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Autoimmune Illness Symptoms – What is The Real Source?

April 23rd, 2012 No comments

You can only submit entirely new text for analysis once every 10 seconds.n out of the bloodstream (to help its survival) and sequestering it into the fatty tissue. This is considered a safer storage than in the bloodstream itself.

Our bodies then release chemicals to convert these fat-soluble poisons into a water-soluble form so that they can be eliminated through the stool and the kidney. However, the higher the toxic load, the more compromised the detoxification pathways and the more overtaxed the organs of elimination. Consequently, this bio-accumulation of contaminants stays stored in the organs and tissue. While there, they compete for the same biological space as many nutrients. Therefore, one becomes both poisoned AND undernourished.

To add insult to injury, these contaminants create a hospitable terrain where opportunistic organisms can thrive. This can lead to a yeast and fungal overgrowth in the small intestine, as well as to the increase of bad bacteria, parasites, and a condition called leaky gut, where more toxins from the gut “leak’ into the bloodstream.

All of this triggers what the Japanese call “diseases of the toxic burden”.

What Is The Autoimmune Reaction To All Of This?

When bio-accumulation in the gut and in the tissue becomes extremely elevated, or when a toxin is introduced into the bloodstream in a condition of “leaky gut”, this triggers a reaction where auto-antibodies are released. The initial intention of these auto-antibodies is to find these toxins, these pathogens, and to inflame them so that the white blood cells can use the inflammation as markers to destroy these invaders. However, because this toxic insult is so prevalent, and because this auto-antibody release is 24/7, surrounding healthy tissue also gets inflamed, a sort of collateral damage. After a while, cellular communication breaks down completely and the auto-antibodies cannot distinguish between a pathogen and one’s own healthy tissue. This is when the full force of the body’s immune function turns on itself – a case of misplaced immunity or autoimmunity.

The more the planet carries this burden, the more human bodies carry this burden – and the more the body adapts in creative and confused ways. Many of the autoimmune disorders that are so prevalent now were not around even 25 or thirty years ago. Thirty-five years ago, did you know anybody with fibromyalgia or environmental sensitivity or Type II diabetes or chronic fatigue? How about Autism or symptoms along that spectrum like attention deficit? How about “dry eye syndrome” or the numerous folks you meet who have a sluggish thyroid or a candida infestation? How about the increasing numbers of people who have gluten, casein, corn or soy sensitivities? How many people did you know 30 years ago who could not eat dairy? Or be in the same room as someone with perfume?

All these are autoimmune in nature. And all these are triggered by the increasing toxic insult by our preserved, make-believe foods and by our environment.

Modern man equals great creative innovations. And modern man also equals a slow destruction of the human organism.

The Final Say

We all believe that we “get” these disorders when, in actuality, we “do” these disorders, unintentional though it may be. Our health, or lack of it, is the by-product of our lifestyle choices: the foods that we eat, the air that we breathe, the water that we drink, the attitudes and the stress that we hold. It is said that “Genetics loads the gun, but environment pulls the trigger” and it is no more true than it is today. We cannot control our genetics, but we can make conscious, informed and loving choices about our environment – both inner and outer terrains.

Very simply, the key lies in taking the poison out of our tissue and brains AND in getting proper, whole food nutrition and supplements to our cells. Address our toxic load and the subsequent undernourishment. This we can control!

The answers do not lie in a laboratory where someone is going to discover “the magic bullet” that saves us all. No one else can give us what we refuse to give ourselves. And no one can deny us what we freely give to ourselves.

There is no magic bullet. Never has been. Technology and the control by the vested interests is not the key. Empowering yourself with honest information and then having the courage and the discipline to implement it into your life IS the key.

Genetics DOES load the gun, but the trigger does not HAVE to be pulled. It is up to each of us, first as individuals, and then as the collective. We can grow more conscious and more healthy together.

Lupus Symptoms in Pregnant Women

September 9th, 2011 No comments

Lupus Symptoms in Women – Pregnancy

lupus symptoms in women

lupus symptoms in women

Lupus Symptoms in women is surely an autoimmune disease which commonly affects women, although men can also have the lupus symptoms,  and often many experts have said that women who have lupus symptoms cannot become pregnant due to their condition. However, this myth has been denied by specialists, approximately 50% of  pregnant women who has lupus symptoms can have a ordinary pregnancy and give birth healthy babies. Conversely, some women might possibly face complications and even lose their fetuses during the pregnancy.

