The Full Wiki

Rheumatoid arthritis: Wikis


Note: Many of our articles have direct quotes from sources you can cite, within the Wikipedia article! This article doesn't yet, but we're working on it! See more info or our list of citable articles.

Did you know ...

More interesting facts on Rheumatoid arthritis

Include this on your site/blog:


From Wikipedia, the free encyclopedia

Rheumatoid arthritis
Classification and external resources

A diagram showing how rheumatoid arthritis affects a joint
ICD-10 M05.-M06.
ICD-9 714
OMIM 180300
DiseasesDB 11506
MedlinePlus 000431
eMedicine med/2024 emerg/48 pmr/124
MeSH D001172

Rheumatoid arthritis (RA) is a chronic, systemic inflammatory disorder that may affect many tissues and organs, but principally attacks the joints producing an inflammatory synovitis that often progresses to destruction of the articular cartilage and ankylosis of the joints. Rheumatoid arthritis can also produce diffuse inflammation in the lungs, pericardium, pleura, and sclera, and also nodular lesions, most common in subcutaneous tissue under the skin. Although the cause of rheumatoid arthritis is unknown, autoimmunity plays a pivotal role in its chronicity and progression.

About 1% of the world's population is afflicted by rheumatoid arthritis, women three times more often than men. Onset is most frequent between the ages of 40 and 50, but people of any age can be affected. It can be a disabling and painful condition, which can lead to substantial loss of functioning and mobility. It is diagnosed chiefly on symptoms and signs, but also with blood tests (especially a test called rheumatoid factor) and X-rays. Diagnosis and long-term management are typically performed by a rheumatologist, an expert in the diseases of joints and connective tissues.[1]

Various treatments are available. Non-pharmacological treatment includes physical therapy, orthoses and occupational therapy. Analgesia (painkillers) and anti-inflammatory drugs, including steroids, are used to suppress the symptoms, while disease-modifying antirheumatic drugs (DMARDs) are often required to inhibit or halt the underlying immune process and prevent long-term damage. In recent times, the newer group of biologics has increased treatment options.[1]

The name is based on the term "rheumatic fever", an illness which includes joint pain and is derived from the Greek word rheumatos ("flowing"). The suffix -oid ("resembling") gives the translation as joint inflammation that resembles rheumatic fever. The first recognized description of rheumatoid arthritis was made in 1800 by Dr Augustin Jacob Landré-Beauvais (1772-1840) of Paris.[2]


Signs and symptoms

While rheumatoid arthritis primarily affects joints, problems involving other organs of the body are known to occur. Extra-articular ("outside the joints") manifestations other than anemia (which is very common) are clinically evident in about 15-25% of individuals with rheumatoid arthritis.[3] It can be difficult to determine whether disease manifestations are directly caused by the rheumatoid process itself, or from side effects of the medications commonly used to treat it - for example, lung fibrosis from methotrexate or osteoporosis from corticosteroids.


The arthritis of joints known as synovitis is inflammation of the synovial membrane that lines joints and tendon sheaths. Joints become swollen, tender and warm, and stiffness limits their movement. With time RA nearly always affects multiple joints (it is a polyarthritis), most commonly small joints of the hands, feet and cervical spine, but larger joints like the shoulder and knee can also be involved. Synovitis can lead to tethering of tissue with loss of movement and erosion of the joint surface causing deformity and loss of function.[1]

Rheumatoid arthritis typically manifests with signs of inflammation, with the affected joints being swollen, warm, painful and stiff, particularly early in the morning on waking or following prolonged inactivity. Increased stiffness early in the morning is often a prominent feature of the disease and may last for more than an hour. Gentle movements may relieve symptoms in early stages of the disease. These signs help distinguish rheumatoid from non-inflammatory problems of the joints, often referred to as osteoarthritis or "wear-and-tear" arthritis. In arthritis of non-inflammatory causes, signs of inflammation and early morning stiffness are absent, and movements induce pain caused by the wear-and-tear.[4] In RA, the joints are often affected in a fairly symmetrical fashion, although this is not specific, and the initial presentation may be asymmetrical.

Hands affected by RA

As the pathology progresses the inflammatory activity leads to tendon tethering and erosion and destruction of the joint surface, which impairs range of movement and leads to deformity. The fingers may suffer from almost any deformity depending on which joints are most involved. Medical students are taught to learn names for specific deformities, such as ulnar deviation, boutonniere deformity, swan neck deformity and "Z-thumb," but these are of no more significance to diagnosis or disability than other variants.


The rheumatoid nodule, which is often subcutaneous, is the feature most characteristic of rheumatoid arthritis. The initial pathologic process in nodule formation is unknown but may be essentially the same as the synovitis, since similar structural features occur in both. The nodule has a central area of fibrinoid necrosis that may be fissured and which corresponds to the fibrin-rich necrotic material found in and around an affected synovial space. Surrounding the necrosis is a layer of palisading macrophages and fibroblasts, corresponding to the intimal layer in synovium and a cuff of connective tissue containing clusters of lymphocytes and plasma cells, corresponding to the subintimal zone in synovitis. The typical rheumatoid nodule may be a few millimetres to a few centimetres in diameter and is usually found over bony prominences, such as the olecranon, the calcaneal tuberosity, the metacarpophalangeal joint, or other areas that sustain repeated mechanical stress. Nodules are associated with a positive RF (rheumatoid factor) titer and severe erosive arthritis. Rarely, these can occur in internal organs or at diverse sites on the body.

Several forms of vasculitis occur in rheumatoid arthritis. A benign form occurs as microinfarcts around the nailfolds. More severe forms include livedo reticularis, which is a network (reticulum) of erythematous to purplish discoloration of the skin caused by the presence of an obliterative cutaneous capillaropathy.

Other, rather rare, skin associated symptoms include:


Fibrosis of the lungs is a recognised response to rheumatoid disease. It is also a rare but well recognised consequence of therapy (for example with methotrexate and leflunomide). Caplan's syndrome describes lung nodules in individuals with rheumatoid arthritis and additional exposure to coal dust. Pleural effusions are also associated with rheumatoid arthritis.


Renal amyloidosis can occur as a consequence of chronic inflammation.[5] Rheumatoid arthritis may affect the kidney glomerulus directly through a vasculopathy or a mesangial infiltrate but this is less well documented. Treatment with Penicillamine and gold salts are recognized causes of membranous nephropathy.

