2. RA
Is a chronic systemic inflammatory disease of
unknown etiology & is considered the
commonest inflammatory arthritis.
Characterized by:
1. Symmetrical inflammatory polyarthritis.
2. It has extra articular features
3.Progressive joint damage causing severe
disability.
3. RA is a worldwide disease affects all racial & ethnic
groups
Affects 1-3% of population
Female: male is 3:1
Females have more articular disease and males have
more systemic presentations.
Age range is 10 – 70y. ( starts 30- 40y)
5-10% having family history & 70% have
HLADR4.
Epidemiology
4. Genetics
1st-degree relatives have 1.5 fold higher risk than
the general population
Twins show heritability of 60%
HLA-DR4 person has increased relative risk 4–5
times.
5. Etiology & Pathogenesis
The cause is unknown & said to be an autoimmune disease
Multifactorial ( i.e. Genetic, environment…)
Cytokines , growth factors , tumor necrosis factors &
metalloproteases have a role .
6.
7.
8. Commonly affected joints are MCPs, PIPs, wrists, MTPs & larger
joints.
Might starts with few joints then progress& become symmetric.
Monoarticular is not uncommon
( episodic)
Thoracolumbar , sacroiliac & DIP joints are very rarely involved.
It has systemic manifestations, extra aricular features.
Clinical Features
9. Symptoms
Joint pain ( More in the morning & might disturb the
sleep).
Morning stiffness. Is a prominent feature , often lasts
>= 1 hour
General symptoms:
weight loss
fever
fatigue, malaise
depression
reduced muscle strength and cachexia
the presence of a fever of >38.3°C at any time during the clinical
course should raise suspicion of systemic vasculitis or infection.
10. Progression of the disease will lead joint
destruction resulting in:
limitation of joint motion
instability
sublaxation &
deformities
Non articular symptoms e.g. carpal tunnel
syndrome.
Signs
Swelling, Warmth,Limitation of movements, Deformities,
Nodules
11. Hand deformities
Radial deviation at wrist
Ulnar deviation at MCP joints
Swan neck deformity ( hyperextension at PIPs)
Boutonniere deformity( flexion at PIPS) or
called Z deformity.
• Feet deformities are like those occur in hands
12.
13. The knees
Synovial effusion
Deformities( valgus, varus &/ or flexion )
Bakers cyst in popliteal fossa which may repture.
( sudden onset of pain & swelling in calf and ankle)
diagnosed by US. & arthrogram.
16. American Rheumatic Association Criteria for the
diagnosis of RA (any 4 of the followings):
1. Morning stiffness for> one hour.
2. Swelling of 3 or more joints( arthritis).
3. Swelling of hand joints ( PIPs , MCPs & wrist ).
4. Symmetrical polyarthritis.
5. Subcutaneous nodules.
6. Serum rheumatoid factor.
7. Radiological changes ( erosion ).
The duration of (1,2,3,4) for 6 weeks or more.
Diagnosis
17. Diagnostic Tests & Interpretation
Initial lab tests
Hematocrit: Mild anemia, leucopenia (may be leucocytosis) &
thrombocytosis.
ESR: Usually elevated
C-reactive protein: Unspecific
Rheumatoid factor (RF): >1:80 in 70–80% of patients with RA (most
commonly IgM Ab):
Doesn’t correlate with disease activity but with extra articular manifistations
Anticyclic citrullinated peptide antibodies (Anti-CCP antibodies) are
highly specific and present early( Linked to erosive RA).
Anti-MCV assay (antibodies against mutated citrullinated Vimentin).
Recently a serological point-of-care test (POCT) for the early detection of
RA has been developed. This assay combines the detection of rheumatoid
factor and anti-MCV for diagnosis of RA and shows a sensitivity of 72%
and specificity of 99.7%.
Antinuclear antibody: Present in 20–30%
Electrolytes, creatinine, liver function, urinalysis to assess comorbid states.
18. Follow-Up & Special Considerations
RF is not useful for monitoring
course of illness.
Radiographs of the hands, wrists, and
feet can be repeated to follow disease
progression.
19. Imaging
Radiographic abnormalities are very useful in the
diagnosis and treatment.
Periarticular osteopenia is the earliest change.
Juxta-articular bone erosions
Symmetrical joint space narrowing.
CT/MRI and ultrasound are useful in cervical-spine
symptoms or detection of early joint erosions.
Bone scan if suspected aseptic necrosis
23. First Line Medication
Nonbiologic DMARDs:
DMARDs within 2 months of diagnosis if patient has ongoing
active disease despite appropriate dose of aspirin or other
NSAIDs.
Offer proton pump inhibitors (PPIs) for chronic NSAID therapy
Nonbiologic DMARD: Methotrexate, sulfasalazine, or
leflunomide
low-dose corticosteroids + NSAIDs to maximize symptoms
management.
24. Biological DMARDs:
Tumor necrosis factor (TNF) inhibitors: infliximab , adalimumab
and etanercept. Check TB prior to treatment and periodic CBC,
Risk of lymphoma, CHF.
Anakinra : an IL-1 receptor antagonist
Abatacept and rituximab : for active moderate to severe RA with
inadequate response to other DMARDs or failed anti-TNF agent.
Two long-acting anti-TNF agents, Certolizumab and golimumab,
25. Older Nonbiologic DMARDs
Have been abandoned in developed countries
for the treatment of RA: Injectable gold,
D-Penicillamine, Cyclosporine, &
Azathioprine.
26. Second Line
Intra-articular steroids: If disease is well
controlled except for a single joint or two,
after establishing that the joint is not
infected
Hyaluronate: Hyaluronic acid , for pain
relief; exact role in RA is unclear.
27. Pregnancy Considerations
Use effective contraception with (DMARDs)
Modify regimen with pregnancy or breast-
feeding.
>75% improve during pregnancy, but relapse
in 6 months.
1st episodes may occur in pregnancy
28. Additional Treatment:
Surgical treatment: synovectomy, tendon
reconstruction, and joint replacement.
Encourage full activity, but avoid heavy work
or exercise during active phases.
Patient Monitoring
• Evaluate for osteoporosis,
• Cardiovascular disease due to accelerated
atherosclerosis.
29. Prognosis
Poor prognostic findings:
Persistent moderate-to-severe disease
Disease onset at early or advanced age
High titre rheumatoid factor
Rheumatoid nodules.
Systemic manifestations
Presence of HLADR4.