Our roundtable experts offer perspectives from their clinical experience in discussing exercise recommendations for patients with RA, considerations for when to switch from anti-TNF agents to biologic therapies, and how to differentiate between RA and fibromyalgia. Without further delay, here is what they had to say.

Q: What types of exercise do you recommend for your RA patients?

A: Charles Pritchard, MD, emphasizes tailoring any exercise recommendations to the specific needs of the patient. For example, when patients have difficulty moving their hands or have RA-related foot pain, Dr. Pritchard says he sends these patients to physical therapy in order to “increase function and decrease pain” in these areas with exercise and modalities such as warm wax treatments, iontophoresis, splinting or ultrasound.

Nathan Wei, MD, agrees with Dr. Pritchard that most patients with RA will benefit from stretching, strengthening exercises and some cardiovascular workout if the patients are able to do it.
When patients have significant pain or difficulty ambulating, Dr. Pritchard says hydrotherapy has been beneficial for these patients. He adds that frequent swimming, especially using strokes like breaststroke, is helpful and enjoyed by patients.

For some patients in pain, it can be difficult to differentiate between rheumatoid arthritis flares and fibromyalgia flares. In these cases, Daniel Malone, MD, urges clinicians to consider clinical, laboratory and imaging data.

Dr. Wei says this is critical as exercise that facilitates an improved sense of well-being helps patients with RA cope with the daily stresses of the disease.

“The role of exercise cannot be underestimated in the comprehensive treatment of rheumatoid arthritis,” states Dr. Wei. “Depending on the degree of physical condition and debility, some patients may pursue a fairly rigorous program of exercise while others will require a gentler approach.”

Dr. Wei notes that a good combination of “stretching, strengthening and non-impact aerobic exercise works well for most patients with RA.”

Q: What criteria do you look for in going from a first-line anti-TNF agent to a second-line biologic agent or second-line agent in general?

A: Norman Koval, MD, usually looks for failure or intolerability to two of the first-line TNF agents.
“I define failure in the same manner as I have read in the advertisement literature for the second-line drugs: i.e. ‘persistent swelling and/or tender joints, persistent pain, prolonged stiffness, significant fatigue or reduced function despite ongoing or past TNF inhibitor therapy,’” notes Dr. Koval.

Patient intolerability to first-line anti-TNF agents may include infection, allergic reaction and severe headaches, according to Dr. Koval. If the patient has a cardiac history, Dr. Koval adds that these agents may increase the risk of symptoms of congestive heart failure.

Even though he might occasionally try a third anti-TNF drug, Dr. Wei says if the patient has not responded well to the first two attempts with anti-TNF medications, it is unlikely a third will be of any significance.

How one defines a “lack of response” also varies among some clinicians, points out Dr. Wei. In addition to the obvious signs and symptoms, a rise in ESR and/or CRP, when it has previously been stable for some time, is a clue that optimal therapy no longer exists. In these situations, Dr. Wei says clinicians should make sure other issues such as undiagnosed infections, unsuspected additional rheumatic disease, malignancy, etc., are not complicating the case. He adds that fibromyalgia is another condition that makes patient evaluation “murky.”

Another critical issue is the timing of starting a patient with a second-line biologic after he or she has been treated with an anti-TNF drug, notes Dr. Wei. He says this is theoretically more of a problem with rituximab (Rituxan, Genentech) than abatacept (Orencia, Bristol Myers Squibb).

“Rituxan acts to deplete B cells. We still do not know how soon we can start Rituxan after a person has failed anti-TNF therapy,” notes Dr. Wei.

Clinicians should also keep in mind that one would administer these second-line biologics intravenously and Dr. Wei notes this could be difficult for some patients with poor venous access. He adds that patient rapport is essential as the potential side effect profile with the second-line biologic agents is something that requires careful explanation to patients.

“Nonetheless, in practice, we are grateful to have some alternatives since about a third or more of our patients either do not respond to anti-TNF agents or lose response over time,” explains Dr. Wei.

