Rheumatoid Arthritis (cont.)
William C. Shiel Jr., MD, FACP, FACR
Dr. Shiel received a Bachelor of Science degree with honors from the University of Notre Dame. There he was involved in research in radiation biology and received the Huisking Scholarship. After graduating from St. Louis University School of Medicine, he completed his Internal Medicine residency and Rheumatology fellowship at the University of California, Irvine. He is board-certified in Internal Medicine and Rheumatology.
Melissa Conrad Stöppler, MD
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
Catherine Burt Driver, MD
Catherine Burt Driver, MD, is board certified in internal medicine and rheumatology by the American Board of Internal Medicine. Dr. Driver is a member of the American College of Rheumatology. She currently is in active practice in the field of rheumatology in Mission Viejo, Calif., where she is a partner in Mission Internal Medical Group.
In this Article
- Rheumatoid arthritis (RA) facts
- What is rheumatoid arthritis (RA)?
- What are causes and risk factors of rheumatoid arthritis?
- What are rheumatoid arthritis symptoms and signs?
- What are complications of rheumatoid disease?
- How do physicians diagnose rheumatoid arthritis?
- What is the treatment for rheumatoid arthritis?
- "First-line" rheumatoid arthritis medications
- "Second-line" or "slow-acting" rheumatoid arthritis drugs (disease-modifying anti-rheumatic drugs or DMARDs)
- What are newer treatments for rheumatoid arthritis?
- Rheumatoid arthritis diet and other treatments
- What about rheumatoid arthritis and pregnancy?
- What is the prognosis (outlook) for patients with rheumatoid arthritis?
- Is it possible to prevent rheumatoid arthritis?
- What research is being done on rheumatoid arthritis?
- Where can people get additional information on rheumatoid arthritis?
- Rheumatoid Arthritis Slideshow
- Take the RA Quiz
- Rheumatoid Arthritis Exercises Slideshow
- Newly Diagnosed Rheumatoid Arthritis Treatment
- Rheumatoid Arthritis FAQs
- Find a local Rheumatologist in your town
What is the treatment for rheumatoid arthritis?
There is no known cure for rheumatoid arthritis. To date, the goal of treatment in rheumatoid arthritis is to reduce joint inflammation and pain, maximize joint function, and prevent joint destruction and deformity. Early medical intervention has been shown to be important in improving outcomes. Aggressive management can improve function, stop damage to joints as monitored on X-rays, and prevent work disability. Optimal RA treatment involves a combination of medications, rest, joint-strengthening exercises, joint protection, and patient (and family) education. Treatment is customized according to many factors such as disease activity, types of joints involved, general health, age, and patient occupation. RA treatment is most successful when there is close cooperation between the doctor, patient, and family members.
Two classes of medications are used in treating rheumatoid arthritis: fast-acting "first-line drugs" and slow-acting "second-line drugs" (also referred to as disease-modifying antirheumatic drugs or DMARDs). The first-line drugs, such as aspirin and cortisone (corticosteroids), are used to reduce pain and inflammation. The slow-acting second-line drugs, such as methotrexate (Rheumatrex, Trexall, Otrexup) and hydroxychloroquine (Plaquenil), promote disease remission and prevent progressive joint destruction.
The degree of destructiveness of rheumatoid arthritis varies among affected individuals. Those with uncommon, less destructive forms of the disease or disease that has quieted after many years of activity ("burned out" rheumatoid arthritis) can be managed with rest plus pain control and anti-inflammatory medications alone. In general, however, function is improved and disability and joint destruction are minimized when the condition is treated earlier with second-line drugs (disease-modifying antirheumatic drugs), even within months of the diagnosis. Most people require more aggressive second-line drugs, such as methotrexate, in addition to anti-inflammatory agents. Sometimes these second-line drugs are used in combination. In some cases with severe joint deformity, surgery may be necessary.
"First-line" rheumatoid arthritis medications
Acetylsalicylate (aspirin), naproxen (Naprosyn), ibuprofen (Advil, Medipren, Motrin), and etodolac (Lodine) are examples of nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs are medications that can reduce tissue inflammation, pain, and swelling. NSAIDs are not cortisone. Aspirin, in doses higher than those used in treating headaches and fever, is an effective anti-inflammatory medication for rheumatoid arthritis. Aspirin has been used for joint problems since the ancient Egyptian era. The newer NSAIDs are just as effective as aspirin in reducing inflammation and pain and require fewer dosages per day. Patients' responses to different NSAID medications vary. Therefore, it is not unusual for a doctor to try several NSAID drugs in order to identify the most effective agent with the fewest side effects. The most common side effects of aspirin and other NSAIDs include stomach upset, abdominal pain, ulcers, and even gastrointestinal bleeding. In order to reduce gastrointestinal side effects, NSAIDs are usually taken with food. Additional medications are frequently recommended to protect the stomach from the ulcer effects of NSAIDs. These medications include antacids, sucralfate (Carafate), proton-pump inhibitors (Prevacid and others), and misoprostol (Cytotec). Newer NSAIDs include selective Cox-2 inhibitors, such as celecoxib (Celebrex), which offer anti-inflammatory effects with less risk of stomach irritation and bleeding risk.
Corticosteroid medications can be given orally or injected directly into tissues and joints. They are more potent than NSAIDs in reducing inflammation and in restoring joint mobility and function. Corticosteroids are useful for short periods during severe flares of disease activity or when the disease is not responding to NSAIDs. However, corticosteroids can have serious side effects, especially when given in high doses for long periods of time. These side effects include weight gain, facial puffiness, thinning of the skin and bone, easy bruising, cataracts, risk of infection, muscle wasting, and destruction of large joints, such as the hips. Corticosteroids also carry some increased risk of contracting infections. These side effects can be partially avoided by gradually tapering the doses of corticosteroids as the individual achieves improvement in symptoms. Abruptly discontinuing corticosteroids can lead to flares of the disease or other symptoms of corticosteroid withdrawal and is discouraged. Thinning of the bones due to osteoporosis may be prevented by calcium and vitamin D supplements.
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