Whilst many pregnancies with lupus are totally natural, women risk to facing problems over their pregnancy. The expectant mother with lupus need to be supervised by an expert doctor (obstetrician) till the end of pregnancy,  in other words, the health risk of the mother’s is definitely diminished and normal babies are usually born. In addition, women with lupus symptoms must obey the doctor’s instruction manuals.

Pregnant women with symptoms of lupus may perhaps face particular symptoms which includes rashes and lupus flare which can appear because of an increased blood flow in the skin, growth of new hair during pregnancy plus severe hair loss after the baby born.

One of the important things we need to notice is that 20% of lupus patients who are pregnant tend to have an abrupt rise in BP (blood pressure), protein in the urine, a condition which you’ll find known as Preeclampsia or toxaemia and degree of serious treatment as well as immediate delivery. The presence of antibody called anti-phospholipid antibody could occur to lupus pregnancies which is another serious complications.  Anti-phospholipid antibody can minimize the function of the placenta by bring about blood clots, as well as blood clots within the placenta, making the placenta to higher risks. Neonatal Lupus Syndrome can occur in lupus pregnancy when the unborn children are exposed to an antibody known as anti-ro or anti-SSA. In many events, women who has severe form of lupus symptoms in pregnancy  have to get through a caesarian section to conserve the premature baby.

Even though, lupus patient in remission generally have less problem when compared with women with activate lupus, a balanced healthy diet could actually help a lot throughout the pregnancy. There are some golden rules to be followed by pregnant woman living with lupus, they are: regularly visits on the doctor, proper prescription of  medication, stay away from pills that can put the baby’s life in danger, a sensible food diet, as well as no bad habits like smoking or drinking.

In conclusion, a normal pregnancy can be carried on by pregnant women who put up with lupus symptoms if  they follow the suitable management and have an equalize standard of living. Moreover, it has been taken into account that most medications for Systemic Lupus Erythematosus (SLE) are safe to be used during the pregnancy given that that they don’t pass through the placenta.

Systemic Lupus Erythematosus Can Create Death

September 6th, 2011 No comments

Nobody passes away from lupus ~ many die from the difficulties.

Systemic Lupus Erythematosus Can Cause Death

Lupus is problematic to detect in addition to more challenging to manage. There is no solitary examination that diagnoses Systemic Lupus Erythematosus (SLE) which is incurable, chronic problem.

Wide spread Lupus Erythematosus happens to be a not curable autoimmune ailments, which holds the potential to disable and take lives therefore invading: healthy and balanced skin cells, tissues, central nerves (CNS), numerous physical systems, blood, and important body organs – brain, heart, lungs, renals and so on

. SLE is not transmittable nor cancerous, and in fact it is quite common. It is pertained to far more frequent than AIDS, Spastic paralysis, Sickle Cell Anemia, Cystic Fibrosis and Multiple Sclerosis (MS) ~ collaborated.

Everybody, men or females, young people, and the aging adults can create lupus – despite the fact that, even more ladies are normally more likely compared to guys for being diagnosed with Systemic Lupus Erythematosus. There are much more Eastern lupus people, rather ased opposed to Caucasians, who require, and are most likely to get, the illness.

There are 4 acknowledged types of lupus, baseding on the American Lupus Foundation:.

    • Cutaneous Lupus Erythematosus
    • Drug-induced Lupus Erythematosus
    • Neonatal Lupus
    • Systemic Lupus Erythematosus

Systemic lupus is the most regular type of lupus, in addition to being exactly what a lot of people mean if they refer to “lupus.” Wide spread Lupus Erythematosus is normally moderate or considerable.

Where Does Systemic Lupus Erythematosus strike?

Systemic lupus erythematosus, which is not treated, could be dangerous. The symptoms are so considerable as the condition itself. Among several saddest facts of the disease is that it’s generally not diagnosed prior to the patient comes to be, in the short-term or entirely, crippled or exists to a dangerous stage on the ailment.

The Symptoms are various from a person to the various other person, consisting of: distressing debilitating joint, and chronic fatigue, seizures and important/vital organ (lungs, kidneys, mind and heart) does not partner correctly, memory issues (aka lupus fog) in addition to confusion, arteriosclerosis, aching throats, hair thinning and even fevers, a breakout over the bridge of the nose and cheeks (butterfly breakout).

