Session Information
Title: Rheumatoid Arthritis - Clinical Aspects (ACR): Comorbidities, Treatment Outcomes and Mortality
Session Type: Abstract Submissions (ACR)
Background/Purpose: Formal educational level is often used as a surrogate for socioeconomic status and in patients with rheumatoid arthritis (RA), low levels have been associated with greater morbidity and worse disease outcomes. Yet, the role of formal educational level and its impact on meaningful clinical response (MCR) in ethnic minorities with RA is unknown. We evaluated the correlation of educational level with meaningful clinical response in ethnic minorities with RA.
Methods: Ethnic Minority RA Consortium (EMRAC) patients with at least one follow up visit were assigned to three educational level categories: high school only (HS), high school with some college, and college graduates. Comparisons between educational categories of demographic (age, gender, race, tobacco use), RA disease status (RF, ACPA, nodules/erosions), and RA treatment (prednisone, DMARD, biologics [anti-TNF, other]) variables were performed between these groups. The frequency of MCR (DRAPID3 [-3.6]) at 3, 6, and 12 months was also evaluated between educational groups.
Results: EMRAC patients (n= 723) with approximately 10 months of follow-up were evaluated (Table 1.). HS patients were significantly older, with longer disease duration and follow-up than those with advanced educational levels. HS patients also had higher baseline RAPID3 scores (p <0.001). Overall, few patients achieved MCR and there was no difference in the frequencies of MCR between education categories at 3, 6 and 12 months. However, in multivariate analyses adjusted for, age, ethnicity, disease duration, and baseline RAPID3 scores, of those who did not achieve MCR, there were more HS patients with significant disease progression (RAPID3 D+0.2) versus college (RAPID3 D-0.5) and college graduates (RAPID3D-0.6)(p= 0.02).
Conclusion: Regardless of race or ethnicity, RA patients with low formal education levels are at risk of disease progression. In clinical practice, this category of patient needs to be identified early, and focused interventions such as self-efficacy and health literacy instituted in order to improve disease outcomes.
Table. 1
|
Clinical Characteristics of Educational Categories in EMRAC cohort
|
||||
|
< High School
|
High School – Some College
|
College Graduate
|
P
|
|
|
N
|
97
|
320
|
306
|
|
|
# of Follow-ups
|
2.9 (2.5) |
3.0 (2.6) |
2.9 (2.6) |
0.681
|
|
Follow-up Length (months) |
11.8 (13.1) |
9.1 (7.4) |
8.8 (6.3) |
0.033
|
|
Age (years) |
63.1 (12.5) |
56.4 (14.3) |
49.5 (15.8) |
<0.001
|
|
Female (N, %) |
72 (75.8%) |
258 (81.9%) |
249 (81.6%) |
0.382
|
|
Duration (years) |
12.0 (11.8) |
9.7 (9.1) |
8.4 (9.2) |
0.016
|
|
Race |
|
|
|
<0.001
|
|
African-American
|
36 (47%) |
118 (42%) |
56 (24%) |
|
|
Caucasian
|
11 (14%) |
99 (35%) |
151 (63%) |
|
|
Hispanic
|
29 (39%) |
65 (23%) |
31 (13%) |
|
|
RAPID3 |
13.7 (7.3) |
12.8 (7.2) |
9.6 (7.0) |
<0.001
|
|
Hx Smoking (N, %) |
25 (33.8%) |
91 (39.1%) |
45 (21.2%) |
<0.001
|
|
RF+ (N, %) |
57 (70.4%) |
152 (57.6%) |
94 (39.7%) |
<0.001
|
|
ACPA+ (N, %) |
41 (50.6%) |
99 (39.9%) |
50 (21.1%) |
<0.001
|
|
Hx Nodules (N, %) |
5 (8.1%) |
24 (11.9%) |
10 (5.8%) |
0.111
|
|
Hx Erosions (N, %) |
22 (33.8%) |
54 (25.2%) |
36 (19.7%) |
0.065
|
|
Prednisone (N, %) |
38 (39.2%) |
119 (37.2%) |
79 (25.8%) |
0.003
|
|
DMARD (N, %) |
73 (75.3%) |
234 (73.1%) |
215 (70.3%) |
0.560
|
|
Biologic (N, %) |
28 (28.9%) |
96 (30.0%) |
119 (38.9%) |
0.036
|
|
RAPID3 -3.6 (N, %) |
27 (27.8%) |
94 (29.4%) |
84 (27.5%) |
0.861
|
|
Response in 3M, (N, %) |
9 (9.3%) |
34 (10.6%) |
32 (10.5%) |
0.928
|
|
Response in 6M, (N, %) |
14 (14.4%) |
66 (20.6%) |
56 (18.3%) |
0.375
|
|
Response in 12M, (N, %) |
19 (19.6%) |
81 (25.3%) |
76 (24.8%) |
0.498
|
|
Average D RAPID3 Predicted from Model* |
0.2 (3.3) |
-0.5 (3.4) |
-0.6 (3.2) |
|
|
*Analysis of variance, adjusted for baseline RAPID3, age, race, disease duration |
||||
Disclosure:
S. Dowell,
Genentech and Biogen IDEC Inc.,
2,
Pfizer,
2,
Bristol-Myers Squibb,
2;
G. S. Kerr,
Genentech and Biogen IDEC Inc.,
2,
Bristol-Myers Squibb,
2,
Pfizer Inc,
2;
Y. Yazici,
Genentech and Biogen IDEC Inc.,
2,
Pfizer Inc,
2,
Bristol-Myers Squibb,
2,
Abbvie,
5,
Bristol-Myers Squibb,
5,
Celgene,
5;
C. Swearingen,
Genentech and Biogen IDEC Inc.,
2,
Pfizer Inc,
2,
Bristol-Myers Squibb,
2;
M. Quinones,
Genentech and Biogen IDEC Inc.,
2,
Pfizer Inc,
2,
Bristol-Myers Squibb,
2;
L. R. Espinoza,
Genentech and Biogen IDEC Inc.,
2,
Pfizer,
2,
Bristol-Myers Squibb,
2;
E. L. Treadwell,
Genentech and Biogen IDEC Inc.,
2,
Pfizer,
2,
Bristol-Myers Squibb,
2;
T. Lawrence-Ford,
Genentech and Biogen IDEC Inc.,
2,
Pfizer Inc,
2,
Bristol-Myers Squibb,
2,
Human Genome Sciences, Inc.,
2,
Abbvie,
2,
Eli Lilly and Company,
2,
Roche Pharmaceuticals,
2,
BMS,
9,
Questcor,
8,
Abbvie,
8,
UCB,
8,
Pfizer Inc,
8,
Amgen,
8,
Takeda,
8,
Actelion Pharmaceuticals US,
8;
Y. Sherrer,
Genentech,
2,
Pfizer Inc,
2,
Bristol-Myers Squibb,
2;
A. Mosley-WIlliams,
Genentech and Biogen IDEC Inc.,
2,
Pfizer Inc,
2,
Bristol-Myers Squibb,
2;
I. Garcia-Valladares,
Genentech and Biogen IDEC Inc.,
2,
Pfizer,
2,
Bristol-Myers Squibb,
2;
R. Perez Alamino,
Genentech and Biogen IDEC Inc.,
2,
Pfizer,
2,
Bristol-Myers Squibb,
2;
C. Luo,
None;
A. Ince,
Genentech and Biogen IDEC Inc.,
2,
Pfizer Inc,
2,
Bristol-Myers Squibb,
2;
A. Godoy,
None;
J. Amatruda,
None.
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