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CHICAGO - Treatment with a biologic agent reduces fatigue in people with rheumatoid arthritis, according to research presented this week at the American College of Rheumatology Annual Scientific Meeting in Chicago.

Rheumatoid arthritis is a chronic disease that causes pain, stiffness, swelling, and limitation in the motion and function of multiple joints. Though joints are the principal body parts affected by RA, inflammation can develop in other organs as well. An estimated 1.3 million Americans have RA, and the disease typically affects women twice as often as men.

In addition to joint pain, people with RA often experience fatigue that diminishes their quality of life and limits their ability to complete even the simplest tasks. Biologics, such as tumor necrosis factor-alpha blockers, which reduce the inflammation caused by the disease, may also reduce accompanying fatigue. Investigators from Germany recently evaluated the effectiveness of several biologic treatments to also relieve fatigue symptoms in people with rheumatoid arthritis.

“Chronic fatigue is a symptom of RA that significantly limits patient’s social life,” says Anja Strangfeld, MD; group leader at Deutsches Rheuma-Forschungszentrum Berlin, Germany and lead investigator in the study. “With data from our German biologics register RABBIT, which observes more than 9,500 patients with RA from start of treatment with either a conventional disease-modifying antirheumatic drug or any approved biologic agent, we were able to investigate the improvement of fatigue under different treatments and demonstrate that biologic agents were best able to improve this symptom.”

Dr. Strangfeld’s team included 5,432 patients from their cohort in the analysis - who were, at baseline, on average 55 years old with an average disease duration of 12 years. They had been unsuccessfully treated with conventional disease-modifying antirheumatic drugs (commonly called DMARDs) before starting a biologic agent, or had been switched from one conventional DMARD to another (control group). Only patients with at least six months of follow up were included in the analysis.

The researchers measured patient-reported fatigue using a scale from zero (no) to 10 (high). Once initial measurements were taken, fatigue was reevaluated at three and six months. While taking into consideration other factors that might affect a person’s fatigue level (e.g., co-existing diseases, use of steroids, and limited functional capacity), they compared the effectiveness of each therapy in fighting fatigue by determining if the therapy was successful in significantly improving it (change in score of three points or more).

At six months, researchers noted that fatigue improved in all participants. However, participants who received biologics reported improvement significantly more frequently when compared with participants who received conventional DMARDs. 

Dr. Strangfeld further comments, “Improvement of fatigue under treatment with biologics was already seen after three months and independent of disease activity. Despite these findings, further studies are needed to evaluate the effectiveness of switching treatments to manage chronic fatigue in people with RA.”

The American College of Rheumatology is an international professional medical society that represents more than 8,000 rheumatologists and rheumatology health professionals around the world. Its mission is to advance rheumatology. The ACR/ARHP Annual Scientific Meeting is the premier meeting in rheumatology. For more information about the meeting, visit Follow the meeting on Twitter by using the official hashtag: #ACR2011.

Editor’s Notes: Anja Strangfeld, MD, will present this research during the ACR Annual Scientific Meeting at McCormick Place Convention Center from 9:00 - 11:00 am on Sunday, November 6 in the Hall F2. Dr. Strangfeld will be available for media questions and briefing at 1:30 pm on Monday, November 7 in the on-site press conference room, W 175C.

Learn more about living well with rheumatic disease as well as rheumatologists and the role they play in health care. Also, discover the ACR’s Simple Tasks campaign, which highlights the severity of rheumatic diseases and the importance of early and appropriate referral to a rheumatologist.

Presentation Number: 461

Impact of Different Biologic Agents on the Improvement of Fatigue

Anja Strangfeld (Deutsches Rheumaforschungszentrum, Berlin, Germany)
Matthias Schneider (Heinrich-Heine-University, Duesseldorf, Germany)
Jörg Kaufmann (Rheumatologist, Ludwigsfelde, Germany)
Andreas Krause (Immanuel Krankenhaus Berlin-Buch, Berlin, Germany)
Angela Zink (Deutsches Rheumaforschungszentrum and Charité University Medicine, Berlin, Germany)
Joachim Listing (German Rheumatism Research Centre, Berlin, Germany)

Background/Purpose: Fatigue is a factor significantly affecting the physical health of patients and limiting their social live. It was reported lately that TNFα leads to prolonged brain activity upon nociceptive stimulation, which is rapidly reversed with TNF-blockade. It was shown that this is not primarily linked to the anti-inflammatory effects of TNF-inhibition. Due to the effects of TNFα in the central nervous system our aim was to examine whether the relative improvement of fatigue is different for the various biologic agents.

Method: We used data from the German biologics register RABBIT which observes more than 9,500 patients with rheumatoid arthritis (RA) from start of treatment with any approved biologic agent or with a new DMARD. In the current analysis, only patients with a follow-up of at least 6 months and a minimum of two DMARD failures were included. Fatigue was measured on a 0 to 10 numerical rating scale (NRS) at baseline, and after 3 and 6 months. Multiple logistic regression was used to compare the treatment with various biologic agents to non-biologic DMARD treatment regarding a) the chance of achieving ‘no fatigue’ (value <= 1) at six months and b) the chance of clinically significant improvement (change in fatigue score of 3 or more) in patients who had a baseline score of at least 3. Adjustment was made for the following baseline variables: fatigue, DAS28, functional capacity (measured by the Hannover Functional Status Questionnaire (FFbH)), co-morbid conditions (4 subgroups), previous treatment with biologics (yes/no), treatment with glucocorticoids (no, <10mg/d >=10mg/d), pain and morning stiffness >=30 minutes.

Result: Data of 5,432 patients with a mean age of 55 years and  disease duration of 12 ± 9 years were available for the analysis.  At baseline, patients had a mean fatigue score of 5.5 ±2.7, a DAS28 of 5.5 ±1.3 and 59% of full function. Fatigue improved to 4.2 ±2.7 at six months. Patients treated with biologics improved significantly more frequently by a score of 3 or higher than DMARD treated patients. This was also found if patients with similar improvement in DAS28 scores were compared (data not shown). Anti-TNF treated patients had compared to DMARD controls a significantly higher chance of achieving ‘no fatigue’ already at three months (data not shown) and at six months (Tab).



‘No fatigue’ at 6 months

Clin. significant improvement


No. of patients

Adj. OR

Adj. frequency (%)

Adj. OR

Adj. frequency (%)




11.7  [10 - 14]


26.6 [23 - 30]



1.7  *

18.3  [16 - 21]

2.1 *

43.8  [40 - 47]



1.6 *

17.4  [14 - 21]

1.8 *

39.3 [34 - 45]



1.4 *

15.6 [14 - 18]

1.9 *

40.2 [37 - 43]




13.8  [11 - 17]

1.7 *

37.5 [33 - 43]




13.1  [8 - 20]

1.6 *

37.0  [28 - 47]




16.6  [12 - 23]

1.9 *

41.3  [32 - 51]

Table.  Adjusted odds ratios (OR) and corresponding adjusted frequencies of patients achieving ‘no fatigue’ (<= 1 on a 0 to 10 scale) or a clinically significant improvement of ≥ 3 points.   * p < 0.05

Conclusion: Treatment with a biologic agent improved fatigue significantly more frequently than with a conventional DMARD. This finding is supported by experimental research in which Hess et al (1) observed that blocking TNFα does not only have anti-inflammatory effects but also an impact on processes in the CNS.

A. Strangfeld
, None.
M. Schneider, None.
J. Kaufmann, None.
A. Krause, None.
A. Zink, None.
J. Listing, None.

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