Problems could not be shown by an un-diagnosed person, while the illness is working surreptitiously attacking the blood circulation by creating blood clots. These embolism could take place in anywhere within the body, featuring the mind and lungs. This might cause a stroke, possibly fatality. Just like any sort of life-altering or perhaps deadly conditions, the morbidity Systemic Lupus Erythematosus applies can be devastating if left without treatment.

Lupus Symptoms: How to Identify

August 3rd, 2011 No comments

Lupus Symptoms– The best ways to Determine

Symptoms of Lupus

Systemic lupus erythematosus (SLE) is a chronic inflamed problem of unidentified cause that could have an effect on the joints, skin, heart, renal systems, nerves, lungs, serous membranes and/or other organs of the body, therefore, lupus symptoms are differ. SLE is characterized by cells and cell damages from pathogenic autoantibodies and immune complexes. Ninety percent of patients are women in childbearing years and the illness is a lot more common in African Americans. Multiple body organ system indications can take place, including musculoskeletal (arthralgias, myalgias), cutaneous (malar breakout, photosensitivity, hair loss), renal (nephritis, nephritic disorder), stressed (seizures, hassles), cardiopulmonary (pericarditis, pleuritis), hematologic (anemia, leukopenia). Immunologic problems, in particular the generation of a quantity of antinuclear antibodies, are another noteworthy attribute of the disorder. There are many kinds of lupus, Systemic lupus erythematosus which influences different physical body parts is the most typical kind, the others are Subacute Cutaneous lupus erythematosus – generates skin sores on components of the body subjected to the sunlight, Discoid lupus erythematosus – causes a skin rash that doesn’t go away entirely, Drug-induced lupus – could be induced by medications, Neonatal lupus – an uncommon type of lupus that impacts newborn babies.

The medical advancement of Wide spread lupus erythematosus is varied and can be represented by patterns of remissions and lasting or severe relapses. Ladies, primarily in their 20s and 30s, are had an effect on much more frequently than guys.

People with SLE are subject to a lot of symptoms, troubles, as well as inflamed participation that might have an impact on virtually every body organ. The most frequent pattern is a mix of constitutional problems with skin, medium hematologic, serologic involvement, in addition to musculoskeletal. On the other individual hand, a number of people have mainly kidney, hematologic, or central nerve fibers manifestations. The particular pattern that dominates through first couple of years of the disease is likely to control later.

Lupus Symptoms, Constitusional – 50 – 100 % of clients has fever, fatigue, and fat burning. Over 50 percent of lupus symptoms is fever that is believed to be because of active illness. 60 % of the fevers were thought to be due to lupus, 23 % to infection, and 17 % to various other reasons. Threat elements for infection: long-lasting disease damage, neutropenia, hypocomplementemia, lymphopenia, energetic lupus disease, renal participation, neuropsychiatric signs, and using glucocorticoids and other immunosuppressive drugs. A lot of fevers as a result of energetic SLE will certainly transmit with usage of acetaminophen, nonsteroidal anti-inflammatory drugs (NSAIDs), and/or low to medium dosages of corticosteroids, if it does not, the suspicion of a contagious or medicine associated etiology is risen.

Lupus symptoms in women

Low Energy or tiredness happens in 80 – 100 % of lupus symptoms, and often the most debilitating. Its existence in not obviously correlated with other measures of disease activity. Hence fatigue is highly correlated with reduced physical exercise tolerance. However, fatigue might not be caused by active SLE, yet to one or more of the following: depression, increased work load, poor habits (smoking, less active living, substance abuse), stress or anxiety, hypothyroidism, anemia, use of specific medications (such as beta-blockers, prednisone), any inflammatory and/or contagious disease, coexistent fibromyalgia, sleeping disturbances and/or deconditioning, or a perception of inadequate social support. Fatigue caused by SLE may respond to antimalarials and glucocorticoids.Weight gain in lupus is commonly caused by one of two factors: salt and water retention associated with hypoalbuminemia, or increased appetite associated with the use of glucocorticoids.Weight loss often occurs before the diagnosis of SLE. Unwilled weight loss could be because of decreased appetite, the side effects of drugs (especially diuretics or antimalarials), and gastrointestinal disease such as (GERD) gastroesophageal reflux disease, abdominal pain, pancreatitis, or peptic ulcer disease.

