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1.
Mark J. Harrison Tracey M. Farragher Alexandra M. Clarke Stephanie C. Manning Diane K. Bunn Deborah P. M. Symmons 《Arthritis care & research》2009,61(10):1297-1304
Objective
To describe the relationship between baseline area‐ and person‐level social inequalities and functional disability at 3 years in patients with early inflammatory polyarthritis (IP).Methods
A total of 1,393 patients with new‐onset IP were recruited and allocated an Index of Multiple Deprivation (IMD) 2004 score based on their area of residence, and a social class based on baseline self‐reported occupation. Differences in the Health Assessment Questionnaire (HAQ) score at baseline and 3 years by IMD or social class were tested. The mean 3‐year change in HAQ score was compared by IMD and social class, and interactions between these measures examined.Results
Patients from more deprived areas had poorer 3‐year HAQ outcome than those from less deprived areas (P = 0.019, adjusted for baseline HAQ score, age, sex, and symptom duration). The mean difference in HAQ change was most notable between the most deprived (IMD4) and least deprived areas (IMD1) (0.22; 95% confidence interval [95% CI] 0.11, 0.34). There was also a significant difference in HAQ score change between patients of the highest (SCI and II) and lowest social class (SCIV and V) (0.11; 95% CI 0.02, 0.20). For the mean (95% CI) 3‐year change in HAQ score, a significant interaction exists between IMD score and social class and their association with HAQ scores (P = 0.001) to modify outcome: IMD1/SC I and II ?0.23 (95% CI ?0.40, ?0.06) versus IMD 4/SC IV and V 0.15 (95% CI ?0.05, 0.34).Conclusion
Person‐ and area‐level inequalities combine to modify outcome for rheumatoid arthritis. A person's social circumstance and residential environment have independent effects on outcome and are not just alternative measures of the same exposure.2.
Tracey M. Farragher Mark Lunt Darren Plant Diane K. Bunn Anne Barton Deborah P. M. Symmons 《Arthritis care & research》2010,62(5):664-675
Objective
To compare the clinical utility of anti–cyclic citrullinated peptide (anti‐CCP) antibodies and rheumatoid factor (RF) testing in predicting both functional outcome and response to treatment in early inflammatory polyarthritis (IP) patients.Methods
A total of 916 IP subjects from a primary care incidence registry (1990–1994) had anti‐CCP antibody and RF status determined at baseline. Mean change in Health Assessment Questionnaire (HAQ) score between baseline and 5 years was compared by antibody status. The effect of treatment with disease‐modifying antirheumatic drugs and/or steroids over 5 years, early (<6 months of symptom onset) versus late initiation, and duration of treatment were also compared by anti‐CCP antibody status. The analysis was adjusted for treatment decisions and censoring over the followup, using marginal structural models.Results
Anti‐CCP antibody–positive patients (n = 268) had more severe disease both at presentation and 5 years of followup, and this was independent of RF. On adjustment, anti‐CCP antibody–negative patients treated early experienced a significant improvement in functional disability compared with anti‐CCP antibody–negative patients who were never treated (?0.31; 95% confidence interval [95% CI] ?0.53, ?0.08), and experienced additional benefit for each additional month of early treatment. Anti‐CCP antibody–positive patients treated early did not have a significant improvement in HAQ score compared with those not treated (?0.14; 95% CI ?0.52, 0.24).Conclusion
In this first observational study to examine the influence of anti‐CCP antibody status on treatment response, anti‐CCP antibody–positive IP patients showed less benefit from treatment, particularly early treatment, than anti‐CCP antibody–negative patients. This provides support for the inclusion of anti‐CCP antibodies as well as RF in the classification criteria for rheumatoid arthritis and for stratification by anti‐CCP antibody status in clinical trials.3.
