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Rheumatoid arthritis joint.gif|
Rheumatoid arthritis
ICD-10 M05-M06
ICD-9 714
OMIM 180300
DiseasesDB 11506
MedlinePlus 000431
eMedicine med/2024 emerg/48 pmr/124
MeSH {{{MeshNumber}}}


Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disorder that most commonly causes inflammation and tissue damage in joints (arthritis) and tendon sheaths, together with anemia. It can also produce diffuse inflammation in the lungs, pericardium, pleura, and the sclera of the eye, and also nodular lesions, most common in subcutaneous tissue under the skin. 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 and occupational therapy. Analgesia (painkillers) and anti-inflammatory drugs, as well as 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 symptomsEdit

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.

JointsEdit

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

Inflammation in the joints manifests itself as a soft, "doughy" swelling, causing pain and tenderness to palpation and movement, a sensation of localized warmth, and restricted movement. Increased stiffness upon waking is often a prominent feature and may last for more than an hour. These signs help distinguish rheumatoid from non-inflammatory problems of the joints, often referred to as osteoarthritis or "wear-and-tear" arthritis. In RA, the joints are often affected in a fairly symmetrical fashion although this is not specific and the initial presentation may be asymmetrical.

File:Arthrite rhumatoide.jpg

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 like ulnar deviation, boutonniere deformity, swan neck deformity and "Z-thumb" but these are of no more significance to diagnosis or disability than other variants.

SkinEdit

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 joints, or other areas that sustain repeated mechanical stress. Nodules are associated with a positive RF (rheumatoid factor) titer and severe erosive arthritis. Rarely, they can occur in internal organs.

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 due to the presence of an obliterative cutaneous capillaropathy.

Other, rather rare, skin associated symtoms include:

LungsEdit

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.

KidneysEdit

Renal amyloidosis can occur as a consequence of chronic inflammation. [4] 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 vesselsEdit

People with rheumatoid arthritis are more prone to atherosclerosis, and risk of myocardial infarction (heart attack) and stroke is markedly increased.[5] Other possible complications that may arise include: pericarditis, endocarditis, left ventricular failure, valvulitis and fibrosis.[How to reference and link to summary or text]

OtherEdit

Ocular
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 due to 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.
Hepatic
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.
Hematological
Anemia is by far the commonest abnormality of the blood cells. The red cells are of normal size and colour (normocytic). A low white blood cell count (neutropenia) or 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.
Neurological
Peripheral neuropathy and mononeuritis multiplex may occur. The most common problem is carpal tunnel syndrome due to 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.
Osteoporosis
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.
Lymphoma
The incidence of lymphoma is increased in RA, although it is still uncommon.[How to reference and link to summary or text]

DiagnosisEdit

X-raysEdit

File:RheumatoideArthritisAP.jpg

X-rays of the hands and feet are generally performed in people with a polyarthritis. In rheumatoid arthritis, these may not show any changes in the early stages of the disease, but more advanced cases demonstrate erosions and bone resorption. X-rays of other joints may be taken if symptoms of pain or swelling occur in those joints.[How to reference and link to summary or text]

Blood testsEdit

When RA is clinically suspected, immunological studies are required, such as testing for the presence of rheumatoid factor (RF, a specific antibody).[6] A negative RF does not rule out RA; rather, the arthritis is called seronegative. This is the case in about 15% of patients.[7] 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, a new serological test has been developed, which tests for the presence of so called anti-citrullinated protein antibodies (ACPAs). Like RF, this test is positive in only a proportion (67%) of all RA cases, but is rarely positive if RA is not present, giving it a specificity of around 95%.[7] As with RF, there is evidence for ACPAs being present in many cases even before onset of clinical disease.[How to reference and link to summary or text] Currently, the most common test for ACPAs 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. Elevated ferritin levels can reveal hemochromatosis, a mimic RA, or be a sign of Still's disease, a seronegative, usually juvenile, variant of rheumatoid.[How to reference and link to summary or text]

Diagnostic criteriaEdit

The American College of Rheumatology has defined (1987) the following criteria for the classification of rheumatoid arthritis:[8]

  • 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.[How to reference and link to summary or text]

Differential diagnosisEdit

Several other medical conditions can resemble RA, and usually need to be distinguished from it at the time of diagnosis:[9]

  • 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:[9]

  • 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.