Heart and blood vessels

People with rheumatoid arthritis are more prone to atherosclerosis, and risk of myocardial infarction (heart attack) and stroke is markedly increased.[6] [7] Other possible complications that may arise include: pericarditis, endocarditis, left ventricular failure, valvulitis and fibrosis.[8] Many people with rheumatoid arthritis do not experience the same chest pain that others feel when they have angina or myocardial infarction. To reduce cardiovascular risk, it is crucial to maintain optimal control of the inflammation caused by rheumatoid arthritis (which may be involved in causing the cardiovascular risk), and to use exercise and medications appropriately to reduce other cardiovascular risk factors such as blood lipids and blood pressure. Doctors who treat rheumatoid arthritis patients should be sensitive to cardiovascular risk when prescribing anti-inflammatory medications, and may want to consider prescribing routine use of low doses of aspirin if the gastrointestinal effects are tolerable.[8]


The eye is directly affected in the form of episcleritis which when severe can very rarely progress to perforating scleromalacia. Rather more common is the indirect effect of keratoconjunctivitis sicca, which is a dryness of eyes and mouth caused by lymphocyte infiltration of lachrymal and salivary glands. When severe, dryness of the cornea can lead to keratitis and loss of vision. Preventive treatment of severe dryness with measures such as nasolacrimal duct occlusion is important.
Cytokine production in joints and/or hepatic Kupffer cells leads to increased activity of hepatocytes with increased production of acute-phase proteins, such as C-reactive protein, and increased release of enzymes such as alkaline phosphatase into the blood. In Felty's syndrome, Kuppfer cell activation is so marked that the resulting increase in hepatocyte activity is associated with nodular hyperplasia of the liver, which may be palpably enlarged. Because Kuppfer cells are not within the liver parenchyma, there is little or no evidence of hepatitis. Hepatic involvement in RA is essentially asymptomatic.
Anemia is by far the most common abnormality of the blood cells. The red cells are of normal size and colour (normocytic). A low white blood cell count (neutropenia) usually only occurs in patients with Felty's syndrome with an enlarged liver and spleen. The mechanism of neutropenia is complex. An increased platelet count (thrombocytosis) occurs when inflammation is uncontrolled, as does the anemia.
Peripheral neuropathy and mononeuritis multiplex may occur. The most common problem is carpal tunnel syndrome caused by compression of the median nerve by swelling around the wrist. Atlanto-axial subluxation can occur, owing to erosion of the odontoid process and or/transverse ligaments in the cervical spine's connection to the skull. Such an erosion (>3mm) can give rise to vertebrae slipping over one another and compressing the spinal cord. Clumsiness is initially experienced, but without due care this can progress to quadriplegia.
Constitutional symptoms
Constitutional symptoms including fatigue, low grade fever, malaise, morning stiffness, loss of appetite and loss of weight are common systemic manifestations seen in patients with active rheumatoid arthritis.
Local osteoporosis occurs in RA around inflamed joints. It is postulated to be partially caused by inflammatory cytokines. More general osteoporosis is probably contributed to by immobility, systemic cytokine effects, local cytokine release in bone marrow and corticosteroid therapy.
The incidence of lymphoma is increased in RA, although it is still uncommon.[citation needed]



X-ray of the hand in rheumatoid arthritis.
Appearance of synovial fluid from a joint with inflammatory arthritis.
Signs of destruction and inflammation on ultrasonography and magnetic resonance imaging in the second metacarpophalangeal joint in established rheumatoid arthritis. Thin arrows indicate an erosive change; thick arrows indicate synovitis. Ultrasonography (left side of image) in the (a) longitudinal and (b) the transverse planes shows both signs of destruction and inflammation. Axial T1-weighted magnetic resonance images were obtained (c) before and (d) after contrast administration, also demonstrating synovitis. Additionally, a coronal T1-weighted magnetic resonance image (e) before contrast administration visualizes the same bone erosion as shown in panels c and d.

X-rays of the hands and feet are generally performed in people with a polyarthritis. In rheumatoid arthritis, there may be no changes in the early stages of the disease, or the x-ray may demonstrate juxta-articular osteopenia, soft tissue swelling and loss of joint space. As the disease advances, there may be bony erosions and sublaxation. X-rays of other joints may be taken if symptoms of pain or swelling occur in those joints.

Other medical imaging techniques such as magnetic resonance imaging and ultrasound are also used in rheumatoid arthritis.

Blood tests

When RA is clinically suspected, immunological studies are required, such as testing for the presence of rheumatoid factor (RF, a specific antibody).[9] A negative RF does not rule out RA; rather, the arthritis is called seronegative. This is the case in about 15% of patients.[10] During the first year of illness, rheumatoid factor is more likely to be negative with some individuals converting to seropositive status over time. RF is also seen in other illnesses, for example Sjögren's syndrome, and in approximately 10% of the healthy population, therefore the test is not very specific.

Because of this low specificity, new serological test have been developed, which tests for the presence of so called anti-citrullinated protein antibodies (ACPAs). Like RF, these tests are positive in only a proportion (67%) of all RA cases, but are rarely positive if RA is not present, giving it a specificity of around 95%.[10] As with RF, there is evidence for ACPAs being present in many cases even before onset of clinical disease.[citation needed]

The most common tests for ACPAs are the anti-CCP (cyclic citrullinated peptide) test and the Anti-MCV assay (antibodies against mutated citrullinated Vimentin). Recently a serological point-of-care test (POCT) for the early detection of RA has been developed. This assay combines the detection of rheumatoid factor and anti-MCV for diagnosis of rheumatoid arthritis and shows a sensitivity of 72% and specificity of 99.7%.[11][12]

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. Elevated ferritin levels can reveal hemochromatosis, a mimic RA, or be a sign of Still's disease, a seronegative, usually juvenile, variant of rheumatoid.[citation needed]

Diagnostic criteria

The American College of Rheumatology has defined (1987) the following criteria for the classification of rheumatoid arthritis:[13]

  • 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. These criteria are not intended for the diagnosis for routine clinical care; they were primarily intended to categorize 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. Most sufferers and rheumatologists would agree that it would be better to treat the condition as early as possible and prevent bone erosion from occurring, even if this means treating people who don't fulfill the ACR criteria. The ACR criteria are, however, very useful for categorising established rheumatoid arthritis, for example for epidemiological purposes.[citation needed]

Differential diagnosis

Several other medical conditions can resemble RA, and usually need to be distinguished from it at the time of diagnosis:[14]

  • Crystal induced arthritis (gout, and pseudogout) - usually involves particular joints and can be distinguished with aspiration of joint fluid if in doubt
  • Osteoarthritis - distinguished with X-rays of the affected joints and blood tests
  • Systemic lupus erythematosus (SLE) - distinguished by specific clinical symptoms and blood tests (antibodies against double-stranded DNA)
  • One of the several types of psoriatic arthritis resembles RA - nail changes and skin symptoms distinguish between them
  • Lyme disease causes erosive arthritis and may closely resemble RA - it may be distinguished by blood test in endemic areas
  • Reactive arthritis (previously Reiter's disease) - asymmetrically involves heel, sacroiliac joints, and large joints of the leg. It is usually associated with urethritis, conjunctivitis, iritis, painless buccal ulcers, and keratoderma blennorrhagica.
  • Ankylosing spondylitis - this involves the spine and is usually diagnosed in males, although a RA-like symmetrical small-joint polyarthritis may occur in the context of this condition.

Rarer causes that usually behave differently but may cause joint pains:[14]

  • Sarcoidosis, amyloidosis, and Whipple's disease can also resemble RA.
  • Hemochromatosis may cause hand joint arthritis.
  • Acute rheumatic fever can be differentiated from RA by a migratory pattern of joint involvement and evidence of antecedent streptococcal infection. Bacterial arthritis (such as streptococcus) is usually asymmetric, while RA usually involves both sides of the body symmetrically.
  • Gonococcal arthritis (another bacterial arthritis) is also initially migratory and can involve tendons around the wrists and ankles.


