Session Information
Date: Sunday, October 21, 2018
Title: Rheumatoid Arthritis – Treatments Poster I: Strategy and Epidemiology
Session Type: ACR Poster Session A
Session Time: 9:00AM-11:00AM
Background/Purpose: Abatacept (ABA), a selective T-cell co-stimulatory modulator, has shown efficacy similar to TNF inhibitors (TNFi) for RA management in clinical trial settings, but different patient (pt) subtypes have shown a differential response to treatments in real-world and clinical trial settings. Additional data comparing the characteristics and associated clinical responses in pts receiving ABA versus other DMARDs in real-world community practice settings are needed.
Methods: We analyzed data from 24,602 pts with RA exposed to DMARDs from January 1, 2014 to September 30, 2017 in the United Rheumatology Database, which provides electronic medical record data from 120 community-based rheumatology providers. Baseline (BL) differences in demographics, disease activity and laboratory measurements were analyzed descriptively between pts receiving ABA versus TNFi, conventional (c)DMARDs and biologic (b) or targeted synthetic (ts)DMARDs of other mechanisms of action (other b/tsDMARDs) as first- or later-line therapy. Mean changes from BL to Year 1 (using records dated closest to Year 1) in CDAI scores were assessed using multivariate linear regressions adjusting for BL covariates (age, sex, smoking status, BMI, Charlson Comorbidity Index, CDAI score and number of prior treatments). Exposure was treated similarly to an intent-to-treat analysis (first observation carried forward).
Results: At BL, ABA pts (vs all other DMARD pts) had higher low- and high-density lipoprotein levels, and were more likely to have a history of type 1 or 2 diabetes (Table 1). ABA pts also had higher BL disease activity (CDAI; mean [SD]: 20.3 [13.0]) versus other b/tsDMARD (19.9 [13.4]), TNFi (18.1 [13.2]) and cDMARD pts (14.4 [12.4]; Table 1). After adjusting for BL covariates, the reduction in least square mean (LSM) CDAI from BL was greater in ABA pts (–5.6) than other b/tsDMARD pts (–3.4); this difference suggested a trend toward significance (2.2 [95% CI: –0.2, 4.6]; p=0.07). The reduction in LSM CDAI was comparable between ABA and TNFi pts (Table 2).
Conclusion: Pts with RA receiving abatacept (vs other DMARDs) in community practice settings tend to have higher disease activity and a history of diabetes, which have been associated with worse clinical response to treatment. Nonetheless, mean changes in disease activity from BL to Year 1 in pts receiving abatacept versus other b/tsDMARDs were larger in magnitude, although the difference was not statistically significant. Additional analyses with a larger pt population are warranted.
Writing support provided by Bu Reinen, PhD (Caudex), funded by Bristol-Myers Squibb.
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Table 1. Baseline Characteristics of Patients With RA in the United Rheumatology Database* |
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|
Baseline characteristics |
Abatacept |
Other b/tsDMARD |
TNFi |
cDMARD |
|
n |
3584 |
3481 |
7711 |
9826 |
|
Age, years, mean (SD) |
61.0 (13.5) |
59.7 (13.2) |
59.4 (13.8) |
63.5 (13.9) |
|
Sex, n (%) |
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|
Female |
2921 (81.5) |
2804 (80.6) |
5812 (75.4) |
7376 (75.1) |
|
History of smoking, n (%) |
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|
No |
706 (19.7) |
824 (23.7) |
1511 (19.6) |
2116 (21.5) |
|
Yes |
994 (27.7) |
1148 (33.0) |
2018 (26.2) |
2826 (28.8) |
|
Unknown |
1884 (52.6) |
1509 (43.3) |
4182 (54.2) |
4884 (49.7) |
|
BMI, kg/m2 |
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|
n |
2094 |
2170 |
4364 |
5142 |
|
Mean (SD) |
30.3 (6.8) |
30.1 (6.7) |
29.7 (6.6) |
29.1 (6.1) |
|
Diabetes, n (%) |
406 (11.3) |
288 (8.3) |
609 (7.9) |
533 (5.4) |
|
Hypertension, n (%) |
881 (24.6) |
943 (27.1) |
1727 (22.4) |
2050 (20.9) |
|
Charlson Comorbidity Index |
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|
n |
3584 |
3481 |
7711 |
9826 |
|
Mean (SD) |
1.0 (1.4) |
1.0 (1.2) |
0.8 (1.1) |
0.6 (0.6) |
|
HDL |
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|
n |
54 |
111 |
60 |
52 |
|
Mean (SD) |
62.0 (20.4) |
60.5 (21.8) |