Q: What kinds of things do you look for when trying to distinguish between a flare of RA versus a flare of fibromyalgia in a patient?

A: This is a very important question since failing to make this distinction results in unnecessary use of antirheumatic drugs, explains Daniel Malone, MD.

He believes that even experienced clinicians often make the mistake of over-treating RA because they fail to recognize that the arthralgia is actually due to fibromyalgia as opposed to RA.

“(As a result), patients with RA and fibromyalgia too often get loaded up with immunosuppressants, biologics, etc., when what they actually need is treatment for the fibromyalgia,” emphasizes Dr. Malone. He notes that he frequently gets referrals from rheumatologists for patients who have been diagnosed with RA but have “failed everything” in terms of treatment for the disease.

If one suspects the possibility of fibromyalgia, Dr. Malone says clinicians should ask these patients how they sleep at night and if they have depression, weight gain, a loss of libido and other typical symptoms of fibromyalgia. He also recommends that clinicians perform a tender point exam.

If the clinician knows that the patient has RA and fibromyalgia, then the complaint of arthralgia in and of itself is useless since fibromyalgia patients often hurt all over all the time as a baseline, and it is not possible to distinguish this common fibromyalgia complaint from pain due to inflammatory arthritis, says Dr. Malone.

In order to differentiate between RA and fibromyalgia, one must consider the use of clinical, laboratory and imaging data. In looking for objective clinical signs, Dr. Malone says it is important to know which ones are helpful and which are not when it comes to diagnosing fibromyalgia. For example, Dr. Malone says grip strength is useless since patients with fibromyalgia often have difficulty performing even the simplest tasks that require strength. Likewise, he says palpating the joints for tenderness is of little help since since most fibromyalgia patients hurt with even light palpation in multiple areas of the body.

Accordingly, Dr. Malone emphasizes that clinicians examine the joints for synovial thickening and effusions, and pay attention to the distribution of the complaints. In other words, Dr. Malone urges clinicians to consider whether the joints with arthralgia are the typical joints affected by RA. However, since obesity is common among patients with fibromyalgia, Dr. Malone cautions that even careful examination of the joints for swelling can be equivocal.

If one is still not sure after a careful joint examination, ordering an erythrocyte sedimentation rate (ESR) or C reactive protein (CRP) might help, according to Dr. Malone, who says the utility of these inflammatory markers is well documented. However, he notes that clinicians must ascertain if the patient’s ESR has been elevated in the past during periods of increased RA activity and returned to normal when treatment suppressed the RA activity. If one cannot document that sort of history, Dr. Malone says the ESR and CRP may not be good tools to assess RA activity.

The use of ultrasound and ultrasound Doppler for checking hypervascularity can be useful but as Dr. Malone points out, many clinicians are not familiar with this technology.

When it comes to obtaining magnetic resonance imaging (MRI), one should ensure gadolinium contrast of the most symptomatic area. If there is an actual RA flare, Dr. Malone says clinicians will see a bright T2 signal in the synovium with enhancement after gadolinium contrast of any synovium that is truly inflamed. If the MRI with gadolinium contrast shows no inflammation, then it is fibromyalgia, not RA, that is causing the trouble, according to Dr. Malone.

While some may criticize the use of MRIs as too expensive, Dr. Malone rejects this assertion. As he points out, “equal, if not much more, money is spent on courses of expensive biologics, disease-modifying antirheumatic agents (DMARDs), monitoring labs, etc.” He adds that the sensitivity of MRI “is very high” for the detection of synovitis.

Dr. Pritchard is a rheumatologist in private practice in Willow Grove, Pa.

Dr. Malone is an Associate Professor of Medicine within the Division of Rheumatology at the University of Wisconsin School of Medicine in Madison, Wisconsin.

Dr. Koval is a rheumatologist in private practice in Wheaton, Md.

Dr. Wei is a board-certified rheumatologist. He is the Clinical Director of the Arthritis and Osteoporosis Center in Frederick, Md.