Rheumatoid arthritis is a form of autoimmunity, the causes of which are still incompletely known. It is a systemic (whole body) disorder principally affecting synovial tissues.


The key pieces of evidence relating to pathogenesis are:

1. A genetic link with HLA-DR4 and related allotypes of MHC Class II and the T cell-associated protein PTPN22.

2. A link with cigarette smoking that appears to be causal.[citation needed]

3. A dramatic response in many cases to blockade of the cytokine TNF (alpha).

4. A similar dramatic response in many cases to depletion of B lymphocytes, but no comparable response to depletion of T lymphocytes.

5. A more or less random pattern of whether and when predisposed individuals are affected.

6. The presence of autoantibodies to IgGFc, known as rheumatoid factors (RF), and antibodies to citrullinated peptides (ACPA).

These data suggest that the disease involves abnormal B cell - T cell interaction, with presentation of antigens by B cells to T cells via HLA-DR eliciting T cell help and consequent production of RF and ACPA. Inflammation is then driven either by B cell or T cell products stimulating release of TNF and other cytokines. The process may be facilitated by an effect of smoking on citrullination but the stochastic (random) epidemiology suggests that the rate limiting step in genesis of disease in predisposed individuals may be an inherent stochastic process within the immune response such as immunoglobulin or T cell receptor gene recombination and mutation. (See entry under autoimmunity for general mechanisms.)

If TNF release is stimulated by B cell products in the form of RF or ACPA - containing immune complexes, through activation of immunoglobulin Fc receptors, then RA can be seen as a form of Type III hypersensitivity.[15] [16] If TNF release is stimulated by T cell products such as interleukin-17 it might be considered closer to type IV hypersensitivity although this terminology may be getting somewhat dated and unhelpful.[17] The debate on the relative roles of immune complexes and T cell products in inflammation in RA has continued for 30 years. There is little doubt that both B and T cells are essential to the disease. However, there is good evidence for neither cell being necessary at the site of inflammation. This tends to favour immune complexes (based on antibody synthesised elsewhere) as the initiators, even if not the sole perpetuators of inflammation. Moreover, work by Thurlings and others in Paul-Peter Tak's group and also by Arthur Kavanagh's group suggest that if any immune cells are relevant locally they are the plasma cells, which derive from B cells and produce in bulk the antibodies selected at the B cell stage.[citation needed]

Although TNF appears to be the dominant, other cytokines (chemical mediators) are likely to be involved in inflammation in RA. Blockade of TNF does not benefit all patients or all tissues (lung disease and nodules may get worse). Blockade of IL-1, IL-15 and IL-6 also have beneficial effects and IL-17 may be important. Constitutional symptoms such as fever, malaise, loss of appetite and weight loss are also caused by cytokines released in to the blood stream.

As with most autoimmune diseases, it is important to distinguish between the cause(s) that trigger the process, and those that may permit it to persist and progress.

Possible infectious triggers

It has long been suspected that certain infections could be triggers for this disease. The "mistaken identity" theory suggests that an infection triggers an immune response, leaving behind antibodies that should be specific to that organism. The antibodies are not sufficiently specific, though, and set off an immune attack against part of the host. Because the normal host molecule "looks like" a molecule on the offending organism that triggered the initial immune reaction - this phenomenon is called molecular mimicry. Some infectious organisms suspected of triggering rheumatoid arthritis include Mycoplasma, Erysipelothrix, parvovirus B19 and rubella, but these associations have never been supported in epidemiological studies. Nor has convincing evidence been presented for other types of triggers such as food allergies.

Epidemiological studies have confirmed a potential association between RA and two herpesvirus infections: Epstein-Barr virus (EBV) and Human Herpes Virus 6 (HHV-6).[18] Individuals with RA are more likely to exhibit an abnormal immune response to the Epstein-Barr virus.[19] [20] The allele HLA-DRB1*0404 is associated with low frequencies of T cells specific for the EBV glycoprotein 110 and predisposes one to develop RA.[21]

Psychological factors

There is no evidence that physical and emotional effects, stress could be a trigger for the disease. The many negative findings suggest that either the trigger varies, or that it might in fact be a chance event inherent with the immune response, as suggested by Edwards et al.[22].

Alimentary antigens

Several studies suspect food-derived antigenes to be involved within a scenario of a "leaky mucosa"[23] and that above all milk-products and cereals (wheat, corn etc.) can trigger the autoimmune response.[24][25][26]

Dairy products & cereals

In 1972, an "infectious agent" was hypothesized to be found in cow's milk[27]. RA can be exacerbated by dairy products (milk and cheese), resulting in an increase in synovitis, changes in immune complexes, IgE antibodies, and heat-damaged red cell clearance rates while exclusion of dairy products produced a considerable improvement.[28] In RA, raised levels of IgA RF are associated with an increased IgG response to antigens which enter the body through the gastrointestinal tract.[29] A high degree of homology between residues 142-156 from bovine albumin and residues 65-78 from human pro-collagen alpha 1 was discovered. The capacity of synoviocytes to bind exogenous antigens and the presence of antibodies to (dietary) bovine proteins suggest a role for type A synoviocytes and an involvement of food antigens in the pathogenesis of RA.[30] Antibodies in serum from some patients with RA recognize bovine serum albumin (BSA) present in milk. In 1991, a molecular mimicry mechanism in RA between this food antigen and other human antigens was elucidated: residues 141-157 of BSA are highly homologous with human collagen type I, C1q and vitamin D binding protein. RA sera display a specific reactivity for a peptide containing the homologous BSA residues. Most epitopes recognized on BSA by the RA sera are conformationally dependent as heat denaturation diminish recognition.[31] A vegan gluten-free diet can improve the symptoms of RA, the effects on arthritis correlating with a reduction in antibodies to food antigens.[32] Because a 2-week "elemental diet", resulting in clinical improvement of active RA, is as effective as oral prednisolone in improving subjective clinical parameters, RA may be a reaction to food antigens and the disease process starts within the intestine.[33]

Impact of raw food diets

In RA patients, an uncooked vegan diet rich in lactobacilli modifies the faecal microbial flora, associated with improvement in RA activity.[34] An uncooked vegan diet rich in lactobacilli decreased subjective symptoms of rheumatoid arthritis.[35]


Raised AGE-levels have been detected in serum and synovial fluid of patients with RA. The Advanced glycation end product (AGE) pentosidine is raised in the articular cartilage, in the serum and synovial fluid of RA patients.[36] In 2002, NE-carboxymethyllysine (CML), an AGE and marker of oxidative stress was detected for the first time in RA synovial tissue.[37]

Continued abnormal immune response

The factors that allow an abnormal immune response, once initiated, to become permanent and chronic, are becoming more clearly understood. The genetic association with HLA-DR4, as well as the newly discovered associations with the gene PTPN22 and with two additional genes[38] , all implicate altered thresholds in regulation of the adaptive immune response. It has also become clear from recent studies that these genetic factors may interact with the most clearly defined environmental risk factor for rheumatoid arthritis, namely cigarette smoking[39] Other environmental factors also appear to modulate the risk of acquiring RA, and hormonal factors in the individual 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. Exactly how altered regulatory thresholds allow the triggering of a specific autoimmune response remains uncertain. However, one possibility is that negative feedback mechanisms that normally maintain tolerance of self are overtaken by aberrant positive feedback mechanisms for certain antigens such as IgG Fc (bound by RF) and citrullinated fibrinogen (bound by ACPA) (see entry on autoimmunity).

