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Rheumatoid Arthritis: Difference between revisions

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■ Rheumatoid arthritis (RA) has an annual incidence of approximately 0.4 per 1000
{{Partial}}
in females and 0.2 per 1000 in males; recent evidence indicates that the incidence
may be rising.
■ A prevalence of 0.4% to 1% is reported in diverse populations worldwide with
evidence for geographic variation.
■ Cigarette smoking remains the strongest environmental risk factor for RA; other
lifestyle factors and exposures such as alcohol use in moderation may be inversely
associated with RA.
■ Childhood and current low socioeconomic status are associated with increased risk
of RA.
■ Hormonal and reproductive factors contribute to the female predominance in RA;
parity, breastfeeding, and exogenous hormones are modifiers of RA risk in women.


Criteria
Rheumatoid arthritis (RA) is an autoimmune disease that has an unknown aetiology. It is characterised by symmetrical erosive synovitis and sometimes multisystem disease. Typically patients have a chronic fluctuating disease course, that if left untreated results in progressive joint destruction, deformity, disability, and premature death.


==Epidemiology==
There is an annual incidence of around 0.4 per 1000 in female and 0.2 per 1000 in males. The prevalence is 0.4-1% with geographical variation, and is ~1% in New Zealand. The strongest risk factor is smoking and this also confers a worse prognosis. Females are more commonly affected than males at a 3-4:1 ratio. Peak onset is 4th and 5th decades but it can occur at any age. 12% of females with RA develop it post-partum.


Pathology
== Aetiology ==
■ Synovial tissue in joints with rheumatoid arthritis (RA) is markedly expanded by the
The aetiology remains unknown. It has a multi-factorial origin, that includes a genetic predisposition.
recruitment and retention of inflammatory cells along with the formation of villous
projections and the generation of pannus tissue that invades and destroys cartilage
and bone.
■ The pathogenic events in RA occur in stages, and mechanisms leading to initiation
of the disease appear to be distinct from those involved in the perpetuation of
inflammation and eventual destruction of joint tissue.
■ Chronic synovitis is maintained by the interactions of cell types native to the joint
and inflammatory cells recruited to the joint, with the subsequent establishment of
cytokine “networks.”
■ Angiogenesis is a feature of RA that is promoted by soluble and cell surface–bound
mediators including growth factors, proinflammatory cytokines, chemokines, matrix
components, cell adhesion molecules, proteases, and others.
■ Cartilage destruction results from the production of enzymes that destroy
components of the cartilage extracellular matrix by cells within synovial tissue
and by chondrocytes; osteoclasts contribute to the destruction of articular bone.


Clinical Features
==Pathology==
Pre-clinical Features
The disease is characterised by immune-driven, chronic inflammation. In the [[Synovial Joints|synovial tissue]], there is recruitment and retention of inflammatory cells, the formation of villous projections, and the generation of pannus tissue that invades and destroys cartilage and bone. The pathology occurs in stages. Mechanisms that initiate disease are distinct from those that perpetuate disease. In chronic synovitis there are interactions of cell types native to the joint and inflammatory cells are recruited. Cytokine "networks" are established. Angiogenesis occurs and this is promoted by mediators that include growth factors, proinflammatory cytokines, chemokines, matrix components, cell adhesion molecules, proteases, and others. Enzymatic destruction of the cartilage matrix occurs. Osteoclasts contribute to articular bone resorption.
■ The current understanding of rheumatoid arthritis (RA) development includes a
preclinical phase that can be defined by the presence of RA-related autoimmunity in
absence of clinically apparent inflammatory arthritis.
■ Growing evidence suggests that RA-related autoimmunity may initially be triggered
outside of the joints and at a mucosal site.
■ RA-related autoantibodies, including rheumatoid factor and antibodies to
citrullinated protein/peptide antigens, can be used to identify with high accuracy
(e.g., positive predictive values of >80%) patients who currently do not have
definable synovitis but will develop RA in the future.
■ Clinical trials are under way testing the hypothesis that preclinical RA can be
interrupted through pharmacologic interventions to prevent the onset of future
clinically apparent RA.


