The goal of treatment is to induce remission. This article is Part 1 on anti-inflammatory drugs and glucocorticoid medicines used to treat RA.



The first group of medicines that are often employed are anti-inflammatory drugs. Salicylates (aspirin), non-steroidal anti-inflammatory drugs (NSAIDs), or selective cyclooxygenase (COX)-2 inhibitors (eg., Celebrex) may reduce joint pain and swelling and improve joint function. These agents have analgesic and anti-inflammatory properties but do not alter the course of the disease or prevent joint destruction. As a result, they should not be used as the only treatment for RA.

Patients with RA are nearly twice as likely as patients with other forms of arthritis, such as osteoarthritis, to have a serious complication from NSAID treatment. Serious gastrointestinal side-effects, such as bleeding, ulcers, and perforation of the stomach, small intestine, or large intestine can occur at any time, with or without warning symptoms, in patients treated with NSAIDs (including COX-2 inhibitors, particularly if patients are taking concurrent aspirin).

Risk factors for the NSAID-associated ulcers affecting the stomach or duodenum (the first part of the small intestine) include age older than 75 years, history of ulcer, associated use of steroids or blood thinners, higher dosage of NSAIDs, use of multiple NSAIDs, and a serious underlying disease.

In 2005 the American College of Rheumatology (ACR) added to their 2002 RA treatment guidelines the warning that some placebo-controlled trials showed an increased risk for cardiovascular events, including nonfatal heart attacks and strokes, with COX-2 selective NSAIDs, particularly when used at higher doses.

Obviously, physicians and patients need to weigh the potential risks and benefits of treatment with these medications.

Glucocorticoids (“steroids”) are often used early in the treatment of active RA. They have potent anti-inflammatory effects and are effective in reducing symptoms quickly.

Glucocorticoids are often started at the same time as other medicines, the disease-modifying anti-rheumatic drugs (DMARDS), are started. The reason is that steroids act quickly while DMARDS act much more slowly.

In this instance, glucocorticoids are used as a “bridge” to help a patient with their symptoms quickly while waiting for DMARDS to kick in.

Frequently, disabling recurrence of joint inflammation returns when glucocorticoids are discontinued, even in patients who are receiving DMARDs. Therefore, many patients with RA are dependent on glucocorticoids and continue them long term. That's the bad news.

The good news is that some recent evidence suggests that low-dose glucocorticoids slow the rate of joint damage and appear to have disease-modifying potential. Joint damage may increase on discontinuation of glucocorticoids. The benefits of low-dose systemic glucocorticoids should always be weighed against their adverse effects. The adverse effects of long-term oral glucocorticoids even at low doses include osteoporosis, hypertension, weight gain, fluid retention, elevated blood sugar, cataracts, and thin skin, as well as the potential for premature hardening of the arteries. These potential side effects should be considered and discussed in detail with the patient before glucocorticoid therapy is begun.

For long-term disease control, the glucocorticoid dosage should be kept to a minimum. For most patients with RA, this means less than 7.5-10 mg of prednisone per day.

RA is associated with an increased risk for osteoporosis independent of glucocorticoid therapy. Some patients may require injections of glucocorticoids into joints to help with painful flares. Joint infection ruled out before local glucocorticoid injections are given. As a rule, the same joint should not be injected more than once within 3 months.

These drugs, while important, must be used in combination with DMARDs and biologic therapies. These drugs will be discussed in parts 2 and 3 of this series.