57.1 (17.2) |
58.9 (16.8) |
|
LDL |
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|
n |
56 |
102 |
54 |
40 |
|
Mean (SD) |
110.0 (38.4) |
106.4 (32.8) |
102.5 (32.9) |
100.1 (37.9) |
|
RF titer |
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|
n |
108 |
91 |
193 |
467 |
|
Mean (SD) |
73.1 (142.4) |
99.9 (127.8) |
75.9 (114.4) |
65.2 (109.7) |
|
ACPA titer ≥20 |
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|
n |
32 |
31 |
97 |
175 |
|
Mean (SD) |
109.7 (138.4) |
87.9 (64.5) |
103.6 (93.6) |
84.7 (77.5) |
|
RAPID3 (0–30) |
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|
n |
1049 |
966 |
1678 |
1679 |
|
Mean (SD) |
8.3 (6.4) |
8.3 (6.5) |
7.3 (6.3) |
6.2 (5.6) |
|
CDAI |
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|
n |
559 |
564 |
820 |
564 |
|
Mean (SD) |
20.3 (13.0) |
19.9 (13.4) |
18.1 (13.2) |
14.4 (12.4) |
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Prior RA treatment (United Rheumatology records only), n (%) |
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|
0 |
1627 (45.4) |
1478 (42.5) |
4047 (52.5) |
7866 (80.1) |
|
1 |
883 (24.6) |
962 (27.6) |
2519 (32.7) |
1662 (16.9) |
|
≥2 |
1074 (30.0) |
1041 (29.9) |
1145 (14.8) |
298 (3.0) |
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*Other b/tsDMARDs: infliximab, etanercept, adalimumab, certolizumab pegol and golimumab; TNFi: tocilizumab, rituximab and tofacitinib; cDMARD: methotrexate, sulfasalazine, azathioprine, tacrolimus, gold thiomalate, leflunomide, aurothioglucose, auranofin, cyclosporine, penicillamine, cyclophosphamide and hydroxychloroquine ACPA=anti-citrullinated protein antibody; b/tsDMARD=biologic or targeted synthetic DMARD; cDMARD=conventional DMARD; HDL=high-density lipoprotein; LDL=low-density lipoprotein; RAPID3=Routine Assessment of Patient Index Data 3; TNFi=TNF inhibitor |
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Table 2. Changes in CDAI Over 12 Months in Patients With RA*,† |
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|
|
n |
Baseline, LSM (95% CI)‡ |
Year 1, LSM (95% CI)‡ |
Change from baseline, LSM (95% CI)‡,§ |
Difference in change, LSM (95% CI)‡,§ |
p value |
|
Abatacept |
164 |
21.0 (18.5, 23.5) |
13.6 (11.7, 15.6) |
−5.6 (−7.4, −3.8) |
Ref |
Ref |
|
Other b/tsDMARD |
108 |
19.8 (17.0, 22.6) |
15.5 (13.3, 17.7) |
−3.4 (−5.5, −1.4) |
2.2 (−0.2, 4.6) |
0.07 |
|
TNFi |
180 |
18.8 (16.4, 21.1) |
12.5 (10.7, 14.3) |
−6.2 (−7.8, −4.5) |
−0.5 (−2.7, 1.7) |
0.64 |
|
cDMARD |
116 |
16.0 (13.2, 18.9) |
12.3 (10.0, 14.5) |
−5.6 (−7.7, −3.5) |
0.0 (−2.6, 2.7) |
0.98 |
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*Includes patients who had CDAI measurements at both baseline and Year 1 †Other b/tsDMARDs: infliximab, etanercept, adalimumab, certolizumab pegol and golimumab; TNFi: tocilizumab, rituximab and tofacitinib; cDMARD: methotrexate, sulfasalazine, azathioprine, tacrolimus, gold thiomalate, leflunomide, aurothioglucose, auranofin, cyclosporine, penicillamine, cyclophosphamide and hydroxychloroquine ‡Calculated by multivariate linear regression adjusted for age, sex, smoking status, BMI, Charlson Comorbidity Index and number of prior treatments §Further adjusted for baseline CDAI b/tsDMARD=biologic or targeted synthetic DMARD; cDMARD=conventional DMARD; LSM=least square mean; TNFi=TNF inhibitor |
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To cite this abstract in AMA style:
Ferri L, Curtis JR, Bao Y, Alemao E, Curtice T, Bryson J, Lozenski K, Balachandar S, Rajagopalan V. Channeling to Treatment and Associated Changes in Disease Activity Over 12 Months in Patients With RA Treated With Abatacept Versus Other DMARDs in Real-World Community Practice Settings [abstract]. Arthritis Rheumatol. 2018; 70 (suppl 9). https://acrabstracts.org/abstract/channeling-to-treatment-and-associated-changes-in-disease-activity-over-12-months-in-patients-with-ra-treated-with-abatacept-versus-other-dmards-in-real-world-community-practice-settings/. Accessed .« Back to 2018 ACR/ARHP Annual Meeting
ACR Meeting Abstracts - https://acrabstracts.org/abstract/channeling-to-treatment-and-associated-changes-in-disease-activity-over-12-months-in-patients-with-ra-treated-with-abatacept-versus-other-dmards-in-real-world-community-practice-settings/