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Rheumatoid arthritis (RA) is traditionally considered a chronic, inflammatory autoimmune disorder that causes the immune system to attack the joints. It is a disabling and painful inflammatory condition, which can lead to substantial loss of mobility due to pain and joint destruction. RA is a systemic disease, often affecting extra-articular tissues throughout the body including the skin, blood vessels, heart, lungs, and muscles.
Autoimmune diseases are illnesses that occur when the body tissues are mistakenly attacked by its own immune system. The immune system is a complex organization of cells and antibodies designed normally to “seek and destroy” invaders of the body, particularly infections. Patients with autoimmune diseases have antibodies in their blood that target their own body tissues, where they can be associated with inflammation. Because it can affect multiple other organs of the body, rheumatoid arthritis is referred to as a systemic illness and is sometimes called rheumatoid disease.
While rheumatoid arthritis is a chronic illness, meaning it can last for years, patients may experience long periods without symptoms. Typically, however, rheumatoid arthritis is a progressive illness that has the potential to cause joint destruction and functional disability.
A joint is where two bones meet to allow movement of body parts. Arthritis means joint inflammation. The joint inflammation of rheumatoid arthritis causes swelling, pain, stiffness, and redness in the joints. The inflammation of rheumatoid disease can also occur in tissues around the joints, such as the tendons, ligaments, and muscles.
In some patients with rheumatoid arthritis, chronic inflammation leads to the destruction of the cartilage, bone and ligaments causing deformity of the joints. Damage to the joints can occur early in the disease and be progressive. Moreover, studies have shown that the progressive damage to the joints does not necessarily correlate with the degree of pain, stiffness, or swelling present in the joints.
Rheumatoid arthritis is a common rheumatic disease, affecting more than two million people in the United States. The disease is three times more common in women as in men. It afflicts people of all races equally. The disease can begin at any age, but most often starts after age forty and before sixty. In some families, multiple members can be affected, suggesting a genetic basis for the disorder.
The cause of rheumatoid arthritis is unknown. Even though infectious agents such as viruses, bacteria, and fungi have long been suspected, none has been proven as the cause. The cause of rheumatoid arthritis is a very active area of worldwide research. Some scientists believe that the tendency to develop rheumatoid arthritis may be genetically inherited. It is suspected that certain infections or factors in the environment might trigger the immune system to attack the body’s own tissues, resulting in inflammation in various organs of the body such as the lungs or eyes.
Regardless of the exact trigger, the result is an immune system that is geared up to promote inflammation in the joints and occasionally other tissues of the body. Immune cells, called lymphocytes, are activated and chemical messengers (cytokines, such as tumor necrosis factor/TNF and interleukin-1/IL-1) are expressed in the inflamed areas.
Environmental factors also seem to play some role in causing rheumatoid arthritis. Recently, scientists have reported that smoking tobacco increases the risk of developing rheumatoid arthritis. Hormonal factors in the individual patients may explain some features of the disease, such as the higher occurrence in women, the not-infrequent onset after child-birth, and the (slight) modulation of disease risk by hormonal medications.
Autoimmune diseases require that the affected individual have a defect in the ability to distinguish foreign molecules from the body’s own. There are markers on many cells that confer this self-identifying feature. However, some classes of markers allow for RA to happen. 90% of patients with RA have the cluster of markers known as the HLA-DR4/DR1 cluster, whereas only 40% of unaffected controls do. Thus, in theory, RA requires susceptibility to the disease through genetic endowment with specific markers and an infectious event that triggers an autoimmune response.
Once triggered, B lymphocytes produce immunoglobins, and rheumatoid factors of the IgG and IgM classes that are deposited in the tissue, this subsequently leads to the activation of the serum complement cascade and the recruitment of the phagocytic arm of the immune response, which further exacerbates the inflammation of the synovium, leading to edema, vasodilation and infiltration by activated T-cells (mainly CD4 in nodular aggregates and CD8 in diffuse infiltrates). Early and intermediate molecular mediators of inflammation include tumor necrosis factor alpha (TNF-Î±), interleukins IL-1, IL-6, IL-8 and IL-15, transforming growth factor beta, fibroblast growth factor and platelet-derived growth factor. Synovial macrophages and dentritic cells further function as antigen presenting cells by expressing MHC class II molecules, leading to an established local immune reaction in the tissue. The disease progresses in concert with formation of granulation tissue at the edges of the synovial lining (pannus) with extensive angiogenesis and production of enzymes that cause tissue damage. Modern pharmacological treatments of RA target these mediators. Once the inflammatory reaction is established, the synovium thickens, the cartilage and the underlying bone begins to disintegrate and evidence of joint destruction accrues .
