Corresponding author: V. Michael Holers, MD, Division of Rheumatology, University of Colorado at Denver and Health Sciences Center, Barbara Davis Center, 1775 North Ursula Street, Aurora, Colorado 80045, Phone: (303) Fax: (303) 724-7581, Michael.Holers@uchsc.edu. Address for reprint requests: Same as above * These two authors contributed equally to the study. COMPETING INTERESTSThe authors declare that they have no competing interests. AUTHORS' CONTRIBUTIONSDM participated in the design and analysis of this study and the writing of this manuscript. KD participated in the analysis of data and preparation of manuscript. LP participated in the analysis of samples and data and preparation of manuscript. AB and AL contributed statistical expertise in the analysis of data for this manuscript. CW participated in subject evaluation and determination of eligibility for this study MR participated in the design of this study and procurement of the serum samples for analysis WG participated in the design of this study and procurement of the serum samples for analysis, as well as subject evaluation and determination of eligibility for this study. JN participated in the design and analysis of this study and preparation of manuscript. VMH participated in the design and analysis of this study, antibody testing, and manuscript preparation. DISCLAIMERThe views expressed in this abstract are those of the authors and do not reflect the official policy of the Department of the Army, Department of Defense, or U.S. Government.The Corresponding Author has the right to grant on behalf of all authors and does grant on behalf of all authors, an exclusive license (or non-exclusive for government employees) on a worldwide basis to the BMJ Publishing Group Ltd and its Licensees to permit this article to be published in Annals of Rheumatic Diseases editions and any other BMJPGL products to exploit all subsidiary rights, as set out in our license http://ard.bmjjournals.com/ifora/licence.pdf. Objectives-This study investigated factors that may influence the prevalence and timing of appearance of rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) antibodies during the pre-clinical phase of rheumatoid arthritis (RA) development. NIH Public AccessMethods-243 serial pre-diagnosis serum samples from 83 subjects with RA were examined for the presence of RF and anti-CCP antibodies.Results-57% and 61% of subjects had at least one pre-diagnosis sample positive for RF or anti-CCP, respectively. Gender and race were not significantly associated with the prevalence or timing of pre-clinical antibody appearance. Pre-clinical anti-CCP positivity was strongly associated with the development of erosive RA (OR 4.64; 95% CI 1.71-12.63; p=0.003), but RF was not (p=0.11). Additionally, as age at the time of diagnosis of RA increased the duration of pre-diagnosis antibody positivity for RF and anti-CCP increased, with the longest duration of preclinical antibody positivity seen in patients diagnosed with RA over the age of 40. In ...

The FFQ shows mostly good agreements with multiple 24-hour recalls and biomarkers in preschool children. In addition, the validity of the FFQ using parental report does not appear to be compromised when there are meal providers in addition to the parents.

Objective. To determine whether shared epitope (SE)-containing HLA-DRB1 alleles are associated with rheumatoid arthritis (RA) in African Americans and whether their presence is associated with higher degrees of global (genome-wide) genetic admixture from the European population.Methods. In this multicenter cohort study, African Americans with early RA and matched control subjects were analyzed. In addition to measurement of serum anti-cyclic citrullinated peptide (anti-CCP) antibodies and HLA-DRB1 genotyping, a panel of >1,200 ancestry-informative markers was analyzed in patients with RA and control subjects, to estimate the proportion of European ancestry.Results. The frequency of SE-containing HLA-DRB1 alleles was 25.2% in African American patients with RA versus 13.6% in control subjects (P ‫؍‬ 0.00005). Of 321 patients with RA, 42.1% had at least 1 SEcontaining allele, compared with 25.3% of 166 control subjects (P ‫؍‬ 0.0004). The mean estimated percent European ancestry was associated with SE-containing HLA-DRB1 alleles in African Americans, regardless of disease status (RA or control). As reported in RA patients of European ancestry, there was a significant association of the SE with the presence of the anti-CCP antibody: 86 (48.9%) of 176 patients with anti-CCP antibody-positive RA had at least 1 SE allele, compared with 36 (32.7%) of 110 patients with anti-CCP antibodynegative RA (P ‫؍‬ 0.01, by chi-square test).Conclusion. HLA-DRB1 alleles containing the SE are strongly associated with susceptibility to RA in African Americans. The absolute contribution is less than that reported in RA among populations of European ancestry, in which ϳ50-70% of patients have at least 1 SE allele. As in Europeans with RA, the SE association was strongest in the subset of African American patients with anti-CCP antibodies. The finding of a higher degree of European ancestry among African

Objective. To examine the association of treatment response and disease duration with changes in rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) antibody levels among patients with rheumatoid arthritis (RA).Methods. The study sample included 66 RA patients who completed double-blind, randomized clinical protocols and for whom baseline and followup serum samples were available. Anti-CCP and RF levels were measured using commercially available assay kits. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were used to describe the association of response and disease duration with declines in antibody levels.Results. Patients had a mean ؎ SD age of 49.9 ؎ 12.0 years and were predominantly female (n ‫؍‬ 51; 77%). The mean ؎ SD duration between the times at which the baseline and followup serum samples were obtained was 13.7 ؎ 8.6 months. Among the 64 subjects with positive antibody at baseline, 33 (52%) experienced a >25% reduction in the anti-CCP antibody level during the course of treatment, and 35 patients (55%) had a >25% reduction in RF. After adjustment for the baseline anti-CCP antibody level, only a shorter disease duration (<12 months) was significantly associated with a decline in the level of anti-CCP antibody (OR 3.0, 95% CI 1.0-8.8), and no association with treatment response was observed. Conversely, treatment response was the only significant determinant of a decrease in RF levels (OR 3.6, 95% CI 1.2-10.4).Conclusion. Shorter disease duration predicts greater declines in anti-CCP antibody levels with treatment in RA. Although treatment response is a robust determinant of a decrease in RF, it does not appear to be associated with declines in the anti-CCP antibody level.

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