continued in the physical abilities of a patient from the beginning rather than relapse-recurrence. Approximately 10% -20% of patients begin with PP-MS.

Patient-passien which began with RR-MS can then enter a phase where the recurrence, relapse is rare but more the inability to accumulate, and is said to have the type of Secondary-Progressive (SP) of multiple sclerosis. Approximately 50% of patients with RR-MS will develop SP-MS within 10 years. Progressive-Relapsing (PR) MS is a type of multiple sclerosis characterized by a continuous decline in abilities accompanied by sporadic attacks (occasionally). There are cases of multiple sclerosis that is lightweight and can be recognized only retrospectively after many years as well as rare cases of multiple sclerosis symptoms that progress very quickly (sometimes fatal) known as malignant or fulminant multiple sclerosis (Marburg variant).

Symptoms of Multiple Sclerosis

The symptoms of multiple sclerosis may be single or multiple and may range from mild to severe in intensity and short to long in duration (duration). Remission is wholly or partly from the initial symptoms occur in approximately 70% of patients with multiple sclerosis.

* Disturbances, visual disturbances may be the first symptoms of multiple sclerosis, but they usually subside. A patient may notice blurred vision, distortion of red-green (color desaturation), or monocular blindness (blindness in one eye) are sudden.
* Muscle weakness with or without difficulties with coordination and balance may occur early.
* Muscle cramps, fatigue, numbness, tingling and pain are common symptoms.
* There may be some loss of sensation, difficulty speaking, shaking, trembling, or dizziness.
Fifty percent of patients experience mental changes such as:

* Decreased concentration,
* Attention deficits,
* Some degree of memory loss (memory),
* Inability to perform tasks sequentially, or
* Disruptions in the decision / judgment.

Other symptoms may include:

* Depression,
* Maniac depression,
* Paranoia, or
* An uncontrollable urge to laugh and cry.

As the disease worsens, patients may experience sexual dysfunction or control the bowels and bladder are reduced. The heat seemed to intensify the symptoms of multiple sclerosis for about 60% of patients. Pregnancy seems to reduce the number of attacks.

Diagnosing Multiple Sclerosis

Caused by the wide limits and subtleties of symptoms, multiple sclerosis may be undiagnosed for many months to years after onset of symptoms. Doctors, especially specialists, neurologists, took detailed histories and perform physical examinations and nerve in full.

* MRI (magnetic resonance imaging) scans with intravenous gadolinium helps to identify, describe, and in some instances fall out wounds in the brain (plaques).
* An electro-physiological tests, which raises the potentials, examine the impulses that travel through the nerves to determine whether the impulses to move normally or too slowly.
* Finally, test the cerebro-spinal fluid that surrounds the brain and spinal cord may identify chemicals (antibodies) or abnormal cells that suggest the presence of multiple sclerosis.

Taken together, three of these tests help the doctor confirm the diagnosis of multiple sclerosis. For a definitive diagnosis of multiple sclerosis, dissemination in time (at least two symptomatic events or changes on a separate MRI) and indoor anatomy (eg, within the central nervous system) must be presented.
Treating Multiple Sclerosis

A lot of things for patients and physicians to consider in treating multiple sclerosis. These goals may include reducing the number of attacks, improve recovery from attacks, and try to slow the progression of the disease even further (treatment with drugs that modify disease). An additional goal is the liberation of the complications caused by loss of function of organs affected (treatment with drugs aimed at specific symptoms). Most experts would consider treatment with nerve drugs that modify the disease once a diagnosis of multiple sclerosis is established. Many will begin treatment at the time of the first attack of multiple sclerosis, because clinical trials have suggested that patients who delayed treatment may not get as much benefit as those patients treated early. Finally, use of support groups or counselors may be useful for patients and their families whose lives may be directly affected by multiple sclerosis.

Once goals have been established, initial treatment may include medications to control attacks, symptoms, or both. An understanding of the side effects of potential drugs are important to patients because of side effects sometimes alone deter patients from drug therapy. Patients may choose to avoid medications altogether, or choosing an alternative drug that may offer an exemption to the side effects are fewer. An ongoing dialogue between patients and physicians about drugs is important in determining the purposes for treatment.
The drugs are known to affect the immune system has become a major focus for controlling multiple sclerosis. Initially, corticosteroids such as prednisone (Deltasone, Liquid Pred, Deltasone, Orasone, Prednicen-M) or methylprednisolone (Medrol, Depo-Medrol), are used widely secar. However, because of their effects on the immune system is non-specific and their use may cause many side effects, corticosteroids are now likely to be used to control only the multiple sclerosis attacks are sudden and severe / severe.
Interferon

Since 1993, drugs that alter the immune system, especially interferon-interferon, have been used to control multiple sclerosis. Interferon-interferon is a protein messengers are created and used by the cells of the immune system to communicate with each other. There are different types of interferons-interferon, such as alpha, beta, and gamma. All of interferon-interferon has the ability to regulate the immune system and plays an important role in protecting against viral infections. Each interferon function differently, but their functions overlap (overlap). Interferon beta-interferon has been found useful in controlling multiple sclerosis. Interferon beta-1b (Betaseron ) is the first interferon approved for the control of RR-MS in 1993. In 1996, interferon beta-1a (Avonex ) received FDA approval for RR-MS.

