History and exam
Key diagnostic factors
common
active symmetrical arthritis lasting >6 weeks
There may be clues that this will develop into rheumatoid arthritis, such as positive blood tests or lack of precipitating infections. There is still a good chance that undifferentiated polyarthritis of <6 weeks' duration will subside spontaneously.
age 50 to 55 years
Most patients present between the ages of 40 and 60.[50] There are cases seen in teenagers and very old people, but alternate diagnosis should be sought before rheumatoid arthritis is definitively diagnosed.
female sex
Usually females outnumber males 2:1, the lifetime risk of rheumatoid arthritis developing in the US has been reported as 3.6% for women and 1.7% for men.[70]
joint pain
Most commonly bilateral metacarpophalangeal (MCP), proximal interphalangeal (PIP), and metatarsophalangeal (MTP) joints are involved. They are painful to touch and when range of motion (ROM) exercises are performed. Wrists, elbows, and ankles are also affected.
joint swelling
Most commonly bilateral metacarpophalangeal (MCP), proximal interphalangeal (PIP), and metatarsophalangeal (MTP) joints are involved. They are painful to touch and when range of motion (ROM) exercises are performed. Wrists, elbows, and ankles are also affected.
Tender and swollen joint count is one of the important outcome measures used in routine care and in randomised controlled clinical trials.
Other diagnostic factors
common
morning stiffness
Even though morning stiffness is not specific to rheumatoid arthritis, >1 hour of morning stiffness is considered a sign of inflammatory disease.[71]
uncommon
swan neck deformity
Seen in advanced rheumatoid arthritis with damage to the ligaments and joints. Classically, there is distal interphalangeal (DIP) hyperflexion with proximal interphalangeal (PIP) hyperextension. No longer common, as most patients are treated with DMARDs at an early stage.
Boutonniere's deformity
Typically, there is proximal interphalangeal (PIP) flexion with distal interphalangeal (DIP) hyperextension. No longer common, as most patients are treated with DMARDs at an early stage.
ulnar deviation
Ulnar deviation, due to inflammation of the metacarpophalangeal (MCP) joints, causes the fingers to become dislocated. As the tendons pull on the dislocated joints, the fingers tend to drift towards the ulnar side.
rheumatoid nodules
Extra-articular features, such as rheumatoid nodules over the extensor surfaces of tendons, can be seen at presentation in some patients who have very active disease with large numbers of joints involved. Now seen less frequently.
vasculitic lesions
Most common vasculitic lesions seen in rheumatoid arthritis are skin rashes. They are rarely seen and are associated with severe disease.
pleuritic chest pain
Pleuritis or pericarditis may occur in severe rheumatoid arthritis.
scleritis and/or uveitis
Inflammatory eye disease may be seen in severe rheumatoid arthritis, although it is an uncommon manifestation. Scleritis and uveitis are the more common presentations.
Risk factors
strong
genetic predisposition
Family history confers a two- to fourfold increased risk for rheumatoid arthritis (RA) in first-degree relatives.[17]
Heritability of RA appears to be approximately 40%, and is higher for seropositive RA than for seronegative RA.[17][39]
The presence of a major histocompatibility complex class II allele human leukocyte antigen (HLA), DRw4, is more common in patients with RA. These HLA alleles code for a shared amino acid sequence that has been named the shared epitope, which may be involved in the pathogenesis of RA.[18]
A role for polymorphisms of genes in both the innate and adaptive immune system have been demonstrated to increase the risk of RA.[19][20][21][22][23][24][25][40][41][42]
weak
smoking
Smoking is associated with the production of rheumatoid factor and anti-CCP antibodies, which are both specific and sensitive antibodies that increase the risk of developing rheumatoid arthritis (RA).[27] The increased risk of RA for people who smoke is dependent on the amount smoked per day combined with number of years they smoked.[10][11][12][13] A gene-environment interaction between heaving smoking and HLA-DRB1 has been demonstrated in patients with HLA-SE seropositive RA risk.[28][29]
Some evidence suggests that childhood exposure to passive smoking increases the risk of developing RA in later life, compared with children not exposed to passive smoking.[43]
overweight or obesity
infection
An infection as a triggering factor for rheumatoid arthritis in genetically susceptible individuals has been proposed, but no specific infectious agent has been identified.[32]
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