Rheumatoid Arthritis Ra

Definition and epidemiology

• Chronic, symmetric, debilitating and destructive polyarthritis caused by inflammatory.

proliferative synovial tissue (pannus) formation in affected joints

• Genetic factors: t incidence in Pis wI shared epitope on Class II MHC DRB1 and DR4

• Environmental factors: smoking, silica dust exposure

• Gready increased risk of developing RA in individuals carrying the shared epitope who smoke due to gene-environment interaction (Arth Wwum 2004:50.3085)

• Prevalence = 1% of adults: female:male 3:1; onset 35-50 y; worldwide Clinical manifestations (lonctt 2001:358.903)

• Pain, swelling, and impaired function of joints (typically PIPs. MCPs, wrists, knees, ankles,

MTPs. and cervical spine) with morning stiffness for si h

• Joint immobilization, muscle shortening, bone & cartilage destruction, joint deformities:

ulnar deviation, swan neck (MCP flexion. PIP hyperextension. DIP flexion) boutonnière (PIP flexion. DIP hyperextension). cock-up deformities (toes)

• C1-C2 instability • myelopathy. . / C-spine flex/ext films prior to elective intubation

• Rheumatoid nodules (20-30%; usually in RF © Pts): SC nodules on extensor surfaces along tendon sheaths and in bursae; also occur in lung, heart, and sclera

• Constitutional symptoms: fever, weight loss, malaise

• Ocular: scleritis. episcleritis, keratoconjunctivitis sicca (associated Sjogren's)

ILD: COP. fibrosis, nodules. Caplan's syndrome (pneumoconiosis + rheumatoid nodules)

pleural disease: pleuritis. pleural effusions (classically low glucose)

airway disease: obstruction (cricoarytenoid arthritis), bronchiolitis, bronchiectasis

• Cardiac pericarditis, myocarditis, nodules can cause valvular and/or conduction disease

• Heme: anemia of chronic disease, leukemia, lymphoma

• Vascular small nail fold infarcts, palpable purpura, leukocytoclastic vasculitis

• Longstanding seropositive, erosive RA:

Felty's syndrome (1%): neutropenia. RF -. splenomegaly; I risk of NHL large granular lymphocyte syndrome: neutropenia, lymphocytosis blood/marrow

• Remember that rheumatoid joints can become superinfected Laboratory and radiologic studies

• RF (IgM anti-IgG Ab) in 85% of Pts; levels correlate only loosely with disease activity nonspecific as also seen in other rheumatic diseases (SLE. Sjogren's), chronic inflammation (SBE. hepatitis. TB). type II cryoglobulinemia, 5% of healthy population

• Anti-CCP (Ab to cydic citrullinated peptide): similar Se ( 80%). more Sp ( 90%) than RF

for RA (Rtam 2006:45:20)

• î ESR and CRP; © ANA in -15%; î globulin during periods of active disease

• Radiographs of hands and wrists: periarticular osteopenia, erosions, and deformities Classification criteria (4 of 7; 90% Se & Sp; Anh R/i«/m 1988:31 315)

• Morning stiffness >1 h x 6 wks • Arthritis -3 joints simultaneously < 6 wks

• Hand joint arthritis < 6 wks • Symmetric joint involvement ■ 6 wks

• Rheumatoid nodules • © Rheumatoid factor

• Radiographic changes c/w RA (ie, erosions and periarticular osteopenia) Management (NqM 2004:350.2591 & 2006:355:704; Lone« 2004:364:263)

• Early dx and Rx w/ frequent follow-up and escalation of Rx as needed -» I disease activity and radiographic progression. T physical fxn and quality of life

• Initial therapy nonselective NSAIDs (? î CV adverse events) or COX-2 inhibitors (î CV adverse events w/ some): sx control as indicated glucocorticoids (joint injection or low-dose oral): acutely i inflammation physical and occupational therapy

• Start Disease-Modifying Anti-Rheumatic Drug (DMARD) therapy w/in 3 mos for any Pt w I established disease and ongoing inflammation (Ann«* 2007.146406) monotherapy with methotrexate, sulfasalazine, leflunomide. or hydroxychloroquine OR combination of DMARD • glucocorticoid or anti-TNF (Anh totum 2005:52.3360 & 3371) escalation therapy add medication (usually a biologic) or change DMARD biologies: never use 2 biologies concurrently in the same Pt anti-TNF (etanercept, infliximab, adalimumab; screen forTB prior to Rx); IL-1 receptor antagonist (anakinra); CTLA4-lgG (3batacept; nejai 2005:353 144); anti-CD20 (rituximab) for anti-TNF nonresponders (NEJM 2006:350:2572) other agents: azathioprine. penicillamine, gold, minocycline, cydosporine

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