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10/27/2017 Rheumatoid arthritis - Wikipedia

Rheumatoid arthritis
Rheumatoid arthritis (RA) is a long-term autoimmune
Rheumatoid arthritis
disorder that primarily affects joints.[1] It typically results in
warm, swollen, and painful joints.[1] Pain and stiffness often
worsen following rest.[1] Most commonly, the wrist and hands are
involved, with the same joints typically involved on both sides of
the body.[1] The disease may also affect other parts of the body.[1]
This may result in a low red blood cell count, inflammation
around the lungs, and inflammation around the heart.[1] Fever
and low energy may also be present.[1] Often, symptoms come on
gradually over weeks to months.[2]

While the cause of rheumatoid arthritis is not clear, it is believed

to involve a combination of genetic and environmental factors.[1]
The underlying mechanism involves the body's immune system A hand affected by rheumatoid arthritis
attacking the joints.[1] This results in inflammation and Specialty Rheumatology
thickening of the joint capsule.[1] It also affects the underlying
Symptoms Warm, swollen, painful joints[1]
bone and cartilage.[1] The diagnosis is made mostly on the basis
of a person's signs and symptoms.[2] X-rays and laboratory Complications Low red blood cells,
testing may support a diagnosis or exclude other diseases with inflammation around the
similar symptoms.[1] Other diseases that may present similarly lungs, inflammation around
include systemic lupus erythematosus, psoriatic arthritis, and the heart[1]
fibromyalgia among others.[2] Usual onset Middle age[1]
Duration Lifelong[1]
The goals of treatment are to reduce pain, decrease inflammation,
and improve a person's overall functioning.[5] This may be helped Causes Unknown[1]
by balancing rest and exercise, the use of splints and braces, or Diagnostic Based on symptoms, medical
the use of assistive devices.[1] Pain medications, steroids, and method imaging, blood tests[2][1]
NSAIDs are frequently used to help with symptoms.[1] Disease- Similar Systemic lupus
modifying antirheumatic drugs (DMARDs), such as conditions erythematosus, psoriatic
hydroxychloroquine and methotrexate, may be used to try to slow arthritis, fibromyalgia[2]
the progression of disease.[1] Biological DMARDs may be used
Medication Pain medications, steroids,
when disease does not respond to other treatments.[6] However,
Nonsteroidal anti-inflammatory
they may have a greater rate of adverse effects.[7] Surgery to
drugs, disease-modifying
repair, replace, or fuse joints may help in certain situations.[1]
antirheumatic drugs[1]
Most alternative medicine treatments are not supported by
evidence.[8][9] Frequency 0.51% (adults in developed
RA affects about 24.5 million people as of 2015.[10] This is
Deaths 30,000 (2015)[4]
between 0.5 and 1% of adults in the developed world with 5 and
50 per 100,000 people newly developing the condition each year.[3] Onset is most frequent during middle age and
women are affected 2.5 times as frequently as men.[1] In 2013, it resulted in 38,000 deaths up from 28,000 deaths in
1990.[11] The first recognized description of RA was made in 1800 by Dr. Augustin Jacob Landr-Beauvais (17721840)
of Paris.[12] The term rheumatoid arthritis is based on the Greek for watery and inflamed joints.[13]

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1 Signs and symptoms

1.1 Joints
1.2 Skin
1.3 Lungs
1.4 Heart and blood vessels
1.5 Blood
1.6 Other
2 Risk factors
2.1 Genetic
2.2 Environmental
2.3 Negative findings
3 Pathophysiology
3.1 Non-specific inflammation
3.2 Amplification in the synovium
3.3 Chronic inflammation
4 Diagnosis
4.1 Imaging
4.2 Blood tests
4.3 Classification Criteria
4.4 Differential diagnoses
4.5 Monitoring progression
5 Prevention
6 Management
6.1 Lifestyle
6.2 Disease modifying agents
6.3 Anti-inflammatory and analgesic agents
6.4 Surgery
6.5 Alternative medicine
6.6 Pregnancy
6.7 Vaccinations
7 Prognosis
7.1 Prognostic factors
7.2 Mortality
8 Epidemiology
9 History
9.1 Etymology
10 Research
11 References
12 External links

Signs and symptoms

RA primarily affects joints, but it also affects other organs in more than 1525% of individuals.[14]

