Body Mass Index and Risk of Rheumatoid Arthritis

Feng, Jian; Chen, Qi; Yu, Feifei; Wang, Zhiyong; Chen, Shuqi; Jin, Zhichao; Cai, Qing; Liu, Yu; He, Jia

doi:10.1097/md.0000000000002859

Cited by 77 publications

(37 citation statements)

References 32 publications

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“…Obesity is one of the described risk factors for the development of RA and it negatively affects disease activity and treatment outcomes [ 3 , 4 , 7–9 ]. Although it has been shown that bariatric surgery–induced weight loss results in decreased disease activity and improved response to treatment, the effect of bariatric surgery on the incidence of RA is not known [ 14 ].…”

Section: Discussionmentioning

confidence: 99%

“…Several factors have been identified that represent a risk for the development of RA, including female sex, genetic predisposition and smoking [ 2 ]. Large meta-analyses have also shown that obesity is among the risk factors for the development of RA, especially among women [ 3–6 ]. Moreover, in subjects with RA, obesity is associated with higher disease activity and lower chance to achieve sustained remission [ 7–10 ].…”

Section: Introductionmentioning

confidence: 99%

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Bariatric surgery and the incidence of rheumatoid arthritis – a Swedish Obese Subjects study

et al. 2019

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Objective The aim of this study was to determine the effect of bariatric surgery on the incidence of RA in participants of the Swedish Obese Subjects (SOS) study. Methods The SOS is a longitudinal study aiming to assess the effect of bariatric surgery on mortality and obesity-related diseases. This report includes 2002 subjects with obesity who underwent bariatric surgery and 2034 matched controls; none of them had RA at baseline. Cases of incident RA were identified through the Swedish National Patient Register by searching for International Classification of Diseases codes. Both intention-to-treat analyses and per-protocol analyses are reported. In the per-protocol analysis, participants from the control group who underwent bariatric surgery later on during follow-up were censored at the time of surgery. Results During follow-up, 92 study participants developed RA. The median follow-up was 21 years (range 0–29). Bariatric surgery was neither associated with the incidence of RA in the intention-to-treat analysis [hazard ratio (HR) 0.92 (95% CI 0.59, 1.46), P = 0.74], nor in the per-protocol analysis [HR 0.86 (95% CI 0.54, 1.38), P = 0.53]. Weight change at the 2 year follow-up, expressed as the change in BMI compared with baseline, did not associate with the development of RA. Higher serum CRP levels and smoking associated with the future development of RA independent of other factors. Conclusions We did not detect any association between bariatric surgery and the incidence of RA in subjects affected by obesity followed up for up to 29 years. ClinicalTrials.gov (http://clinicaltrials.gov): NCT01479452.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Bariatric surgery and the incidence of rheumatoid arthritis – a Swedish Obese Subjects study

et al. 2019

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“…Wnt5a is markedly upregulated in visceral adipose tissue (VAT) and correlates strongly with indices of inflammation and diabetes mellitus [10, 51]. Despite the existence of “rheumatoid cachexia” in late-stage disease, large scale meta-analysis reveals that obesity is a risk factor for RA that is associated with disease severity [52, 53]. It has been proposed that adipokines, cytokines secreted by adipose tissue, are molecular drivers of both diseases [52, 54].…”

Section: Discussionmentioning

confidence: 99%

Genetic deficiency of Wnt5a diminishes disease severity in a murine model of rheumatoid arthritis

et al. 2017

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BackgroundRheumatoid arthritis (RA) is a common autoimmune disease characterized by chronic inflammation of the joints, leading to bone erosion and joint dysfunction. Despite the recent successes of disease-modifying anti-rheumatic drugs (DMARDs), there is still clinical need for understanding the development and molecular etiology of RA. Wnts are developmental morphogens whose roles in adult pathology are poorly characterized. Wnt5a is a member of the non-canonical family of Wnts that modulates a wide range of cell processes, including differentiation, migration, and inflammation. Wnt5a has been implicated as a possible contributor to arthritis and it is upregulated in synovial fibroblasts from RA patients.MethodsWe investigated the role of endogenous Wnt5a in RA. Tamoxifen-inducible, Wnt5a knockout (Wnt5a cKO) mice and littermate controls were monitored for arthritis development and joint pathology using the K/BxN serum transfer-induced arthritis (STIA) model. To explore a role of Wnt5a in osteoclast fusion, bone marrow-derived monocytes (BMDMs) were differentiated in vitro.ResultsWnt5a cKO mice were resistant to arthritis development compared to control littermates as assessed by ankle thickness and histologic measurements. Some parameters of inflammation were reduced in the Wnt5a cKO mice, including the extent of polymononuclear cell infiltration and extra-articular inflammation. Wnt5a cKO mice also exhibited less cartilage destruction and a reduction in osteoclast activity with concomitant reduction in tartrate-resistant acid phosphatase (TRAP), cathepsin K (CTSK), macrophage colony-stimulating factor (MCSF), matrix metalloproteinase (MMP)2 and MMP9 in the arthritic joints. Treatment of BMDMs with Wnt5a enhanced osteoclast fusion and increased the expression of dendrocyte-expressed seven transmembrane protein (DCSTAMP) and MMP9, that are necessary for osteoclast formation and activity.ConclusionsThese data suggest that Wnt5a modulates the development of arthritis by promoting inflammation and osteoclast fusion, and provide the first mouse genetic evidence of a role for endogenous Wnt5a in autoimmune disease.Electronic supplementary materialThe online version of this article (doi:10.1186/s13075-017-1375-0) contains supplementary material, which is available to authorized users.