Here is a list of Lupus Symptoms 

General Symptoms : Photosensitivity (sensitive to the sun light), Fatigue, Malaise, Hair Loss, Weight gain or loss, Fever
Central Nervous System : Lupus Headaches, Fibromyalgia, CNS Vasculitis
Cardio-Vascular System : Antiphospolipid Syndrome, Anemia, Chest Pain when taking a deep breath, Myocarditis, Endocarditis
Gastrointestinal Tract : Gastroesophageal Reflux Disease, Lupus Hepatitis, Chronic Diarrhoea, Nausea and Vomitting, Ascites
Musculoskletal System : Arthritis, Muscle Pain, Fibromyalgia
Reproductive System : Lesion(s) in genital area, Loss of Libido, Increase Miscarriage rate
Kidney : Lupus Nephritis
Skin : Discoid Lupus Erytemathosus, Malar Rash / Butterfly Rash, Tumid Lupus Erythematosus, Raynaud’s Phenomenon, Lupus Panniculitis, Purpura, Subacute Cutaneus Lupus
Mouth and Nose : Mucosal Discoid Lupus, Mouth and Nose Ulcers, Bullous Systemic Lupus Erythematosus
Lungs : Pleuritis, Shortness of breath, Chest Pain
Other Organs : Eye Problem, Lupus Thyroiditis, Swollen Glands, Rhinitis nonallergica

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How Is Lupus Diagnosed?

Lupus is not diagnosed with single test only. The diagnosis might take several months or years, as your doctor has to piece together the puzzle of symptoms of this complex disease in order to be diagnosed accurately. Knowledge and awareness of  the doctor and also good communication from the patient are important so that the correct diagnosis can be made. Some test for lupus or tools may be required by your doctor to make the diagnosis of lupus, such as :

  • Medical history
  • Complete physical examination
  • Complete blood count (CBC)
  • Blood chemistries
  • Erythrocyte sedimentation rate (ESR)
  • Urinalysis
  • Complement levels
  • Antinuclear antibody test (ANA)
  • Other autoantibody tests (anti-DNA, anti-Sm, anti-RNP, anti-Ro [SSA], anti‑La [SSB])
  • Anticardiolipin antibody test
  • Skin biopsy (looking at skin samples under a microscope)
  • Kidney biopsy (looking at tissue from your kidney under a microscope).
  • X rays and other imaging tests can help doctors see the organs affected lupus

Criteria for classification of SLE
(SLE = 4 or more of these 11 criteria)

  • Malar (butterfly) rash
  • Discoid rash
  • Photosensitivity
  • Arthritis
  • Oraulcers
  • Serositis (pleurisy or pericarditis)
  • Renadisorders (proteinuria or casts)
  • Neurologicadisorders (intractable headache, seizures or psychosis)
  • Haematologicadisorders (haemolytic anaemia, leucopenia, lymphopenia or thrombocytopenia)
  • Immunologicadisorders (positive LE cells, anti-DNA, anti-Sm or false positive syphilis serology)
  • Positive antinuclear antibody

Diagnostic tests

  • ESR—elevated in proportion to disease activity
  • antinuclear antibodies (ANA)—positive in 95% (key test)
  • double stranded DNA antibodies—90% specific for SLE but present in only 60% (key test)
  • rheumatoid factor—positive in 50%
  • LE test—inefficient and not used

The diagnosis cannot be made on blood tests alone. Supportive clinicaevidence is necessary.

Management

Appropriate explanation, support and reassurance, use of sunscreens
Refer to consultant for shared care
Drug treatments

  • mild: NSAIDs (for arthralgia)
  • moderate (esp. skin, joint serosa involved): low-dose antimalarials, e.g.
  • hydroxychloroquine up to 6 mg/kg once daily
  • severe: corticosteroids are the mainstay immunosuppressive drugs, e.g. azathioprine

Avoid drugs in those in clinicaremission and with normacomplement levels
Other treatments such as plasma exchange and immunosuppressive regimens available for severe disease

 

Related Article you might like Lupus symptoms in women, Rheumatoid Arthritis Symptoms and Diagnosis

Recommended Books for Lupus

Rheumatoid Arthritis Manifestations and Diagnosis

May 23rd, 2011 No comments

Rheumatoid Arthritis

Exactly what is Rheumatoid arthritis – Rheumatoid arthritis (RA) is among autoimmune ailments which is a chronic or long-term inflammatory problem. RA is the commonest chronic inflammatory polyarthritis and affects about 3 % of the populace. The symptoms create slowly, and could differ from a mild to a most extreme debilitating expression. It might consist of joint pain, tightness, and swelling. The condition can influence numerous cells throughout the body, yet the joints are typically most severely impacted. The cause of rheumatoid arthritis is unknown.

