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Rheumatoid Arthritis

arthritis is a chronic inflammatory disease, primarily involving the peripheral joints (finger joints, wrists, toes and knees) and surrounding muscles, tendons, ligaments and blood vessels.

This disease is among the autoimmune disorders (an abnormal immune response to oneself which leads to a sequence of tissue reactions and damage that may produce diffuse, systemic signs and symptoms).

Description

Rheumatoid Arthritis (RA) can be one of the most disabling types of arthritis. It occurs worldwide, affecting more than 6.5 million people in the U.S. alone. The disease strikes women three times more often than men. Although it can occur at any age, the peak onset period is between the ages of 35 and 50. The disease may come on slowly or appear suddenly.

RA usually requires lifelong treatment and sometimes, surgery. In most people with RA, the disease follows an intermittent course with a variety of symptoms, from just a few symptoms to severe and painful deformities that may be disabling.

Much more is known about the pathophysiology of RA than its causes. If unarrested, joint inflammation occurs in four stages:

1. First stage, synovitis (inflammation of the synovial membrane) develops from congestion and edema of the synovial membrane (membrane lining the capsule of a joint) and the joint capsule.

2. Formation of pannus (thickened layers of granulation tissue) marks the onset of the second stage. Pannus covers and invades cartilage and eventually destroys the joint capsule and bone.

3. Progression to the third stage is characterized by fibrous ankylosis - fibrous invasion of the pannus and scar formation that occludes the joint space. Bone atrophy and misalignment causes visible deformities and disrupts the articulation of opposing bones, causing muscle atrophy and imbalance and possibly, partial dislocations or subluxations.

4. In the fourth stage, fibrous tissue calcifies, resulting in bony ankylosis and total immobility.

Risks and Factors

What causes RA is unknown, but various theories point to infections, genetics and endocrine factors.

This disease is not contagious. A genetically susceptible person may develop abnormal or altered antibodies when exposed to a virus or antigen (a substance which induces the formation of antibodies). The body doesn't recognize these altered antibodies as "self," and the person forms an antibody (known as a rheumatoid factor) against them. This rheumatoid factor then generates inflammation of the joint lining.

Symptoms

The onset may be insidious with nonspecific symptoms, including fatigue, malaise, anorexia, persistent low-grade fever, weight loss, and vague articular symptoms; or it may have an abrupt onset with simultaneous inflammation in multiple joints. The symptoms usually occur bilaterally and symmetrically, and may extend to the wrists, elbows, knees and ankles.

The person may have stiff joints after inactivity, especially on rising in the morning. The person may also complain that joints are tender and painful, at first only when he/she moves them, but eventually even at rest. Ultimately, joint function is diminished.

Other complaints include stiff, weak or painful muscles. If the patient has peripheral neuropathy, he/she may report numbness or tingling in the feet or weakness or loss of sensation in the fingers.

Inspection of the person's joints may show deformities and contractures, especially if active disease continues. The fingers may appear spindle-shaped from marked edema and congestion in the joints. The joints may even be hot to the touch.

Treatment

Treatment requires a multidisciplinary health care team to reduce the patient's pain and inflammation, preserve functional capacity, resolve pathologic processes and bring about improvement.

The most effective treatment program for arthritis consists of drug therapy, exercise and rest. Many different drugs are now used to treat rheumatoid arthritis. Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen (Motrin and others), naproxen (Naprosyn and others) and most recently, dicolfenac (Voltaren), have immediate analgesic and anti-inflammatory effects. As many as 75 percent of all RA patients improve somewhat with conservative treatment during the first year of disease.

Salicylates (particularly aspirin) are the mainstay of therapy, because they decrease inflammation, relieve joint pain and are relatively safe. Aspirin in high doses is as effective as any other NSAID and much less expensive. However, as effective as it is, some people develop a gastrointestinal toxicity, tinnitus (ringing sound in the ear), and rarely, hepatitis or renal damage.

It also may interfere with platelet function, causing bleeding problems. If stomach irritation is a problem, enteric-coated aspirin is safer, but may not be fully absorbed. Nonacetylated salicylates, such as sodium salicylate, salsalate (Disalcid and others) and choline magnesium salicylate (Trillisate and others), do not interfere with platelet function and may be safer than acetylated salicylates for aspirin-sensitive patients. There are several situations when use of a nonsalicylate NSAID concurrently with aspirin is appropriate. Some patients get relief from aspirin yet develop tinnitus at blood levels inadequate for full anti-inflammatory activity.