PathophysiologyEdit

File:Rheumatoid arthritis joint.gif

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.

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.[10][11] 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.[12] 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.

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 due to cytokines released in to the blood stream.

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

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.

There is also no clear evidence that physical and emotional effects, stress and improper diet 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 [13].

Epidemiological studies have confirmed a potential association between RA and two herpesvirus infections: Epstein-Barr virus (EBV) and Human Herpes Virus 6 (HHV-6). [14] Individuals with RA are more likely to exhibit an abnormal immune response to the Epstein-Barr virus. [15][16] 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.[17]

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 [18], 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 [19] 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.

TreatmentEdit

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.[How to reference and link to summary or text]Cortisone therapy has offered relief in the past, but its long-term effects have been deemed undesirable.[20]. 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.[How to reference and link to summary or text]Pharmacological treatment of RA can be divided into disease-modifying antirheumatic drugs (DMARDs), anti-inflammatory agents and analgesics.[21][22] Treatment also includes rest and physical activity.

Disease modifying anti-rheumatic drugs (DMARDs)Edit

Main article: Disease-modifying antirheumatic drug

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.[23]

Traditional small molecular mass drugs Edit

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.

Many rheumatologists consider methotrexate 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). 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.

Biological agentsEdit

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

Anti-inflammatory agents and analgesicsEdit

Anti-inflammatory agents include:

Analgesics include:

The Prosorba column blood filtering device was approved by the FDA for treatment of RA in 1999 [25] However, the results have been very modest.[How to reference and link to summary or text]

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, rest, extractions of teeth, fasting, honey, vitamins, insulin, magnets, and electroconvulsive therapy (ECT).[26]. Most of these have either had no effect at all, or their effects have been modest and transient, while not being generalizable.

Other therapiesEdit

Other therapies are weight loss, occupational therapy, podiatry, physiotherapy, 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. 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 ibuprofen or other anti-inflammatory. Other areas of the body, such as the eyes and lining of the heart, are treated individually. Fish oil may have anti-inflammatory effects.

Radon therapy, popular in Germany and Eastern Europe, can induce beneficial long-term effects for rheumatoid arthritis.[27]

A survey in the United Kingdom between 1998 and 2002 found arthritis to be reported among the five most common reasons for the medicinal use of cannabis.[28]

Patients with rheumatoid arthritis do not benefit from acupuncture.[29] Severely affected joints may require joint replacement surgery, such as knee replacement.

PrognosisEdit

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.

DisabilityEdit

Prognostic factorsEdit

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.

MortalityEdit

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".[30] 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,[31] 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.[32]

EpidemiologyEdit

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%.[How to reference and link to summary or text]

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.[How to reference and link to summary or text]

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.[33] 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.

HistoryEdit

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.[34] In the Old World the disease is vanishingly rare before the 1600s.[35] 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.[36] 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.[37] 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.[38][39] Rheumatoid arthritis appears to some to have been depicted in 16th century paintings.[40] 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.[41]


