From Publishers Weekly
Type 1 diabetes, Crohn’s disease, lupus, rheumatoid arthritis—all these increasingly common illnesses are autoimmune diseases in which the immune system attacks the body’s own tissues or nervous system. Equally alarming, as journalist Nakazawa tells us, is researchers’ growing suspicion that autism may be an autoimmune disease, brought on in part by genetic predisposition, exposure of young bodies to man-made chemicals and perhaps viral triggers. Nakazawa (D (more…)

Review
“…provides valuable information on managing one’s own disorder and lists treatments and possible new ways to alter immune responses.” — New York Times, July 1, 2003″These disorders pose unique treatment challenges, and this up-to-date information provided will be welcome in women’s health collections.” — Library Journal, February 2003…delivers a comprehensive picture of the disease… — Associated Press, 2003 Health & Fitness Book Feature
–This text refers to an o (more…)

Symptoms associated with Sjögren’s are caused by the infiltration of immune-system cells, usually B and T lymphocytes, into the glands responsible for secreting fluid. This condition can affect people of any age, but symptoms usually appear between the ages of 45 and 55. In Sjogren’s syndrome, your immune system attacks the glands that make tears and saliva. Sjögren’s may also cause dryness of other organs, affecting the kidneys, GI tract, blood vessels, lung, liver, pancreas, and the central nervous system. Many patients experience debilitating fatigue and joint pain. Symptoms can plateau, worsen, or go into remission. While some people experience mild symptoms, others suffer debilitating symptoms that greatly impair their quality of life. Virtually all organs may be involved. The disease commonly affects the eyes, mouth, parotid gland, lungs, kidneys, skin, and nervous system. Sjogren’s syndrome can also cause problems in other parts of the body, including the joints, lungs, muscles, kidneys, nerves, thyroid gland, liver, pancreas, stomach and brain.

Sjögren’s occurs in all age groups in both women and men. It is estimated to strike as many as 4 million people in the United States. Sjogren’s Syndrome is also found more commonly in families that have members with other autoimmune illnesses, such as systemic lupus erythematosus, autoimmune thyroid disease, juvenile diabetes, etc. Sjögren’s syndrome—dryness, fatigue, pain, head and neck complaints, hoarseness, or hearing loss—can also occur as a result of medication use, anxiety and depression, or normal aging. The majority of the patients with Sjögren’s syndrome have symptoms related to diminished lacrimal and salivary gland functions. The initial manifestations may be nonspecific, such as arthralgias, Raynaud’s phenomenon and fatigue, and usually 8 to 10 years elapse from the initial symptoms to the full-blown development of the disease. Patients usually complain of difficulty in eating dry food (like trying to eat crackers without water), inability to speak continuously, oral soreness, changes in tasting and smelling and fissures of the tongue and lips (angular queilitis).

Treatment is generally symptomatic and supportive. Infections are treated with anti-fungal or antibiotic preparations. Hydroxychloroquine (Plaquenil) has been helpful for some manifestations of Sjogren’s syndrome. Moisture replacement therapies may ease the symptoms of dryness. Nonsteroidal anti-inflammatory drugs may be used to treat musculoskeletal symptoms. Lacriserts, is used by some to alleviate dry eyes. Two prescription medications, Salagen (pilocarpine hydrochloride) and Evoxac (cevimeline), are available to treat dry mouth.. Serious complications, such as vasculitis, can require immune suppression medications, including cortisone (prednisone and others) and/or azathioprine (Imuran) or cyclophosphamide (Cytoxan). Many of these types of agents are available as over-the-counter products including toothpaste, gum, and mouthwash (Biotene). Vitamin E oil has been used with some success. Infections of the mouth and teeth should be addressed as early as possible in order to avoid more severe complications.

Autoimmune hemolytic anemia is a rare group of disorders that can happen at any age. These disorders impact women more frequently than men. Destruction of crimson blood cells by autoantibodies may happen abruptly, or it may produce gradually. In some people, the destruction may stop after a period of time, whereas in other people, it persists and becomes chronic. When the cause of autoimmune hemolytic anemia is another disease, symptoms of the underlying disease, such as swollen and tender lymph nodes and fever, may dominate. Autoimmune hemolytic anemia can also be induced by several drugs including methyl-dopa and fluarabine. In people with hemolytic anemia, red blood cells have an abnormally short life span. Hemolytic antibodies also may be induced by incompatible blood transfusions and be encountered in isoimmune anemias of newborn piglets, puppies, or foals.