Once the abnormal immune response has become established (which may take several years before any symptoms occur), plasma cells derived from B lymphocytes produce rheumatoid factors and ACPA of the IgG and IgM classes in large quantities. These are not deposited in the way that they are in systemic lupus. Rather, they appear to activate macrophages through Fc receptor and perhaps complement binding. This can contribute to inflammation of the synovium, in terms of edema, vasodilation and infiltration by activated T-cells (mainly CD4 in nodular aggregates and CD8 in diffuse infiltrates). Synovial macrophages and dendritic 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.


There is no known cure for rheumatoid arthritis, but many different types of treatment can alleviate symptoms and/or modify the disease process.

The goal of treatment is two-fold: alleviating the current symptoms, and preventing the future destruction of the joints with the 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 most RA should be treated 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.[citation needed]

Cortisone therapy has offered relief in the past, but its long-term effects have been deemed undesirable.[40]. 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.[citation needed]

Pharmacological treatment of RA can be divided into disease-modifying antirheumatic drugs (DMARDs), anti-inflammatory agents and analgesics.[41][42] Treatment also includes rest and physical activity.

Disease modifying anti-rheumatic drugs (DMARDs)

The term Disease modifying anti-rheumatic drug (DMARD) originally meant a drug that affects biological measures such as ESR and haemoglobin and autoantibody levels, but is now usually used to mean a drug that reduces the rate of damage to bone and cartilage. DMARDs have been found both to produce durable symptomatic remissions and to delay or halt progression. 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 among rheumatologists that permanent damage to the joints occurs at a very early stage in the disease. In the past it was common 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. Ultrasound and MRI are more sensitive methods of imaging the joints and have demonstrated that joint damage occurs much earlier and in more sufferers than was previously thought. People with normal X-rays will often have erosions detectable by ultrasound that X ray could not demonstrate. The aim now is to treat before damage occurs.

There may be other reasons why starting DMARDs early is beneficial as well as prevention of structural joint damage. From the earliest stages of the disease, the joints are infiltrated by cells of the immune system that signal to one another in ways that may involve a variety of positive feedback loops (it has long been observed that a single corticosteroid injection may abort synovitis in a particular joint for long periods). 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 with early arthritis, when they are most responsive to therapy and have the most to gain.[43]

Traditional small molecular mass drugs

Chemically synthesised DMARDs:

Cytotoxic drugs:

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 is usually insufficient to control symptoms on its own.[citation needed]

Methotrexate is considered by many rheumatologists to be the most important and useful DMARD, largely because of lower drop-out rates for reasons of toxicity. Nevertheless, methotrexate is often considered as a very 'toxic' drug. This reputation is not entirely justified, and at times can result in people being denied the most effective treatment for their arthritis. Although methotrexate does have the potential to suppress 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, where one of a range of different DMARDs were used, people who were prescribed methotrexate stayed on their medication the longest (the others stopped because of either side-effects or failure of the drug to control the arthritis).[citation needed] 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 as safe in combination with biological agents.[citation needed]

Biological agents

Biological agents (biologics) are produced through genetic engineering, and include:

As of December 2007 Numerous biologics are in clinical trials (eg. Ocrelizumab, Ofatumumab).[48]

Anti-inflammatory agents and analgesics

Anti-inflammatory agents include:

Analgesics include:

Historic treatments for RA have also included: rest, ice , compression and elevation, acupuncture, apple diet, nutmeg, some light exercise every now and then, nettles, bee venom, copper bracelets, rhubarb diet, extractions of teeth, fasting, honey, vitamins, insulin, magnets, and electroconvulsive therapy (ECT).[49]. Most of these have either had no effect at all, or their effects have been modest and transient, while not being generalizable.

Other therapies

Other therapies are weight loss, orthoses, occupational therapy, podiatry, physiotherapy, immunoadsorption therapy, joint injections, and special tools to improve hard movements (e.g. special tin-openers). Regular exercise is important for maintaining joint mobility and making the joint muscles stronger.

Ayurveda, mostly in southern India, is another source of treatment, and while it is popular in India there are no studies to show that it benefits patients with RA.

A survey in the United Kingdom between 1998 and 2002 found that arthritis, in its various forms, was among the five most common reasons for the medicinal use of cannabis.[50]

The Prosorba column blood filtering device (removing IgG) was approved by the FDA in 1999 for treatment of RA[51] However it was discontinued at the end of 2006.[52]

The effectiveness of treating RA with acupuncture is inconclusive, and "more rigorous research seems to be warranted" according to one study.[53]

Severely affected joints may require joint replacement surgery, such as knee replacement.


The course of the disease varies greatly. Some people 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 individuals.
  • After 5 years of disease, approximately 33% of sufferers will not be working.[citation needed]
  • After 10 years, approximately half will have substantial functional disability.[citation needed]

Prognostic factors

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.


Estimates of the life-shortening effect of RA vary; most sources cite a lifespan reduction of 5 to 10 years. According to the UK's National Rheumatoid Arthritis Society, "Young age at onset, long disease duration, the concurrent presence of other health problems (called co-morbidity), and characteristics of severe RA – such as poor functional ability or overall health status, a lot of joint damage on x-rays, the need for hospitalisation or involvement of organs other than the joints – have been shown to associate with higher mortality".[54] Positive responses to treatment may indicate a better prognosis. A 2005 study by the Mayo Clinic noted that RA sufferers suffer a doubled risk of heart disease,[55] independent of other risk factors such as diabetes, alcohol abuse, and elevated cholesterol, blood pressure and body mass index. The mechanism by which RA causes this increased risk remains unknown; the presence of chronic inflammation has been proposed as a contributing factor.[56]


Disability-adjusted life year for rheumatoid arthritis per 100,000 inhabitants in 2004.[57]
     no data      less than 40      40-50      50-60      60-70      70-80      80-90      90-100      100-110      110-120      120-130      130-140      more than 140

The incidence of RA is in the region of 3 cases per 10,000 population per annum. Onset is uncommon under the age of 15 and from then on the incidence rises with age until the age of 80. The prevalence rate is 1%, with women affected three to five times as often as men. It is 4 times more common in smokers than non-smokers. Some Native American groups have higher prevalence rates (5-6%) and people from the Caribbean region have lower prevalence rates. First-degree relatives prevalence rate is 2-3% and disease genetic concordance in monozygotic twins is approximately 15-20%.[citation needed]

It is strongly associated with the inherited tissue type Major histocompatibility complex (MHC) antigen HLA-DR4 (most specifically DR0401 and 0404) — hence family history is an important risk factor.[citation needed]

Rheumatoid arthritis affects women three times more often than men, and it can first develop at any age. The risk of first developing the disease (the disease incidence) appears to be greatest for women between 40 and 50 years of age, and for men somewhat later.[58] RA is a chronic disease, and although rarely, a spontaneous remission may occur, the natural course is almost invariably one of persistent symptoms, waxing and waning in intensity, and a progressive deterioration of joint structures leading to deformations and disability.


