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Rheumatoid arthritis

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What is Rheumatoid Arthritis (RA)?

Rheumatoid arthritis (RA) is a chronic, systemic, autoimmune inflammatory disease primarily characterized by inflammation of the synovium (the lining of the joints). This inflammation leads to pain, swelling, stiffness, and eventual destruction of the cartilage and bone within the joints, potentially causing joint deformity and loss of function (1, 2).

As an autoimmune disease, RA occurs when the body's immune system mistakenly attacks its own healthy tissues, primarily targeting the joints. While the exact cause (etiology) is unknown, it likely involves a combination of genetic predisposition and environmental factors (e.g., smoking, certain infections) (1, 3).

RA typically affects joints symmetrically (e.g., both wrists, both knees) and most commonly involves the small joints of the hands (metacarpophalangeal - MCP, proximal interphalangeal - PIP joints) and feet (metatarsophalangeal - MTP joints), as well as wrists, elbows, shoulders, knees, and ankles (2, 4).

Because RA is a systemic disease, it can also affect other parts of the body beyond the joints, including the skin (rheumatoid nodules), eyes, lungs, heart, blood vessels, and nerves (1, 2). Early diagnosis and aggressive treatment are crucial to control inflammation, prevent joint damage, maintain function, and manage systemic effects.

Rheumatoid arthritis typically affects multiple joints symmetrically, especially the wrists, hands (MCP, PIP joints), and feet (MTP joints) (2, 4).

Note: The description of "volatile" arthritis migrating between joints and the primary pathology being in the heart is characteristic of Acute Rheumatic Fever, not Rheumatoid Arthritis. RA involves persistent inflammation in affected joints (1).

Large joints like the knees can also be significantly affected by rheumatoid arthritis, leading to pain, swelling, and functional limitation (2).

Symptoms of Rheumatoid Arthritis

The presentation of RA can vary, but common symptoms include (1, 2, 4):

  • Joint Pain, Swelling, and Tenderness: Affecting multiple joints, often symmetrically.
  • Morning Stiffness: Prolonged stiffness (typically lasting more than 30-60 minutes) upon waking or after periods of inactivity, which gradually improves with movement.
  • Reduced Range of Motion: Difficulty moving affected joints fully.
  • Fatigue and Malaise: Feeling generally unwell, tired, or lacking energy.
  • Low-Grade Fever: Sometimes present, reflecting systemic inflammation.
  • Weight Loss: Unintentional weight loss can occur.
  • Rheumatoid Nodules: Firm lumps under the skin, often found over pressure points like elbows or fingers (occur in about 20-30% of patients, usually those positive for rheumatoid factor).
  • Systemic Manifestations: Inflammation can affect other organs, leading to symptoms like dry eyes/mouth (Sjögren's syndrome), lung inflammation (pleuritis, interstitial lung disease), inflammation around the heart (pericarditis), or inflammation of blood vessels (vasculitis).

Diagnosis of Rheumatoid Arthritis

Diagnosing RA involves a combination of clinical evaluation, laboratory tests, and imaging studies. There isn't a single definitive test (1, 5).

  • Medical History and Physical Examination: Assessing the pattern of joint involvement (number, symmetry, specific joints), duration of symptoms (especially morning stiffness), presence of systemic symptoms, and family history. Examination focuses on identifying swollen, tender joints, reduced range of motion, and potential deformities or nodules.
  • Laboratory Tests:
    • Rheumatoid Factor (RF): An antibody found in the blood of about 70-80% of RA patients. However, it can be present in other conditions and absent in some RA patients (seronegative RA) (1, 5).
    • Anti-Cyclic Citrullinated Peptide (anti-CCP) Antibodies: More specific for RA than RF and often present early in the disease. Positive anti-CCP is associated with a higher likelihood of erosive disease (1, 5).
    • Inflammatory Markers: Erythrocyte Sedimentation Rate (ESR) and C-Reactive Protein (CRP) levels are usually elevated, indicating systemic inflammation, but are not specific to RA (1, 5).
    • Complete Blood Count (CBC): May show normocytic anemia (anemia of chronic disease) or thrombocytosis (elevated platelets) related to inflammation.
  • Imaging Studies:
    • X-rays: May be normal early on. Later, can show characteristic findings like soft tissue swelling, periarticular osteopenia (bone thinning near joints), joint space narrowing, and bony erosions (damage to the bone at the joint margins) (1, 5). Used to assess damage and monitor progression.
    • Ultrasound or MRI: More sensitive than X-rays for detecting early inflammation (synovitis, tenosynovitis, effusions) and early erosions (1).
  • Classification Criteria: The 2010 American College of Rheumatology (ACR) / European League Against Rheumatism (EULAR) classification criteria are often used to aid diagnosis, particularly in early RA. These criteria assign points based on the pattern of joint involvement, serology (RF/anti-CCP), inflammatory markers (ESR/CRP), and duration of symptoms (5). A score of 6 or more out of 10 is consistent with definite RA.
Characteristic hand deformities, like ulnar deviation and finger subluxations, can develop in chronic, untreated, or poorly controlled rheumatoid arthritis (1).