■ Morning stiffness and swelling in the wrists and proximal interphalangeal and
==Clinical Assessment==
metacarpophalangeal joints are the typical features of rheumatoid arthritis (RA).
History is used to assess for inflammatory rhythm and extraarticular features, examination is used to detect swelling and tenderness, blood tests are used to detect inflammation (CRP, ESR) and autoantibodies (RF, anti-CCP), and imaging is used to detect radiographic signs of disease (XR, US, MRI).
■ Early diagnosis of RA is critical, but many cases of “early arthritis” are not RA.
■ The 2010 American College of Rheumatology/European League Against Rheumatism
classification criteria for RA provide a framework for accurate diagnosis of
early RA.
■ Anticitrullinated peptide antibodies occur earlier than rheumatoid factor and are
more specific for RA.
■ Aggressive early administration of disease-modifying antirheumatic drugs is critical
to a good outcome.


Extra-articular features
The preclinical phase is defined by an RA-related autoimmunity without clinically apparent inflammatory arthritis. This RA-related autoimmunity can be triggered initially outside the joints in a mucosal site. The RA-related autoantibodies that include RF and anti-CCF can be used to identify those at risk of developing RA in the future.
Rheumatoid arthritis (RA) may be associated with inflammation in extraarticular
organs.
■ Features of systemic involvement in RA include constitutional symptoms, distinct
organ manifestations, and severe multiorgan disease.
■ Systemic features may be associated with a poor prognosis, especially vasculitis and
rheumatoid lung disease.


Imaging
In clinically apparent disease, the typical features are morning stiffness along with swelling in the wrists, PIPJs and MCPJs. The early diagnosis is critical, however many cases of early arthritis are not RA.
■ Symmetric bilateral rheumatoid arthritis (RA) is commonly seen in the hands and
feet, but asymmetric disease is frequently found in large joints.
■ Hands and feet show the earliest radiographic changes in RA, which include soft
tissue swelling, erosions, and diffuse joint space narrowing.
■ Radiographic damage to large joints is seen most frequently in the elbow, shoulder,
and knee.
■ Sacroiliac joint disease in a patient with RA is relatively insignificant and
uncommon.
■ Long-term complications such as atlantoaxial subluxation and basilar invagination
can be present and serious but are seen less frequently today in the modern
therapeutic era. The lateral cervical spine in flexion is the best way to evaluate
patients for atlantoaxial subluxation. Basilar invagination is best appreciated on
magnetic resonance imaging (MRI) and computed tomography.
■ Ultrasonography and MRI are becoming popular imaging modalities in clinical
rheumatology to detect subclinical disease and potentially provide an additional
outcome target for remission.


Antibodies
Extra-articular features may occur including constitutional symptoms, distinct organ manifestations, and severe multiorgan disease. Systemic features may have a poor prognosis, especially the presence of vasculitis and rheumatoid lung disease.
■ Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by the
presence of autoantibodies in peripheral blood and synovial fluid. Most
autoantibodies are not directed to joint-specific antigens.
■ Autoantibodies are already present in the earliest stages of the disease and may
precede onset by several years.
■ Rheumatoid factors (RFs), or autoantibodies to the Fc portion of IgG, are the
longest-known marker antibodies in RA. High-titer IgM-RF and also IgA-RF are of
high diagnostic and prognostic value because they are associated with erosive and
more severe disease.
■ Anti-citrullinated citrullinated protein antibodies (ACPAs) are directed to antigens
containing the unusual amino acid citrulline. They are the most specific marker
antibodies for RA and, similar to high-titer RF, are linked to erosive RA.
Autoantibodies to carbamylated antigens containing the unusual amino acid
homocitrulline may have prognostic value next to ACPAs.
■ Autoantibodies may contribute to the pathophysiology of RA by inducing,
maintaining, or modulating the disease process. Although there is increasing
evidence for a direct pathogenetic role of ACPAs and RF, the primary
(disease-inducing) autoimmune targets remain to be identified.