The symptoms of rheumatoid arthritis come and go, depending on the degree of tissue inflammation. When body tissues are inflamed, the disease is active. When tissue inflammation subsides, the disease is inactive (in remission). Remissions can occur spontaneously or with treatment, and can last weeks, months, or years. During remissions, symptoms of the disease disappear, and patients generally feel well. When the disease becomes active again (relapse), symptoms return. The return of disease activity and symptoms is called a flare. The course of rheumatoid arthritis varies from patient to patient, and periods of flares and remissions are typical.
When the disease is active, symptoms can include fatigue, lack of appetite, low grade fever, muscle and joint aches, and stiffness. Muscle and joint stiffness are usually most notable in the morning and after periods of inactivity. Arthritis is common during disease flares. Also during flares, joints frequently become red, swollen, painful, and tender. This occurs because the lining tissue of the joint (synovium) becomes inflamed, resulting in the production of excessive joint fluid (synovial fluid). The synovium also thickens with inflammation (synovitis).
Synovitis affecting synovial joints is the most prominent feature in rheumatoid arthritis. Joint synovitis could evolve in to a chronic arthritis and deformities in rheumatoid arthritis. Rheumatoid arthritis is a systemic disorder due to an abnormal immune reaction associated with constitutional symptoms which can affect the other organ systems as well. However the joint synovitis leading to arthritis affecting multiple joints remains the key clinical feature in rheumatoid arthritis.
Inflammation in the joints manifests itself as a soft, “doughy” swelling, pain, tenderness to palpation and movement, local warmth, and functional impairment. Morning stiffness is often a prominent feature and may last for more than an hour. These signs help distinguish rheumatoid and other inflammatory arthritides from non-inflammatory diseases of the joints such as osteoarthritis (sometimes referred to as the “wear-and-tear” of the joints). In RA, the joints are usually affected in a fairly symmetrical fashion although the initial presentation may be asymmetrical.
Rheumatoid arthritis is a systemic disorder mainly affecting synovial joints. Chemical mediators (Cytokines) released as a result of an abnormal immune reaction triggered by yet undetermined agent/ agents, immune system releases cytokines which gives rise to inflammation of joint synovium (Synovitis). Constitutional symptoms such as fever, malaise, loss of appetite and loss weight are also due to cytokines released in to the blood stream due to an abnormal immune reaction. Vasculitis affecting many other organ systems often gives rise to systemic complications. Most common and disabling clinical feature in Rheumatoid arthritis is chronic, deforming, often symmetrical polyarthritis (affecting multiple joints) due to joint Synovitis triggered by an autoimmune reaction in genetically susceptible individuals.
In rheumatoid arthritis, multiple joints are usually inflamed in a symmetrical pattern (both sides of the body affected). The small joints of both the hands and wrists are often involved. Simple tasks of daily living, such as turning door knobs and opening jars can become difficult during flares. The small joints of the feet are also commonly involved. Occasionally, only one joint is inflamed. When only one joint is involved, the arthritis can mimic the joint inflammation caused by other forms of arthritis, such as gout or joint infection. Chronic inflammation can cause damage to body tissues, cartilage and bone. This leads to a loss of cartilage and erosion and weakness of the bones as well as the muscles, resulting in joint deformity, destruction, and loss of function. Rarely, rheumatoid arthritis can even affect the joint that is responsible for the tightening our vocal cords to change the tone of our voice, the cricoarytenoid joint. When this joint is inflamed, it can cause hoarseness of voice.