Some folk with autoimmune hemolytic anemia may get no symptoms, particularly when the devastation of crimson blood cells is balmy and develops gradually. Autoimmune hemolytic anemia is characterized by a malfunction of the exempt structure that produces autoantibodies, which assault crimson blood cells as if they were substances international to the system. Others have symptoms similar to those that occur with other types of anemia, especially when the destruction is more severe or rapid. When severe or rapid destruction of red blood cells occurs, mild jaundice may also develop. Penicillin, quinine, quinidine, L-dopa, and other agents may cause immune hemolysis. A patient who needs a transfusion but does not show evidence of blood loss or bone marrow suppression may have hemolytic anemia. The onset of the disease may be quite rapid and very serious.

If symptoms are balmy or if devastation of crimson blood cells seems to be slowing on its own, no handling is needed. If crimson blood cubicle devastation is worsening, a corticosteroid drug such as prednisone is normally the best selection for handling. If prednisone does not improve the condition, a splenectomy may be considered. High doses are used at first, followed by a gradual tapering of the dose over many weeks or months. When destruction of red blood cells persists after removal of the spleen or when surgery cannot be performed, immunosuppressive drugs, such as cyclophosphamide or azathioprine, are used. Plasmapheresis, which involves filtering blood to remove antibodies, is occasionally helpful when other treatments fail. Blood transfusions are given with caution, if indicated for severe anemia, because of the potential that blood may not be compatible and may bring on a reaction.

Autoimmune inner ear disease is a rare disease occurring in less than one percent of the 28 million Americans with a hearing loss. Both allergy and traditional autoimmune disease such as ankylosing spondylitis, systemic lupus erythematosus, Sjoegren’s syndrome, cogan’s disease, ulcerative colitis, wegener’s granulomatosis, rheumatoid arthritis, and scleroderma can cause or be associated with AIED. The condition has been suggested to be more common in female patients who may or may not have concomitant systemic autoimmune disease than in male patients. Autoimmunity occurs with loss of homeostatic control in the immune system. Host tissues become recognized as foreign and induce damaging vasculitis and fibrosis. Veldman described a continuum of autoimmunity. On one end, organ specific responses with organ specific autoantibodies and T cells produce tissue alteration.

The symptoms of autoimmune inner ear disease are abrupt hearing departure in one ear progressing quickly to the second ear. The hearing departure can advance over weeks or months. Vestibular role may be lost gradually so that intense symptoms do not happen, but patients may produce ataxia and unsteadiness more evident in dark with long-term, multilateral vestibular hypofunction. More experience with the disease has revealed this to be a rare finding and it is not considered a routine occurrence in the syndrome. Outer Ear symptoms that may be attributed to allergy include chronic itching or frequent infections of the ear canal. Meniere’s disease in one or both ears may sometimes be aggravated by allergies. Diagnosis of autoimmune inner ear disease is difficult and is often mistaken for otitis media until the patient develops a loss in the second ear.

There are several protocols for treatment of autoimmune inner ear disease. Treatment goals in autoimmune inner ear disease include improving speech thresholds to levels treatable with hearing aids in severely affected patients and recovery of hearing to near normal levels in those with mild to moderate losses. Most patients with autoimmune inner ear disease respond to the initial treatment of steroids, prednisone, and methotrexate, a chemotherapy agent. Some patients may benefit from the use of hearing aids. In persons with response to steroids, in most cases a chemotherapy type of medication such as cytoxan or will be used over the long term. The medicine can be put right into the inner ear under local anesthesia, or through the use of tiny ear tubes put in place surgically. Not all people respond to steroid therapy the same way. Treatment in some people results in better hearing, or better discrimination or both.

Folic acid deficiency anemia. Folic acid is a member of the vitamin B family. It is used in the production of new red blood cells. Some people do not get enough folic acid in their normal diet, so their bodies are unable to produce enough red blood cells. In other cases, the body may not be able to properly use the folic acid eaten.

Causes

Idiopathic autoimmune hemolytic anemia is an acquired disease that occurs when antibodies form against a person’s own red blood cells. In the idiopathic form of this disease, the cause is unknown.

There are other types of immune hemolytic anemias where the cause may result from an underlying disease or medication. Idiopathic autoimmune hemolytic anemia accounts for one-half of all immune hemolytic anemias. The onset of the disease may be quite rapid and very serious.

Symptoms

Symptoms in AIHA vary according to the severity of the condition. Common symptoms include fever, fatigue, pale skin, weakness, dizziness, confusion, low blood pressure, intolerance to physical activity, enlarged liver, increased heart rate and heart murmur. When RBC destruction is rapid, mild jaundice, a yellowing of the skin and eyes associated with dark urine can occur. If RBC destruction persists for extended periods, the spleen can become enlarged, causing symptoms of abdominal fullness or bloating.

When the cause of autoimmune hemolytic anemia is another disease, symptoms of the underlying disease, such as swollen and tender lymph nodes and fever, may dominate.