Tracey M. Farragher Nicola J. Goodson Haris Naseem Alan J. Silman Wendy Thomson Deborah Symmons Anne Barton 《Arthritis \u0026amp; Rheumatology》2008,58(2):359-369
Objective
To examine the role of the variants of the PTPN22 and HLA–DRB1 genes as predictors of mortality in inflammatory polyarthritis (IP) and rheumatoid arthritis (RA).Methods
Patients were recruited from a primary care–based inception cohort of patients with IP and were followed up prospectively. For patients who died, the cause and date of death was obtained. Cox proportional hazards regression models were used to assess the association of the HLA–DRB1 (including the shared epitope [SE]) and PTPN22 genes with the risk of death from all causes and from cardiovascular disease (CVD) and to assess the interactions between SE, smoking, and anti–cyclic citrullinated peptide (anti‐CCP) status, adjusted by age at symptom onset and sex.Results
DNA samples were available from 1,022 IP patients. During followup, 751 of them (74%) satisfied the American College of Rheumatology 1987 criteria for RA, and 242 of them (24%) died. Carriage of 2 copies of SE alleles predicted death from all causes (hazard ratio [HR] 1.57 [95% confidence interval (95% CI) 1.1–2.2]) and from CVD (HR 1.68 [95% CI 1.1–2.7]). This effect was most marked for individuals with the HLA–DRB1*01/*04 combination. An interaction of smoking, SE alleles, and anti‐CCP antibodies was observed and was associated with the greatest risk of death from CVD (HR 7.81 [95% CI 2.6–23.2]). No association of the PTPN22 gene with mortality was detected.Conclusion
SE alleles, particularly compound heterozygotes, are associated with death from all causes and from CVD, independently of autoantibody status. However, the combination of SE, smoking, and anti‐CCP antibodies is associated with a high risk of premature death in patients with IP and RA, which raises the possibility of a targeted strategy to prevent CVD in these patients.4.
Sophia M. Naz Tracey M. Farragher Diane K. Bunn Deborah P. M. Symmons Ian N. Bruce 《Arthritis \u0026amp; Rheumatology》2008,58(4):985-989
Objective
To investigate the influence of age at symptom onset and length of followup on mortality in patients with recent‐onset inflammatory polyarthritis (IP), and to examine predictors of mortality in relation to disease duration.Methods
From 1990 to 1994, patients with recent‐onset IP were registered with the Norfolk Arthritis Register (NOAR) and followed up prospectively. Standardized mortality ratios (SMRs) were calculated for all‐cause and cardiovascular disease (CVD) mortality and for those who were younger than age 55 years at disease onset and for the first 5 and 10 years of followup. Cox proportional hazards models were developed to assess predictors of early and later mortality.Results
Of 1,098 patients, 224 (20%) had died by the end of 2004. All‐cause and CVD mortality were increased in rheumatoid factor (RF)–positive patients and in this subgroup, CVD mortality was increased at both early and later followup (SMR 5‐year followup 1.93 [95% confidence interval 1.08–3.19]; SMR 10‐year followup 2.00 [95% confidence interval 1.37–2.80]). CVD mortality was highest in seropositive patients <55 years of age at disease onset (SMR 5.58 [95% confidence interval 2.24–11.50]). In multivariate models, age at onset, male sex, RF positivity, Health Assessment Questionnaire score ≥1.5, and nodules were predictors of early and later mortality.Conclusion
Patients with IP had higher rates of CVD mortality throughout the followup period studied, and this was highest in seropositive patients who were <55 years of age at symptom onset. This subgroup deserves particular attention in terms of disease and risk factor modification. Nodules were independent predictors of CVD mortality, suggesting that extraarticular/vascular inflammation identifies patients at particularly high CVD risk.5.