Since rheumatoid arthritis is a systemic disease, its inflammation can affect organs and areas of the body other than the joints. Inflammation of the glands of the eyes and mouth can cause dryness of these areas and is referred to as Sjogren’s syndrome. Rheumatoid inflammation of the lung lining (pleuritis) causes chest pain with deep breathing or coughing. The lung tissue itself can also become inflamed and sometimes nodules of inflammation (rheumatoid nodules) develop within the lungs. Inflammation of the tissue (pericardium) surrounding the heart, called pericarditis, can cause a chest pain that typically changes in intensity when lying down or leaning forward. The rheumatoid disease can reduce the number of red blood cells (anemia), and white blood cells. Decreased white cells can be associated with an enlarged spleen (referred to as Felty’s syndrome) and can increase the risk of infections. Firm lumps under the skin (rheumatoid nodules) can occur around the elbows and fingers where there is frequent pressure. Even though these nodules usually do not cause symptoms, occasionally they can become infected. A rare, serious complication, usually with long-standing rheumatoid disease, is blood vessel inflammation (vasculitis). Vasculitis can impair blood supply to tissues and lead to tissue death. This is most often initially visible as tiny black areas around the nail beds or as leg ulcers.
As the pathology progresses the inflammatory activity leads to erosion and destruction of the joint surface, which impairs their range of movement and leads to deformity.
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The fingers are typically deviated towards the little finger (ulnar deviation) and can assume unnatural shapes. Classical deformities in rheumatoid arthritis are the Boutonniere deformity (Hyperflexion at the proximal interphalangeal joint with hyperextension at the distal interphalangeal joint), swan neck deformity (Hyperextension at the proximal interphalangeal joint, hyperflexion at the distal interphalangeal joint). The thumb may develop a “Z-Thumb” deformity with fixed flexion and subluxation at the metacarpophalangeal joint, and hyperextension at the IP joint.
Patients with RA usually exhibit signs of systemic inflammation, that is, the inflammatory process in the joint leaves its marks on other organs as well (and this may also help distinguish it from osteoarthritis). Examples are a general tiredness and lassitude, sometimes low-grade fever, and some abnormalities on blood tests such as an elevated erythrocyte sedimentation rate (ESR), and anemia, which is often seen as a consequence of the disease itself (anaemia of chronic disease) although it may also be caused by gastrointestinal bleeding as a side effect of drugs used in treatment.
1.The rheumatoid nodule is the cutaneous (strictly speaking subcutaneous) feature most characteristic of rheumatoid arthritis. The initial pathologic process in nodule formation is unknown but is thought to be related to small-vessel inflammation.
2.Several forms of vasculitis are also cutaneous manifestations associated with rheumatoid arthritis. A benign form occurs as microinfarcts around the nailfolds.
Other, rather rare, cutaneous features include:
*pyoderma gangrenosum, a necrotizing, ulcerative, noninfectious neutrophilic dermatosis.
*Sweet’s syndrome, a neutrophilic dermatosis usually associated with myeloproliferative disorders
*atrophy of digital skin
*diffuse thinning (rice paper skin), and skin fragility.
The American College of Rheumatology has defined (1987) the following criteria for the classification of rheumatoid arthritis:
*Morning stiffness of >1 hour most mornings for at least 6 weeks.
*Arthritis and soft-tissue swelling of >3 of 14 joints/joint groups, present for at least 6 weeks
*Arthritis of hand joints, present for at least 6 weeks
*Symmetric arthritis, present for at least 6 weeks
*Subcutaneous nodules in specific places
*Rheumatoid factor at a level above the 95th percentile
*Radiological changes suggestive of joint erosion
At least four criteria have to be met for classification as RA.
It is important to note that these criteria are not intended for the diagnosis of patients for routine clinical care. They were primarily intended to categorize patients for research. For example: one of the criteria is the presence of bone erosion on X-Ray. Prevention of bone erosion is one of the main aims of treatment because it is generally irreversible. To wait until all of the ACR criteria for rheumatoid arthritis are met may sometimes result in a worse outcome for the patient. Most patients and rheumatologists would agree that it would be better to treat the patient as early as possible and prevent bone erosion from occurring, even if this means treating patients who don’t fulfill the ACR criteria. The ACR criteria are, however, very useful for categorising patients with established rheumatoid arthritis, for example for epidemiological purposes.