RHEUMATOID ARTHRITIS DANGER ELEMENTS – The particular reason for rheumatoid arthritis is still not understood yet. Sensitivity aspects and Launching elements, nonetheless, have been presumed as elements that can affect an individual’s danger.

Susceptibility factors— RA more than likely creates when a prone person is subjected to factors that begin the inflammatory process. Heredity, gender, and genes mostly figure out an individual’s possibility of developing rheumatoid arthritis. Around 1 per 100 individuals has actually rheumatoid arthritis.

  • Heredity – RA is not a received disease. Genes do not trigger rheumatoid arthritis, they just affect the risk of illness’ advancement.
  • Gender – Gender appears to take part in a major duty in an individual’s susceptibility to rheumatoid arthritis. Ladies are about 3 times more likely than males.
  • Specific genes – Person with specific variants of human leukocyte antigen (HLA) genes are most likely to get rheumatoid arthritis.

Starting aspects – Many individuals who have HLA genes never ever create the condition. As a matter of fact, when one identical twin has rheumatoid arthritis signs, the probability that the other individual will certainly establish illness is just approximately 1 in 3. This shows that aspects must be essential for a person to establish RA.

  • Infection – Bacteria or viruses could be just one of the elements that start rheumatoid arthritis.
  • Smoking – Smoking might raise the risk of creating RA and also could enhance the probability the intensity need to it happens.
  • Anxiety – Taxing occasions such as mishaps, separation and sorrow are more common in individuals with RA in the 6 months prior their diagnosis.

RHEUMATOID ARTHRITIS SYMPTOMS— In the majority of people RA starts with the perilous start of discomfort and stiffness of the little joints of the hands and feet which is on-going as opposed to short lived and mostly has an effect on the fingers where symmetrical participation of the PIP joints produces spindling while the metacarpophalangeal joints (joints in the center of the fingers) establish diffuse thickening as does the arm. Early symptoms could feature tiredness, muscle pain, a low-grade fever, fat burning, and numbness and tingling in the hands. Sometimes, these signs take place prior to joint discomfort or stiffness is obvious. In 25 % of cases Rheumatoid arthritis signs present as arthritis of a solitary joint such as the knee, a circumstance causing complication with Lyme illness or a spondyloarthropathy.

rheumatoid arthritis pictures, rheumatoid arthritis symptoms,

Joi.nts involved

  • Hands : MCP and PIP joints, DIP joints (30%)
  • Wrist and elbows
  • Feet : MTP joints, tarsal joints (not IP joints), ankle
  • Knees (common) and hip (delayed—up to 50%)
  • Shoulder (glenohumeral) joints
  • Temporomandibular joints
  • Cervical spine

Joint symptoms – These Rheumatoid Arthritis symptoms Usually begin gradually and include pain and stiffness, redness, warmth to the touch, and joint swelling. The joint stiffness is most bothersome in the morning and after sitting still for a period of time. The stiffness can persist for more than one hour.

rheumatoid arthritis symptoms

  • Hands – The joints of the hands are often the very first joints affected by rheumatoid arthritis. Between 1 and 5 % of people with rheumatoid arthritis develop carpal tunnel syndrome because swelling compresses a nerve that runs through the wrist which is characterized by weakness, tingling, and numbness of certain areas of the hand.

Rheumatoid Arthritis SymptomsCertain characteristic hand deformities can occur with long-standing rheumatoid arthritis. swan neck deformities and boutonniere deformities, and may drift together in the direction of the small finger. The tendons on the back of the hand may become very prominent and tight, called the bow string sign.