The first known traces of arthritis date back at least as far as 4500 BC. A text dated 123 AD first describes symptoms very similar to rheumatoid arthritis. It was noted in skeletal remains of Native Americans found in Tennessee.[59] In the Old World the disease is vanishingly rare before the 1600s.[60] and on this basis investigators believe it spread across the Atlantic during the Age of Exploration. In 1859 the disease acquired its current name.

An anomaly has been noticed from investigation of Precolumbian bones. The bones from the Tennessee site show no signs of tuberculosis even though it was prevalent at the time throughout the Americas.[61] Jim Mobley, at Pfizer, has discovered a historical pattern of epidemics of tuberculosis followed by a surge in the number of rheumatoid arthritis cases a few generations later.[62] Mobley attributes the spikes in arthritis to selective pressure caused by tuberculosis. A hypervigilant immune system is protective against tuberculosis at the cost of an increased risk of autoimmune disease.

The art of Peter Paul Rubens may possibly depict the effects of rheumatoid arthritis. In his later paintings, his rendered hands show, in the opinion of some physicians, increasing deformity consistent with the symptoms of the disease.[63][64] Rheumatoid arthritis appears to some to have been depicted in 16th century paintings.[65] However, it is generally recognised in art historical circles that the painting of hands in the sixteenth and seventeenth century followed certain stylised conventions, most clearly seen in the Mannerist movement. It was conventional, for instance to show the upheld right hand of Christ in what now appears a deformed posture. These conventions are easily misinterpreted as portrayals of disease. They are much too widespread for this to be plausible.

The first recognized description of rheumatoid arthritis was in 1800 by the French physician Dr Augustin Jacob Landré-Beauvais (1772-1840) who was based in the famed Salpêtrière Hospital in Paris.[2] The name "rheumatoid arthritis" itself was coined in 1859 by British rheumatologist Dr Alfred Baring Garrod.[66]

Notable cases

  • Dorothy Hodgkin, Nobel prize winning scientist, developed severe deforming rheumatoid arthritis at age 28. In spite of this she continued her career and developed X-ray crystallography, which underpins much of the information known about rheumatoid arthritis. She also discovered the structure of insulin and enabled the discovery of the genetic code.
  • Auguste Renoir, impressionist painter, whose later 'softer' style might have reflected in some way his severe disability.
  • Christiaan Barnard, the first surgeon to perform a human-to-human heart transplant had to retire owing to the condition. He also wrote a book on living with arthritis.
  • James Coburn claimed to have healed the condition using pills containing a sulfur-containing compound on his return to acting.
  • Erik Lindbergh, aviator and member of the X-Prize administration. Erik has been a spokesman for the arthritis drug Enbrel, as a result of his success with the treatment.[67]
  • Bob Mortimer British comedian and actor.[68]
  • Kathleen Turner and Aida Turturro have worked to raise public awareness of the condition[69]
  • Billy Bowden, international cricket umpire who had to retire from active play because of rheumatoid arhtirits.
  • Melvin Franklin, bass singer of the Temptations. He treated RA with cortisone shots so he could perform.
  • Jamie Farr, American actor, famous for his role as Max Klinger on the 1970s television series M*A*S*H.
  • Gabi Rojas, An American dancer, She appeared on So You Think You Can Dance Season 5 making the top 54 in Vegas.
  • Sandy Koufax, An American Hall-of-Fame baseball pitcher who played from 1955 to 1966 for the Los Angeles Dodgers.