Arthritis of joints involves inflammation of the synovial membrane. Joints become swollen, tender and warm, and
stiffness limits their movement. With time, multiple joints are affected (polyarthritis). Most commonly involved are the
small joints of the hands, feet and cervical spine, but larger joints like the shoulder and knee can also be involved.[15]:1098
Synovitis can lead to tethering of tissue with loss of movement and erosion of the joint surface causing deformity and loss
of function.[2]

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RA 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 typically lasts 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,
such as osteoarthritis. In arthritis of non-inflammatory causes, signs of
inflammation and early morning stiffness are less prominent with
stiffness typically less than one hour, and movements induce pain
caused by mechanical arthritis.[16] The pain associated with RA is
induced at the site of inflammation and classified as nociceptive as
opposed to neuropathic.[17] The joints are often affected in a fairly
symmetrical fashion, although this is not specific, and the initial
presentation may be asymmetrical.[15]:1098

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. Specific deformities, which also occur in osteoarthritis,
include ulnar deviation, boutonniere deformity (also "buttonhole
deformity", flexion of proximal interphalangeal joint and extension of
distal interphalangeal joint of the hand), swan neck deformity
(hyperextension at proximal interphalangeal joint and flexion at distal
interphalangeal joint) and "Z-thumb." "Z-thumb" or "Z-deformity" A diagram showing how rheumatoid
consists of hyperextension of the interphalangeal joint, fixed flexion arthritis affects a joint
and subluxation of the metacarpophalangeal joint and gives a "Z"
appearance to the thumb.[15]:1098 The hammer toe deformity may be
seen. In the worst case, joints are known as arthritis mutilans due to the mutilating nature of the deformities.[18]

The rheumatoid nodule, which is sometimes in the skin, is the most common non-joint feature and occurs in 30% of
people who have RA.[19] It is a type of inflammatory reaction known to pathologists as a "necrotizing granuloma". 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 elbow, the heel, the knuckles, or other areas that sustain repeated mechanical stress. Nodules
are associated with a positive RF (rheumatoid factor) titer, ACPA, and severe erosive arthritis. Rarely, these can occur in
internal organs or at diverse sites on the body.

Several forms of vasculitis occur in RA, but are mostly seen with long-standing and untreated disease. The most common
presentation is due to involvement of small- and medium-sized vessels. Rheumatoid vasculitis can thus commonly
present with skin ulceration and vasculitic nerve infarction known as mononeuritis multiplex.[20]

Other, rather rare, skin associated symptoms include pyoderma gangrenosum, Sweet's syndrome, drug reactions,
erythema nodosum, lobe panniculitis, atrophy of finger skin, palmar erythema, and skin fragility (often worsened by
corticosteroid use).
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Lung fibrosis is a recognized complication of rheumatoid arthritis. It is also a rare but well-recognized consequence of
therapy (for example with methotrexate and leflunomide). Caplan's syndrome describes lung nodules in individuals with
RA and additional exposure to coal dust. Exudative pleural effusions are also associated with RA.[21][22]

Heart and blood vessels

People with RA are more prone to atherosclerosis, and risk of myocardial infarction (heart attack) and stroke is markedly
increased.[23][24][25] Other possible complications that may arise include: pericarditis, endocarditis, left ventricular
failure, valvulitis and fibrosis.[26] Many people with RA 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 RA (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 people with RA 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.[26]

Anemia is by far the most common abnormality of the blood cells which can be caused by a variety of mechanisms. The
chronic inflammation caused by RA leads to raised hepcidin levels, leading to anemia of chronic disease where iron is
poorly absorbed and also sequestered into macrophages. RA may also cause a warm autoimmune hemolytic anemia.[27]
The red cells are of normal size and color (normocytic and normochromic). A low white blood cell count usually only
occurs in people with Felty's syndrome with an enlarged liver and spleen. The mechanism of neutropenia is complex. An
increased platelet count occurs when inflammation is uncontrolled.



Renal amyloidosis can occur as a consequence of untreated chronic inflammation.[28] Treatment with penicillamine and
gold salts are recognized causes of membranous nephropathy.

The eye can be directly affected in the form of episcleritis or scleritis, 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 lacrimal 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 blockage is important.

Liver problems in people with rheumatoid arthritis may be due to the underlying disease
process or as a result of the medications used to treat the disease.[29] A coexisting
autoimmune liver disease, such as primary biliary cirrhosis or autoimmune hepatitis may also
cause problems.[29]

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. Rheumatoid disease of the spine can lead to myelopathy. 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

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over one another and compressing the spinal cord. Clumsiness is initially experienced, but
without due care, this can progress to quadriplegia or even death.[30]

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 people with active

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, although it is uncommon and associated with the
chronic inflammation, not the treatment of RA.[31][32]

Risk factors
RA is a systemic (whole body) autoimmune disease. Some genetic and environmental factors impact on the risk for RA.