See alsoEdit

ReferencesEdit

  1. 1.0 1.1 1.2 Majithia V, Geraci SA (2007). Rheumatoid arthritis: diagnosis and management. Am. J. Med. 120 (11): 936–9.
  2. 2.0 2.1 Landré-Beauvais AJ (1800). La goutte asthénique primitive (doctoral thesis). 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.
  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.
  4. de Groot K (August 2007). [Renal manifestations in rheumatic diseases]. Internist (Berl) 48 (8): 779–85.
  5. Wolfe F, Mitchell DM, Sibley JT, et al (April 1994). The mortality of rheumatoid arthritis. Arthritis Rheum. 37 (4): 481–94.
  6. Westwood OM, Nelson PN, Hay FC (April 2006). Rheumatoid factors: what's new?. Rheumatology (Oxford) 45 (4): 379–85.
  7. 7.0 7.1 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. Ann. Intern. Med. 146 (11): 797–808.
  8. 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.
  9. 9.0 9.1 (1992) Berkow R The Merck Manual, 16th, 1307–08, Merck Publishing Group.
  10. SUNY Stony Brook Pathology Department HBP310 Immunology. URL accessed on 2008-09-20.
  11. Hypersensitivity reactions. URL accessed on 2008-09-20.
  12. Lecture 14: Hypersensitivity. URL accessed on 2008-09-20.
  13. Edwards JC, Cambridge G, Abrahams VM. Do self-perpetuating B lymphocytes drive human autoimmune disease? Immunology. 1999;97:188-96.
  14. 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.
  15. 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.
  16. 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.
  17. Balandraud N, Roudier J, Roudier C (July 2004). Epstein-Barr virus and rheumatoid arthritis. Autoimmun Rev 3 (5): 362–7.
  18. 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.
  19. 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.
  20. Boland EW, Headley NE (June 1951). Results of long-continued cortisone administration in rheumatoid arthritis. Calif Med 74 (6): 416–423.
  21. O'Dell J (2004). Therapeutic strategies for rheumatoid arthritis.. N Engl J Med 350 (25): 2591–602.
  22. Hasler P (June 2006). Biological therapies directed against cells in autoimmune disease.. Springer Semin Immunopathol 27 (4): 443–56.
  23. Vital E, Emery P (Sep 15 2005). Advances in the treatment of early rheumatoid arthritis.. Am Fam Physician 72 (6): 1002, 1004.
  24. 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.
  25. Fresenius HemoCare, Inc., "New Hope for Rheumatoid Arthritis Patients," press release, September 17, 1999.
  26. Hart FD (March 1976). History of the treatment of rheumatoid arthritis. Br Med J 1 (6012): 763–5.
  27. Franke A, Reiner L, Pratzel HG, Franke T, Resch KL (August 2000). Long-term efficacy of radon spa therapy in rheumatoid arthritis--a randomized, sham-controlled study and follow-up. Rheumatology (Oxford) 39 (8): 894–902.
  28. 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).
  29. Lee1 MS, Shin B-C, Ernst E (2008). Acupuncture for rheumatoid arthritis: a systematic review. Rheumatology 47: 1747–53.
  30. Excess mortality in rheumatoid arthritis
  31. The second largest contributor of mortality is cerebrovascular disease. Increased risk of heart disease in rheumatoid arthritis patients
  32. Cardiac disease in rheumatoid arthritis
  33. 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.
  34. http://mcclungmuseum.utk.edu/research/renotes/rn-05txt.htm Tennessee Origins of Rheumatoid Arthritis
  35. http://www.arc.org.uk/newsviews/arctdy/104/bones.htm Bones of Contention
  36. 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.
  37. Scientist finds surprising links between arthritis and tuberculosis
  38. Appelboom T, de Boelpaepe C, Ehrlich GE, Famaey JP (1981). Rubens and the question of antiquity of rheumatoid arthritis. JAMA 245 (5): 483–6.
  39. http://japan.medscape.com/viewarticle/538251 Did RA travel from New World to Old? The Rubens connection
  40. Dequeker J., Rico H. (1992). Rheumatoid arthritis-like deformities in an early 16th-century painting of the Flemish-Dutch school. JAMA 268: 249–251.
  41. Garrod AB (1859). The Nature and Treatment of Gout and Rheumatic Gout, London: Walton and Maberly.

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