Corticosteroids (Prednisone and others), are the most dramatically effective short-term anti-inflammatory drugs. RA, however, is usually active for years, therefore this drug should be reserved for "bridge" therapy between the time when the decision is made to start a disease-modifying anti-rheumatic drug (DMARD: such as gold) and when the drug becomes effective. Because of their side effects, corticosteroids should be given only after careful evaluation and conclusion that the benefits far outweigh the costs. Intra-articular injections of corticosteroid may temporarily help to control local synovitis in one or two particularly painful joints.

A major decision for the physician treating RA is when to begin therapy with second line or slow-acting disease modifying drugs (DMARDs). Hydroxychloroquine or sulfasalazine are the best drugs to begin with, since they have the least toxicity. One study claims that over a two-year period, patients treated with sulfasalazine had less progression of erosions than patients treated otherwise. The patient must not have false expectations about rapid responses, for as much as six months may be needed before a response to gold salts is manifested.

Gold compounds usually are given, in addition to salicylates or other NSAIDs if they do not provide sufficient relief or suppression of active joint inflammation. In some patients, gold may produce clinical remission and decrease the formation of new bony erosions. Improvement often can be sustained for several years with prolonged maintenance administration.

Gold is given either as an injectable or oral drug (auranofin). Before receiving gold, the patient should have several lab tests and should be repeated while continuing this drug therapy. There are risks of toxic reactions with gold salts, along with side effects.

Penicillamine given orally may have beneficial effects similar to that of gold. Because of its varied and unpredictable toxicity, D-penicillamine should probably be used after a trial, if gold has failed.

Cytotoxic or immunosuppressive drugs, such as methotrexate (MTX) and azathioprine are increasingly used in management of severe, active RA. Some rheumatologists use MTX early, after gold has failed and before D-penicillamine. Others use it instead of gold in patients with proteinuria or thrombocytopenia.

The true place in therapy of MTX is uncertain and is the subject of many studies. These drugs can suppress inflammation and may allow reduction of corticosteroid doses. The onset of action of the drug appears to occur within three to four weeks after beginning therapy.

The most common side effect is gastrointestinal distress, with stomatitis, nausea and pain leading the list. There are other major side effects which can occur with these drugs and the patient should be fully informed of these potential side effects.

Supportive measures include increased sleep (eight to 10 hours every night) frequent rest periods between daily activities and splinting to rest inflamed joints (although, with corticosteroid therapy, immobilization can cause osteoporosis). Occasionally, complete bedrest is indicated for a short period during the most active painful stage of severe disease.

Moderate daily exercise, such as swimming, walking or physical therapy, is critical to maintaining mobility. To lessen pain while increasing movement, moist heat (hot soaks, paraffin baths and whirlpools) often help patients with chronic disease.

Some severe cases of rheumatoid arthritis may require surgery to remove inflamed synovial tissue. Useful surgical procedures include metatarsal head and distal ulnar resectional arthroplasty, and insertion of a Silastic prosthesis between the metacarpophalangeal and proximal interphalangeal joints. Arthrodesis (joint fusion) may bring about stability and relieve pain, but only at the price of decreased joint mobility. Synovectomy (removal of destructive, proliferating synovium, usually in the wrists, fingers, and knees) may halt or delay the course of the disease.

Osteotomy (the cutting of bone or excision of a wedge of bone) can realign joint surfaces and redistribute stresses.

Given that no specific cause of RA is likely to be identified soon, and that even the best current therapies cannot stop the proliferative and destructive component of the disease, there are both opportunities and need for better therapy. There are several experimental treatments and therapies being studied presently. Most remain investigational with no conclusive results.

Questions To Ask Your Doctor

What tests will you be prescribing and what will they tell you?
How are the tests performed?
Is there evidence of rheumatoid arthritis and what stage is it at?
What drug therapy program will you start with?
What are the side effects?
What should I expect?
Should a physical therapist be consulted to set up an exercise program?
Are there any signs or symptoms that need to be reported immediately?
Are there any support groups or counselors to help with the stress and emotions of this disease?
Is there information on additional measures that can be done at home to help relieve symptoms or to prevent complications?








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