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Radiographic joint damage in early rheumatoid arthritis is highly dependent on body mass index

✍ Scribed by Gisela Westhoff; Rolf Rau; Angela Zink


Publisher
John Wiley and Sons
Year
2007
Tongue
English
Weight
87 KB
Volume
56
Category
Article
ISSN
0004-3591

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✦ Synopsis


Abstract

Objective

To investigate the association between body mass index (BMI) and radiographic joint damage (using the Ratingen Score [RS]) in early rheumatoid arthritis (RA).

Methods

The study was carried out in 767 patients with early RA. Standard clinical data, RS, and BMI were evaluated at baseline and after 3 years. Multivariate logistic regression analyses were performed in rheumatoid factor (RF)–positive and RF‐negative patients to determine the influence of BMI (<25 versus ≥30 kg/m^2^) on considerable joint damage (RS ≥7) after 3 years, adjusting for sex, age, disease duration, and disease activity (using the Disease Activity Scale in 28 joints [DAS28]).

Results

Patients of normal weight already had significantly more joint damage at study entry than obese patients (mean RS 4.5 versus 2.4; P = 0.004) and experienced significantly more progression than obese patients (RS 3.4 versus 1.3; P = 0.011). At 3 years, their RS score was twice as high as that of the obese patients (7.5 versus 3.7; P < 0.001). Multivariate regression analyses in both serologic groups revealed significantly higher odds of RS ≥7 in RF‐positive patients of normal weight than in RF‐positive obese patients (odds ratio [OR] 3.3), but not in RF‐negative patients. Male sex (OR 1.6), osteoporosis (OR 2.0), C‐reactive protein levels >15 mg/liter versus <5 mg/liter (OR 2.6), and disease activity (DAS28 ≥5.1 versus <3.2; OR 1.9) were independently associated with RS ≥7.

Conclusion

BMI provides a risk estimate of joint damage in RA patients. Further studies are needed to elucidate the association between BMI, RF, and joint damage in RA and the possible role of adipose tissue.


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## Objective Recent evidence has highlighted a major genetic contribution to radiographic damage in rheumatoid arthritis (RA). The objective of this study was to determine whether genetic variants in the loci for interleukin-1 (IL-1), IL-6, IL-10, protein tyrosine phosphatase N22 (PTPN22), and sele