A family history of RA increases the risk around three to five times; as of 2016 it was estimated that genetics may account
for between 40 and 65% of cases of seropositive RA, but only around 20% for seronegative RA.[3] RA is strongly
associated with genes of the inherited tissue type major histocompatibility complex (MHC) antigen HLA-DR4 is the
major genetic factor implicated the relative importance varies across ethnic groups.[33] Genome-wide association
studies examining single-nucleotide polymorphisms have found around one hundred genes associated with RA risk, with
most of them involving the HLA system (particularly HLA-DRB1) which controls recognition of self versus nonself
molecules; other mutations affecting co-stimulatory immune pathways, for example CD28 and CD40), cytokine
signaling, lymphocyte receptor activation threshold (e.g., PTPN22), and innate immune activation appear to have less
influence than HLA mutations.[3]

There are established epigenetic and environmental risk factors for RA.[34][3] Smoking is an established risk factor for RA
in Caucasian populations, increasing the risk three times compared to non-smokers, particularly in men, heavy smokers,
and those who are rheumatoid factor positive.[35] Modest alcohol consumption may be protective.[36]

Silica exposure has been linked to RA.[37]

Negative findings
No infectious agent has been consistently linked with RA and there is no evidence of disease clustering to indicate its
infectious cause,[33] but periodontal disease has been consistently associated with RA.[3]

As of 1999, there was no evidence that physical and emotional effects or 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.[38]


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RA primarily starts as a state of persistent cellular activation leading to autoimmunity and immune complexes in both
joints and other organs where it manifests. The initial site of disease is the synovial membrane, where swelling and
congestion leads to infiltration by immune cells. Three phases of progression of RA are an initiation phase, due to non-
specific inflammation, an amplification phase, due to T cell activation and chronic inflammatory phase with tissue injury,
due to cytokines IL1, TNF-alpha and IL6.[18]

Non-specific inflammation
Factors allowing an abnormal immune response once initiated to become permanent and chronic are genetic mutations
for example, which change regulation of the adaptive immune response.[3] Genetic factors interact with environmental
risk factor for RA, the most clearly defined being cigarette smoking.[35][39]

Other environmental and hormonal factors in an individual may explain the higher risk in women, onset after childbirth,
and the (slight) modulation of disease risk by hormonal medications. Exactly how altered regulatory thresholds allow
triggering of a specific autoimmune response remains uncertain.

One possibility is that negative feedback mechanisms, which normally maintain tolerance of the self are overtaken by
positive feedback mechanisms for certain antigens, such as IgG Fc bound by Rheumatoid Factor and citrullinated
fibrinogen bound by antibodies to citrullinated peptides (ACPA). A debate on the relative roles of B-cell produced
immune complexes and T cell products in inflammation in RA has continued for 30 years, but neither cell is necessary at
the site of inflammation, only autoantibodies to IgGFc, known as rheumatoid factors (RF), and (ACPA). As with other
autoimmune diseases, people with RA have abnormally glycosylated antibodies, which are believed to promote joint

Amplification in the synovium

Once the generalized 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 activate macrophages through Fc receptor and complement binding, which is part of the
intense inflammation in RA.[41] Binding of an autoreactive antibody to the Fc receptors is mediated through the
antibody's N-glycans, which are altered to promote inflammation in people with RA.[40]

This contributes to local inflammation in a joint, specifically the synovium with edema, vasodilation and entry of
activated T-cells, mainly CD4 in microscopically nodular aggregates and CD8 in microscopically diffuse infiltrates.

Synovial macrophages and dendritic cells function as antigen-presenting cells by expressing MHC class II molecules,
which establishes the immune reaction in the tissue.

Chronic inflammation
The disease progresses by forming granulation tissue at the edges of the synovial lining, pannus with extensive
angiogenesis and enzymes causing tissue damage. The synovium thickens, cartilage and underlying bone begin to
disintegrate and the joint is getting destroyed.