Objective
It has been found that women with rheumatoid arthritis (RA) have a poorer prognosis than men. However, the impact of age at symptom onset is unclear. We investigated the relationship between these factors and functional disability in patients with recent‐onset inflammatory polyarthritis (IP).Methods
A total of 3,666 patients (66% women) were registered with the Norfolk Arthritis Register between 1990 and 2008. Functional disability was assessed using the Health Assessment Questionnaire (HAQ), adjusted for age at HAQ completion. Linear random‐effects models were used to examine HAQ score over time, by sex and age at symptom onset (early = age <55 years, late = age 55–74 years, very late = age ≥75 years).Results
Women had higher HAQ scores over time than men (mean difference 0.29; 95% confidence interval [95% CI] 0.25, 0.34). Men with late‐onset IP had lower baseline HAQ scores than men with early onset (mean difference ?0.14; 95% CI ?0.29, ?0.001). Women had comparable baseline HAQ scores at all ages of onset. Both sexes showed the greatest rate of disability progression in patients with very late onset. Those with early onset had a steady level of disability over time. Adjustment for treatment received, comorbidities, and RA subgroup analysis produced results that were largely similar to the initial analysis.Conclusion
Female patients have higher HAQ scores than male patients; patients with early symptom onset show the smallest sex difference. Older age at symptom onset is associated with an increasingly steep trajectory of disability progression. The impact of sex on outcome is evident at baseline, whereas the impact of age at symptom onset becomes apparent during long‐term followup.6.
M. Bukhari W. Thomson H. Naseem D. Bunn A. Silman D. Symmons A. Barton 《Arthritis \u0026amp; Rheumatology》2007,56(9):2929-2935
Objective
Anti–cyclic citrullinated peptide (anti‐CCP) antibodies are a stronger predictor of the severity of rheumatoid arthritis than is rheumatoid factor (RF). Their role in predicting outcome in unselected patients with new‐onset inflammatory polyarthritis (IP) has not been examined. The aims of this study were to examine the role of baseline RF and anti‐CCP antibodies in determining the likelihood of patients having erosions at presentation or in predicting future radiologic damage, and to determine whether anti‐CCP antibodies or RF is sufficiently robust to be clinically useful in guiding treatment decisions in early IP.Methods
Patients were recruited from the Norfolk Arthritis Register. Logistic regression models were fitted to test the ability of anti‐CCP antibodies and RF to predict erosions. Further models were investigated to examine the role of anti‐CCP antibodies in patients stratified by RF status.Results
The presence of anti‐CCP antibodies at baseline was strongly associated with both prevalent erosions (odds ratio [OR] 2.53 [95% confidence interval (95% CI) 1.48–4.30]) and developing erosions at 5 years (OR 10.2 [95% CI 6.2–16.9]). These ORs were higher than those for RF (OR 1.63 [95% CI 0.94–2.82] and OR 3.4 [95% CI 2.2–5.2], respectively). The likelihood ratio (LR) for the prediction of prevalent erosions and erosions at 5 years was highest in the RF−subgroup (LR 2.2 and 5.8, respectively). However, 27% of anti‐CCP−patients had developed erosions by 5 years.Conclusion
Despite their strong association with the presence, development, and extent of erosions, anti‐CCP antibodies alone are not a sufficiently accurate measure upon which to base clinical treatment decisions. Knowledge of anti‐CCP antibody status is most informative in RF−negative patients.7.
E. M. Camacho M. Lunt T. M. Farragher S. M. M. Verstappen D. K. Bunn D. P. M. Symmons 《Arthritis \u0026amp; Rheumatology》2011,63(8):2183-2191
Objective
Use of oral contraceptives (OCs) may prevent the development of rheumatoid arthritis, but the influence of OC use on disease outcome is unresolved. The purpose of this study was to examine functional outcome and OC use in women with inflammatory polyarthritis (IP).Methods
The Norfolk Arthritis Register (NOAR) is an inception cohort of patients with recent‐onset IP. We studied patient‐reported history of OC use in 663 women who were born after 1945 and who had not used OCs during followup. OC use during followup was additionally investigated in 265 women who were <50 years old and had not undergone menopause or hysterectomy during followup. All patients were recruited to the NOAR between 1990 and 2004. Functional ability was assessed using the Health Assessment Questionnaire (HAQ), with adjustment for age at symptom onset.Results
The median followup was 4.9 years. In the investigation analyzing OC use before symptom onset, patients who had used OCs before symptom onset had lower HAQ scores throughout followup than patients who had not taken OCs before symptom onset (difference in score at 5‐year followup −0.35; 95% confidence interval [95% CI] −0.51, −0.19). Patients who were taking OCs at baseline had lower HAQ scores over time than women who were not taking OCs at baseline but had previously done so (mean difference −0.21; 95% CI −0.40, −0.02). In the investigation analyzing OC use during followup, OC use during followup was associated with lower HAQ scores over time than no OC use during followup (mean difference −0.06; 95% CI −0.16, 0.03); however, this was only significant for women with moderate or severe functional disability at the previous assessment (mean difference −0.23; 95% CI −0.40, −0.07). Further adjustment for potential confounders and exclusion of hormone replacement therapy users had little impact.Conclusion
OC use is generally associated with a beneficial functional outcome in IP, and use before and at symptom onset appeared to have the most consistent benefit.8.