 

Treatment of Rheumatoid Arthritis

The primary goals of RA treatment are to (1, 6):

  • Control inflammation (achieve remission or low disease activity).
  • Relieve pain and other symptoms.
  • Prevent or slow joint damage and deformity.
  • Maintain or improve physical function and quality of life.
  • Manage systemic complications.

Treatment typically involves a combination of medications, physical therapy, lifestyle modifications, and sometimes surgery. Early and aggressive treatment, often managed by a rheumatologist, is associated with better long-term outcomes (1, 6). The "treat-to-target" strategy aims to reach a specific goal (remission or low disease activity) by regularly monitoring disease activity and adjusting treatment accordingly (6).

Medications:

  • Disease-Modifying Antirheumatic Drugs (DMARDs): These are the cornerstone of RA treatment, as they target the underlying immune processes to slow disease progression and prevent joint damage.
    • Conventional Synthetic DMARDs (csDMARDs): Methotrexate is typically the first-line choice. Others include sulfasalazine, leflunomide, and hydroxychloroquine (1, 6).
    • Biologic DMARDs (bDMARDs): These are genetically engineered proteins targeting specific inflammatory molecules or cells (e.g., TNF inhibitors like adalimumab, etanercept; IL-6 inhibitors like tocilizumab; T-cell co-stimulation inhibitors like abatacept; B-cell depleting agents like rituximab) (1, 6). Used if csDMARDs are insufficient or not tolerated.
    • Targeted Synthetic DMARDs (tsDMARDs): Small molecule drugs taken orally that target specific intracellular pathways (e.g., JAK inhibitors like tofacitinib, baricitinib, upadacitinib) (1, 6). Often used after csDMARDs or sometimes biologics.
  • Nonsteroidal Anti-Inflammatory Drugs (NSAIDs): Such as ibuprofen or naproxen. Help reduce pain and inflammation but do *not* slow disease progression. Used for symptom relief, often alongside DMARDs (1).
  • Corticosteroids (e.g., Prednisone): Potent anti-inflammatory drugs. Can provide rapid symptom relief. Often used as a "bridge" therapy while waiting for DMARDs to take effect or during disease flares. Long-term use is limited due to potential side effects; low doses may be used in some cases (1, 6). Intra-articular steroid injections can target specific inflamed joints.

Non-Pharmacological Therapies:

  • Physical Therapy: Exercises to maintain joint flexibility, strengthen supporting muscles, and improve function (1).
  • Occupational Therapy: Strategies and assistive devices to protect joints and manage daily activities.
  • Patient Education and Self-Management Programs: Understanding the disease and treatment strategies.
  • Lifestyle: Smoking cessation (smoking worsens RA), healthy diet, stress management.
Physiotherapy modalities may be used adjunctively to help manage pain, swelling, and maintain function in affected joints like the ankle during RA treatment (1).

Physiotherapy and occupational therapy are important for managing symptoms and maintaining function in commonly affected areas like the wrists and hands in RA (1).

Surgical Treatment:

  • Considered for severe joint damage or deformity unresponsive to medical management. Procedures include synovectomy (removal of inflamed synovium), tendon repair, joint fusion (arthrodesis), or joint replacement (arthroplasty) (1).

Management often requires a multidisciplinary team including rheumatologists, primary care physicians, physical/occupational therapists, and sometimes orthopedic surgeons.