See also


  1. ^ a b c Majithia V, Geraci SA (2007). "Rheumatoid arthritis: diagnosis and management". Am. J. Med. 120 (11): 936–9. doi:10.1016/j.amjmed.2007.04.005. PMID 17976416. 
  2. ^ a b Landré-Beauvais AJ (1800). La goutte asthénique primitive (doctoral thesis). Paris.  reproduced in Landré-Beauvais AJ (March 2001). "The first description of rheumatoid arthritis. Unabridged text of the doctoral dissertation presented in 1800". Joint Bone Spine 68 (2): 130–43. doi:10.1016/S1297-319X(00)00247-5. PMID 11324929. 
  3. ^ Turesson C, O'Fallon WM, Crowson CS, Gabriel SE, Matteson EL (2003). "Extra-articular disease manifestations in rheumatoid arthritis: incidence trends and risk factors over 46 years". Ann. Rheum. Dis. 62 (8): 722–7. doi:10.1136/ard.62.8.722. PMID 12860726. 
  4. ^ Jijith Krishnan,Document on Rhuematoid arthritis
  5. ^ de Groot K (August 2007). "[Renal manifestations in rheumatic diseases]". Internist (Berl) 48 (8): 779–85. doi:10.1007/s00108-007-1887-9. PMID 17571244. 
  6. ^ Wolfe F, Mitchell DM, Sibley JT, et al (April 1994). "The mortality of rheumatoid arthritis". Arthritis Rheum. 37 (4): 481–94. doi:10.1002/art.1780370408. PMID 8147925. 
  7. ^ Aviña-Zubieta JA, Choi HK, Sadatsafavi M et al (Dec 2008). "Risk of cardiovascular mortality in patients with rheumatoid arthritis: a meta-analysis of observational studies". Arthritis Rheum. 59: 1690-1697. PMID 19035419. 
  8. ^ a b Gupta A and Fomberstein B (August 2009). "Evaluating cardiovascular risk in rheumatoid arthritis". Journal of Musculoskeletal Medicine 26 (8): 481–94. 
  9. ^ Westwood OM, Nelson PN, Hay FC (April 2006). "Rheumatoid factors: what's new?". Rheumatology (Oxford) 45 (4): 379–85. doi:10.1093/rheumatology/kei228. PMID 16418203. 
  10. ^ a b Nishimura K, Sugiyama D, Kogata Y, et al (June 2007). "Meta-analysis: diagnostic accuracy of anti-cyclic citrullinated peptide antibody and rheumatoid factor for rheumatoid arthritis" (PDF). Ann. Intern. Med. 146 (11): 797–808. PMID 17548411. 
  11. ^ Renger F, Bang H, Fredenhagen G, Natusch A, Backhaus M, Feist E, Egerer K, Burmester GR. "Anti-MCV Antibody Test for the Diagnosis of Rheumatoid Arthritis Using a POCT-Immunoassay". American College of Rheumatology, 2008 Annual Scientific Meeting, poster presentation. 
  12. ^ Luime JJ, Colin EM, Hazes JM, Lubberts E. (2009). "Does anti-MCV has additional value as serological marker in the diagnostic and prognostic work-up of patients with rheumatoid arthritis? A systematic review.". Ann Rheum Dis. 2009 Mar 15. [Epub ahead of print]. doi:ard.2008.103283v1 (inactive 2009-11-06). PMID 19289382 PMID: 19289382. 
  13. ^ Arnett F, Edworthy S, Bloch D, McShane D, Fries J, Cooper N, Healey L, Kaplan S, Liang M, Luthra H (1988). "The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis.". Arthritis Rheum 31 (3): 315–24. doi:10.1002/art.1780310302. PMID 3358796. 
  14. ^ a b Berkow R, ed (1992). The Merck Manual (16th ed.). Merck Publishing Group. pp. 1307–08. ISBN 0-91191-016-6. 
  15. ^ "SUNY Stony Brook Pathology Department HBP310 Immunology". Retrieved 2008-09-20. 
  16. ^ "Hypersensitivity reactions". Retrieved 2008-09-20. 
  17. ^ "Lecture 14: Hypersensitivity". Retrieved 2008-09-20. 
  18. ^ Alvarez-Lafuente R, Fernández-Gutiérrez B, de Miguel S, et al (September 2005). "Potential relationship between herpes viruses and rheumatoid arthritis: analysis with quantitative real time polymerase chain reaction". Ann. Rheum. Dis. 64 (9): 1357–9. doi:10.1136/ard.2004.033514. PMID 16100341.& PMC 1755640. 
  19. ^ Ferrell PB, Aitcheson CT, Pearson GR, Tan EM (March 1981). "Seroepidemiological study of relationships between Epstein-Barr virus and rheumatoid arthritis". J. Clin. Invest. 67 (3): 681–7. doi:10.1172/JCI110083. PMID 6259207. 
  20. ^ Catalano MA, Carson DA, Slovin SF, Richman DD, Vaughan JH (November 1979). "Antibodies to Epstein-Barr virus-determined antigens in normal subjects and in patients with seropositive rheumatoid arthritis". Proc. Natl. Acad. Sci. U.S.A. 76 (11): 5825–8. doi:10.1073/pnas.76.11.5825. PMID 230491. 
  21. ^ Balandraud N, Roudier J, Roudier C (July 2004). "Epstein-Barr virus and rheumatoid arthritis". Autoimmun Rev 3 (5): 362–7. doi:10.1016/j.autrev.2004.02.002. PMID 15288002. 
  22. ^ Edwards JC, Cambridge G, Abrahams VM (June 1999). "Do self-perpetuating B lymphocytes drive human autoimmune disease?". Immunology 97 (2): 188–96. doi:10.1046/j.1365-2567.1999.00772.x. PMID 10447731. 
  23. ^ Is diet important in rheumatoid arthritis? Buchanan HM, Preston SJ, Brooks PM, Buchanan WW. Br J Rheumatol. 1991 Apr;30(2):125-34.
  24. ^ The gut-joint axis: cross reactive food antibodies in rheumatoid arthritis. Hvatum M, Kanerud L, Hällgren R, Brandtzaeg P. Gut. 2006 Sep;55(9):1240-7.
  25. ^ Preliminary results of a wheat-free and milk-free diet in rheumatoid arthritis. Seignalet J, Pauthe C, Reynier J, Moens P, Simon L. Presse Med. 1989 Nov 25;18(39):1931-2.
  26. ^ Effect of dietary restrictions on disease activity in rheumatoid arthritis. Beri D, Malaviya AN, Shandilya R, Singh RR. Ann Rheum Dis. 1988 Jan;47(1):69-72.
  27. ^ Svartz N. The primary cause of rheumatoid arthritis is an infection--the infectious agent exists in milk. Acta Med Scand. 1972; 192(3): 231-9.
  28. ^ Parke AL, Hughes GR. 1981; 282(6281): 2027-9. Rheumatoid arthritis and food: a case study. Br Med J (Clin Res Ed).
  29. ^ O'Farrelly C, Price R, McGillivray AJ, Fernandes L. IgA rheumatoid factor and IgG dietary protein antibodies are associated in rheumatoid arthritis. Immunol Invest. 1989; 18(6): 753-64.
  30. ^ Bellon T, Pérez-Maceda B, Marquet A, López-Bote JP, Larraga V, Langa C, de Blas E, Bernabeu C. Synoviocytes type A bind exogenous antigens recognized by antibodies present in rheumatoid arthritis. Scand J Immunol. 1989 Nov;30(5):563-71.
  31. ^ Pérez-Maceda B, López-Bote JP, Langa C, Bernabeu C. Antibodies to dietary antigens in rheumatoid arthritis--possible molecular mimicry mechanism. Clin Chim Acta. 1991 Dec 16;203(2-3):153-65.
  32. ^ Hafström I, Ringertz B, Spångberg A, von Zweigbergk L, Brannemark S, Nylander I, Rönnelid J, Laasonen L, Klareskog L. A vegan diet free of gluten improves the signs and symptoms of rheumatoid arthritis: the effects on arthritis correlate with a reduction in antibodies to food antigens. Rheumatology (Oxford). 2001; 40(10): 1175-9.
  33. ^ Podas T, Nightingale JM, Oldham R, Roy S, Sheehan NJ, Mayberry JF. Is rheumatoid arthritis a disease that starts in the intestine? A pilot study comparing an elemental diet with oral prednisolone. Postgrad Med J. 2007 Feb;83(976):128-31.
  34. ^ Peltonen R, Nenonen M, Helve T, Hänninen O, Toivanen P, Eerola E. Faecal microbial flora and disease activity in rheumatoid arthritis during a vegan diet. Br J Rheumatol. 1997; 36(1): 64-8.
  35. ^ Nenonen MT, Helve TA, Rauma AL, Hänninen OO. Uncooked, lactobacilli-rich, vegan food and rheumatoid arthritis. Br J Rheumatol. 1998; 37(3): 274-81.
  36. ^ Miyata T, Ishiguro N, Yasuda Y. Increased pentosidine, an advanced glycation end product, in plasma and synovial fluid from patients with rheumatoid arthritis and its relation with inflammatory markers. Biochem Biophys Res Commun 1998; 244: 49–9.
  37. ^ S Drinda, S Franke, C C Canet, P Petrow, R Bräuer, C Hüttich, G Stein, G Hein. Identification of the advanced glycation end products NE-carboxymethyllysine in the synovial tissue of patients with rheumatoid arthritis. Ann Rheum Dis 2002; 61: 488–492.
  38. ^ Plenge RM, Seielstad M, Padyukov L, et al (September 2007). "TRAF1-C5 as a risk locus for rheumatoid arthritis--a genomewide study". N. Engl. J. Med. 357 (12): 1199–209. doi:10.1056/NEJMoa073491. PMID 17804836. 
  39. ^ Padyukov L, Silva C, Stolt P, Alfredsson L, Klareskog L (October 2004). "A gene-environment interaction between smoking and shared epitope genes in HLA-DR provides a high risk of seropositive rheumatoid arthritis". Arthritis Rheum. 50 (10): 3085–92. doi:10.1002/art.20553. PMID 15476204. 
  40. ^ Boland EW, Headley NE (June 1951). "Results of long-continued cortisone administration in rheumatoid arthritis". Calif Med 74 (6): 416–423. PMID 14848703. 
  41. ^ O'Dell J (2004). "Therapeutic strategies for rheumatoid arthritis.". N Engl J Med 350 (25): 2591–602. doi:10.1056/NEJMra040226. PMID 15201416. 
  42. ^ Hasler P (June 2006). "Biological therapies directed against cells in autoimmune disease.". Springer Semin Immunopathol 27 (4): 443–56. doi:10.1007/s00281-006-0013-8. PMID 16738955. 
  43. ^ Vital E, Emery P (Sep 15 2005). "Advances in the treatment of early rheumatoid arthritis.". Am Fam Physician 72 (6): 1002, 1004. PMID 16190499. 
  44. ^
  45. ^
  46. ^
  47. ^ Edwards J, Szczepanski L, Szechinski J, Filipowicz-Sosnowska A, Emery P, Close D, Stevens R, Shaw T (2004). "Efficacy of B-cell-targeted therapy with rituximab in patients with rheumatoid arthritis.". N Engl J Med 350 (25): 2572–81. doi:10.1056/NEJMoa032534. PMID 15201414. 
  48. ^ "New RA Drugs in the Pipeline"
  49. ^ Hart FD (March 1976). "History of the treatment of rheumatoid arthritis". Br Med J 1 (6012): 763–5. doi:10.1136/bmj.1.6012.763. PMID 177148. 
  50. ^ S. Wright, M. Ware and G. Guy (2006). "The use of a cannabis-based medicine (Sativex) in the treatment of pain caused by rheumatoid arthritis (LTE)". Rheumatology (Oxford) 45 (6): 781. doi:10.1093/rheumatology/kel114. PMID 16621924. 
  51. ^ Fresenius HemoCare, Inc., "New Hope for Rheumatoid Arthritis Patients," press release, September 17, 1999.
  52. ^
  53. ^ Lee1 MS, Shin B-C, Ernst E (2008). "Acupuncture for rheumatoid arthritis: a systematic review". Rheumatology 47 (12): 1747–53. doi:10.1093/rheumatology/ken330. PMID 18710899. 
  54. ^ Excess mortality in rheumatoid arthritis
  55. ^ The second largest contributor of mortality is cerebrovascular disease. Increased risk of heart disease in rheumatoid arthritis patients
  56. ^ Cardiac disease in rheumatoid arthritis
  57. ^ "WHO Disease and injury country estimates". World Health Organization. 2009. Retrieved Nov. 11, 2009. 
  58. ^ Alamanos Y, Voulgari PV, Drosos AA (2006). "Incidence and prevalence of rheumatoid arthritis, based on the 1987 American College of Rheumatology criteria: a systematic review". Semin. Arthritis Rheum. 36 (3): 182–8. doi:10.1016/j.semarthrit.2006.08.006. PMID 17045630. 
  59. ^ Tennessee Origins of Rheumatoid Arthritis
  60. ^ Bones of Contention
  61. ^ Rothschild BM, Rothschild C, Helbling M (2003). "Unified theory of the origins of erosive arthritis: conditioning as a protective/directing mechanism?". J. Rheumatol. 30 (10): 2095–102. PMID 14528501. 
  62. ^ Scientist finds surprising links between arthritis and tuberculosis
  63. ^ Appelboom T, de Boelpaepe C, Ehrlich GE, Famaey JP (1981). "Rubens and the question of antiquity of rheumatoid arthritis". JAMA 245 (5): 483–6. doi:10.1001/jama.245.5.483. PMID 7005475. 
  64. ^ Did RA travel from New World to Old? The Rubens connection
  65. ^ Dequeker J., Rico H. (1992). "Rheumatoid arthritis-like deformities in an early 16th-century painting of the Flemish-Dutch school". JAMA 268 (2): 249–251. doi:10.1001/jama.268.2.249. PMID 1608144. 
  66. ^ Garrod AB (1859). The Nature and Treatment of Gout and Rheumatic Gout. London: Walton and Maberly. 
  67. ^ "The Insider: Amgen recruits high-flier to help Enbrel sales take off". Seattle Post-Intelligencer. 2007-11-07. Retrieved 2003-03-24. 
  68. ^
  69. ^ ""Sopranos" Star Aida Turturro Brings Rheumatoid Arthritis Awareness Campaign to Philadelphia". Retrieved 2007-12-18. 

