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Abstract Number: 1370

The Association of Body Mass Index (BMI) and Radiographic Progression of Joint Disease in Rheumatoid Arthritis (RA)

Christine K. Iannaccone1, Jing Cui2, K P Liao3, Jonathan S. Coblyn3, Michael Weinblatt4 and Nancy A. Shadick5, 1Department of Medicine, Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, MA, 2Rheumatology, Brigham and Womens Hospital, Boston, MA, 3Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, MA, 4Rheumatology, Brigham & Women's Hospital, Harvard Medical School, Boston, MA, 5Brigham and Women's Hospital/Harvard University, Cambridge, MA

Meeting: 2014 ACR/ARHP Annual Meeting

Keywords: body mass, joint damage and rheumatoid arthritis (RA)

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Session Information

Session Title: Rheumatoid Arthritis - Clinical Aspects (ACR): Comorbidities, Treatment Outcomes and Mortality

Session Type: Abstract Submissions (ACR)

Background/Purpose

Previous studies suggest that lower BMI is associated with progression of radiographic joint damage in RA but little is known about the biological role BMI plays in radiographic joint damage and research outcomes of the association have varied. Whether the association of BMI and radiographic joint damage may be mediated by disease activity variables is currently unknown. Using a cohort of RA patients, this study aims to examine the relationship between BMI and radiographic joint damage and disease activity.

Methods

We analyzed data from a longitudinal RA cohort study. The data collection included joint examinations, blood draws and patient reported outcome measures over 10 years. Hand and wrist radiographs were acquired at baseline and 2 years and scored by the van der Heijde-modified Sharp score method (vdHSs) (n=543). We created a dichotomous outcome variable for radiologic progression; defining patients with radiographic progression as having a change of ≥ 10 units in total vdHSs over two years. We conducted univariate analyses to assess predictors of radiographic joint damage progression that included age, gender, BMI group (underweight BMI <20kg/m2, normal BMI 20-24.9 kg/m2, overweight BMI 25-29.9 kg/m2, obese BMI ≥30kg/m2 (Baker et al, 2011)), DAS28-CRP4, anti-TNF use and anti-CCP status. For our primary analysis, we constructed a multivariate logistic regression model to study the effect between BMI and radiographic progression.

Results

We studied 543 patients with a mean age (SD) of 57.6 (12.7) years and a mean disease duration of 14.4 (12.2) years. Eighty-three percent were female and 68.3% were anti-CCP+; 69 (12.7%) of the patients had progression of joint damage. In the univariate analysis, BMI (group), anti-CCP+, and DAS28-CRP4 were all associated with radiographic joint damage, but age, gender and anti-TNF use did not show any association. The multivariate logistic regression analyses showed that patients who were underweight or normal weight had a significantly increased odds (OR=4.85, 95%CI 1.76-9.05; OR=3.99, 95%CI 1.76-9.05) of having radiographic progression compared to patients who were obese. Having a higher DAS28-CRP4 score was associated with greater odds of having radiographic joint damage (Table).

Conclusion

We found that lower BMI was associated with radiographic joint damage progression in RA, independent of disease activity. Further work is necessary to understand the biological role BMI plays in radiographic joint damage progression, as well as the involvement of inflammation in the relationship between BMI and progression of joint disease in RA. 

Association of BMI and radiologic progression of joint disease in RA

Multivariate Logistic Regression Model*

Odds Ratios

Confidence Intervals

BMI (underweight vs. Obese)

4.85

1.34-17.53**

BMI (Normal vs. Obese)

3.99

1.76-9.05

BMI (Overweight vs. Obese)

1.65

0.68-4.02

DAS28-CRP4 (continuous)

1.28

1.08-1.51

Anti-CCP Positive

1.85

0.96-3.57

*adjusted for age and gender

**test for trend of BMI group and radiologic progression p=0.0006


Disclosure:

C. K. Iannaccone,
None;

J. Cui,
None;

K. P. Liao,
None;

J. S. Coblyn,

CVS caremark,

5;

M. Weinblatt,

BMS, UCB, Crescendo Bioscience,

2,

Medimmune, AstraZeneca, Amgen, Abbvie, BMS, Crescendo Bioscience, Lilly, Pfizer, UCB, Roche,

5;

N. A. Shadick,

Crescendo Bioscience,

2,

Amgen,

2,

UCB,

2,

Abbvie,

2,

Bristol Myers Squibb,

2,

Genentech ,

2.

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