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Rheumatoid Arthritis

Clinical features, Diagnosis, Management, Prognosis,

Rheumatoid arthritis (RA) is the commonest form of chronic inflammatory joint disease. In its typical form RA is a symmetrical, destructive and deforming polyarthritis affecting small and large peripheral joint with associated systemic disturbances, a variety of extra-articular features and the presence of circulating autoantibodies that target the Fc portions of normal IgG antibodies (rheumatoid factors). Rheumatoid factors bind with their target self-antigens in blood and joint synovial membranes, forming immune complexes that initiate an inflammatory reaction.

Rheumatoid arthritis occurs throughout the world and in all ethnic groups. Climate, altitude and geography do not appear to influence its prevalence. The overall prevalence of RA in Caucasian populations is about 1% with female to male of 3:1. The disease starts most commonly between the third and fifth decade.

Although the cause of rheumatoid arthritis remains unknown, there is increasing evidence that the disease is triggered by T lymphocyte activation in genetically predisposed individuals with defined HLA Class II tissue types (HLA-DR4 is the major susceptibility type). However it is not known which antigen (exogenous or endogenous) initiates and perpetuates the disease, but certain retroviruses and parvoviruses might be responsible, at least in initial stages of the disease. Alternatively, it has been suggested that sensitisation to self antigens could be a consequence of enzymatic or free radical damage to proteins such as immunoglobulin (IgG) or collagen, which results in minor structural abnormality.

Whatever the initiating stimulus, RA is characterised by persistent activation of immune cells and the presence of immune complexes at sites of articular and extra-articular lesions. Thus rheumatoid arthritis is both an extravascular immune complex disease and a disorder of cell-mediated immunity. The severity of tissue damage is related to joint movement and physical stress as well as the activity of the inflammatory disease indicating that mechanical factors are also important in its pathogenesis.

The earliest change is swelling and hyperaemia (redness) of the synovial membrane and the underlying connective tissues, which become infiltrated with lymphocytes (especially CD4 T helper cells responsible for starting an inflammatory response), plasma cells and macrophages (macrophages secrete cytokines such as tumour necrosis factor now through to play an important role in tissue inflammation). Damage of joint tissues appears to be the result of action of released lysosomal enzymes from macrophages and neutrophils

Accumulation of inflammatory fluid (exudate) in the joint space takes place during active phases of the disease. Thickening of the synovial membrane occurs with the formation of lymphoid aggregates resembling an immunologically active lymph node. Hyperplastic and oedematous synovial inflammatory tissue (pannus) is formed, spreading over and under the articular cartilage, which is progressively eroded and destroyed, but some damage of articular capsule and ligaments also occurs. Later, fibrous adhesions may form between the layers of pannus across the joint space. These adhesions can undergo partial calcification eventually forming fibrous or bony ankylosis (joint immobility).

Clinical features:  < BACK TO TOP >

  • In the majority of patients the onset is insidious with joint pain, stiffness and symmetrical swelling f a number of peripheral joints, usually first small joints of the fingers and toes.
  • Swelling of proximal, but not distal, interphalangeal joint gives the fingers a characteristic 'spindled' appearance, and swelling of the metatarsophalangeal joints results in 'broadening' of the forefoot (patients may need to buy bigger shoes).
  • Rest pain in the joints and especially early morning stiffness are characteristic features, and the pain seems to improve on joint movement (exercise or mild work).
  • In time the disease spreads to involve the wrists, elbows, shoulders, ankles, knees, other foot joints, cervical spine with neck pain and stiffness.
  • The temporomandibular, acromioclavicular and sternoclavicular joints are sometimes involed, hip joints also but only in very advanced disease.
  • As the disease advances tendon sheath and joint destruction result in limitation of joint motion with consequent muscle atrophy, instability, subluxation (incomplete dislocation) and deformities such as very characteristic ulnar drift (deviation) of the fingers.
  • Hyperextension of the proximal interphalangeal joint with fixed flexion at the distal interphalangeal joint leads to 'swan neck' deformity.
  • Fixed flexion of the proximal interphalangeal joint and extension of the distal interphalangeal joint forms 'button-hole' (boutonniere) deformity.
  • In the foot hyperextension of the toes ('clawing') develop as well exposed metatarsal heads with a painful sensation of 'walking on pebbles'.
  • Subcutaneous rheumatoid nodules develop in 20% of patients at sites of pressure or friction such as dorsal side of the hands, elbow area, sacrum and Achilles tendon: they are composed of central area of tissue necrosis surrounded by the layers of lymphocytes and connective tissue.
  • Extra-articular features are various: fever, weight loss, fatigue, susceptibility to infection, muscle wasting, tenosynovitis, osteoporosis, anaemia, lymphadenopathy, splenomegaly, episcleritis and keratoconjunctivitis, peripheral vasculitis, pericarditis, myocarditis, conduction defects in the heart (various types of heart block), pleurisy with pleural effusions and peripheral neuropathy (the patient may complain of burning sensation or numbness).
  • Characteristically the course of the disease is prolonged with exacerbations and remissions, but resulting in significant disability in many patients.