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“…We dichotomized BMI <25 vs. ≥25 kg/m 2 based on the World Health Organization definition of normal vs. overweight/obese [15], as well as literature supporting this as a clinically important cutoff for RA risk [10, 11, 17, 44, 45]. Subjects were also cross-classified into four groups according to their BMI (<25 vs. ≥25 kg/m 2 ) and ACPA status (<2 vs. ≥2 subtypes).…”

Section: Methodsmentioning

confidence: 99%

“…Recent meta-analyses of BMI’s effect on RA risk reported that BMI ≥25 kg/m 2 (the World Health Organization definition of overweight/obese) significantly increased RA risk by 15%, compared to BMI <25 kg/m 2 ; BMI ≥30 kg/m 2 (obesity) significantly increased RA risk by 21% to 31% compared to normal BMI [15-17]. Obesity may increase RA risk via systemic inflammation, as adipose tissue secretes pro-inflammatory adipokines [18].…”

Section: Introductionmentioning

confidence: 99%

Elevated BMI and antibodies to citrullinated proteins interact to increase rheumatoid arthritis risk and shorten time to diagnosis: A nested case–control study of women in the Nursesʼ Health Studies

Tedeschi

Cui

Arkema

et al. 2017

Seminars in Arthritis and Rheumatism

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Objective Overweight/obesity and anti-citrullinated protein antibodies (ACPA) increase RA risk. We investigated the relationship between body mass index (BMI) and ACPA, tested for an interaction between BMI and ACPA for RA risk, and examined effects of BMI and ACPA on time to RA diagnosis. Design Within the Nurses’ Health Studies, blood samples were collected before diagnosis from medical record-confirmed incident RA cases and matched controls. Multiplex assays measured seven ACPA subtypes (biglycan, clusterin, enolase, fibrinogen, histone 2A, histone 2B, vimentin). Logistic regression analyses tested the association of BMI and ACPA and for a multiplicative interaction between BMI groups (≥25 vs. <25 kg/m2) and ACPA positivity (≥2 vs. <2 subtypes), adjusting for age, smoking, alcohol use, and HLA-shared epitope. In case-only analyses, log-rank tests compared time from blood draw to RA onset by cross-classified BMI/ACPA status. Results Among 255 pre-RA cases and 778 matched controls, 15.7% vs. 2.1% (p<0.001) had ≥2 ACPA and 49.4% vs. 40.2% (p<0.01) were overweight/obese. Continuous BMI was not associated with presence of ≥2 ACPA (OR per kg/m2 unit BMI: 1.03 [95% CI 0.97-1.09]). However, there was a multiplicative interaction between elevated BMI and presence of ≥2 ACPA for RA risk (p=0.027). Women with BMI ≥25 kg/m2 and ≥2 ACPA had OR 22.7 (95% CI [6.64-77.72]) for RA. Median time to RA differed by BMI/ACPA group (overall log-rank p<0.001) and was shortest among women with ≥2 ACPA and BMI ≥25 kg/m2 (45.0 months, IQR [17.5-72.5]) and longest in women with <2 ACPA and BMI <25 kg/m2 (125.0 months, IQR [72.0-161.0]) (pairwise log-rank p=0.002). Conclusion Elevated BMI and presence of ACPA interacted to increase RA risk. Time to RA onset was shortest among overweight/obese women with ≥2 ACPA.

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Body Mass Index and Risk of Rheumatoid Arthritis

Cited by 77 publications

References 32 publications

Bariatric surgery and the incidence of rheumatoid arthritis – a Swedish Obese Subjects study

Bariatric surgery and the incidence of rheumatoid arthritis – a Swedish Obese Subjects study

Genetic deficiency of Wnt5a diminishes disease severity in a murine model of rheumatoid arthritis

Elevated BMI and antibodies to citrullinated proteins interact to increase rheumatoid arthritis risk and shorten time to diagnosis: A nested case–control study of women in the Nursesʼ Health Studies

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