Cytokines and chemokines attract and accumulate immune cells, i.e. activated T- and B cells, monocytes and
macrophages from activated fibroblasts, in the joint space. By signalling through RANKL and RANK they eventually
trigger osteoclast production, which degrades bone tissue.[3][42]

Tumor necrosis factors (TNF alpha) plays a major role and several theories exist on how TNF release happens in RA. 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.[43][44]26 October
2017 As of 1999, if TNF release is stimulated by T cell products such as interleukin-17 it might be closer to type IV
hypersensitivity although this terminology may be getting somewhat dated and unhelpful.[45]

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Although TNF appears to be the dominant chemical mediator other cytokines are involved in inflammation in RA,
because blocking TNF does not benefit all persons and all tissues, particualarly lung disease and nodules may get worse.
Blocking IL-1, IL-15 and IL-6 have beneficial effects and IL-17 may be important.[46]


X-rays of the hands and feet are generally performed when many joints
affected. In RA, there may be no changes in the early stages of the disease or
the x-ray may show osteopenia near the joint, soft tissue swelling, and a
smaller than normal joint space. As the disease advances, there may be bony
erosions and subluxation.Other medical imaging techniques such as magnetic
resonance imaging (MRI) and ultrasound are also used in RA.[18]

Technical advances in ultrasonography like high-frequency transducers

(10 MHz or higher) have improved the spatial resolution of ultrasound images
depicting 20% more erosions than conventional radiography. Color Doppler
and power Doppler ultrasound are useful in assessing the degree of synovial
inflammation as they can show vascular signals of active synovitis. This is
important, since in the early stages of RA, the synovium is primarily affected,
and synovitis seems to be the best predictive marker of future joint

Blood tests
When RA is clinically suspected, a physician may test for rheumatoid factor X-ray of the hand in rheumatoid
(RF) and anti-citrullinated protein antibodies (ACPAs measured as anti-CCP arthritis.
antibodies).[49] It is positive in 75-85%, but a negative RF or CCP antibody
does not rule out RA, rather, the arthritis is called seronegative, which is in
about 15-25% of people with RA.[50] During the first year of illness,
rheumatoid factor is more likely to be negative with some individuals
becoming seropositive over time. RF is a non-specific antibody and seen in
about 10% of healthy people, in many other chronic infections like hepatitis C,
and chronic autoimmune diseases such as Sjgren's syndrome and systemic
lupus erythematosus. Therefore, the test is not specific for RA.[18]

Hence, new serological tests check for anti-citrullinated protein antibodies

ACPAs . These tests are again positive in 61-75% of all RA cases, but with a
specificity of around 95%.[51] As with RF, ACPAs are many times present
before symptoms have started.[18]

The by far most common clinical test for ACPAs is the anti-cyclic citrullinated
peptide (anti CCP) ELISA. In 2008 a serological point-of-care test for the
early detection of RA combined the detection of RF and anti-MCV with a
Appearance of synovial fluid from a
sensitivity of 72% and specificity of 99.7%.[52][53]
joint with inflammatory arthritis.
Other blood tests are usually done to differentiate from other causes of
arthritis, like the erythrocyte sedimentation rate (ESR), C-reactive protein,
full blood count, kidney function, liver enzymes and other immunological tests (e.g., antinuclear antibody/ANA) are all

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performed at this stage. Elevated ferritin levels can reveal hemochromatosis,

a mimic of RA, or be a sign of Still's disease, a seronegative, usually juvenile,
variant of rheumatoid arthritis.

Classification Criteria
In 2010 the 2010 ACR / EULAR Rheumatoid Arthritis Classification Criteria
were introduced.[54]

The new criterion is not a diagnostic criterion but a classification criterion to

identify disease with a high likelihood of developing a chronic form.[18]
However a score of 6 or greater unequivocally classifies a person with a
diagnosis of rheumatoid arthritis.

These new classification criteria overruled the "old" ACR criteria of 1987 and Closeup of bone erosions in
are adapted for early RA diagnosis. The "new" classification criteria, jointly rheumatoid arthritis.[47]
published by the American College of Rheumatology (ACR) and the European
League Against Rheumatism (EULAR) establish a point value between 0 and
10. Four areas are covered in the diagnosis:[54]

joint involvement, designating the metacarpophalangeal joints, proximal interphalangeal joints, the interphalangeal
joint of the thumb, second through fifth metatarsophalangeal joint and wrist as small joints, and shoulders, elbows,
hip joints, knees, and ankles as large joints:

Involvement of 1 large joint gives 0 points

Involvement of 210 large joints gives 1 point
Involvement of 13 small joints (with or without involvement of large joints) gives 2 points
Involvement of 410 small joints (with or without involvement of large joints) gives 3 points
Involvement of more than 10 joints (with involvement of at least 1 small joint) gives 5 points
serological parameters including the rheumatoid factor as well as ACPA "ACPA" stands for "anti-citrullinated
protein antibody":

Negative RF and negative ACPA gives 0 points

Low-positive RF or low-positive ACPA gives 2 points
High-positive RF or high-positive ACPA gives 3 points
acute phase reactants: 1 point for elevated erythrocyte sedimentation rate, ESR, or elevated CRP value (c-reactive
duration of arthritis: 1 point for symptoms lasting six weeks or longer
The new criteria accommodate to the growing understanding of RA and the improvements in diagnosing RA and disease
treatment. In the "new" criteria serology and autoimmune diagnostics carries major weight, as ACPA detection is
appropriate to diagnose the disease in an early state, before joints destructions occur. Destruction of the joints viewed in
radiological images was a significant point of the ACR criteria from 1987.[55] This criterion no longer is regarded to be
relevant, as this is just the type of damage that treatment is meant to avoid.

In clinical practice, the following criteria apply:

two or more swollen joints

morning stiffness lasting more than one hour for at least six weeks
the detection of rheumatoid factors or autoantibodies against ACPA such as autoantibodies to mutated citrullinated
vimentin can confirm the suspicion of RA. A negative autoantibody result does not exclude a diagnosis of RA.

Differential diagnoses
Several other medical conditions can resemble RA, and need to be distinguished from it at the time of diagnosis:[56][57]

Crystal induced arthritis (gout, and pseudogout) usually involves particular joints (knee, MTP1, heels) and can be
distinguished with an aspiration of joint fluid if in doubt. Redness, asymmetric distribution of affected joints, pain

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occurs at night and the starting pain is less than an hour with gout.
Osteoarthritis distinguished with X-rays of the affected joints and blood tests, older age, starting pain less than an
hour, asymmetric distribution of affected joints and pain worsens when using joint for longer periods.
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
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
Axial spondyloarthritis (including ankylosing spondylitis) this involves the spine, although an RA-like symmetrical
small-joint polyarthritis may occur in the context of this condition.
Hepatitis C RA-like symmetrical small-joint polyarthritis may occur in the context of this condition. Hepatitis C may
also induce Rheumatoid Factor auto-antibodies
Rarer causes which usually behave differently but may cause joint pains:[56]

Sarcoidosis, amyloidosis, and Whipple's disease can also resemble RA.

Hemochromatosis may cause hand joint arthritis.
Acute rheumatic fever can be differentiated by a migratory pattern of joint involvement and evidence of antecedent
streptococcal infection.
Bacterial arthritis (such as by Streptococcus) is usually asymmetric, while RA usually involves both sides of the body
Gonococcal arthritis (a bacterial arthritis) is also initially migratory and can involve tendons around the wrists and
Sometimes arthritis is in an undifferentiated stage (i.e. none of the above criteria is positive), even if synovitis is
witnessed and assessed with ultrasound imaging.

Monitoring progression
Many tools can be used to monitor remission in rheumatoid arthritis.

Disease Activity Score of 28 joints (DAS28) is widely used as an indicator of RA disease
activity and response to treatment. Joints included are (bilaterally): proximal interphalangeal
joints (10 joints), metacarpophalangeal joints (10), wrists (2), elbows (2), shoulders (2) and
knees (2). When looking at these joints, both the number of joints with tenderness upon
touching (TEN28) and swelling (SW28) are counted. The erythrocyte sedimentation rate (ESR)
is measured and the affected person makes a subjective assessment (SA) of disease activity
during the preceding 7 days on a scale between 0 and 100, where 0 is "no activity" and 100 is
"highest activity possible". With these parameters, DAS28 is calculated as:[58]

From this, the disease activity of the affected person can be classified as follows:[58]

Current DAS28 decrease from initial value

DAS28 > 1.2 > 0.6 but 1.2 0.6
3.2 Inactive Good improvement Moderate improvement No improvement
> 3.2 but 5.1 Moderate Moderate improvement Moderate improvement No improvement
> 5.1 Very active Moderate improvement No improvement No improvement

It is not always a reliable indicator of treatment effect.[59] One major limitation is that low-grade synovitis may be