 

Components of RA Management

A comprehensive approach to managing RA involves several integrated components (1, 6):

  • Pharmacological Therapy: Using appropriate DMARDs, NSAIDs, and corticosteroids as needed, guided by disease activity and the treat-to-target strategy.
  • Monitoring Disease Activity: Regular assessment using composite scores (e.g., DAS28, CDAI, SDAI), patient-reported outcomes, and physician evaluation to guide treatment adjustments (clinical examination and follow-up) (6).
  • Physical and Occupational Therapy: Including therapeutic exercise, joint protection techniques, and use of assistive devices.
  • Pain Management: Utilizing medications, physical modalities, and sometimes complementary therapies. Intra-articular injections can provide targeted relief.
  • Patient Education and Support: Empowering patients to actively participate in their care.
  • Management of Comorbidities: Addressing associated conditions like cardiovascular disease, osteoporosis, infections, and depression.
  • Surgical Intervention: Surgical treatment when indicated for joint damage or functional impairment.
  • Rehabilitation: Rehabilitation programs post-surgery or to improve overall function. (Note: Spa treatment and general massage (massage) may offer symptom relief for some but are not core evidence-based treatments for modifying the RA disease process itself (1)).

Differential Diagnosis

Several conditions can mimic RA, requiring careful differentiation (1, 7):

Condition Key Differentiating Features
Osteoarthritis (OA) Degenerative ("wear and tear"). Affects weight-bearing joints (knees, hips) and DIP/PIP joints of hands. Pain worsens with activity, improves with rest. Morning stiffness brief (<30 min). Systemic inflammation absent (ESR/CRP normal). X-rays show osteophytes, joint space narrowing. RF/anti-CCP negative.
Psoriatic Arthritis (PsA) Associated with psoriasis (skin/nail changes). Can affect DIP joints, spine (spondylitis), and cause dactylitis ("sausage digits"), enthesitis (inflammation where tendons attach). Pattern can be asymmetric. RF often negative.
Systemic Lupus Erythematosus (SLE) Systemic autoimmune disease with multi-organ involvement (skin rash, kidney, CNS, blood cells). Arthritis is common but usually non-erosive. Specific autoantibodies (e.g., anti-dsDNA, anti-Sm) present.
Gout / Pseudogout Crystal arthropathies causing acute, severe, episodic joint inflammation (often monoarticular initially, e.g., big toe in gout). Diagnosis by identifying crystals (urate/CPPD) in synovial fluid. Chronic gout can mimic RA (tophaceous gout).
Reactive Arthritis Develops after infection (often GI or GU). Typically asymmetric oligoarthritis (few joints), often lower limbs. May have associated urethritis, conjunctivitis.
Septic Arthritis Bacterial infection of a joint. Presents acutely with severe pain, swelling, redness, warmth, fever, inability to move the joint. Requires urgent diagnosis (synovial fluid analysis/culture) and treatment (antibiotics, drainage).
Fibromyalgia Widespread musculoskeletal pain, fatigue, sleep disturbance, tender points. Joints themselves are not typically swollen or inflamed. Inflammatory markers normal.
Lyme Disease Can cause arthritis (often knee) weeks to months after tick bite/rash. Diagnosis via serology.

References

  1. Smolen JS, Aletaha D, McInnes IB. Rheumatoid arthritis. Lancet. 2016;388(10055):2023-2038. doi:10.1016/S0140-6736(16)30173-8
  2. Firestein GS, McInnes IB. Immunopathogenesis of Rheumatoid Arthritis. Immunity. 2017;46(2):183-196. doi:10.1016/j.immuni.2017.02.006
  3. Deane KD, Demoruelle MK, Kelmenson LB, et al. Genetic and environmental risk factors for rheumatoid arthritis. Best Pract Res Clin Rheumatol. 2017;31(1):3-18. doi:10.1016/j.berh.2017.08.003
  4. Scott DL, Wolfe F, Huizinga TW. Rheumatoid arthritis. Lancet. 2010;376(9746):1094-1108. doi:10.1016/S0140-6736(10)60826-4
  5. Aletaha D, Neogi T, Silman AJ, et al. 2010 Rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Arthritis Rheum. 2010;62(9):2569-2581. doi:10.1002/art.27584
  6. Smolen JS, Landewé RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2019 update. Ann Rheum Dis. 2020;79(6):685-699. doi:10.1136/annrheumdis-2019-216655
  7. Wasserman AM. Diagnosis and Management of Rheumatoid Arthritis. Am Fam Physician. 2011;84(11):1245-1252. Available from: https://www.aafp.org/pubs/afp/issues/2011/1201/p1245.html