Conventional medical treatments may help relieve the symptoms of autoimmune hemolytic anemia but they do not address the root of the problem. Generally, by undergoing comprehensive natural medicine testing, the reasons the body is producing antibodies against itself can be found. Some of these reasons include sensitivities or allergies to foods, inhalants and chemicals and various infections.

Diagnosis

Your doctor will ask about your symptoms, medications, and medical history, and perform a physical exam. You will most likely be referred to a hematologist.

Tests may include the following:

Extensive blood testing

Urinalysis

Treatment

In cases where symptoms of autoimmune hemolytic anemia are mild, or when the destruction of red blood cells seems to be decreasing on its own, individuals may not require any medical treatment.

However, in cases when anemia is caused by an underlying source, such as mononucleosis or viral medications used to treat mono, treatment will usually involve dealing with this underlying cause. Treatment may also involve taking immune system suppressant drugs such as steroids or gamma globulin to help suppress the system’s attack of red blood cells.

The most frequent course of therapy for AIHA is the administration of high doses of corticosteroids such as prednisone, which have a pronounced anti-inflammatory and immunosupressive action that impairs functions of various components of the immune system. Once the disease is in remission, low dose, intermittent therapy is continued for several months. Some dogs, however, do not respond to corticosteroid treatment and require more potent immunosuppressive drugs that are often combined with corticosteroid treatment. Such drugs include cytotoxic agents such as azathioprine and cyclophosphamide.

Review”The authors use first-person accounts to illustrate their advice on coping simultaneously with symptoms and the challenges of the workplace; developing a financial plan; communicating with coworkers, employers, and loved ones; building a support team; and balancing work and family responsibilities. A little book with lots of useful advice; recommended.”— Library Journal”An essential resource and guide for women living with autoimmune diseases, such as rheumatoid arthritis, lu (more…)

The most common form of hyperthyroidism is Graves’ disease. In newborns, the most common cause of an overactive thyroid is called neonatal Graves disease, which can be life threatening. However, hyperthyroidism rarely occurs in children and adolescents. It is named after Robert Graves, the 19th century Irish physician who first discovered the condition. In Graves’ disease, the thyroid gland in the neck is diffusely enlarged and hyperactive, producing excessive thyroid hormones. Graves’ disease can have an effect on many parts of the body such as the nervous system, eyes, skin, hair/nails, lungs, digestive system, muscles/bones and reproductive system.

Graves disease can run in families. The rate of concordance for Graves disease is about 20% among monozygotic (identical) twins, and the rate is much lower among dizygotic (nonidentical) twins, indicating that genes make only a moderate contribution to the susceptibility to Graves disease. No single gene is known to cause the disease or to be necessary for its development. There are well-established associations with certain HLA types. Linkage analysis has identified gene loci on chromosomes 14q31, 20q11.2, and Xq21 that are associated with susceptibility to Graves disease.

Causes

Graves’ disease involves the immune system of the body. Normally, the immune system protects you from infection and abnormal body cells by recognizing and destroying cells using antibodies, which are produced by blood cells known as lymphocytes. In Graves’ disease, the lymphocytes in the body’s immune system produce antibodies that actually attack the body’s own tissue instead of protecting. Due to a result of this attack, the antibodies cause the thyroid gland to overproduce thyroid hormones.

Symptoms

Classic symptoms include goiter (an enlarged thyroid), nervousness, heat intolerance, weight loss despite increased appetite, sweating, diarrhea, tremor, and palpitations.

Abnormally protruding eyeballs are a classic sign but don’t occur in all cases.

Treatment

Currently there is no treatment available to halt production of the antibodies that cause hyperthyroidism. However, there are three courses of study of treatment available to assist Graves’ disease patients have more normal grades of thyroid internal secretion and to command their symptoms. Anti-thyroid drugs are utilized to diminish the production of thyroid internal secretion. This treatment will consequence in prolonged remittal of the disease in about 20 to 30 percentage of patients and usually those with milder disease at the beginning of treatment.

Anti-thyroid drugs which inhibit production or conversion of the active thyroid hormone.

Surgical removal of most of the thyroid gland is the other alternative for severe cases of Graves’ disease.

Fevers are treated with cooling measures and antipyretics.

Radioactive iodine. The radioactive iodine damages thyroid cells, shrinking and eventually destroying the thyroid gland in order to reduce hormone levels. Like surgery, this condition usually leads to hypothyroidism, so that thyroid hormone supplement medication is needed for the rest of the patient’s life.

Crohn’s disease (also known as regional enteritis) is a chronic, episodic, inflammatory bowel disease (IBD) and is generally classified as an autoimmune disease. Crohn’s disease can affect any part of the gastrointestinal tract from mouth to anus as a result, the symptoms of Crohn’s disease vary among afflicted individuals. The disease is characterized by areas of inflammation with areas of normal lining between in a symptom known as skip lesions. The main gastrointestinal symptoms are abdominal pain, diarrhea (which may be bloody, though this may not be visible to the naked eye), constipation, vomiting, weight loss or weight gain.