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Other tools to monitor remission in rheumatoid arthritis are: ACR-EULAR Provisional Definition
of Remission of Rheumatoid arthritis, Simplified Disease Activity Index (SDAI) and Clinical
Disease Activity Index (CDAI).[61] Some scores do not require input from a healthcare
professional and allow self-monitoring by the person, like HAQ-DI.[62]

There is no known prevention for the condition other than the reduction of risk factors.[63]

There is no cure for RA, but treatments can improve symptoms and slow the progress of the disease. Disease-modifying
treatment has the best results when it is started early and aggressively.[64]

The goals of treatment are to minimize symptoms such as pain and swelling, to prevent bone deformity (for example,
bone erosions visible in X-rays), and to maintain day-to-day functioning.[65] This is primarily addressed with disease-
modifying antirheumatic drugs (DMARDs); analgesics may be used to help manage pain.[5] RA should generally be
treated with at least one specific anti-rheumatic medication.[6] The use of benzodiazepines (such as diazepam) to treat the
pain is not recommended as it does not appear to help and is associated with risks.[66]

Regular exercise is recommended as both safe and useful to maintain muscles strength and overall physical function.[67]
It is uncertain if specific dietary measures have an effect.[68] Physical activity is beneficial for persons with Rheumatoid
arthritis complaining of fatigue.[69] Occupational therapy has a positive role to play in improving functional ability of
persons with rheumatoid arthritis.[70]

Disease modifying agents

Disease-modifying antirheumatic drugs (DMARDs) are the primary treatment for RA.[6] They are a diverse collection of
drugs, grouped by use and convention. They have been found to improve symptoms, decrease joint damage, and improve
overall functional abilities.[6] DMARDs should be started early in the disease as they result in disease remission in
approximately half of people and improved outcomes overall.[6]

The following drugs are considered as DMARDs: methotrexate, hydroxychloroquine, sulfasalazine, leflunomide, TNF-
alpha inhibitors (certolizumab, infliximab and etanercept), abatacept, and anakinra. Rituximab and tocilizumab are
monoclonal antibodies and are also DMARDs.[6]

The most commonly used agent is methotrexate with other frequently used agents including sulfasalazine and
leflunomide.[6] Sodium aurothiomalate (gold) and cyclosporin are less commonly used due to more common adverse
effects.[6] Agents may be used in combinations.[6] Methotrexate is the most important and useful DMARD and is usually
the first treatment.[6][5][71] Adverse effects should be monitored regularly with toxicity including gastrointestinal,
hematologic, pulmonary, and hepatic.[71] Side effects such as nausea, vomiting or abdominal pain can be reduced by
taking folic acid.[72]

A 2015 Cochrane review found rituximab with methotrexate to be effective in improving symptoms compared to
methotrexate alone.[73] Rituximab works by depicting levels of B-cells (immune cell that is involved in inflammation).
People taking rituximab had improved pain, function, reduced disease activity and reduced joint damage based on x-ray
images. After 6 months, 21% more people had improvement in their symptoms using rituximab and methotrexate.[73]

Biological agents should generally only be used if methotrexate and other conventional agents are not effective after a
trial of three months.[6] They are associated with a higher rate of serious infections as compared to other DMARDs.[74]
Biological DMARD agents used to treat rheumatoid arthritis include: tumor necrosis factor alpha (TNF) blockers such

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as infliximab; interleukin 1 blockers such as anakinra, monoclonal antibodies against B cells such as rituximab, and
tocilizumab T cell co-stimulation blocker such as abatacept. They are often used in combination with either methotrexate
or leflunomide.[6][3] Abatacept should not be used at the same time as other biologics.[75] In those who are well controlled
on TNF blockers decreasing the dose does not appear to affect overall function.[76] Persons should be screened for latent
tuberculosis before starting any TNF blockers therapy to avoid reactivation.[18]

TNF blockers and methotrexate appear to have similar effectiveness when used alone and better results are obtained
when used together. TNF blockers appear to have equivalent effectiveness with etanercept appearing to be the safest.[77]
Abatacept appears effective for RA with 20% more people improving with treatment than without but long term safety
studies are yet unavailable.[78] However, there is a lack of evidence to distinguish between the biologics available for
RA.[79] Issues with the biologics include their high cost and association with infections including tuberculosis.[3]

Anti-inflammatory and analgesic agents

Glucocorticoids can be used in the short term and at the lowest dose possible for flare-ups and while waiting for slow-
onset drugs to take effect.[6][3]

Non-NSAID drugs to relieve pain, like paracetamol may be used to help relieve the pain symptoms; they do not change
the underlying disease.[5]