Diagnosis:  < BACK TO TOP >

  • Diagnosis of rheumatoid arthritis can be established if any four or more of the follwing criteria are identified:
    • morning stiffness lasting more that 1 hour (duration of six weeks or more)
    • arthritis f 3 or more joint areas - polyarthritis (duration of six weeks or more)
    • arthritis of hand joints (duration of six weeks or more)
    • rheumatoid subcutaneous nodules
    • positive rheumatoid factor
    • characteristic X ray changes (loss of bine cartilage, bone erosions, subluxations, deformations, ankylosis)
  • Markers of active inflammatory disease in blood are important supportive findings:
    • normochromic-normocytic anaemia of chronic disease (not iron deficient)
    • thrombocytosis (increased platelet count)
    • increased erythrocyte sedimentation rate (found in 90% of cases)
    • C reactive protein (more sensitive than ESR) which is an abnormal protein produced in the liver, that resembles immunoglobulins in structure
  • Serological tests can detect rheumatoid factors by testing the ability of the patient's serum to agglutinate certain carrier particles coated with IgG, and they readily demonstrate IgM rheumatoid factors (IgM molecules are composed of 5 units that can bind different particles).
    • Polystyrene plastic beads coated with human IgG are used in the latex fixation test and IgM rheumatoid factors readily agglutinate these particles.
    • Sheep or human erythrocytes coated with rabbit anti-erythrocyte antibodies are used in the Rose Waaler sheep-cell agglutination test (SCAT) and the human erythrocyte agglutination test (HEAT).
    • The latex fixation test is simple and sensitive but less specific so that it is frequently used as a screening test. The erythrocyte tests are less sensitive but more specific to rheumatoid arthritis, and therefore are carried out after the latex test has returned a positive result.
    • The agglutination tests are positive in 70% of patients with rheumatoid arthritis but may not become so for 1-2 years, However, positive tests are also found in other autoimmune diseases (e.g., systemic lupus erythematosus) and chronic infections (e.g., chronic hepatitis).
    • Rheumatoid factor, including IgG type, can be identified by nephelometry technique that measures the turbidity of the patient's serum after IgG has been added that serves as an antigen (turbidity is due to formed immune complexes).
    • Up to 30% of patients with RA have positive tests for antinuclear factor (antibodies against various nuclear components), which is more commonly associated with systemic lupus erythematosus.