Assessment
Examination findings are synovitis, nodules, tenosynovitis, and bursitis. see [https://www.youtube.com/watch?v=RnvsbD6NKoc Joint Assessment Video] for examination method.
■ Assessment of patients with rheumatoid arthritis (RA) is aimed at evaluating or
prognosticating the disease process or disease outcome.
■ The 2010 classification criteria for RA were developed jointly by the American
College of Rheumatology and the European League Against Rheumatism to allow
assessment and timely institution of treatment in patients with very early and
established disease.
■ Core sets of individual measures of the disease process have been defined and
include joint swelling and tenderness, the acute-phase response, pain, patient global
assessment, and evaluator global assessment.
■ These individual measures can be effectively integrated into composite indices that
allow determination of actual disease activity, as well as disease activity states.
■ For therapeutic targeting of low disease activity or remission, clinical disease activity
assessment by composite measures has proven to be of at least similar validity as
assessment by sonography and thus remains to be the gold standard, targeting
sonographic outcomes being afflicted with costly overtreatment without any clinical
benefit.
■ In clinical practice, disease activity (the disease process) is the immediate target of
therapeutic interventions, but the ultimate goal of treatment is optimal disease
outcome, including health-related quality of life.
■ In clinical trials, disease activity states and responses, as well as their time of onset
and sustainment, should be reported.
■ The typical proxy for disease outcome is radiographic damage, which is a surrogate
for the accrued joint destruction and can be assessed by quantitative scoring.
■ Impairment of physical function (disability) is another important outcome and can
be assessed with questionnaires, typically the Health Assessment Questionnaire, or
direct functional performance tests, such as grip strength.
■ Physical function is influenced by both disease activity and joint damage; functional
disability related to joint damage is currently considered to be irreversible.


Management
Clinical disease activity using composite measures is of at least similar validity to ultrasonographic assessment without any clinical benefit.  
■ Early diagnosis and treatment are important for optimal outcomes in rheumatoid
arthritis (RA).
■ Disease-modifying antirheumatic drugs (DMARDs) with or without glucocorticoids
should be commenced at the earliest opportunity.
■ Disease activity should be monitored regularly and treatment increased until a target
(ideally remission) is reached.
■ Biologic DMARD-free and drug-free remission is achievable in a proportion of
patients with early RA


■ Disease-modifying antirheumatic drugs (DMARDs) are effective in slowing or halting
Function can be assessed with the Health Assessment Questionnaire or direct functional performance tests. Function is influenced by disease activity as well as joint damage. Any functional disability from joint damage is irreversible.
rheumatoid arthritis (RA) progression and are the mainstays of treatment.
 
■ Treating RA to the target of complete disease remission is the ultimate goal of RA
==Antibodies==
therapy.
Most autoantibodies are not joint-specific. Autoantibodies are present in the earliest stages of disease, and there may be years before clinical disease manifestation.
■ The management of RA must encompass the patient as a whole and consider
 
comorbid conditions, desire for pregnancy, patient preference, and cost in
Rheumatoid factors (RFs) are autoantibodies to the Fc portion of IgG. High-titre IgM-RF and IgA-RF are associated with erosive and more severe disease. RF is positive in ~80% with longstanding disease, but is also found in post vaccination, viral infection, malignancy, healthy elderly, and others.
management decisions.
 
■ The effective treatment of RA has been shown to help mitigate the risk of
Anti-citrullinated citrullinated protein antibodies (anti-CCPs) are autoantibodies to atigens containing the unusual amino acid citrulline. They are more specific (~96%) than RF but less sensitive (~75%). Similar to high-titre RF are associated with erosive RA with a poor prognosis.
developing complications from RA such as cardiovascular disease and cancers.
 
■ Eventual withdrawal of DMARD therapy may be possible in select patients, but it
==Imaging==
does carry a high risk of disease relapse.
Symmetric bilateral RA is commonly seen in the hands and feet, but asymmetric disease is frequently found in large joints.
 
The typical change seen on plain films is erosion. The earliest radiographic changes occur in the hands and feet: tissue swelling, erosions, and diffuse joint space narrowing. Radiographic evidence of disease in the large joints is most common in the elbow, shoulder, and knee. Sacroiliac joint disease is uncommon.
 
Rare late-term complications are atlantoaxial subluxation and basilar invagination. The best view for atlantoaxial subluxation is a lateral film of the cervical spine in flexion. For basilar invagination MRI and CT are best. Ultrasound and MRI are increasingly commonly used to detect subclinical disease.
 