NSAIDs reduce both pain and stiffness in those with RA but do not affect the underlying disease and appear to have no
effect on people's long term disease course and thus are no longer first line agents.[3][80] NSAIDs should be used with
caution in those with gastrointestinal, cardiovascular, or kidney problems.[81][82][83] Use of methotrexate together with
NSAIDS is safe, if adequate monitoring is done.[84] COX-2 inhibitors, such as celecoxib, and NSAIDs are equally

Especially for affected fingers, hands, and wrists, synovectomy may be needed to prevent pain or tendon rupture when
drug treatment has failed. Severely affected joints may require joint replacement surgery, such as knee replacement.
Postoperatively, physiotherapy is always necessary.[15]:1080, 1103

Alternative medicine
In general, there is not enough evidence to support any complementary health approaches for RA, with safety concerns
for some of them. Some mind and body practices and dietary supplements may help people with symptoms and therefore
may be beneficial additions to conventional treatments, but there is not enough evidence to draw conclusions.[9] A
systematic review of CAM modalities (excluding fish oil) found that " The available evidence does not support their
current use in the management of RA.".[86] Studies showing beneficial effects in RA on a wide variety of CAM modalities
are often affected by publication bias and are generally not high quality evidence such as randomized controlled trials

A 2005 Cochrane review states that low level laser therapy can be tried to improve pain and morning stiffness due to
rheumatoid arthritis as there are few side-effects.[87]

There is some evidence that Tai Chi improves the range of motion of a joint in persons with rheumatoid arthritis.[88] The
evidence for acupuncture is inconclusive[89] with it appearing to be equivalent to sham acupuncture.[90]

Dietary supplements

Some evidence supports omega-3 fatty acids and gamma-linolenic acid in RA.[91] The benefit
from omega-3 appears modest but consistent,[92] though the current evidence is not strong
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enough to determine that supplementation with omega-3 polyunsaturated fatty acids (found in
fish oil) is an effective treatment for RA.[93] Gamma-linolenic acid, which may reduce pain,
tender joint count and stiffness, is generally safe.[94]

The American College of Rheumatology states that no herbal medicines have health claims
supported by high-quality evidence and thus they do not recommend their use.[95] There is no
scientific basis to suggest that herbal supplements advertised as "natural" are safer for use
than conventional medications as both are chemicals. Herbal medications, although labelled
"natural", may be toxic or fatal if consumed.[95]

Due to the false belief that herbal supplements are always safe, there is sometimes a hesitancy to report their use which
may increase the risk of adverse reaction.[8]

The following are under investigation for treatments for RA, based on preliminary promising results (not recommended
for clinical use yet): boswellic acid,[96] curcumin,[97] devil's claw,[98][99] Euonymus alatus,[100] and thunder god vine
(Tripterygium wilfordii).[101] NCCIH has noted that, "In particular, the herb thunder god vine (Tripterygium wilfordii)
can have serious side effects."[9]

There is conflicting evidence on the role of erythropoiesis-stimulating agents for treatment of anemia in persons with
rheumatoid arthritis.[102]

More than 75% of women with rheumatoid arthritis have symptoms improve during pregnancy but might have
symptoms worsen after delivery.[18] Methotrexate and leflunomide are teratogenic (harmful to foetus) and not used in
pregnancy. It is recommended women of childbearing age should use contraceptives to avoid pregnancy and to
discontinue its use if pregnancy is planned.[65][71] Low dose of prednisolone, hydroxychloroquine and sulfasalazine are
considered safe in pregnant persons with rheumatoid arthritis.

People with RA have an increased risk of infections and mortality and recommended vaccinations can reduce these
risks.[103] The inactivated influenza vaccine should be received annually.[104] The pneumococcal vaccine should be
administered twice for people under the age 65 and once for those over 65.[105] Lastly, the live-attenuated zoster vaccine
should be administered once after the age 60, but is not recommended in people on a tumor necrosis factor alpha

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.

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

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Family history of RA
Poor functional status
Socioeconomic factors
Elevated acute phase response (erythrocyte sedimentation
rate [ESR], C-reactive protein [CRP])
Increased clinical severity.

