Rheumatoid arthritis therapy

by Nathan Wei, MD, FACP, FACR

Nathan Wei is a nationally known board-certified rheumatologist and author of the Second Opinion Arthritis Treatment Kit. It's available exclusively at this website... not available in stores.

Click here: Second Opinion Arthritis Treatment Kit

What is rheumatoid arthritis?

Rheumatoid arthritis (RA) is the most common inflammatory form of arthritis. It is characterized by inflammation of the synovial (joint) lining of multiple joints, usually presenting in a symmetric manner (meaning one side is like the other).

Early on, small joints such as the hands, wrists, ankles, and feet are involved. As the disease progresses, larger joints also are affected. Virtually, any joint can be involved.

Rheumatoid arthritis is an acquired autoimmune disease with a genetic predisposition. About 70% of patients have the genetic markers, HLA-DR4 or HLA-DR1.

Rheumatoid factors, which are antibodies to IgG, occur in 60-80% of adult RA patients. The level of rheumatoid factor in the blood seems to correlate with prognosis.

The three abnormal factors that seem to be associated with the development of RA are an environmental trigger (the exact trigger is still unknown), genetic predisposition, and a hyper normal immune response.

RA affects about 1-2% of the population (2 million people) with a female to male ratio of about 3:1. Mortality in patients with RA is increased compared with the general population. Life expectancy is reduced about 7 years in men and 4 years in women.

The economic impact is staggering! Direct costs are $14 billion per year in the United States. After 5 years of disease, 27% of people are disabled. After 10 years between 40 to 60% of people are disabled.

How does the damage occur in RA?

What happens is that various white blood cells including polymorphonuclear leukocytes, macrophages, and specific lymphocytes called T cells and B cells become hyperactive and cause inflammation.

This inflammation leads to and is perpetuated by the production of chemical messengers, called cytokines. Cytokines cause damage by attracting more inflammatory cells to the area, causing more cytokines to be produced. Cytokines promote the release of destructive enzymes that destroy cartilage and other tissues.

As inflammation progresses, the synovium becomes swollen and takes on a life of its own.

At this stage it is called pannus and invades and destroys cartilage, bone, tendons, and ligaments resulting in joint deformity and loss of mobility. Some experts have compared the destructive potential of pannus to a slow-growing malignanacy. Synovial inflammation causes joint pain, stiffness, swelling, warmth, and redness.

Tell me about the symptoms…

The most common symptoms are morning stiffness, joint pain and swelling, nodules under the skin in about 20% of patients, and fatigue.

Since rheumatoid arthritis is a systemic illness it can lead to damage involving the brain and peripheral nervous system, skin, lungs, heart, and eyes.

Further, treatment with many of the medicines used in rheumatoid arthritis can lead to side-effects that affect the gastrointestinal system, the lungs, heart, and bones.

The course of RA is variable but progressive if untreated.

Causes of death include infection, malignancies, and vascular disease. There is some evidence that atherosclerosis (hardening of the arteries) is accelerated and that certain cancers such as multiple myeloma and lymphoma occur more often.

“I want to know how it’s diagnosed…”

The most important part of evaluating the patient is the history and physical examination. Helpful diagnostic laboratory tests include the rheumatoid factor, anti- CCP, erythrocyte sedimentation test (ESR), and C-reactive protein (CRP).

Imaging procedures such as magnetic resonance imaging and ultrasound are helpful. Diagnostic x-rays are of limited use because significant damage can occur before it shows up on x-ray.

The goals of management include: aggressive and early treatment, reduction of signs and symptoms, prevention of deformities, maintenance of joint function, control of co-morbidities (other associated disease such as hypertension, diabetes, etc., a patient might have), and possibly... cure. While this last option is still not quite achievable, it is becoming more of a possibility.

In addition to medications, treatment of RA includes diet, exercise, joint protection, occasionally joint surgery.

The approach to RA treatment has changed dramatically in the last 15 years.

“What do you have that will put my arthritis into remission?”

Current treatment options involving medications include:

Non steroidal anti inflammatory drugs: These help to reduce pain and improve function. They do not have an effect on the underlying disease. Examples include ibuprofen, naproxyn, sulindac, etodolac, nabumatone, celecoxib, and meloxicam.

These drugs are usually effective for mild symptoms but they have potential side effects including peptic ulcer disease, kidney and liver damage, rashes, and fluid retention. Another problem associated with these drugs is the slight increase in cardiovascular events such as heart attack and stroke. These drugs require careful monitoring.

Corticosteroids: These drugs suppress inflammation but also have no effect on the underlying disease. Examples include prednisone, methylprednisolone, and prednisolone. Used long term they may have undesirable side effects including ulcers, cataracts, osteoporosis, adrenal gland suppression, thinning of the skin, and diabetes.

Disease-modifying anti-rheumatic drugs (DMARDS): These drugs slow down the progression of rheumatoid arthritis. Examples would be medicines such as methotrexate, sulfasalazine (Azulfidine), leflunomide (Arava), hydroxychloroquine (Plaquenil), and cyclosporine (Sandimmune).

Most DMARDS act slowly.

The workhorse of DMARDS is probably methotrexate. All DMARDS have the potential for significant side-effects and must be monitored slowly.

Biologics: Most recently, biologic therapies such as Enbrel, Humira, Remicade, Cimzia, Simponi, Kineret, Actemra. Orencia, Rituxan, and Xeljanz have helped tremendously.

These drugs target the cells and cytokines that are the primary cause of rheumatoid arthritis. These drugs work quickly. These drugs have a different mechanism of action from each other but they essentially all do the same thing. And they do it well. These drugs have revolutionized our approach to RA.

Rheumatologists are using this group of drugs earlier in the course of disease to hopefully prevent damage from occurring. There is also some evidence that early aggressive treatment may prevent some of the long term complications of rheumatoid arthritis such as lymphoma and cardiovascular events.

Potential side-effects of anti-TNF therapy include an increased susceptibility to infection, the reactivation of latent tuberculosis and other fungal infections, and the development of lupus-like or MS-like syndromes.

Kineret, unfortunately, does not have the same salutary effect and is not used very often.

More biologic therapies are on the horizon. These new drugs may prove to be more effective and safer than what is currently available.

In patients with more severe disease, a procedure where blood is passed through a special filter (Prosorba column) may be of use. As one might guess, it is not used very often.


Rheumatoid arthritis is a chronic inflammatory disease with the potential to cripple and shorten life-span. Fortunately, with the treatment protocols available today, this disease is extremely controllable.

Still, there are some patients who don’t respond to any of these treatments. At the same time we have been able to put more people into sustained remission than at any other time before.

The development of a cure is a definite possibility. Research into what are called synovial biomarkers, specific characteristics that can be targeted with therapies, may be the answer. Until that day arrives, the key remains early diagnosis and aggressive treatment.

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