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"rheumatoid arthritis"[MeSH Terms] AND treatment
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Rheumatoid Arthritis (RA)
You likely mean Rheumatoid Arthritis - one of the most common autoimmune inflammatory diseases. Here is a full clinical overview.
Definition
Rheumatoid Arthritis is a chronic, systemic autoimmune disease in which cellular and autoimmune mechanisms cause persistent synovial inflammation, leading to progressive destruction of joints and, in severe cases, extra-articular organ involvement. - Textbook of Family Medicine 9e
Epidemiology
- Prevalence: 1-2% of adults worldwide
- Women are affected 3 times more often than men
- Peak onset: ages 20-50 years, but occurs across all age groups
- Prevalence rises to ~10% in those over age 65
- Higher concordance in monozygotic vs. dizygotic twins, indicating a genetic contribution via HLA-DR (MHC class II) genes
- Textbook of Family Medicine 9e, p. 1603
Pathogenesis
The exact trigger is unknown, but the process is well characterized:
- Genetic predisposition - HLA-DR alleles (particularly the "shared epitope") increase susceptibility
- Environmental triggers - Smoking is the strongest environmental risk factor; others include infection, microbiome changes, and periodontal disease
- Autoantibody formation - Rheumatoid Factor (RF) is an autoantibody against IgG Fc fragments. Anti-cyclic citrullinated peptide (anti-CCP) antibodies are more specific and can appear years before symptoms
- Synovial inflammation - The synovial lining proliferates, forming an invasive pannus (fibrovascular granulation tissue). Leukocytes invade; a cascade of proteases and cytokines (especially TNF-alpha, IL-1, IL-6) drives cartilage and bone erosion
- RF is not specific to RA - it can appear in healthy individuals and other conditions
Clinical Features
Articular (Joint) Manifestations
- Symmetric polyarthritis - hallmark of RA; affects joints symmetrically on both sides
- Morning stiffness lasting >1 hour (key distinguishing feature from OA, where stiffness resolves in <30 min)
- Commonly affected joints: MCPs, PIPs (proximal interphalangeal joints), wrists, knees, ankles, MTPs - notably sparing DIP joints
- Classic deformities (late disease):
- Ulnar deviation of fingers at MCP joints
- Swan neck deformity (PIP hyperextension, DIP flexion)
- Boutonniere deformity (PIP flexion, DIP hyperextension)
- Z-deformity of thumb
- Hallux valgus and forefoot deformities
Constitutional Symptoms
- Fatigue, low-grade fever, weight loss, malaise - common and often precede joint symptoms by months
Extra-articular Manifestations
- Rheumatoid nodules - firm subcutaneous nodules over pressure points (elbows, fingers); seen in ~20% of RF-positive patients
- Pulmonary: interstitial lung disease, pleuritis, pulmonary nodules
- Cardiovascular: accelerated atherosclerosis, pericarditis - RA significantly increases cardiovascular risk
- Neurological: cervical myelopathy (C1-C2 subluxation), peripheral neuropathy, carpal tunnel syndrome
- Ocular: keratoconjunctivitis sicca (dry eyes), scleritis, episcleritis
- Renal: secondary amyloidosis in long-standing disease
- Felty's syndrome: RA + splenomegaly + neutropenia (rare)
Diagnosis
RA is primarily a clinical diagnosis. The 2010 ACR/EULAR Classification Criteria (which replaced the 1987 criteria) score patients across four domains - a score of ≥6/10 classifies as RA:
| Domain | Points |
|---|---|
| Joint involvement (number and size) | 0-5 |
| Serology (RF, anti-CCP) | 0-3 |
| Acute-phase reactants (CRP, ESR) | 0-1 |
| Duration of symptoms ≥6 weeks | 0-1 |
Laboratory Tests
| Test | Notes |
|---|---|
| RF (Rheumatoid Factor) | Positive in ~70-80%; not specific |
| Anti-CCP antibodies | More specific (~95%); can be present years before symptoms |
| ESR, CRP | Elevated, indicate inflammation activity |
| CBC | Normocytic anemia, thrombocytosis common |
| Synovial fluid | >2000 WBCs/mm3 (inflammatory pattern) |
Imaging
-
X-ray: Periarticular osteopenia and joint space narrowing (early); marginal erosions (later - typically after 6-12 months)
-
MRI / Ultrasound: More sensitive for early synovitis and erosions before X-ray changes appear
-
Textbook of Family Medicine 9e, Harrison's 22E
Treatment
General Principles
- Early aggressive treatment is essential - patients with active, polyarticular, RF-positive RA have >70% chance of developing joint erosion within 2 years without treatment
- Treat-to-target (T2T): aim for remission or low disease activity, reassess every 1-3 months
- Harrison's Principles of Internal Medicine 22E, p. 2892
Pharmacotherapy
1. NSAIDs (e.g. ibuprofen, naproxen)
- Provide symptomatic relief only - do NOT slow disease progression
- Now considered adjunctive agents, not core therapy
- Chronic use carries risk of GI ulcers and renal injury
2. Glucocorticoids (e.g. prednisone)
- Used as a bridge while DMARDs take effect (which may take weeks to months)
- Low-dose prednisone (5-10 mg/day) may provide ongoing benefit in some patients
- Short bursts for acute flares
- Risk of osteoporosis, infection, metabolic effects with long-term use
3. Conventional DMARDs (disease-modifying antirheumatic drugs)
| Drug | Notes |
|---|---|
| Methotrexate (MTX) | First-line DMARD of choice; most widely used; weekly dosing |
| Hydroxychloroquine | Least toxic DMARD; used for mild disease; requires ophthalmology monitoring |
| Sulfasalazine | 2-3 g/day; monitor CBC and LFTs |
| Leflunomide | Alternative to MTX; teratogenic |
4. Biologic DMARDs (for inadequate response to conventional DMARDs)
| Class | Examples |
|---|---|
| TNF inhibitors | Etanercept, infliximab, adalimumab, certolizumab, golimumab |
| IL-6 receptor inhibitors | Tocilizumab, sarilumab |
| CTLA-4-Ig (co-stimulation blocker) | Abatacept |
| Anti-CD20 (B-cell depletion) | Rituximab |
5. JAK inhibitors (targeted synthetic DMARDs)
- Tofacitinib, baricitinib, upadacitinib
- Oral small molecules; monitor for infections, thrombosis, and cardiovascular risk
Non-Pharmacological
- Physical therapy: joint protection, range-of-motion exercises, splints
- Occupational therapy: adaptive devices, activity modification
- Patient education: adherence to DMARDs is critical
- Surgery: joint replacement or synovectomy for severe, refractory cases
Prognosis & Monitoring
- Disease activity is tracked using composite indices: DAS28, SDAI, CDAI, RAPID3
- ACR 20/50/70 response criteria are used in clinical trials
- Poor prognostic factors: high RF/anti-CCP titers, many swollen joints, elevated inflammatory markers, early radiographic erosions, functional limitation, extra-articular disease
- Optimal management requires close follow-up with a rheumatologist
In summary, Rheumatoid Arthritis is a systemic autoimmune inflammatory arthritis causing symmetric joint destruction driven by pannus formation. Early diagnosis and prompt initiation of DMARD therapy - ideally methotrexate - is the cornerstone of modern management. Biologics and JAK inhibitors provide additional options when conventional DMARDs fail.
Sources: Textbook of Family Medicine 9e; Harrison's Principles of Internal Medicine 22E (2025)
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