When RA is being clinically suspected, immunological studies are required, such as rheumatoid factor (RF, a specific antibody). A negative RF does not rule out RA; rather, the arthritis is called seronegative. During the first year of illness, rheumatoid factor is frequently negative. 80% of patients eventually convert to seropositive status. RF is also seen in other illnesses, like SjÃ¶gren’s syndrome, and in approximately 10% of the healthy population, therefore the test is not very specific.
Because of this low specificity, a new serological test has been developed in recent years, which tests for the presence of so called anti-citrullinated protein antibodies (ACPA). Like RF, this test can detect approximately 80% of all RA patients, but is rarely positive in non-RA patients, giving it a specificity of around 98%. In addition, ACP antibodies can be often detected in early stages of the disease, or even before disease onset. Currently, the most common test for ACP antibodies is the anti-CCP (cyclic citrullinated peptide) test.
Also, several other blood tests are usually done to allow for other causes of arthritis, such as lupus erythematosus. The erythrocyte sedimentation rate (ESR), C-reactive protein,full blood count, renal function, liver enzymes and other immunological tests (e.g. antinuclear antibody/ANA) are all performed at this stage. Ferritin can reveal hemochromatosis, which can mimic RA.
Joint x-rays may be normal or only show swelling of soft tissues early in the disease. As the disease progresses x-rays can show bony erosions typical of rheumatoid arthritis in the joints. Joint x-rays can also be helpful in monitoring the progression of disease and joint damage over time. Bone scanning, a radioactive test procedure, can demonstrate the inflamed joints.
The doctor may elect to perform an office procedure called arthrocentesis. In this procedure, a sterile needle and syringe are used to drain joint fluid out of the joint for study in the laboratory. Analysis of the joint fluid, in the laboratory, can help to exclude other causes of arthritis, such as infection and gout. Arthrocentesis can also be helpful in relieving joint swelling and pain. Occasionally, cortisone medications are injected into the joint during the arthrocentesis in order to rapidly relieve joint inflammation and further reduce symptoms.
There is no known cure for rheumatoid arthritis. However, many different types of treatment can be used to alleviate symptoms and/or to modify the disease process.
The goal of treatment in this chronic disease must be two-fold: to alleviate the suffering of the patient here and now, and to prevent the future destruction of the joints and resulting handicap if the disease is left unchecked. These two goals may not always coincide: while pain relievers may achieve the first goal, they do not have any impact on the long-term consequences. For these reasons, most authorities believe that RA should be treated, in the vast majority of patients, by at least one specific anti-rheumatic medication, also named DMARD (see below), to which other medications and non-medical interventions can be added as needed.
Cortisone therapy has offered relief to many patients in the past, but its long-term effects have been deemed undesirable. However, cortisone injections can be valuable adjuncts to a long-term treatment plan, and using low dosages of daily cortisone (e.g., prednisone or prednisolone, 5-7.5 mg daily) can also have an important benefit if added to a proper specific anti-rheumatic treatment.
Pharmacological treatment of RA can be divided into disease-modifying antirheumatic drugs (DMARDs), anti-inflammatory agents and analgesics. DMARDs have been found to produce durable remissions and delay or halt disease progression. In particular they prevent bone and joint damage from occurring secondary to the uncontrolled inflammation. This is important as such damage is usually irreversible. Anti-inflammatories and analgesics improve pain and stiffness but do not prevent joint damage or slow the disease progression.
There is an increasing recognition amongst rheumatologists that permanent damage to the joints occurs at a very early stage in the disease. In the past the strategy used was to start with just an anti-inflammatory drug, and assess progression clinically and using X-rays. If there was evidence that joint damage was starting to occur then a more potent DMARD would be prescribed. Tools such as ultrasound and MRI are more sensitive methods of imaging the joints and have demonstrated that joint damage occurs much earlier and in more patients than was previously thought. Patients with normal X-rays will often have erosions detectable by ultrasound that X ray could not demonstrate.
There may be other reasons why starting DMARDs early is beneficial as well as prevention of structural joint damage. In the early stage of the disease, the joints are increasingly infiltrated by cells of the immune system that signal to one another and are thought to set up self-perpetuating chronic inflammation. Interrupting this process as early as possible with an effective DMARD (such as methotrexate) appears to improve the outcome from the RA for years afterwards. Delaying therapy for as little as a few months after the onset of symptoms can result in worse outcomes in the long term. There is therefore considerable interest in establishing the most effective therapy in patients with early arthritis, when they are most responsive to therapy and have the most to gain.
