The diagnosis of rheumatoid arthritis (RA) starts with a careful history and physical examination. Answers to questions such as:

How did the symptoms begin?
When did they begin?
What joints are involved?
How long does the stiffness in the morning last?
How has your level of fatigue changed?
What do you have difficulty doing that you could do without trouble before your symptoms began?

... are very helpful.

Valuable diagnostic laboratory tests include the rheumatoid factor, anti-CCP, erythrocyte sedimentation test (ESR), and C-reactive protein (CRP).

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

It's important to realize that progression of RA is closely associated with the development of disability. It is also associated with the development of other potential problems such as early cardiovascular events such as heart attacks and strokes.

Before discussing treatment, let's look at the goals of treatment. These include: control of signs and symptoms, prevention of deformity, maintenance of joint function, control of co-morbidities (other associated disease such as hypertension, diabetes, etc.), and restoration of normal activities of daily living.

Current treatment options involving medications include:

Non-steroidal anti inflammatory drugs help reduce pain and improve function. They do not have an effect on slowing the underlying disease. Examples include ibuprofen (Motrin), naproxyn (Naprosyn), sulindac (Clinoril), etodolac (Lodine), nabumatone (Relafen), ketoprofen (Orudis), meloxicam (Mobic), and celecoxib (Celebrex).

These drugs are effective but they have potential side effects including peptic ulcer disease, kidney and liver damage, rashes, and fluid retention, and possibly a slight increase in cardiovascular events such as heart attack and stroke. These drugs require careful monitoring.

Corticosteroids suppress inflammation but also have no effect on the underlying disease. Examples include prednisone, methylprednisolone, and prednisolone. They have potential side effects including ulcers, cataracts, osteoporosis, adrenal gland suppression, thinning of the skin, and diabetes.

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

DMARDS act slowly. They may also not stop the progression of RA.

All DMARDS have potential side-effects and must be monitored slowly.

Most recently, biologic therapies such as etanercept (Enbrel), adalimumab (Humira), infliximab (Remicade), and anakinra (Kineret) have helped tremendously.

These drugs target the cells and cytokines that are the primary cause of rheumatoid arthritis. Etanercept, adalimumab, and infliximab block tumor necrosis factor- the primary cytokine responsible for the damage in RA

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

A second wave of biologic therapies are available and offers hope for patients who fail anti-TNF treatment. The two newest drugs are abatacept (Orencia) and rituximab (Rituxan).

Abatacept is a co-stimulatory blocker. It prevents T cells from being activated to produce cytokines. Rituximab is a B-cell depleter. It removes B cells from a patient's system. B-cells are felt to play a big role in the development of RA by some experts.

Both drugs are given by intravenous infusion. Side effects include infusion reactions and rashes.

Potentially helpful new drugs such as Actemra and Cimzia are on the horizon as this article is written.