Anthropometric Measures and Risk of Rheumatoid Arthritis in the French E3N Cohort Study.

Carine Salliot,Raphaèle Seror,Marie-Christine Boutron-Ruault,Xavier Mariette,Yann Nguyen

doi:10.3390/nu14050934

Abstract

We aimed to assess the relationships between anthropometric measures and risk of rheumatoid arthritis (RA). The E3N cohort included 98,995 women (aged 40–65 years at the recruitment) who completed mailed questionnaires on reproductive factors, lifestyle, and health-related information, including anthropometric measures, every 2–3 years. Cox proportional hazards regression models with age as the time scale and adjusted on known RA risk factors were used to estimate hazard ratios (HRs) and 95% confidence intervals for the risk of incident RA in the overall population (n = 78,452) and after stratification on smoking exposure. Incident RA diagnosis was validated in 698 women. Abdominal obesity (waist circumference >88 cm) was associated with RA (HR = 1.2 (1.0–1.5)), independent of BMI; whereas obesity, defined as BMI ≥ 30 kg/m2, was marginally associated with RA (HR = 1.26 (0.9–1.5), ptrend = 0.0559). Taking lean body shape (BS) as reference, medium BS at puberty (HR = 1.3 (1.0–1.7)) and medium-large BS at perimenopausal period (HR = 1.5 (1.1–1.9)) were associated with the risk of RA among never-smoker women, independent of BMI. Regarding BS trajectory, taking constantly lean BS as reference, constantly large BS from puberty to perimenopause was associated with RA among non-smokers (HR = 2.10 (1.2–3.6)), independent of BMI.

Highlights

Publisher’s Note: MDPI stays neutralRheumatoid arthritis (RA) is the most common inflammatory rheumatic disease
Some alleles of HLA-DRB1 are associated with the development of a subset of rheumatoid arthritis (RA) characterized by presence of ACPA [2]
HRs: hazard ratios; 95% confidence intervals (95% CIs): 95% confidence interval; Ref: reference

Summary

Introduction

Publisher’s Note: MDPI stays neutralRheumatoid arthritis (RA) is the most common inflammatory rheumatic disease. Both environmental and genetic factors are involved in its pathophysiology. They interact in the pathogenesis by triggering autoimmunity [1]. Some alleles of HLA-DRB1 (so called shared epitope) are associated with the development of a subset of RA characterized by presence of ACPA (auto-antibodies directed against the citrullinated peptide) [2]. These autoantibodies could be detected years before RA onset (so called preclinical stage). Active smoking has been reproducibly and strongly associated with an increased risk of ACPA-positive RA, especially in individuals carrying the shared epitope [1,2]

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