Treatment also includes rest and physical activity. Regular exercise is important for maintaining joint mobility and making the joint muscles stronger. Swimming is especially good, as it allows for exercise with a minimum of stress on the joints. Heat and cold applications are modalities that can ease symptoms before and after exercise. Pain in the joints is sometimes alleviated by oral acetaminophen (paracetamol). Other areas of the body, such as the eyes and lining of the heart, are treated individually. However, there is no diet that has been shown to alleviate rheumatoid arthritis, although fish oil may have anti-inflammatory effects.
Disease modifying anti-rheumatic drugs (DMARDs)
The term Disease Modifying Anti-Rheumatic Agent was originally introduced to indicate a drug that reduced evidence of processes thought to underly the disease, such as a raised erythrocyte sedimentation rate, reduced haemoglobin level, raised rheumatoid factor level and more recently, raised C-reactive protein level. More recently, the term has been used to indicate a drug that reduces the rate of damage to bone and cartilage. DMARDs can be further subdivided into traditional small molecular mass drugs synthesised chemically and newer ‘biological’ agents produced through genetic engineering.
Traditional small molecular mass drugs:
*ciclosporin (cyclosporine A)
The most important and most common adverse events relate to liver and bone marrow toxicity (MTX, SSZ, leflunomide, azathioprine, gold compounds, D-penicillamine), renal toxicity (cyclosporine A, parenteral gold salts, D-penicillamine), pneumonitis (MTX), allergic skin reactions (gold compounds, SSZ), autoimmunity (D-penicillamine, SSZ, minocycline) and infections (azathioprine, cyclosporine A). Hydroxychloroquine may cause ocular toxicity, although this is rare, and because hydroxychloroquine does not affect the bone marrow or liver it is often considered to be the DMARD with the least toxicity. Unfortunately hydroxychloroquine is not very potent, and for most patients hydroxychloroquine alone is insufficient to control symptoms.
Many rheumatologists consider methotrexate to be the most important and useful DMARD, largely because of lower rates of stopping the drug through toxicity. Nevertheless, methotrexate is often considered by patients and even other doctors as a very “toxic” drug. This reputation is not entirely justified, and at times can result in patients being denied the most effective treatment for their arthritis. Although methotrexate does indeed have the potential to suppress the bone marrow or cause hepatitis, these effects can be monitored using regular blood tests, and the drug withdrawn at an early stage if the tests are abnormal, before any serious harm is done (typically the blood tests return to normal after stopping the drug). In clinical trials in which patients with RA were treated with one of a range of different DMARDs, patients who were prescribed methotrexate were those who stayed on their medication the longest (the others stopped theirs because of either side-effects or failure of the drug to control the arthritis). Lastly, methotrexate is often preferred by rheumatologists because if it does not control arthritis on its own then it works well in combination with many other drugs, especially the biological agents. Other DMARDs may not be as effective or safe in combination with biological agents.
Biological agents (biologics include:
*tumor necrosis factor alpha (TNFÎ±) blockers – etanercept (Enbrel), infliximab (Remicade), adalimumab (Humira)
*Interleukin 1 blockers – anakinra
*monoclonal antibodies against B cells – rituximab (Rituxan)
*T cell activation blocker abatacept (Orencia)
Anti-inflammatory agents and analgesics
Anti-inflammatory agents include:
*Non-steroidal anti-inflammatory drug (NSAIDs, most also act as analgesics)
acetaminophen (Paracetamol outside US)
The Prosorba column blood filtering device was approved by the FDA for treatment of RA in 1999 However, in most patients the results have been very modest.
Other therapies are weight loss, occupational therapy, podiatry, physiotherapy, joint injections, and special tools to improve hard movements (e.g. special tin-openers).
The areas of the body, other than the joints, that are affected by rheumatoid inflammation are treated individually. Sjogren’s syndrome (described above, see symptoms) can be helped by artificial tears and humidifying rooms of the home or office. Medicated eye drops, cortisporine ophthalmic drops (Restasis), are also available to help the dry eyes in those affected. Regular eye check-ups and early antibiotic treatment for infection of the eyes are important. Inflammation of the tendons (tendinitis), bursae (bursitis) and rheumatoid nodules can be injected with cortisone. Inflammation of the lining of the heart and/or lungs may require high doses of oral cortisone.
