• Chronic symmetrical arthritis affecting mainly peripheral joints
  • In addition it has non articular features

 

Aetiology

  • Most common age of onset is 30-50
  • Women before the menopause are 3 times more likely to be affected than men. After then menopause the frequency of onset is the same
  • Familial component
  • Associated with HLA-DR4 and HLA-DRb1

 

Immunology

  • T cell mediated
  • Temporary B cell ablation induces remission – suggesting the role of rheumatoid factor is producing and maintaining inflammation
  • Antibodies against TNF and IL-1 produce short term improvement in synovitis
  • High affinity antibody production is not a feature

 

Pathology

  • Widespread synovitis
  • Role of rheumatoid factor by plasma cells in the synovium and local formation of immune complexes
  • Synovium becomes greatly thickened and becomes palpable as a ‘boggy’ swelling around joints and tendons
  • Synovium proliferates into folds and frounds and is infiltrated with neutrophils, macrophages, T cells and B cells
  • Form disorganised lymphoid structures
  • Increased permeability of blood vessels and synovial lining leads to joint effusions
  • Synovium spreads from the joint margins onto the cartilage surface, damaging it by blocking it normal nutrition
  • Contributes to juxta-articular osteoporosis
  • Rheumatoid factor – IgM recognising the Fc region of IgG
  • Aggregate into immune complexes and activated complement

 

Clinical features

  • Typically presents as a slowly progressive, symmetrical peripheral polyarthritis evolving over weeks to months
  • Patients who develop quickly with a severe symmetrical polyarthritis have a better prognosis

 

DDx

  • Postviral arthritis – rubella, hep B or parvovirus
  • Seronegative spondyloarthopathy
  • Polymyalgia rheumatica
  • Acute nodal osteoarthritis

 

Symptoms/signs

  • Pain and stiffness of the small joints of the hand and feet
  • Wrists, elbows, shoulders, knees and ankles are also affected
  • Hips are rarely affected
  • Pain and stiffness worse in the morning
  • Joints are usually warm and tender with some swelling

 

Complications

  • Ruptured tendons
  • Ruptured joints
  • Joint infections
  • Spinal cord compression
  • Amyloidosis

 

Joint involvement

 

Hands and wrists

  • In early disease fingers and swollen painful and stiff
  • Inflamed flexor tendon sheaths may cause carpal tunnel syndrome
  • Joint damage results in ulnar drift and palmer subluxation of the MCP
  • PIP joint deformities include fixed flexion – Boutonniere deformity or fixed extension – Swan-neck deformity
  • Dorsal subluxation of the ulnar styloid may cause rupture of the finger extensor tendons leading to a sudden onset of finger drop in the ring and little fingers

 

Shoulders

  • Commonly affected
  • Initially mimic rotator cuff tendonitis with painful arc syndrome and pain in the upper arms at night
  • Stiffening occurs as the joint becomes more damaged
  • Rotator cuff tears are common

 

Elbows

  • Swelling and painful fixed flexion deformities

 

Feet

  • Painful swelling of the MTP joints
  • Foot becomes broader and hammer toe deformity develops
  • Pain is caused by exposure of the metatarsal heads due to movement of protective fibro-fatty pad
  • Flat medial arch and loss of flexion of the foot
  • Ankle assumes valgus formation

 

Knees

  • Synovitis and effusion
  • Risk of popliteal cyst formation and rupture
  • Erosion of cartilage and bone causes loss of joint space and damage to the medial/lateral/retropatellar compartments
  • Knees may develop valgus or varus deformity
  • Secondary OA follows

 

Cervical spine

  • Synovitis may affect the synovial joints of the upper cervical spine and the bursae which separates the ondontoid peg from the anterior arch or the atlas
  • May cause atlanto-axial or upper cervical instability
  • May result in damage to the spinal cord resulting in pyramidal and sensory signs

 

Nonarticular manifestations

 

Soft tissue surrounding joints

  • Subcutaneous nodules, firm, intradermal and generally occur over pressure points
  • May ulcerate and become infected
  • May can bursitis of the olecranon
  • Tenosynovitis of the flexor tendons of the hand can cause finger trigger
  • Muscle wasting of the hands – corticosteroid induced myopathy may occur

 

Lungs

  • Peripheral intrapulmonary nodules are usually asymptomatic but may cavitate
  • When pneumoconiosis in present (Caplan’s syndrome), large cavitating lung nodules develop

 

Vasculitis

  • Caused by immune complex deposition in the blood vessel walls
  • Manifestations include;
  • Nail-fold infarcts due to cutaneous vasculitis
  • Cutaneous vasculitis with skin necrosis
  • Mononeuritis multiplex
  • Bowel infarction

 

Heart and peripheral vessels

  • Pericarditis
  • Endocarditis
  • Myocardial disease
  • Raynaud’s syndrome

 

Spleen, lymph nodes and blood

  • Felty’s syndrome is splenomegaly and neutropenia in a patient with RA
  • May be peripheral lymphadenopathy
  • Anaemia is common and is the normochromic, normocytic anaemia of chronic disease

 

Investigations

  • Blood counts – anaemia may be present, raised inflammatory markers
  • Serology – rheumatoid factor and ANA
  • X-rays of affected joints
  • Aspiration of joint

 

Criteria for diagnosis of rheumatoid disease

  • Four or more criteria required for diagnosis
    • Morning stiffness >1hr for 6 weeks or more
    • Arthritis of 3 or more joints for 6 weeks or more
    • Arthritis of wrists and hands for 6 weeks or more
    • Symmetrical arthritis
    • Subcutaneous nodules
    • A positive serum rheumatoid factors
    • Typical radiological changes  - erosions or periarticular osteopenia

 

Management

  • 25% of patients will recover completely
  • Use NSAIDs and analgesics to control symptoms
  • Try to induce remission with im depot of methylprednisolone if synovitis persists
  • Treat recurrence of synovitis with sulfasalazine or methotrexate
  • Give second i.m depot of methylprednisolone
  • Refer for physiotherapy
  • If no significant improvement give methotrexate with sulfasalazine
  • If no improvement, use gold, d-penicillamine, leflunamide or anti-TNF

 

  • Use of DMARDs early in disease prevent long term irreversible damage of the joints
  • DMARDs may act through cytokine inhibition
  • Include;
    • Methotrexate
    • Sulfasalazine
    • Leflunamide (blocks pyrimidine production in proliferating lymphocytes by blocking dyhydro-orotate dehydrogenase). Shouldn’t be used in premenopausal women
    • TNF blocker
    • ciclosporin
 

Leave a Reply

Your email address will not be published. Required fields are marked *

*

You may use these HTML tags and attributes: <a href="" title=""> <abbr title=""> <acronym title=""> <b> <blockquote cite=""> <cite> <code> <del datetime=""> <em> <i> <q cite=""> <strike> <strong>