==Diagnostic Criteria==
{| class="wikitable"
|+2010 American College of Rheumatology/European League Against Rheumatism criteria for rheumatoid arthritis
| colspan="2" |Target population (those who should be tested): Patients
 
#Who have at least 1 joint with definite clinical synovitis (swelling)<ref group="Note">The criteria are aimed at classification of newly presenting patients. In addition, patients with erosive disease typical of rheumatoid arthritis (RA) with a history compatible with prior fulfillment of the 2010  criteria should be classified as having RA. Patients with long-standing disease, including those whose disease is inactive (with or without treatment) who, based on retrospectively available data, have previously fulfilled the 2010 criteria should be classified as having RA.
</ref>
#Whose synovitis is not better explained by another disease<ref group="Note">Differential diagnoses vary among patients with different presentations but may include conditions such as systemic lupus erythematosus, psoriatic arthritis, and gout. If it is unclear about the relevant differential diagnoses to consider, an expert rheumatologist should be consulted.</ref>
 
Classification criteria for RA (score-based algorithm: add score of categories A–D; a score of ≥6/10 is needed to classify a patient as having definite RA)<ref group="Note">Although patients with a score of <6 of 10 are not classifiable as having RA, their status can be reassessed, and the criteria might be fulfilled cumulatively over time.</ref>
|-
!A. Joint involvement<ref group="Note">Joint involvement refers to any swollen or tender joint on examination, which may be confirmed by imaging evidence of synovitis. Distal interphalangeal joints, first carpometacarpal joints, and first metatarsophalangeal joints are excluded from assessment. Categories of joint distribution are classified according to the location and number of involved joints, with placement into the highest category possible based on the pattern of joint involvement.</ref>
!Score
|-
|1 large joint<ref group="Note">“Large joints” refers to shoulders, elbows, hips, knees, and ankles.</ref>
|0
|-
|2–10 large joints
|1
|-
|1–3 small joints (with or without involvement of large joints)<ref group="Note">∥“Small joints” refers to the metacarpophalangeal joints, proximal interphalangeal joints, second through fifth metatarsophalangeal joints, thumb interphalangeal joints, and wrists.</ref>
|2
|-
|4–10 small joints (with or without involvement of large joints)
|3
|-
|>10 joints (at least 1 small joint)<ref group="Note">In this category, at least one of the involved joints must be a small joint; the other joints can include any combination of large and additional small joints, as well as other joints not specifically listed
elsewhere (e.g., temporomandibular, acromioclavicular, sternoclavicular).</ref>
|5
|-
!B. Serologic results (at least 1 test result is needed for classification<ref group="Note">“Negative” refers to international unit (IU) values that are less than or equal to the upper limit of normal (ULN) for the laboratory and assay; “low-positive” refers to IU values that are higher than the ULN but three times or less the ULN for the laboratory and assay. Where rheumatoid factor (RF) information is available only as positive or negative, a positive result should be scored as low positive for
RF.</ref>
!Score
|-
|Negative RF and negative ACPA
|0
|-
|Low-positive RF or low-positive ACPA
|2
|-
|High-positive RF or high-positive ACPA
|3
|-
!C. Acute-phase reactants (≥1 test result is needed for classification)<ref group="Note">Normal and abnormal is determined by local laboratory standards.</ref>
!Score
|-
|Normal CRP and normal ESR
|0
|-
|Abnormal CRP or abnormal ESR
|1
|-
!D. Duration of symptoms<ref group="Note">“Duration of symptoms” refers to patient self-report of the duration of signs or symptoms of synovitis (e.g., pain, swelling, tenderness) of joints that are clinically involved at the time of assessment regardless of treatment status.</ref>
!Score
|-
|<6/wk
|0
|-
|≥6/wk
|1
|-
| colspan="2" |
<small>ACPA, Anti–citrullinated protein antibody; CRP, C-reactive protein; ESR, erythrocyte sedimentation rate.<br>
From Aletaha D, Neogi T, Silman AJ, et al. 2010 Rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Arthritis Rheum 2010;62:2569-81.</small>
|}
===Criteria Notes===
<references group="Note" />
 
== Management ==
Early diagnosis and treatment are critical for optimal outcomes.
 
