Body Mass Index and Clinical Response to Infliximab in Rheumatoid Arthritis

被引:162
作者
Klaasen, Ruth [1 ]
Wijbrandts, Carla A. [1 ]
Gerlag, Danielle M. [1 ]
Tak, Paul P. [1 ]
机构
[1] Univ Amsterdam, Acad Med Ctr, Div Clin Immunol & Rheumatol, NL-1105 AZ Amsterdam, Netherlands
来源
ARTHRITIS AND RHEUMATISM | 2011年 / 63卷 / 02期
关键词
TUMOR-NECROSIS-FACTOR; RADIOGRAPHIC JOINT DAMAGE; C-REACTIVE PROTEIN; INFLAMMATION; ASSOCIATION; CRITERIA; ADIPOCYTOKINES; ADIPONECTIN; DESTRUCTION; VALIDATION;
D O I
10.1002/art.30136
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective. Adipose tissue has immunomodulating effects in rheumatoid arthritis (RA), although the exact role is, at present, unclear. The purpose of this study was to determine whether body mass index (BMI) affects response to infliximab in RA patients investigated prospectively. Methods. In 89 patients with active RA, the BMI was calculated before initiation of infliximab treatment (3 mg/kg intravenously). After 16 weeks of treatment, changes in disease activity were assessed with the Disease Activity Score in 28 joints (DAS28). Results. The mean +/- SD BMI was 26 +/- 5 kg/m(2) (range 17-42). The BMI correlated positively with the DAS28 at baseline (r = 0.34, P = 0.001). Since selection of study patients according to DAS28 values could influence the clinical response to tumor necrosis factor (TNF) blockade due to regression to the mean because the clinical response is itself based on the change in the DAS28 values, analysis of covariance was used to correct for the baseline DAS28. A highly significant, negative association between the BMI and the absolute decrease in the DAS28 after 16 weeks (P = 0.001) was found also when adjusted for anti-citrullinated protein antibodies. Conclusion. Although the infliximab dosage is based on body weight, RA patients with a high BMI responded less well to infliximab, a finding that held true when adjusted for the baseline DAS28 or anti-citrullinated protein antibody status. These results support the notion that adipose tissue may be involved in the pathophysiology of RA and could have implications for other immune-mediated inflammatory conditions treated with TNF antagonists.
引用
收藏
页码:359 / 364
页数:6
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