What are the symptoms?

The most common symptoms of Crohn’s disease are abdominal pain, often in the lower right area, and diarrhea. Rectal bleeding, weight loss, arthritis, skin problems, and fever may also occur. Bleeding may be serious and persistent, leading to anemia. Children with Crohn’s disease may suffer delayed development and stunted growth. The range and severity of symptoms varies.

Blood in your stool. Food moving through your digestive tract can cause inflamed tissue to bleed, or your bowel may also bleed on its own.

Feeling generally unwell – fever and extreme tiredness,

Loss of appetite and weight,

What causes Crohn’s disease?

The cause of Crohn’s disease is unknown. Some scientists suspect that infection by certain bacteria, such as strains of mycobacterium, may be the cause of Crohn’s disease. To date, however, there has been no convincing evidence that the disease is caused by infection. Crohn’s disease is not contagious.

The body’s immune system, which protects it against many different infections, is known to be a factor. There are still a number of unknowns about the cause of the disease. Fortunately, a great deal is known about the disease and especially its treatment.

Treatment of Crohn’s disease

Biologic therapies. In August 1998, the FDA approved the first biologic therapy for Crohn’s disease. This was infliximab (Remicade®), which is indicated for moderately to severely active Crohn’s in patients who have not responded adequately to conventional therapy.

Crohn’s disease makes it hard for your body to absorb nutrients from food. A meal plan that focuses on high-calorie, high-protein foods can help you get the nutrients you need. Eating this way may be easier if you have regular meals plus two or three snacks each day.

Steroids are generally used for people who have more severe disease. In more aggressive disease, steroids may be used with immunosuppressants or with a newer medicine called infliximab (brand name: Remicade). If you have very severe Crohn’s disease, you may need to stay in the hospital. Sometimes surgery is needed, but it cannot cure the disease.

Drug Therapy

Drugs are used to suppress the inflammatory response associated with Crohn’s disease, which in turn helps the intestines to heal and relieves symptoms. Once symptoms are under control, medications are used to decrease the frequency of flare-ups and prevent symptoms from recurring. There are several types of drugs available to treat Crohn’s disease including aminosalicylates, corticosteroids, immune modifiers and biologic therapy.

Diabetes is caused by the body resistance to, or deficiency of the hormone insulin which helps in removal of excess sugar from the blood stream into the body cells so that it can be used as a source of energy.

If this hormone insulin is deficient or ineffective, blood sugar rises causing excessive urination, hunger and thirst. Apart from excess urine, additional symptoms may include weight loss, nausea, vomiting, blurred vision, irritability, weakness and fatigue.

There are two main types of diabetes:

Type 1: Insulin dependent diabetes mellitus (IDDM) or otherwise known as juvenile onset diabetes, this type normally starts at childhood or early adulthood and has a very strong genetic components. This type is characterized by a complete lack of insulin as the name implies and must be treated with regular insulin injections.

This type 1 diabetes is also an autoimmune disease (that is a condition whereby the body disease fighting immune system attacks the healthy tissues and cells). In this case the immune system attacks and destroys insulin producing cells in the pancreas.

Type 2: Non-insulin dependent diabetes mellitus (NIDDM) or maturity onset diabetes tends to develop in middle age or older individuals particularly those who are obese.

In this case the pancreas secrets enough insulin, but the body cells seem resistant to the effects making the body to release more insulin in the blood by trying to overcome the resistance.

Most cases of type 2 diabetes can be managed with a combination of diet, exercise and oral medication. Symptoms include repeated infections or skin sore that heals slowly or not at all, numbness in the hand or feet, tiredness and nausea.

For women, it is particularly important because diabetes seems to affect the female hormone and as a result, many women with diabetes develop coronary heart disease. Diabetes may cause blockage of large blood vessels that can lead to severe cardiovascular problems.

Studies have shown that some environmental factors can trigger type 1 diabetes in people with genetic predisposition for the disease.

Researchers attribute type 2 diabetes to obesity. So every pound of excess weight you gain increases your chance by 5 per cent at least.

Treatment includes controlling the amount of glucose in your blood stream depending on the type of diabetes, physical exercise, controlled diet and medication makes it less common. Most importantly, check your blood sugar regularly and see your physician for a more qualified advice.

A couple of drugs like, Glucophage, Actos, Precose, Avandis and many others have been developed to help with type 2 diabetes. Consult your doctor for a detailed and proper form of treatment.

To learn more about diabetes and heart diseases http://www.heartcares.blogspot.com

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