  • Wrist – The wrist is the most commonly affected joint of the arm in people with rheumatoid arthritis. In the early stages of RA, it might be not easy to bend the wrist backward.
  • Elbow – Rheumatoid arthritis may cause inflammation of the elbow. Swelling of this joint may compress nerves that travel through the arm and cause numbness or tingling in the fingers.
  • Shoulder – The shoulder may be inflamed in the later stages of rheumatoid arthritis, causing pain and limited motion.
  • Foot – The joints of the feet are often affected in the early stages of rheumatoid arthritis symptoms, especially the joints at the base of the toes.
  • Ankle – Rheumatoid arthritis may cause inflammation of the ankle. Inflammation of this joint may cause nerve damage, leading to numbness and tingling in the foot.
  • Knee – Rheumatoid arthritis may cause swelling of the knee, difficulty bending the knee, excessive looseness of the ligaments that surround and support the knee, and damage of the ends of the bones that meet at the knee. RA may cause the formation of a Baker’s cyst (a cyst filled with joint fluid and located in the hollow space at the back of the knee).
  • Hips – The hips may become inflamed in the later stages of rheumatoid arthritis symptoms. Pain in the hips may make it difficult to walk.
  • Cervical spine – Rheumatoid arthritis symptoms may present as an inflammation of the cervical spine, which is the area between the shoulders and the base of the head.
  • Cricoarytenoid joint -In about 30 % of people with rheumatoid arthritis symptoms, there is inflammation of a joint near the windpipe called the cricoarytenoid joint. Inflammation of this joint can cause hoarseness and difficulty breathing.

Other Rheumatoid Arthritis Symptoms  – Although joint problems are the most commonly known issues in rheumatoid arthritis, the condition can be associated with a variety of other problems.

  • Rheumatoid nodule – Rheumatoid nodule is painless lumps that appear beneath the skin. The nodule may move easily when touched or they may be fixed to deeper tissues.
  • Felty’s Syndrome : Characterized by an abnormally enlarged spleen (splenomegaly).
  • Amyloidosis : Infiltration of the liver, kidneys, spleen and other tissues with amyloid (starch like substance).
  • Inflammatory conditions – Rheumatoid arthritis may produce a variety of other symptoms, depending on which tissues are inflamed.
  • Pericarditis : Inflammation of the pericardium, tissue lining the chest cavity and surrounding the heart that may cause chest pain and difficulty breathing.
  • Fibrosing Alveolitis : Inflammation of the lung that is not due to infection may cause shortness of breath and a dry cough.
  • Peripheral sensory neuropathy, mononeuritis multiplex : Abnormal nerve function may cause numbness, tingling, or weakness.
  • Sjögren’s syndrome : Dry eyes and dry mouth. women may develop vaginal dryness due to Sjögren’s syndrome, which can cause pain with sexual intercourse.
  • Inflammation of the white part of the eye may cause pain or vision problems.
  • Vasculitis – Inflammation of the blood vessels, may cause a wide variety of symptoms, depends on the location.

RHEUMATOID ARTHRITIS DIAGNOSIS – There is no single test used to diagnose rheumatoid arthritis. Instead, the diagnosis is based upon many factors, including the characteristic signs and symptoms, the results of laboratory tests, and the results of x-rays.

American Rheumatism Association: criteria for the diagnosis of rheumatoid arthritis

  1. Morning stiffness
  2. Pain on motion or tenderness in at least one joint
  3. Swelling of one joint, representing soft tissue or fluid
  4. Swelling of at least one other joint (soft tissue or fluid) with an interval free of symptoms no longer than three (3) months
  5. Symmetrical joint swelling (simultaneous involvement of the same joint, right and left)
  6. Subcutaneous nodules over bony prominences, extensor surfaces or near joints
  7. Typical X-ray changes that must include demineralisation in periarticular bone as an index of inflammation
  8. Positive test for rheumatoid factor in the serum
  9. Synovial fluid – a poor mucin clot formation on adding synovial fluid to dilute acetic acid
  10. Characteristic histopathology of rheumatoid nodules biopsied from any site
  11. Synovial histopathology consistent with RA:

(a)    marked villous hypertrophy

(b)   proliferation of synovial cells

(c)    lymphocyte plus plasma cell infiltration in subsynovium

(d)   fibrin deposition within or upon microvilli

• For classical RA 7 criteria needed

• For definite RA 5 criteria needed

• For probable RA 3 criteria needed

 

Autoimmune disease – Diagnosis, Symptoms, Investigation, Definition,

May 17th, 2011 No comments

Autoimmune disease

Autoimmune diseaseAutoimmune disease is a pathological condition which is caused by an adaptive autoimmune response directed against an antigen within the body of the host. In other words, the body mistakenly attacks its own cells. The disease can affect every part of the human body. It may be systemic, affect single organs or organ systems or attacking several organ systems simultaneously. Thus, the symptoms are vary correspondingly depend on which parts of the body are attacked by the immune system and on the development of the disease. However, these definitions can be unclear since it is often difficult to differentiate the causality when dealing with a human disease. It is very beneficial to consider the evidence of an autoimmune etiology of a human disease with three degrees of stringency.

