Counseling Points - October 2007 - (Page 11) that reduce inflammation and pain and inhibit disease progression is optimal.3,10,19 Medications that are used to treat RA are divided into three primary classes: nonsteroidal anti-inflammatory drugs (NSAIDs), glucocorticoids (corticosteroids), and DMARDs, which include both synthetic and biologic agents.1 NSAIDs NSAIDs are particularly helpful to patients during the first few weeks of symptom onset because the drugs provide partial relief of pain and stiffness.3,19 Commonly used agents include aspirin, ibuprofen, acetaminophen, and COX-2 inhibitors. NSAIDs have antiinflammatory and analgesic properties; however, they have not been demonstrated to alter disease course or slow progression of RA. Therefore, in long-term treatment of the disease, these agents should be used in combination with DMARDs.3 Patients with RA are twice as likely to have serious complications from NSAID treatment than others and should be monitored for gastrointestinal adverse effects.3 Gastroprotective medications, such as proton-pump inhibitors, taken with NSAIDs may be effective in decreasing gastrointestinal side effects. Glucocorticoids as medications that slow or stop the progression of disease. 3,19 The ACR RA Guidelines state that DMARD therapy should not be delayed beyond 3 months for any patient with established RA who continues to experience joint pain and significant morning stiffness (regardless of NSAID therapy), fatigue, active synovitis, radiographic joint damage, or elevations in CRP or ESR.3 Table 3 lists some of the commonly and uncommonly used conventional (synthetic) DMARDs.24 Although these agents have been used for years to provide enhanced disease-modifying therapy and other significant therapeutic benefits to RA patients, they do have disadvantages. First, conventional DMARDs take an extended time to work and have a 1- to 6-month window before a benefit can been seen in RA course.1,19,24 Also, because treatment with a single conventional DMARD often fails, combinations of two or three of these agents are used to improve efficacy.1,19,24 Patients treated with conventional DMARDs may also experience many possible toxicities, such as myelosuppression, hepatotoxicity, and anemia. Furthermore, dosing schedules of these drugs range from treatment once to twice daily to once weekly, depending on the specific agent.1,19,24 Oral and injectable steroids are potent suppressors of inflammation in RA as well as in many other diseases. There is also some evidence that steroids in low doses slow joint damage. Unfortunately, these agents produce dose-dependent side effects, such as cataracts, weight gain, osteoporosis, hypertension, and hyperlipidemia.3,19 For long-term RA control, steroids should be selectively used in low dosages, such as ≤10 mg of prednisone per day, and their benefits should be weighed against their adverse effects.3,19 DMARDs Table 3. Conventional (Synthetic) DMARDs Commonly Used DMARDs • Hydroxychloroquine (Plaquenil®) or chloroquine (Aralen®) • Leflunomide (Arava®) • Methotrexate (Rheumatrex®) • Sulfasalazine (Azulfidine®) Less Commonly Used DMARDs • Azathioprine (Imuran®) • Cyclophosphamide (Cytoxan® or Neosar®) • Cyclosporine (Neoral® or Sandimmune®) • Gold salts (Ridaura® or Aurolate®) • Minocycline (Dynacin® or Minocin®) • Penicillamine (Cuprimine® or Depen®) DMARDs=disease-modifying antirheumatic drugs. Although steroids and NSAIDs relieve symptoms of pain, stiffness, and swelling in RA patients, joint destruction may continue to occur.Therefore, optimal management of the disorder requires prompt and sustained use of DMARDs.3,19 These agents are defined 11 OCTOBER 2007
Table of Contents Feed for the Digital Edition of Counseling Points - October 2007 Counseling Points - October 2007 Welcome Introduction Overview of RA RA Morbidity and Mortality RA Costs and Quality of Life RA Risk Factors Pathophysiology of RA Diagnosis and Natural History of RA Diagnostic Tests and Radiography Natural History and Progression of RA Disease Management Treatment Strategies Summary Continuing Education Posttest Evaluation Form Counseling Points - October 2007 Counseling Points - October 2007 - Counseling Points - October 2007 (Page 1) Counseling Points - October 2007 - Counseling Points - October 2007 (Page 2) Counseling Points - October 2007 - Welcome (Page 3) Counseling Points - October 2007 - RA Morbidity and Mortality (Page 4) Counseling Points - October 2007 - RA Risk Factors (Page 5) Counseling Points - October 2007 - Pathophysiology of RA (Page 6) Counseling Points - October 2007 - Diagnosis and Natural History of RA (Page 7) Counseling Points - October 2007 - Diagnostic Tests and Radiography (Page 8) Counseling Points - October 2007 - Disease Management (Page 9) Counseling Points - October 2007 - Treatment Strategies (Page 10) Counseling Points - October 2007 - Treatment Strategies (Page 11) Counseling Points - October 2007 - Summary (Page 12) Counseling Points - October 2007 - Summary (Page 13) Counseling Points - October 2007 - Continuing Education Posttest (Page 14) Counseling Points - October 2007 - Evaluation Form (Page 15) Counseling Points - October 2007 - Evaluation Form (Page 16)
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