461 - Impact of Different Biologic Agents on the Improvement of Fatigue

Sunday, November 6, 2011: 9:00 AM-6:00 PM
Hall F2 - Poster Hall (McCormick Place West)
Anja Strangfeld, Deutsches Rheumaforschungszentrum, Berlin, Germany, Matthias Schneider, Heinrich-Heine-University, Duesseldorf, Germany, J÷rg Kaufmann, Rheumatologist, Ludwigsfelde, Germany, Andreas Krause, Immanuel Krankenhaus Berlin-Buch, Berlin, Germany, Angela Zink, Deutsches Rheumaforschungszentrum and CharitÚ University Medicine, Berlin, Germany and Joachim Listing, German Rheumatism Research Centre, Berlin, Germany
Presentation Number: 461

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 (%)

DMARD

1,068

Referent

11.7  [10 - 14]

Referent

26.6 [23 - 30]

Etanercept

1,249

1.7  *

18.3  [16 - 21]

2.1 *

43.8  [40 - 47]

Infliximab

516

1.6 *

17.4  [14 - 21]

1.8 *

39.3 [34 - 45]

Adalimumab

1,389

1.4 *

15.6 [14 - 18]

1.9 *

40.2 [37 - 43]

Rituximab

840

1.2

13.8  [11 - 17]

1.7 *

37.5 [33 - 43]

Abatacept

182

1.1

13.1  [8 - 20]

1.6 *

37.0  [28 - 47]

Tocilizumab

188

1.5

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.


Keywords: DMARDs, quality of life and rheumatoid arthritis (RA)

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