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Rheumatoid Arthritis

Definition

Autoimmune inflammation of the joints, particularly the synovium, also characterised by extra-articular features.

 

Risk Factors

  • Smoking
  • Very low genetic component
  • Other autoimmune disease
  •  

 

Differential diagnosis

  • Osteoarthritis
  • SLE
  • Psoriatic arthritis
  • Gonorrhoeal arthritis
  • Gout

 

Epidemiology

  • 1% worldwide
  • 3:1 women:men, but reduces with age
  • Any age of onset, increasing frequency 30-60
  • Is found worldwide, more prevalent in Native American (5-6%), less prevalent in Black Caribbean

 

Aetiology

  • Aetiology is unclear, some evidence of differences in HLA alleles and predisposition genes
  • Autoimmune destruction of synovium by antibodies, leads to inflammatory response
  • Rheumatoid factor (autoantibody): is IgM that is usually for removing immune complexes, becomes reactive to self IgG (Fc region)
  • Immune complexes have higher affinity in RA, and more persistent production

 

Clinical features

  • Symmetrical polyarthropathy
  • Affects small joints, most commonly:
    • PIP
    • MCP/MTP
    • Carpals/ankle
    • Knee
  • Rapid onset (weeks to months)
  • Morning stiffness >30 mins
  • Hot, swollen ‘boggy’ joints
  • Pain and stiffness relieved on exercise
  • Systemic illness before and during onset of articular features
    • Fatigue, malaise, fever, sweats, weight loss, aches
  • Longer-term:
    • Extra articular features
      • Lung (nodules, pleural effusions, fibrosis)
      • Rheumatoid nodules on places with high mechanical use eg elbow, highly associated with rheumatoid factor
      • Vasculitis
      • Cardiovascular disease from inflammation
      • Skin manifestations (palpable purpura, skin ulcers, palmar erythema)
      • Episcleritis
    • Joint deformity
      • Ulnar deviation
      • Swan neck, Boutonniere’s deformity, Z-thumb
      • Ankylosis of small bones (eg carpals)
      • Muscle wasting around joints
      • Tendon rupture
      • Subluxation and dislocation
  • Symptoms improve in pregnancy, and worsen postpartum (as with many autoimmune inflammatory conditions)

 

Pathophysiology

  • Macrophage infiltration of synovium, as signalled by autoantibodies – phagocytosis and cytokine signalling (dominant = TNF and IL-1) à inflammatory response: neutrophils, basophils, eosinophils, lymphocytes
  • Macrophages and cytokines activate osteoclasts, which leads to bone erosion
  • Proteases secreted à cartilage degradation
  • Thickening/hyperplasia of synovium – forms a pannus which covers the articular cartilage, and prevents nutrients being delivered, leads to destruction of cartilage
  • Neovascularisation allows more immune cells access

 

Investigations

  • X-ray (likely to appear normal at onset)
    • Bone erosion
    • Joint space narrowing
    • Subluxation and conformational deformity eg ulnar deviation
  • Rheumatoid factor (present in about 70% of RA, and present in 5% of non-RA, so not very selective or specific)
  • Anti-CCP (in 70-80% of RA)
  • ESR, CRP to signal inflammation
  • Clinical history and examination

 

Management

  • For mild to moderate: disease modifying anti-rheumatic drugs:
    • Methotrexate (prevents DNA replication) plus folic acid is first line
    • Other DMARDS available
  • Biologicals for severe or non-responsive, possibly in addition to DMARDS:
    • Anti -TNF-alpha eg adalimumab
    • B-cell inhibitor eg rituximab
  • Corticosteroids as adjunct
  • Surgical management for joints, such as fusions of bones and removal of all/parts of bones

 

Prognosis

  • RF, anti-CCP, extra-articular feature, bony erosions are all poor prognostic indicators, but unlikely to dramatically reduce life expectancy
Rheumatoid Arthritis.docx
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