Severely affected joints may require joint replacement surgery, such as knee replacement.
Proper, regular exercise is important in maintaining joint mobility, and in strengthening the muscles around the joints. Swimming is particularly helpful because it allows exercise with minimal stress on the joints. Physical and occupational therapists are trained to provide specific exercise instructions and can offer splinting supports. For example, wrist and finger splints can be helpful in reducing inflammation and maintaining joint alignment. Devices, such as canes, toilet seat raisers, and jar grippers can assist daily living. Heat and cold applications are modalities that can ease symptoms before and after exercise.
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Historic treatments for RA have also included: RICE, acupuncture, apple diet, nutmeg, some light exercise every now and then, nettles, bee venom, copper bracelets, rhubarb diet, rest, extractions of teeth, fasting, honey, vitamins, insulin, magnets, and electroconvulsive therapy (ECT). Most of these have either had no effect at all, or their effects have been modest and transient in some individual patients, while not being generalizable.
Future treatments Option
Scientists throughout the world are studying many promising areas of new treatment approaches for rheumatoid arthritis. These areas include treatments that block the action of the special inflammation factors, such as tumor necrosis factor (TNFalpha) and interleukin-1 (IL-1), as described above. Many other drugs are being developed that act against certain critical white blood cells involved in rheumatoid inflammation. Also, new NSAIDs with mechanisms of action that are different from current drugs are on the horizon.
Better methods of more accurately defining which patients are more likely to develop more aggressive disease are becoming available. Recent antibody research has found that the presence of citrulline antibodies in the blood has been associated with a greater tendency toward more destructive forms of rheumatoid arthritis.
Studies involving various types of the connective tissue collagen are in progress and show encouraging signs of reducing rheumatoid disease activity. Finally, genetic research and engineering is likely to bring forth many new avenues of earlier diagnosis and accurate treatment in the near future. Gene profiling, also known as gene array analysis, is being identified as a helpful method of defining which people will respond to which medications. Studies are underway that are using gene array analysis to determine which patients will be at more risk for more aggressive disease. This is all occurring because of technology improvements. We are at the threshold of tremendous improvements in the way rheumatoid arthritis is managed.
The course of the disease varies greatly from patient to patient. Some patients have mild short-term symptoms, but in most the disease is progressive for life. Around 20%-30% will have subcutaneous nodules (known as rheumatoid nodules); this is associated with a poor prognosis.
Daily living activities are impaired in most patients.
After 5 years of disease, approximately 33% of patients will not be working
After 10 years, approximately half will have substantial functional disability.
Poor prognostic factors include persistent synovitis, early erosive disease, extra-articular findings (including subcutaneous rheumatoid nodules), positive serum RF findings, positive serum anti-CCP autoantibodies, carriership of HLA-DR4 “Shared Epitope” alleles, family history of RA, poor functional status, socioeconomic factors, elevated acute phase response (erythrocyte sedimentation rate [ESR], C-reactive protein [CRP]), and increased clinical severity.
Rheumatoid Arthritis At A Glance:
*Rheumatoid arthritis is an autoimmune disease that can cause chronic inflammation of the joints and other areas of the body.
*Rheumatoid arthritis can affect persons of all ages.
*The cause of rheumatoid arthritis is not known.
*Rheumatoid arthritis is a chronic disease, characterized by periods of disease flares and remissions.
*In rheumatoid arthritis, multiple joints are usually, but not always, affected in a symmetrical pattern.
*Chronic inflammation of rheumatoid arthritis can cause permanent joint destruction and deformity.
*Damage to joints can occur early and does not correlate with symptoms.
*The “rheumatoid factor” is an antibody blood test that can be found in 80 % of patients with rheumatoid arthritis.
*There is no known cure for rheumatoid arthritis.
*The treatment of rheumatoid arthritis optimally involves a combination of patient education, rest and exercise, joint
*protection, medications, and occasionally surgery.
Early treatment of rheumatoid arthritis results in better outcomes.
For further information about rheumatoid arthritis, please visit the following sites:
The Arthritis Foundation (http://www.arthritis.org)
Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose