Session Information
Session Type: Abstract Submissions (ACR)
Background/Purpose: Although the etiology of rheumatoid arthritis (RA) is unknown, there are reported interactions of genetic and environmental factors. Tobacco exposure is a well-documented risk factor, both in Caucasian and African American (AA) RA cohorts for disease susceptibility and severity. Yet there are no data addressing the association of tobacco use with RA-phenotypic expression, particularly within multi-ethnic cohort, specifically Hispanic patients. We examined the association of tobacco exposure and RA phenotype in a diverse ethnic RA cohort.
Methods: Patients enrolled in EMRAC, with baseline demographics data (age, gender, tobacco use), RA disease status (severity [RF, ACPA, nodules, erosions], activity [TJC, SJC, ESR, CRP, CDAI, DAS28, RAPID3], and extra-articular manifestations) were available for analysis. Smoking status was categorized as current, former, or never use. Comparisons of RA-features with smoking status between ethnic groups were analyzed using Cochran-Mantel-Haenzel test. Any association between tobacco exposure and clinical disease activity measures and outcomes were estimated using logistic regression adjusting for race (Caucasian vs. Non-Caucasian), age and disease duration.
Results: Of 861 EMRAC patients available for analysis, the mean age was 56.3 (sd 13.5) years, and disease duration 10.2 (sd 10.1) years. 405 (47%) were Caucasians, 287 (33%) AA and 169 (20%) Hispanics. Erosions were reported in 10%, predominantly in AA (25%). Only 20% reported tobacco use (ever), and exposure was not associated with disease activity [high CDAI score: non-smokers (49%) vs. former (53%) and current smokers (62%) (p=0.253); high DAS 28 score: non-smokers (61%) vs. former (62%) and current smokers (78%) (p=0.205); high RAPID3: non-smokers (74%) vs. former (75%) and current smokers (75%) (p=0.713)] or frequency of extra-articular disease in the cohort.
Smoking ever (former or current) was associated with erosive disease, adjusting for ethnic groups (p=0.002). Smoking ever had a 144% increase in odds of having erosions compared to never smoking (OR=2.44, p=0.003), and non-Caucasians had 638% increase in odds for erosions compared to Caucasians (OR=7.38, p<0.001) in a multiple logistic regression adjusting for disease duration, age and disease activity (Table).
Conclusion: In a diverse ethnic RA cohort, cigarette smoking and non-Caucasian ethnicity were independently associated with higher risk of erosive disease. While further studies are developed to better understand the relationship of tobacco exposure and RA, more aggressive anti-smoking efforts and counseling, as well as more aggresive RA therapy, appears warranted in ethnic minorities with the disease.
Table: Multiple Logistic Regression Model (Dependent Variable: Erosion)
|
Variables
|
OR (95% CI)
|
p
|
|
Smoking (Reference=Never)
|
2.44 (1.34-4.39)
|
0.003
|
|
Race (Reference=White)
|
7.38 (3.44-18.04)
|
<0.001
|
|
Disease duration (years)
|
1.05 (1.03-1.08)
|
<0.001
|
|
Age (years)
|
1.01 (1.00-1.04)
|
0.142
|
|
RAPID3
|
0.97 (0.93-1.01)
|
0.100
|
Disclosure:
R. Perez Alamino,
None;
L. R. Espinoza,
None;
G. S. Kerr,
Genentech and Biogen IDEC Inc., 2, Pfizer Inc, 2, Bristol Myers Squibb, 2,
2;
C. Swearingen,
None;
C. Luo,
None;
Y. Yazici,
BMS, Genentech, Celgene, 2, Abbvie, Pfizer, UCB Pharma, 5,
2;
Y. R. S. Sherrer,
UCB, lilly, GSK, Astrazeneca,
2,
AspraZeneca, GSK, Amgen, Pfizer,
8;
E. L. Treadwell,
None;
A. D. Mosley-Williams,
None;
S. Dowell,
None;
I. Garcia-Valladares,
None;
T. Lawrence-Ford,
Amgen, Pfizer, UCB, Abbvie, Takeda.GSK,
8;
A. Godoy,
None;
A. Ince,
None;
C. Flower,
None.
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