Disease activity is the immediate target of therapeutic intervention. The ultimate goal is optimal disease outcome which encompasses health-related quality of life. The proxy measure for disease outcome is radiographic damage.
 
NSAIDs can reduce joint pain and swelling, but have no effect on disease progression. They can however be a useful first line analgesic.
 
DMARDs should be used at the earliest opportunity (within 6-12 weeks of diagnosis). The disease activity is monitored regularly until a target is reached, which is ideally remission. A proportion of patients can achieve remission in early RA without medication, however DMARDs are effective in slowing or stopping RA progression and are the mainstays of treatment. Effective management also reduces the risk of complications including cardiovascular disease and cancers. Eventual withdrawal of DMARDs is potentially possible in some patients but there is a high risk of relapse.
 
The most commonly used DMARDs are methotrexate and sulfasalazine at initiation. Leflunomide is a second or third line agent. Other DMARDs include hydroxychloroquine, IM gold, cyclosporin, and azathioprine. Most agents require regular monitoring (FBC, LFTs, UECs). Methotrexate has the best continuation rate. Combinations of DMARDs may be used.
 
the biological DMARDs include anti-TNFα therapies (adalimumab, etanercept, infliximab), anti-B cell therapy (rituximab), and anti-IL6 therapy (tociluzumab).
 
Glucocorticoids are used for local intra-articular injections. Prednisone is only used for those who are resistant or unable to tolerate NSAIDs. They can also be useful for short term flares.
 
Surgery is indicated in the setting of uncontrolled pain and functional limitation secondary to joint damage.
 
== Prognosis ==
The median years of life lost for men is 10, and for women is 11.
 
== Core Reading ==
{{PDF|Imaging the spine in arthritis - Jurik 2011.pdf}}
* {{#pmid:27156434}}
* {{#pmid:26545940}}
* {{#pmid:19506586}}
* {{#pmid:26282936}}
* {{#pmid:22150039}}
[[Category:Rheumatology]]

Latest revision as of 20:36, 7 April 2022

This article is still missing information.

Rheumatoid arthritis (RA) is an autoimmune disease that has an unknown aetiology. It is characterised by symmetrical erosive synovitis and sometimes multisystem disease. Typically patients have a chronic fluctuating disease course, that if left untreated results in progressive joint destruction, deformity, disability, and premature death.

Epidemiology

There is an annual incidence of around 0.4 per 1000 in female and 0.2 per 1000 in males. The prevalence is 0.4-1% with geographical variation, and is ~1% in New Zealand. The strongest risk factor is smoking and this also confers a worse prognosis. Females are more commonly affected than males at a 3-4:1 ratio. Peak onset is 4th and 5th decades but it can occur at any age. 12% of females with RA develop it post-partum.

Aetiology

The aetiology remains unknown. It has a multi-factorial origin, that includes a genetic predisposition.

Pathology

The disease is characterised by immune-driven, chronic inflammation. In the synovial tissue, there is recruitment and retention of inflammatory cells, the formation of villous projections, and the generation of pannus tissue that invades and destroys cartilage and bone. The pathology occurs in stages. Mechanisms that initiate disease are distinct from those that perpetuate disease. In chronic synovitis there are interactions of cell types native to the joint and inflammatory cells are recruited. Cytokine "networks" are established. Angiogenesis occurs and this is promoted by mediators that include growth factors, proinflammatory cytokines, chemokines, matrix components, cell adhesion molecules, proteases, and others. Enzymatic destruction of the cartilage matrix occurs. Osteoclasts contribute to articular bone resorption.

Clinical Assessment

History is used to assess for inflammatory rhythm and extraarticular features, examination is used to detect swelling and tenderness, blood tests are used to detect inflammation (CRP, ESR) and autoantibodies (RF, anti-CCP), and imaging is used to detect radiographic signs of disease (XR, US, MRI).

The preclinical phase is defined by an RA-related autoimmunity without clinically apparent inflammatory arthritis. This RA-related autoimmunity can be triggered initially outside the joints in a mucosal site. The RA-related autoantibodies that include RF and anti-CCF can be used to identify those at risk of developing RA in the future.

In clinically apparent disease, the typical features are morning stiffness along with swelling in the wrists, PIPJs and MCPJs. The early diagnosis is critical, however many cases of early arthritis are not RA.