External links

Study guide

Up to date as of January 14, 2010

From Wikiversity

What is rheumatoid arthritis?

Rheumatoid arthritis, or RA for short, is a chronic inflammatory disease. It is also thought to be an autoimmune disease. Its exact cause is unknown. It mainly affects the synovium, the membrane surrounding the movable joints of the skeleton. However it can also affect other organs, such as the skin, lungs, nerves, blood vessels and heart. The inflamed membrane eventually forms pannus tissue. This invades the bone and cartillage, damaging and deforming it.

RA mainly affects joints in the wrist (the metacarpal phalangeal and proximal interphalangeal joints), and those in the foot. it also affects the joints of the wrist, elbow, shoulder, neck, jaw, hip, knee and ankle.

In about 10% of cases, the onset of RA is sudden and severe. This is called acute onset.

In 20% of cases, RA develops relatively quickly over a few weeks. This is called sub-acute onset.

In the majority of cases, (approximately 70%), the conditions develop more slowly, over a long period of time. This is called insidious onset.


Approximately 0.8% of the U.K.'s adult population have rheumatoid arthritis. other sources have estimated about 400,000 people with the condition in the country.

Approximately 12,000 children under 16 have JIA (Juvenile Idiopathic Arthritis).

It most frequently occurs between the ages of 35 and 45, and affects women more than men, in the ratio of 3:1.

Genetic Factors

Genetic factors have been linked to incidence of rheumatoid arthritis. RA tends to run in families. the condition is often linked with the gene HLA-DR4. However this gene occurs in about 20-30 per cent of the population, and so is thought to make one only more susceptible to an external trigger that sets off the disease.

