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Abstract Number: 2651

Evaluation of the Impact of Disease-Modifying Antirheumatic Drugs on Anti-Cyclic Citrullinated Peptide Autoantibody Levels in Clinical Practice

E Alemao1, KK Gandhi1, C Iannaccone2, M Frits2, JS Coblyn2, N Shadick2 and Michael Weinblatt2, 1Bristol-Myers Squibb, Princeton, NJ, 2Brigham and Women's Hospital, Boston, MA

Meeting: 2015 ACR/ARHP Annual Meeting

Date of first publication: September 29, 2015

Keywords: Abatacept, anti-CCP antibodies and disease-modifying antirheumatic drugs

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Session Information

Date: Tuesday, November 10, 2015

Title: Rheumatoid Arthritis - Clinical Aspects Poster Session III

Session Type: ACR Poster Session C

Session Time: 9:00AM-11:00AM

Background/Purpose: Testing for anti-citrullinated
peptide antibodies (ACPA) is included in the 2010 ACR classification criteria
for RA. ACPA concentration, beyond ACPA positivity, is indicative of more
aggressive radiographic progression. Biologic (b)DMARDs such as abatacept have been
shown to reduce ACPA levels in clinical trials; however, there are limited data
on the impact of DMARDs on ACPA in clinical practice.   Methods: Data were analyzed from patients (pts) enrolled in a large, US RA registry established in 2003. The registry comprises
pts with established RA who were evaluated annually for
multiple clinical and laboratory measures, and semi-annually for multiple pt-reported
outcomes and resource utilization parameters. The current analysis is based on pts
enrolled in the registry with ACPA values at the time of initiating DMARDs
(baseline ACPA levels). Baseline and follow-up ACPA levels were measured using
a validated ELISA (Inova Diagnostics) until its
discontinuation in 2011; the Euro-Diagnostica assay (distributed by IBL-America,
Minneapolis, MN), which
supplied the ‘capture’ antibody for the original Inova Diagnostics ELISA, has
been used since (correlation between the two assays: 0.984).
Mean ACPA level and mean
change from baseline to Year (Yr) 1 and Yr 2 were compared between conventional
(c)DMARDs, TNF-inhibitors (TNF-Is) and abatacept. To control for baseline
differences in clinical and laboratory measures, additional ACPA comparisons between
groups were conducted based on a 1:1 matched cohort of TNF-I and abatacept pts.   Results:   Overall, 1316 (98%) registry pts with ACPA levels
at therapy initiation were included in the analysis; 45, 49 and 6% of pts were
initiated on cDMARDs, TNF-Is or abatacept, respectively. The mean (SD) age (yrs) was 58.7 (14.1), 54.7 (13.6)
and 59.3 (11.4) for cDMARD, TNF-Is and abatacept cohorts, respectively. The
average (SD) disease duration (yrs) in the abatacept cohort was 20.5 (12.0) (vs
12.5 [12.6] for cDMARDs and 14.2 [11.4] for TNF-Is). The abatacept group also
had higher mean (SD) disease activity (24.3 [15.7] vs 19.9 [15.5] in cDMARDs
and 20.1 [17.3] in TNF-Is). ACPA values at baseline, Yr 1 and Yr 2 by treatment
group are shown in Table 1. The pt characteristics of the matched abatacept and
TNF-I groups, and ACPA values in Yr 1 and Yr 2 are shown in Table 2. Pts treated with abatacept showed a lowering of the
ACPA values during follow-up, while similar reductions in ACPA values were not
seen in pts treated with TNF-Is or cDMARDs.

Conclusion:

These results from a real-world clinical
setting support observations from clinical trials that abatacept treatment
leads to a reduction of ACPA levels, which is not seen with TNF inhibitors.

 

Table 1. Baseline and follow-up ACPA levels (U/mL) in pts treated with cDMARDs, TNF-Is and abatacept
  N Mean (SD) Change from baseline
      Median Mean (SE)
cDMARDs        
Baseline 591 99.8 (133.0) – –
Yr 1 333 103.7 (138.8) 0.00 2.1 (3.0)
Yr 2 263 130.6 (168.1) 1.34 29.0 (4.2)
TNF-Is        
Baseline 651 157.1 (162.5) – –
Yr 1 380 155.8 (151.5) –0.01 3.3 (3.6)
Yr 2 323 175.0 (162.4) 3.40 26.2 (4.6)
Abatacept        
Baseline 74 169.1 (225.3) – –
Yr 1 30 89.7 (122.9) –0.47 –20.5 (20.3)
Yr 2 19 112.5 (135.4) –11.18 –55.1 (29.4)

Table 2. Baseline characteristics and follow-up ACPA levels in matched cohorts of pts treated with TNF-Is and abatacept

 

TNF-Is

(n=66)

Abatacept

(n=66)

p-value

Baseline age, mean (SD)

57.0 (11.7)

58.9 (11.4)

0.34

Female, %

84.8

81.8

0.64

Baseline disease duration, mean (SD)

19.1 (11.3)

20.0 (11.3)

0.64

Baseline DAS28 (CRP), mean (SD)

3.9 (1.5)

4.0 (1.5)

0.51

Baseline SDAI, mean (SD)

24.3 (16.5)

24.3 (15.7)

0.99

Baseline ACPA, mean (SD)

167.7 (227.2)

167.1 (227.1)

0.99

Follow-up ACPA levels (U/mL)

TNF-Is

Abatacept

1-yr follow-up ACPA

 

 

N

33

27

Mean (SE)

165.8 (36.7)

84.5 (23.8)

Median

78.8

29.4

Interquartile range (IQR)

12.3 to 272.7

3.7 to 97.0

ACPA change from baseline to Yr 1

 

 

N

33

27

Mean (SE)

4.20 (23.2)

–11.4 (19.3)

Median

–0.23

–0.45

IQR

–12.7 to 20.1

–12.3 to 4.8

2-yr follow-up ACPA

 

 

N

29

16

Mean (SE)

155.1 (30.4)

97.5 (32.2)

Median

113.8

48.7

IQR

3.3 to 310.2

11.2 to 97.2

ACPA change from baseline to Yr 2

 

 

N

29

16

Mean (SE)

18.2 (14.4)

–40.5 (27.7)

Median

0.0

–40.5

IQR

–6.1 to 49.2

–33.0 to 0.23

   


Disclosure: E. Alemao, Bristol-Myers Squibb, 3,Bristol-Myers Squibb, 1; K. Gandhi, Bristol-Myers Squibb, 1,Bristol-Myers Squibb, 3; C. Iannaccone, None; M. Frits, None; J. Coblyn, None; N. Shadick, Amgen, Questcor, Crescendo Biosciences, UCB, Bristol-Myers Squibb, 2; M. Weinblatt, Amgen, Abbvie, Bristol-Myers Squibb, Lilly, Novartis, Merck, Pfizer, Roche, Crescendo, Myriad Genetics, UCB, 5,Bristol-Myers Squibb, Myriad Genetics, UCB, 2.

To cite this abstract in AMA style:

Alemao E, Gandhi K, Iannaccone C, Frits M, Coblyn J, Shadick N, Weinblatt M. Evaluation of the Impact of Disease-Modifying Antirheumatic Drugs on Anti-Cyclic Citrullinated Peptide Autoantibody Levels in Clinical Practice [abstract]. Arthritis Rheumatol. 2015; 67 (suppl 10). https://acrabstracts.org/abstract/evaluation-of-the-impact-of-disease-modifying-antirheumatic-drugs-on-anti-cyclic-citrullinated-peptide-autoantibody-levels-in-clinical-practice/. Accessed .
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