Management  < BACK TO TOP >

  • Because the aetiology of rheumatoid arthritis is unknown the treatment is empirically directed towards relief of symptoms, suppression of active and progressive disease and conservation and restoration of function in affected joints.
  • This can be achieved by combining treatment of the patient (drugs, rest, physiotherapy, surgery) with modification of the environment (appropriate aids, appliances, housing, occupation, statutory social benefits etc).
  • NSAIDs (non-steroidal anti-inflammatory drugs) provide important symptomatic relief but they do not appear to alter the lomg-term course of the disease. Drugs commonly given are ibuprofen [Brufen, Nurofen], ketoprofen [Orudis, Oruvail], naproxen[Naprosyn, Naprogesic], indomomethacin [ Indocid], piroxicam [Feldene], diclofenec [Voltaren], tenoxicam [Tilcotil].
  • Currently available NSAIDs frequently cause side effects such as gastrointestinal disturbances, bleeding or even peptic ulcer disease, and impairment of kidney function known as analgesic nephropathy (roughly in 25% of treated patients).
  • New NSAIDs such as celecoxib [Celebrex] have highly selective anti-COX-2 activity (most NSAIDs mentioned earlier block both types of cyclo-oxygenase COX-1 and COX-2) and much less incidence of gastrointestinal and renal side effects have been approved.
  • Recent studies have suggested that more aggressive therapy started early can delay the crippling portion of rheumatoid factor and has been diagnosed as new rheumatoid arthritis, the drug of choice currently may be immuno-suppressive drug methotrexate [Methotrexate, Ledertrexate, Methoblastin], usually once a week, when a response occurs in about 1 month.
  • Recently a new immunosuppressive/immuno modulatory drug leflunomide [Arava] has been approved for treatment of rheumatoid arthritis. It is gived orally once a day and its results are comparable to methotrexate, although it appears to be better tolerated.
  • Other drugs that might be considered are:
    • oral and parenteral gold compounds such as auranofin [Ridaura], aurothioglucose [Gold-50] and autothiomalate [Myocrisin]
    • immuno-suppressant azathioprine [Imuran]
    • penicillamine [D-Penamine]
    • corticosteroid drugs in low doses, usually prednisolone [Delta-Cortef, Panafcortelone, Solone] or prednisone [Panafcort, Sone]
    • sulfasalazine [Salazopyrin]
  • Recently monoclonal antibodies against TNF (tumour necrosis factor) such as etanercept and infliximab have been approved for in USA (not yet available in Australia) and they act as anti-inflammatory agents (given subcutaneously).

Prognosis  < BACK TO TOP >

  • The course and prognosis in rheumatoid arthritis is very variable. Review after ten years show that:
    • 25% will have almost complete remission of symptoms and remain fit for all normal activities.
    • 40% will have only moderate impairment of function despite exacerbations and remissions of disease
    • 25% will be more severely disabled.
    • 10% will be severely crippled
  • A poor prognosis may be associated with:
    • high concentrations of rheumatoid factor
    • insidious onset of disease
    • more than a year active disease without remission despite treatment
    • early development of subcutaneous and bone erosions
    • extra articular manifestations

Juvenile Rheumatoid Arthritis

Juvenile rheumatoid arthritis is similar to adult RA. There are three main clinical patterns:

  • Systemic onset (also known as Still's disease) occurs in about 20% of patients with high fever, macular rash (usually seen when fever is present), splenomegaly, generalised lymphadenopathy, pleurisy, pericarditis, with myalgia, arthralgia and eventually polyarthritis. This pattern most common between the ages of 1 and 5 years. There is usually weight loss and retardation of growth. Rheumatoid factor and antinuclear antibodies are absent.
  • Pauciaticular onset occurs in about 40% of patients, usually young girls, involving four or less joints and usually no systemic features. Antinuclear antibodies are found in up to 75% of affected children.
  • Polyarticular onset occurs in the remaining 40% of patients and often is similar to adult RA Rheumatoid factor is usually negative, but in adolescent girls it can be positive.

The overall prognosis for juvenile rheumatoid arthritis is generally better than for adult one, with complete remissions developing in 50-75% of patients. Patients with polyarticular onset and positive rheumatoid factor have less favourable prognosis.
Therapy is similar to adult RA. Various non-steroidal anti-inflammatory drugs are given, but in contrast to adult RA corticosteroids are reserved for children with severe systemic disease only. Immunosuppressants may be necessary for managing more serious polyarticular disease. Other measures such as hydrotherapy in a warm pool, exercises, and other physiotherapy measures are also useful.

(source : Dr Zoran Pletikosa)

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