Mortality Disability-adjusted life year for RA per

100,000 inhabitants in 2004.[107]
RA reduces lifespan on average from three to twelve years.[65]
no data 90100
According to the UK's National Rheumatoid Arthritis Society,
Young age at onset, long disease duration, the concurrent <40 100110
presence of other health problems (called co-morbidity), and 4050 110120
characteristics of severe RAsuch as poor functional ability or 5060 120130
overall health status, a lot of joint damage on x-rays, the need for 6070 130140
hospitalisation or involvement of organs other than the joints
7080 >140
have been shown to associate with higher mortality".[108] 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,[109] 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.[110] It is possible that the use of new biologic drug therapies extend the lifespan of people with RA and reduce the
risk and progression of atherosclerosis.[111] This is based on cohort and registry studies, and still remains hypothetical. It
is still uncertain whether biologics improve vascular function in RA or not. There was an increase in total cholesterol and
HDLc levels and no improvement of the atherogenic index.[112]

RA affects between 0.5 and 1% of adults in the developed world
with between 5 and 50 per 100,000 people newly developing the
condition each year.[3] In 2010 it resulted in about 49,000 deaths

Onset is uncommon under the age of 15 and from then on the

incidence rises with age until the age of 80. Women are affected
three to five times as often as men.[18] Deaths from rheumatoid arthritis per million
persons in 2012
The age at which the disease most commonly starts is in women
00 66 1320
between 40 and 50 years of age, and for men somewhat later.[114]
11 78 2155
RA is a chronic disease, and although rarely, a spontaneous
remission may occur, the natural course is almost invariably one 23 99
of the persistent symptoms, waxing and waning in intensity, and a 45 1012
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 RA. It was noted in skeletal remains of Native Americans found in Tennessee.[115] In Europe, the disease is
vanishingly rare before the 17th century.[116] The first recognized description of RA in modern medicine was in 1800 by

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the French physician Dr Augustin Jacob Landr-Beauvais (17721840) who was based in the famed Salptrire Hospital
in Paris.[12] The name "rheumatoid arthritis" itself was coined in 1859 by British rheumatologist Dr Alfred Baring

An anomaly has been noticed from the investigation of Pre-Columbian bones. The bones from the Tennessee site show
no signs of tuberculosis even though it was prevalent at the time throughout the Americas.[118]

The art of Peter Paul Rubens may possibly depict the effects of RA. In his later paintings, his rendered hands show, in the
opinion of some physicians, increasing deformity consistent with the symptoms of the disease.[119][120] RA appears to
some to have been depicted in 16th-century paintings.[121] However, it is generally recognized in art historical circles that
the painting of hands in the 16th and 17th century followed certain stylized 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.

Historic treatments for RA have also included: rest, ice, compression and elevation, 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).[122]

Rheumatoid arthritis is derived from the Greek word -rheuma (nom.), -rheumatos (gen.) ("flow,
current"). The suffix -oid ("resembling") gives the translation as joint inflammation that resembles rheumatic fever.
Rhuma which means watery discharge might refer to the fact that the joints are swollen or that the disease may be made
worse by wet weather.[13]

Meta-analysis found an association between periodontal disease and RA, but the mechanism of this association remains
unclear.[123] Two bacterial species associated with periodontitis are implicated as mediators of protein citrullination in
the gums of people with RA.[3]

Vitamin D deficiency is more common in people with rheumatoid arthritis than in the general population.[124][125]
However, whether vitamin D deficiency is a cause or a consequence of the disease remains unclear.[126] One meta-
analysis found that vitamin D levels are low in people with rheumatoid arthritis and that vitamin D status correlates
inversely with prevalence of rheumatoid arthritis, suggesting that vitamin D deficiency is associated with susceptibility to
rheumatoid arthritis.[127]

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External links
Classification ICD-10: M05 VTD
Rheumatoid arthritis (https://dmoztools.net/Health/Conditions_and_Disease
s/Musculoskeletal_Disorders/Arthritis/Rheumatoid) at DMOZ assifications/icd10/br
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Charles Weber. "History of rheumatoid arthritis" (http://charles_w.tripod.co owse/2016/en#/M05)-

m/arthritis2.html). M06 (http://apps.wh
#/M06), M45 (http://a
016/en#/M45) ICD-
9-CM: 714 (http://ww
=714) OMIM:
180300 (https://omi
MeSH: D001172 (ht
DiseasesDB: 11506
External MedlinePlus:
resources 000431 (https://www.
31.htm) eMedicine:
article/331715 (http://
tm) article/1266195
article/305417 (http://
article/401271 (http://
article/335186 (http://
article/808419 (http://

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-overview) Patient
UK: Rheumatoid
arthritis (https://patie

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