Overall, patients treated with interferon-interferon had fewer relapses, a relapse or longer intervals between relapse-recurrence. Experiments have also shown effects on slowing accumulation of disability. Side effects The most common is a syndrome such as influenza, including fever, tiredness, weakness, chills, and muscle aches. This syndrome tends to occur less frequently when therapy continues. Other side effects are common are injection site reactions, changes in blood cell counts, and abnormalities of liver tests. Liver tests and blood counts are regularly recommended remedy those patients who were receiving interferon beta-1b. With the simultaneous use of analgesics and the actions of local skin, lenience in interferon-interferon has increased.

Clinical trials of beta interferon drugs in patients with first attack of multiple sclerosis showed that in this early patient population, these drugs delay the onset of the second attack. Avonex  is given intramuscularly once a week, Betaseron  administered subcutaneously every other day, and Rebif administered subcutaneously three times per week.
Interferon Beta available include:
IFN beta-1b (Betaseron ) used for the treatment of relapsing forms of multiple sclerosis, to reduce the frequency of recurrence, clinical recurrence. Patients with multiple sclerosis that its effectiveness has been demonstrated include patients who have experienced a first clinical episode and have MRI features consistent with multiple sclerosis.

IFN beta-1a (Rebif ) used for the treatment of patients with relapsing forms of multiple sclerosis to reduce the frequency of recurrence, clinical recurrence and delay the accumulation of physical disability. The effectiveness of Rebif  in chronic progressive multiple sclerosis who still has not been established.

IFN beta-1a (Avonex ) used for the treatment of patients with relapsing forms of multiple sclerosis uto slow accumulation of physical disability and reduce relapse-recurrence frekwenai from the clinic. Patients with multiple sclerosis that its effectiveness has been demonstrated include patients who have experienced a first clinical episode and MRI have features consistent with multiple sclerosis. Safety and efficacy in patients with chronic progressive multiple sclerosis who still has not been established.

Other Medications
Glatiramer acetate

Glatiramer acetate (Copaxone) is another drug approved to modify the disease to reduce the frequency of relapse-recurrence in RR-MS. Glatiramer acetate is a synthetic amino acid mixture (manmade) that might resemble a protein component of myelin. It is estimated that the immune system reaction against myelin in multiple sclerosis might be thwarted by glatiramer acetate. A reaction that occurs immediately after the injection of glatiramer acetate is common, affecting one in 10 patients. The reaction may involve flushing, chest pain or tightness, palpitations, fear, shortness of breath, tightness in the throat, or hives. The reaction usually disappears within 30 minutes and requires no maintenance. Some patients may be at risk of developing lipoatrophy, inflammation and damage of the tissue under the skin at the injection site. Glatiramer acetate is used to reduce the frequency of relapse-recurrence in patients with relapsing-remitting multiple sclerosis.
Natalizumab
Natalizumab (Tysabri ) is a drug approved by FDA for treating multiple sclerosis. Natalizumab is a monoclonal antibody against VLA-4, a molecule required for immune cells to attach to other cells, penetrate the blood-brain barrier and enters the brain. He administered via monthly intravenous infusions. He carried a warning for a potentially fatal disease, progressive multifocal leukoencephalopathy (PML), a viral infection of the brain that usually leads to death or severe disability. For this reason only those patients who had signed a contract for this treatment under a controlled drug distribution program can obtain this treatment.

Natalizumab is used as a monotherapy for the treatment of patients with relapsing forms of multiple sclerosis to delay the progression of physical disability and reduce relapse-recurrence frequency of clinic. Safety and efficacy of natalizumab for more than two years is unknown. Because natalizumab increases the risk of PML, it is generally recommended only for patients who have had an inadequate response to, or unable to tolerate multiple sclerosis therapies are changing.
Mitoxantrone

Mitoxantrone (Novantrone) is also approved by the FDA for the treatment of multiple sclerosis. Mitoxantrone is a chemotherapeutic drug that bring in the risk of side effects serious cardiac or cancer. Because side effects are serious, doctors tended to reserve its use for cases of more advanced or worsening of multiple sclerosis.

Mitoxantrone is used to reduce neurological disability and or frequency of recurrence, clinical recurrence in patients with secondary (chronic) progressive, progressive relapsing, or worsening relapsing-remitting multiple sclerosis (eg, patients with state of nerves is significantly abnormal between relapses -recurrence). Mitoxantrone is used in the treatment of patients with primary progressive multiple sclerosis.

Direction-Future Directions for Controlling Multiple Sclerosis

There is a great deal of ongoing research on multiple sclerosis, and they continue to be a focus on immune system therapies in the investigation. In addition, scientists are trying to develop techniques that allow brain cells to produce new myelin or the nerve to prevent death. Other approaches are promising including the use of precursor cells (neuronal stem or progenitor) that can be implanted into the brain or spinal cord (spinal cord) to re-inhabit areas that lose cells. Future therapies might involve methods that are designed to improve the impulses that travel through the nerves are damaged. Scientists also are investigating the effects of diet in multiple sclerosis.