Extra-articular features may occur including constitutional symptoms, distinct organ manifestations, and severe multiorgan disease. Systemic features may have a poor prognosis, especially the presence of vasculitis and rheumatoid lung disease.

Examination findings are synovitis, nodules, tenosynovitis, and bursitis. see Joint Assessment Video for examination method.

Clinical disease activity using composite measures is of at least similar validity to ultrasonographic assessment without any clinical benefit.

Function can be assessed with the Health Assessment Questionnaire or direct functional performance tests. Function is influenced by disease activity as well as joint damage. Any functional disability from joint damage is irreversible.

Antibodies

Most autoantibodies are not joint-specific. Autoantibodies are present in the earliest stages of disease, and there may be years before clinical disease manifestation.

Rheumatoid factors (RFs) are autoantibodies to the Fc portion of IgG. High-titre IgM-RF and IgA-RF are associated with erosive and more severe disease. RF is positive in ~80% with longstanding disease, but is also found in post vaccination, viral infection, malignancy, healthy elderly, and others.

Anti-citrullinated citrullinated protein antibodies (anti-CCPs) are autoantibodies to atigens containing the unusual amino acid citrulline. They are more specific (~96%) than RF but less sensitive (~75%). Similar to high-titre RF are associated with erosive RA with a poor prognosis.

Imaging

Symmetric bilateral RA is commonly seen in the hands and feet, but asymmetric disease is frequently found in large joints.

The typical change seen on plain films is erosion. The earliest radiographic changes occur in the hands and feet: tissue swelling, erosions, and diffuse joint space narrowing. Radiographic evidence of disease in the large joints is most common in the elbow, shoulder, and knee. Sacroiliac joint disease is uncommon.

Rare late-term complications are atlantoaxial subluxation and basilar invagination. The best view for atlantoaxial subluxation is a lateral film of the cervical spine in flexion. For basilar invagination MRI and CT are best. Ultrasound and MRI are increasingly commonly used to detect subclinical disease.

Diagnostic Criteria

2010 American College of Rheumatology/European League Against Rheumatism criteria for rheumatoid arthritis
Target population (those who should be tested): Patients
  1. Who have at least 1 joint with definite clinical synovitis (swelling)[Note 1]
  2. Whose synovitis is not better explained by another disease[Note 2]

Classification criteria for RA (score-based algorithm: add score of categories A–D; a score of ≥6/10 is needed to classify a patient as having definite RA)[Note 3]

A. Joint involvement[Note 4] Score
1 large joint[Note 5] 0
2–10 large joints 1
1–3 small joints (with or without involvement of large joints)[Note 6] 2
4–10 small joints (with or without involvement of large joints) 3
>10 joints (at least 1 small joint)[Note 7] 5
B. Serologic results (at least 1 test result is needed for classification[Note 8] Score
Negative RF and negative ACPA 0
Low-positive RF or low-positive ACPA 2
High-positive RF or high-positive ACPA 3
C. Acute-phase reactants (≥1 test result is needed for classification)[Note 9] Score
Normal CRP and normal ESR 0
Abnormal CRP or abnormal ESR 1
D. Duration of symptoms[Note 10] Score
<6/wk 0
≥6/wk 1

ACPA, Anti–citrullinated protein antibody; CRP, C-reactive protein; ESR, erythrocyte sedimentation rate.
From Aletaha D, Neogi T, Silman AJ, et al. 2010 Rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Arthritis Rheum 2010;62:2569-81.

