Rheumatoid arthritis

From Academic Kids

Rheumatoid arthritis (RA) is a chronic, inflammatory autoimmune disorder that causes the immune system to attack the joints. It is a disabling and painful inflammatory condition, which can lead to substantial loss of mobility due to pain and joint destruction. The disease is also systemic in that it often also affects many extra-articular tissues throughout the body including the skin, blood vessels, heart, lungs, and muscles.

Derived from the Greek rheumatos= flowing, -oid= in the shape of, arthr= joint, itis= condition involving inflammation

Contents

Features

The American College of Rheumatology has defined (1987) the following criteria for Rheumatoid Arthritis [1] (http://www.rheumatology.org/publications/classification/ra/ra.asp?aud=mem):

  • Morning stiffness of >1 hour.
  • Arthritis and soft-tissue swelling of >3 of 14 joints/joint groups
  • Arthritis of hand joints
  • Symmetric arthritis
  • Subcutaneous nodules in specific places
  • Rheumatoid factor at a level above the 95th percentile
  • Radiological changes suggestive of joint erosion

Four criteria have to be met, although many patients are treated despite not meeting the criteria.

The symptoms that distinguish rheumatoid arthritis are inflammation and soft-tissue swelling of many joints at the same time (polyarthritis). The hands are generally affected in a symmetric fashion. The pain generally improves with use of the affected joints, and there is usually stiffness of all joints in the morning that lasts over 1 hour.

If the arthritis has been longstanding, the inflammatory activity has led to erosion and destruction of the joint surface, which impairs their range of movement and leads to deformity. The fingers are typically deviated towards the little finger (ulnar deviation) and can assume unnatural shapes.

Subcutaneous nodules on extensor surfaces, e.g. the elbows, are often present.

Diagnosis

When RA is being clinically suspected, immunological studies are required, such as rheumatoid factor[2] (http://www.labtestsonline.org/understanding/analytes/rheumatoid/test.html) (RF, a specific antibody). A negative RF does not rule out RA; rather, the arthritis is called seronegative. During the first year of illness, rheumatoid factor is frequently negative. 80% patients eventually convert to seropositive status. RF is also seen in other illnesses, like Sjögren's syndrome, therefore the test is not very specific. Because of this low specificity, a new serological test has been developed in recent years, which tests for the presence of so called anti-citrullinated protein (ACP) antibodies. Like RF, this test can detect approximately 80% of all RA patients, but is rarely positive in non-RA patients, giving it a specificity of around 98%. In addition, ACP antibodies can be often detected in early stages of the disease, or even before disease onset. Currently, most common test for ACP antibodies is the anti-CCP[3] (http://www.labtestsonline.org/understanding/analytes/ccp/test.html) (cyclic citrulinated 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[4] (http://www.labtestsonline.org/understanding/analytes/crp/test.html), full blood count, renal function, liver enzymes and immunological tests (e.g. antinuclear antibody/ANA)[5] (http://www.labtestsonline.org/understanding/analytes/ana/test.html) are all performed at this stage. Ferritin can reveal hemochromatosis, which can mimic RA.

Pathophysiology

The cause of RA is unknown, but long suspected to be infectious. Mycoplasma, Erysipelothrix, Epstein-Barr virus, parvovirus and rubella have been suspected but never supported in epidemiological studies. As in other autoimmune diseases, the "mistaken identity" theory suggests that an offending organism causes an immune response that leaves behind antibodies that are specific to that organism. The antibodies are not specific enough, though. They begin an immune attack against, in this case, the synovium, because some molecule in the synovium "looks like" a molecule on the offending organism that created the initial immune reaction.

Autoimmune diseases require that the affected individual have a defect in the ability to distinguish self from foreign molecules. This ability is acquired in the first year of life. There are markers on many cells that confer this self-identifying feature. However, some classes of markers allow for RA to happen. 90% of patients with RA have the cluster of markers known as the HLA-DR4/DR1 cluster, whereas only 40% of controls do. Thus, in theory, RA requires susceptibility to the disease through genetic endowment with specific markers and an infectious event that triggers an autoimmune response.

Once triggered, the immune response causes inflammation of the synovium. Modern pharmacological treatments of RA target these early and intermediate molecular mediators of inflammation, including tumor necrosis factor alpha (TNF-α), interleukin (IL)–1, IL-6, transforming growth factor beta, IL-8, fibroblast growth factor and platelet-derived growth factor. Once the inflammatory reaction is established, the synovium thickens, the cartilage and the underlying bone begins to disintegrate and evidence of joint destruction accrues.

Treatment

Pharmacological treatment of RA can be divided into disease-modifying antirheumatic drugs (DMARDs), anti-inflammatory agents and analgesics. DMARDs have been found to produce durable remissions and delay or halt disease progression. This is not true of anti-inflammatories and analgesics.

DMARDs can be further subdivided into xenobiotic agents and biological agents. Xenobiotic agents are those DMARDs that do not occur naturally in the body, as opposed to biologicals.

Xenobiotics

Xenobiotics include:

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.

Biological agents

Biological agents include:

Anti-inflammatory agents and analgesics

Anti-inflammatory agents include:

Analgesics include:

Other therapies

Other therapies are weight loss, physiotherapy , joint injections, and special tools to improve hard movements (e.g. special tin-openers).

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

Epidemiology

  • Incidence 3 cases per 10,000 population
  • Prevalence rate is 1%
  • Higher prevalence rates, 5-6%, in some Native American groups
  • Lower prevalence rates in black persons from the Caribbean region
  • First-degree relatives prevalence rate is 2-3%
  • Disease concordance in monozygotic twins is approximately 15-20%

Prognosis

Disability

  • Daily living activities are impaired in most patients.
  • After 5 years of disease, approximately 33% of patients will not be working
  • After 10 years, approximately half will have substantial functional disability.

Prognostic factors

  • Poor prognostic factors include persistent synovitis, early erosive disease, extra-articular findings (including subcutaneous rheumatoid nodules), positive serum RF findings, family history of RA, male sex, advanced age, poor functional status, socioeconomic factors, elevated acute phase response (erythrocyte sedimentation rate [ESR], C-reactive protein [CRP]), and increased clinical severity.

Mortality

  • Life expectancy for patients with RA is shortened by 5-10 years, although those who respond to therapy may have lower mortality rates.

Prevention

Regular exercise and carefully controlled diet can help lessen the pain and stiffness associated with arthritic flare-ups.

History

"to be written"

See also

External links

fr:Arthrite rhumatoïde pl:Reumatoidalne zapalenie stawów

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