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RA Population (ra + population)
Selected AbstractsOutcomes generated by patients with rheumatoid arthritis: how important are they?MUSCULOSKELETAL CARE, Issue 3 2005Sarah Hewlett PhD MA RGN Arc Senior Lecturer Abstract Background: It has been shown previously that patients with rheumatoid arthritis (RA) can generate a wide range of outcomes that they consider important in treatment. It is not known if these outcomes are generally important in the wider RA patient community. Objectives: (1) To examine whether recent patient-generated outcomes are generalizable within a wider RA population; (2) to assess the relative importance of each outcome; and(3) to explore whether any important outcomes have been omitted. Methods: A questionnaire, listing 23 outcomes previously generated by RA patients, was distributed through three rheumatology centres in the UK. Patients gave an importance score to each outcome (0,3), selected their top three most important outcomes, and then listed any outcomes of personal importance that were missing. Results: 323 questionnaires were returned (65%). All outcomes were deemed important. Independence, pain, and mobility were most frequently selected by patients in their top three outcomes but were not chosen by 61,66% of patients. The next most commonly chosen outcomes related to feeling well and fatigue. Factor analysis revealed six reasonably distinct groupings: general well-being (11.9% explained variance), day-to-day functioning(10.6%), emotional and psychological well-being (10.6%), social role and confidence (10%), physical symptoms (9.5%) and medication issues (7.9%). Conclusion: Outcomes generated by patients as important in RA, are generalizable and inclusive. The most important (independence, pain and mobility) are routinely treated and measured. The next most important (feeling well, fatigue) are infrequently addressed and deserve urgent consideration for measurement, treatment and research. Copyright © 2005 John Wiley & Sons, Ltd. [source] Could accelerated aging explain the excess mortality in patients with seropositive rheumatoid arthritis?ARTHRITIS & RHEUMATISM, Issue 2 2010Cynthia S. Crowson Objective To determine whether the mortality pattern in patients with seropositive rheumatoid arthritis (RA) is consistent with the concept of accelerated aging, by comparing the observed mortality rates in patients with RA with the age-accelerated mortality rates from the general population. Methods A population-based inception cohort of patients with seropositive RA (according to the American College of Rheumatology 1987 criteria) was assembled and followed up for vital status until July 1, 2008. The expected mortality rate was obtained by applying the death rates from the general population to the age, sex, and calendar year distribution of the RA population. The observed mortality was estimated using Kaplan-Meier methods. Acceleration factors for the expected mortality were estimated in accelerated failure time models. Results A total of 755 patients with seropositive RA (mean age 55.6 years, 69% women) were followed up for a mean of 12.5 years, during which 315 patients died. The expected median survival was age 82.4 years, whereas the median survival of the RA patients was age 76.7 years. Results of statistical modeling suggested that, in terms of mortality rates, patients with RA were effectively 2 years older than actual age at RA incidence, and thereafter the patients underwent 11.4 effective years of aging for each 10 years of calendar time. Conclusion The overall observed mortality experience of patients with seropositive RA is consistent with the hypothesis of accelerated aging. The causes of accelerated aging in RA deserve further investigation. [source] Genetic analysis of collagen-induced arthritis in rats: a polygenic model for rheumatoid arthritis predicts a common framework of cross-species inflammatory/autoimmune disease lociIMMUNOLOGICAL REVIEWS, Issue 1 2001Marie M. Griffiths Summary: Collagen-induced arthritis (CIA) is a useful model for dissecting the genetic patterns underlying susceptibility to rheumatoid arthritis (RA) and related chronic/inflammatory autoimmune diseases. CIA exhibits three phenotypes characteristic of autoimmune disease pathogenesis: abnormal levels of immune reactivity to self antigens; chronic inflammation of target organs expressing that specific autoantigen; activation and direct participation of invading mononuclear cells and resident tissue fibroblasts in organ damage. Over 25 different quantitative trait loci (QTL) regulating arthritis severity and autoantibody in rats with CIA are mapped. QTL-congenic strains show that certain CIA,QTLs can modulate arthritis independently. These monogenic models are proving to be highly informative for fine mapping and function studies, revealing gender effects and evidence of gene clusters. Recent genome scans of RA populations identified RA-susceptibility loci in chromosome regions homologous to rat chromosomal segments housing CIA,QTLs. Also, CIA,QTLs frequently co-localize with susceptibility QTLs mapped in other rat arthritis models induced with non-immunogenic adjuvant oils and/or in rat autoimmune models of multiple sclerosis and diabetes. Common autoimmunity genes and inflammation genes important to several human diseases are likely being detected in the various rat disease models. Continued dissection of the genetic underpinnings of rat arthritis models should provide candidate genes for investigation in human patients and lead to a clearer understanding of the complex genetics of RA. [source] Rheumatoid arthritis association with the FCRL3 ,169C polymorphism is restricted to PTPN22 1858T,homozygous individuals in a Canadian populationARTHRITIS & RHEUMATISM, Issue 12 2006William G. Newman Objective Variants in genes encoding the Fc receptor,like 3 (FcRL-3) and the class II major histocompatibility complex (MHC) transactivator proteins have been associated with an increased risk of rheumatoid arthritis (RA) in Japanese and Nordic populations, respectively. The aim of this study was to investigate these associations in a Canadian Caucasian cohort of RA cases and healthy controls. Methods A total of 1,187 RA patients and 462 healthy controls were genotyped for FCRL3 and MHC2TA gene variants associated with RA. Epistasis between the FCRL3 ,169C and the PTPN22 1858T variants was also examined. Results An association was detected between RA and both the FCRL3 ,169C allele (OR 1.19, P = 0.023) and the homozygous genotype (OR 1.41, P = 0.027), but association of the MHC2TA promoter region variant (,168G) with RA was not replicated. Stratification of the RA cohort by PTPN22 genotypes revealed the FCRL3 risk variant and RA association was stronger in the patient subgroup lacking PTPN22 1858T variants (P = 0.004) and was not detectable in the subgroup with PTPN22 1858T variants (P = 0.52). The PTPN22 association with RA was greater in the absence than in the presence of the FCRL3 ,169C allele (P = 0.0008 versus P = 0.001). The PTPN22 1858T variant also increased the risk of autoimmune thyroid disease (AITD) in the RA patients, whereas the FCRL3 risk variant was protective against AITD. Conclusion Our findings support an association of RA with an FCRL3 functional polymorphism and reveal that this association is stronger in the absence of PTPN22 risk genotypes. These findings support a genetic heterogeneity across RA populations, suggesting that both the FCRL3 and PTPN22 genes play roles in RA susceptibility, but in different individuals. [source] | ||||||||||