Criteria Notes

  1. ↑ The criteria are aimed at classification of newly presenting patients. In addition, patients with erosive disease typical of rheumatoid arthritis (RA) with a history compatible with prior fulfillment of the 2010 criteria should be classified as having RA. Patients with long-standing disease, including those whose disease is inactive (with or without treatment) who, based on retrospectively available data, have previously fulfilled the 2010 criteria should be classified as having RA.
  2. ↑ Differential diagnoses vary among patients with different presentations but may include conditions such as systemic lupus erythematosus, psoriatic arthritis, and gout. If it is unclear about the relevant differential diagnoses to consider, an expert rheumatologist should be consulted.
  3. ↑ Although patients with a score of <6 of 10 are not classifiable as having RA, their status can be reassessed, and the criteria might be fulfilled cumulatively over time.
  4. ↑ Joint involvement refers to any swollen or tender joint on examination, which may be confirmed by imaging evidence of synovitis. Distal interphalangeal joints, first carpometacarpal joints, and first metatarsophalangeal joints are excluded from assessment. Categories of joint distribution are classified according to the location and number of involved joints, with placement into the highest category possible based on the pattern of joint involvement.
  5. ↑ “Large joints” refers to shoulders, elbows, hips, knees, and ankles.
  6. ↑ ∥“Small joints” refers to the metacarpophalangeal joints, proximal interphalangeal joints, second through fifth metatarsophalangeal joints, thumb interphalangeal joints, and wrists.
  7. ↑ In this category, at least one of the involved joints must be a small joint; the other joints can include any combination of large and additional small joints, as well as other joints not specifically listed elsewhere (e.g., temporomandibular, acromioclavicular, sternoclavicular).
  8. ↑ “Negative” refers to international unit (IU) values that are less than or equal to the upper limit of normal (ULN) for the laboratory and assay; “low-positive” refers to IU values that are higher than the ULN but three times or less the ULN for the laboratory and assay. Where rheumatoid factor (RF) information is available only as positive or negative, a positive result should be scored as low positive for RF.
  9. ↑ Normal and abnormal is determined by local laboratory standards.
  10. ↑ “Duration of symptoms” refers to patient self-report of the duration of signs or symptoms of synovitis (e.g., pain, swelling, tenderness) of joints that are clinically involved at the time of assessment regardless of treatment status.

Management

Early diagnosis and treatment are critical for optimal outcomes.

Disease activity is the immediate target of therapeutic intervention. The ultimate goal is optimal disease outcome which encompasses health-related quality of life. The proxy measure for disease outcome is radiographic damage.

NSAIDs can reduce joint pain and swelling, but have no effect on disease progression. They can however be a useful first line analgesic.

DMARDs should be used at the earliest opportunity (within 6-12 weeks of diagnosis). The disease activity is monitored regularly until a target is reached, which is ideally remission. A proportion of patients can achieve remission in early RA without medication, however DMARDs are effective in slowing or stopping RA progression and are the mainstays of treatment. Effective management also reduces the risk of complications including cardiovascular disease and cancers. Eventual withdrawal of DMARDs is potentially possible in some patients but there is a high risk of relapse.

The most commonly used DMARDs are methotrexate and sulfasalazine at initiation. Leflunomide is a second or third line agent. Other DMARDs include hydroxychloroquine, IM gold, cyclosporin, and azathioprine. Most agents require regular monitoring (FBC, LFTs, UECs). Methotrexate has the best continuation rate. Combinations of DMARDs may be used.

the biological DMARDs include anti-TNFα therapies (adalimumab, etanercept, infliximab), anti-B cell therapy (rituximab), and anti-IL6 therapy (tociluzumab).

Glucocorticoids are used for local intra-articular injections. Prednisone is only used for those who are resistant or unable to tolerate NSAIDs. They can also be useful for short term flares.

Surgery is indicated in the setting of uncontrolled pain and functional limitation secondary to joint damage.

Prognosis

The median years of life lost for men is 10, and for women is 11.

Core Reading

Imaging the spine in arthritis - Jurik 2011.pdf
  • Smolen et al.. Rheumatoid arthritis. Lancet (London, England) 2016. 388:2023-2038. PMID: 27156434. DOI.
  • Singh et al.. 2015 American College of Rheumatology Guideline for the Treatment of Rheumatoid Arthritis. Arthritis & rheumatology (Hoboken, N.J.) 2016. 68:1-26. PMID: 26545940. DOI.
  • Østensen & Förger. Management of RA medications in pregnant patients. Nature reviews. Rheumatology 2009. 5:382-90. PMID: 19506586. DOI.
  • Richards et al.. How to use biologic agents in patients with rheumatoid arthritis who have comorbid disease. BMJ (Clinical research ed.) 2015. 351:h3658. PMID: 26282936. DOI.
  • McInnes & Schett. The pathogenesis of rheumatoid arthritis. The New England journal of medicine 2011. 365:2205-19. PMID: 22150039. DOI.
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