1911 encyclopedia

Up to date as of January 14, 2010

From LoveToKnow 1911

RHEUMATOID ARTHRITIS (OSTEO-ARTHRITIS, ARTHRITIS Deformans), terms employed to designate a disease or group of diseases characterized by destructive changes in the joints. Though it is only in comparatively recent times that the disease was definitely recognized as separate clinically from either rheumatism or gout, it is certain that it prevailed in ancient times. Characteristic changes in the bones have been found in remains in tombs in Egypt attributed by Petrie to 1300 B.C., and ancient Roman as well as British graves have held bones showing distinct traces of the diseases. Of early medical writers, Paulus Aeginata observed the lesions and seemed to consider them distinctive. Landre Beauvais in 1800 published a description of the disease under the title of Goutte asthenique primitif. The first endeavour, however, to separate rheumatoid arthritis as a distinct disease was made by William Heberden in 1803; while in 1805 John Haygarth recognized the difference between it and rheumatism, and suggested the term "nodosity of the joints." A wide divergence of opinion during the 19th century as to its relation to rheumatism and to gout gave rise to the unfortunate term "rheumatic gout." The name arthritis deformans was suggested by Virchow in 1859. Various causes, such as nervous origin, inherited arthritic diathesis, a relationship to rheumatism or gout, and reflex irritation, have been put foward as giving rise to the disease, but in the present state of medical knowledge two are most favoured. The first ascribes the disease to an infective process arising from micro-organisms. Several observers have found bacteria in the synovial fluid and membranes of affected joints, - Max Schuller finding both bacilli and cocci, while in 1896 Gilbert Bannatyne, Wohlmann and Blaxall isolated a micro-organism, a bacillus with a bipolar staining, which they stated to be almost constantly present in the joints of patients with true rheumatoid arthritis. The second view is that the disease is the result of a chronic toxaemia produced by absorption of toxines from the intestine, with perhaps some error in metabolism. In many cases there seems to be a distinct evidence of a local infection, injury being a determining factor, and some families seem to have joints which are specially liable to degeneration. The disease may begin at any age, for there is no doubt that persistent cases have been met with in quite young children; but it usually begins in early middle-age, and statistics seem to confirm the impression of the greater liability of females. Conditions which tend to lower the general health seem to act as a predisposing cause to rheumatoid arthritis, e.g. mental worry, uterine disorders and various lowering diseases, prominent among which are influenza and tonsillitis. In a number of cases in women the onset occurs about the time of the menopause.

The method of onset varies according to the form. There are four well-marked types - (t) the peri-articular form, in which the most marked changes are in the synovial membrane and peri-articular tissues, and the cartilage may be involved to a lesser degree. In this variety is found every grade of severity. The onset may be acute, resembling an attack of rheumatic fever, for which it may be mistaken; the joints, one or more, are swollen, tender and painful to the touch; the temperature elevated to ioo; 101°; but unlike rheumatic fever, sweating and hyperpyrexia are uncommon. The acute stage may then subside, a slight thickening remaining in the capsule of the joint, and the contours of the limb scarcely regaining the normal; or the attack may gradually develop into the chronic form. The pain varies greatly, and is not necessarily in ratio to the amount of arthritis present. Various joints may be involved, the spinal vertebrae not infrequently sharing in an arthritis; the most usual joints to be attacked, however, are`the knee and shoulder. When the knee is attacked there is commonly effusion into the joint. Muscular atrophy is usually present, but varies greatly in its extent. In most cases it is present to a much greater degree than can be accounted for by disuse of the muscles. The skin has in these cases a curious glossy appearance, and pigmentations may be noticed. In chronic forms the onset is gradual, one joint becoming painful and swelling, and then the others successively; in these slow forms the outlook for the recovery of the joint is not so good as in the acute, and some cases may proceed to extreme deformity with little or no pain. Gradually the shape of the joint is altered; this is in a great measure due to synovial thickening, and partly to the presence of osteophytes in the joint. When the affected joint is moved a distinct crepitation can be felt. The muscles about the joint atrophy often to an extreme degree, and contractures supervene, flexing the leg upon the thigh if the knees should be affected, and the thigh upon the abdomen should the hip be affected. In extreme degrees the patient may become a complete cripple. Later, in many cases a quiescent stage of the disease is reached, the patients cease to suffer pain, and are inconvenienced only by the deformities in the limbs, in which a considerable degree of motion may be retained. Remarkable deformities are seen in hands in which a considerable amount of usefulness still, remains. Dyspepsia and anaemia are frequently associated with arthritis. Monarticular arthritis more particularly affects the aged; and when it affects the hip is known as morbus coxae senilis. (2) The atrophic form of arthritis is not very common. The chief anatomical change is due to atrophy in the bone and cartilage. The disease occurs at an earlier period in life than the peri-articular form, from which the initial symptoms do not markedly differ; but the disorganization in the joint is greater, dislocations frequently occur, and ankylosis of the joints follows. This is the most serious form of arthritis.

(3) In the hypertrophic form the anatomical changes include the formation of new bone as well as changes in the cartilage. This new-bone formation may lead to progressive ankylosis in the joints. Should the vertebral column be affected a rigid condition of the spine known as spondylitis deformans (" poker back") may ensue. What are termed "Heberden's nodes" are small hard knobs about the size of a pea frequently found upon the fingers near the terminal phalangeal joints; they rarely give rise to symptoms. Popularly ascribed to gout, these nodes are in reality a manifestation of arthritis.

(4) A variety of arthritis occurring in children is known as Still's disease; in which the swelling of the joints is associated with swelling of the lymph glands and of the spleen. The onset is often acute, with fever and rigors; sweating is profuse and the joints are enlarged and painful. There may be much muscular wasting and limitation of movement in the joints, and anaemia is associated with the disease.

The treatment of rheumatoid arthritis is rarely curative, once the disease has been permanently established; and it is therefore important to begin treatment before destructive changes have taken place in the joints. In the acute febrile form, which is frequently taken for rheumatism, the essential treatment is rest to the affected joints, with the application of oil of wintergreen; the joint should not be fixed but supported. In the more chronic forms medicinal treatments are usually of little value. Potassium iodide is useful in some cases by promoting absorption of the hypertrophied fibrous tissue, and guaiacol if administered for a sufficiently long time is said to be capable of arresting the disease, diminishing the size of the joint and helping movement. Where anaemia accompanies the disease iron and arsenic are of value. The general health of a patient suffering from rheumatoid arthritis must be maintained, and he should live upon a dry soil. Visits to Aix-les-Bains, Buxton, Bath or Droitwich, with their baths and shampooings, often prove useful, particularly when combined with gentle massage. It is a mistake to keep the joints entirely at rest in the chronic forms, as this tends to the formation of contractures and ankylosis. Moderate exercise without undue fatigue is desirable. Patients should go early to bed and have plenty of rest, sunshine and fresh air. It is important that the diet should be nourishing and plentiful, and should there be intestinal putrefaction fermented milk is useful. As regards the local treatment, it will be well in the majority of cases to determine by the X-rays the exact state of the affected joints. Radiant heat, vibration and hot-air baths are among the best treatments. The active hyperaemia induced by hot air favours restoration of movement and alleviates pain, but where there is pronounced destruction of bone and cartilage full restoration of a joint cannot take place. Systematic exercises of the joints tend to prevent the atrophy of the adjacent muscles, .,nd Bier's passive hyperaemia induced by the temporary use of an elastic bandage has the same results. Should an X-ray photograph reveal the presence of spurs or loose bodies in the joints interfering with free movement their removal is called for. Sometimes the breaking down of adhesions under an anaesthetic is necessary, and gentle passive and later active movements of the joints should follow if freedom of use is to be gained. Recently treatment by radium has taken a definite place in the therapeutics of chronic arthritis, its analgesic properties seeming of great benefit. (H. L. H.)

<< Rheumatism

Rheydt >>

Got something to say? Make a comment.
Your name
Your email address