  • Direct evidence
  • Indirect evidence
  • Circumstantial evidence

AUTOIMMUNE DISEASE – CRITERIA

How to determine if autoimmunity is the cause of the disease rather than an accompanying feature or an outcome? The demonstration of auto-antibodies is the first step in the diagnosis of these diseases, however the antibodies might not be the actual pathogens of the disease. Autoantibodies can occur naturally and are common in all immunologically competent person and might even increase nonspecifically while in the course of disease or injury. Hence, the miniscule presence of autoantibodies does not automatically determine a cause-and-effect relationship, because the autoantibodies might be the result, not the cause, of the disease process. However it is important to emphasize, that the presence of autoantibody responses has great value in diagnosing and prognosing numerous human diseases.

Autoantibodies may be present many years before the diagnosis of diseases such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), Type 1 diabetes mellitus (DM) and antiphospholipid syndrome. Combined with genetic information or family history, the presence of autoantibodies may be highly predictive of the later onset of an autoimmune disorder.

Direct evidence – The disease can be produced by showing autoimmune response. Direct evidence usually involves transfer of autoantibody from a patient to a healthy recipient, either an animal or a human. A few instances of such transfers have been successfully performed.

  • Reproduction of pemphigus by injection of patient serum into a neonatal mouse.
  • Maternal-fetal transmission (transplacental transmission) of myastenia gravis, Graves’ disease, and the complete heart block associated with lupus and Sjögren’s disease. The clinical manifestations in the offspring are temporary, because the autoantibody in these cases is provided through passive transfer of serum from the mother.

Indirect evidence – The second level of proof of causality is indirect evidence which requires the availability of an appropriate animal model where the necessary transfer studies can be carried out. Different animal models are implemented :

  • Reproduction of disease in animals via immunization with the appropriate antigen.
  • Autoimmune thyroiditis in the mouse after immunization with thyroglobulin – Hashimoto’s thyroiditis (chronic autoimmune thyroiditis).
  • Myocarditis after immunization of susceptible mice with murine myosin.
  • Naturally occurring disease in animals that resembles its human counterpart.
  • Many aspects that resemble human SLE (Systemic Lupus Erythematosus) have been found in particular genetic strains of mice.
  • A disease closely resembling Type 1 (autoimmune) diabetes.
  • Disease resulting from manipulation of the immune system.
  • Models of inflammatory bowel disease have been described in animals in which particular cytokines such as interleukin (IL)-2 and IL-10 have been eliminated.
  • Autoimmune dilated cardiomyopathy develop in mice which are deficient in programmed cell death-1 (PD-) immuno-inhibitory coreceptor.

Circumstantial evidence – This is the lowest level of proof, which is the one most commonly available to connect a mysterious human disease to autoimmunity.

  • The hazards of using this kind of evidence as the basis for concluding that a disease is caused by autoimmunity have been previously described. Natural autoantibodies are common and might rise nonspecifically in the course of a disease process.
  • Autoimmune diseases tend to cluster, maybe simply because they share a number of genetic susceptibility traits. For examples, a single person will have more than one autoimmune disease, and family members share the very same or even other autoimmune diseases.
  • Most, but not all, autoimmune diseases are more common in women than men. Therefore, a sex bias provides increased circumstantial evidence of an autoimmune etiology. In addition, new information on the differing pathogenic mechanisms involved in men and women has been provided by comparing of the sex-based differences in autoimmune diseases.
  • A disease’s response to immunosuppressive therapy is usually an important clinical indicator of autoimmune etiology. If effective symptomatic therapy can be obtained by immunosuppression, therefore, demonstrating the etiologic agent of the disease may seem less essential.
  • A particular bias to certain HLA haplotypes is shown by most of the autoimmune diseases, usually the Class II category. Because genes that are important in regulating the immune response are encoded by the Class II Major Histocompability Complex (MHC), some rational association may exist between the genetic constitution and susceptibility to a specific autoimmune disease.