Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a chronic autoimmune disease of persistent synovial inflammation that, untreated, causes progressive joint destruction, disability and excess cardiovascular mortality.

It typically presents as a symmetrical inflammatory polyarthritis of the small joints of the hands and feet, with prolonged morning stiffness and fatigue. It is 2 to 4 times more common in women, and in the UK incidence peaks in the 70s, although any age can be affected.

Early treatment matters most. Disease-modifying anti-rheumatic drugs (DMARDs) started within 3 months of persistent symptoms give the best chance of remission and of preventing irreversible damage, so suspected persistent synovitis is referred promptly.

In genetically susceptible people (the HLA-DRB1 shared epitope, including HLA-DR4), environmental triggers drive autoimmunity. Smoking is the main modifiable risk factor, particularly for seropositive disease.

• •Citrullination of self-proteins generates anti-citrullinated protein antibodies (anti-CCP), often years before symptoms
• •Rheumatoid factor (RF) is present in around 70% but also occurs in infection, other autoimmune disease and some healthy adults

The inflamed synovium thickens into invasive pannus, driven by tumour necrosis factor alpha (TNF-alpha) with interleukin-6 (IL-6) amplifying systemic disease. Osteoclasts at the bare areas produce marginal erosions. Circulating cytokines cause anaemia, fatigue and accelerated atherosclerosis, the leading cause of death in RA.

Typical joints are the metacarpophalangeal (MCP), proximal interphalangeal (PIP), wrist and metatarsophalangeal (MTP) joints and the cervical spine (C1 and C2). The distal interphalangeal (DIP) joints, lumbar spine and sacroiliac joints are usually spared.