Jiunn‐Yih Wu Si‐Huei Lee Chih‐Jung Shen Yueh‐Che Hsieh Ping‐Hsiung Yo Hsiang‐Yun Cheng Rai‐Chi Chan Chien‐Chang Lee Shy‐Shin Chang 《Arthritis \u0026amp; Rheumatology》2012,64(9):3034-3042
Objective
To systematically review evidence of the accuracy of the procalcitonin test for diagnosis of bacterial infection in patients with autoimmune disease.Methods
The major databases Medline, EMBase, and the Cochrane Library were searched for studies published between January 1966 and October 2011 that evaluated procalcitonin, alone or in comparison with other laboratory markers such as C‐reactive protein (CRP), as a diagnostic marker for bacterial infection in patients with autoimmune disease and provided sufficient data to permit construction of 2 × 2 tables.Results
Nine studies were included in the final meta‐analysis. The area under the summary receiver operating characteristic curve values were 0.91 (95% confidence interval [95% CI] 0.88–0.93) for procalcitonin and 0.81 (95% CI 0.78–0.84) for CRP. In general, testing for procalcitonin was highly specific for identifying infectious complications, although it was not as sensitive as testing for CRP. Pooled sensitivity was 0.75 (95% CI 0.63–0.84) for procalcitonin tests and 0.77 (95% CI 0.67–0.85) for CRP tests. Pooled specificity was 0.90 (95% CI 0.85–0.93) for procalcitonin tests and 0.56 (95% CI 0.25–0.83) for CRP tests. The positive likelihood ratio for procalcitonin (7.28 [95% CI 5.10–10.38]) was sufficiently high to qualify procalcitonin testing as a rule‐in diagnostic tool, while the negative likelihood ratio (0.28 [95% CI 0.18–0.40]) was not sufficiently low to qualify procalcitonin testing as a reliable rule‐out diagnostic tool.Conclusion
Procalcitonin has higher diagnostic value than CRP for the detection of bacterial sepsis in patients with autoimmune disease, and the test for procalcitonin is more specific than sensitive. A procalcitonin test is not recommended to be used in isolation as a rule‐out tool.9.
Objective
To examine predictors of progression of disability in rheumatoid arthritis (RA), as measured by the Health Assessment Questionnaire disability index (HAQ), and to determine rates of progression during biologic treatment.Methods
We followed 18,485 RA patients for up to 11 years (mean 3.7 years) in a longitudinal study of RA outcomes. Patients were characterized as having moderate or severe RA versus less severe RA at study entry. Annualized progression rates were determined in multivariable analyses using generalized estimating equations.Results
Although all of the demographic and severity characteristics were associated with baseline differences in HAQ score, progression was only associated with age, comorbidity, initial severity, and treatment. HAQ score increased fastest in patients ages >65 years (0.031; 95% confidence interval [95% CI] 0.028, 0.034). HAQ progression was independently associated with the presence of baseline cardiovascular disease, hypertension, diabetes mellitus, and the number of comorbid conditions. Annualized progression rates were greater in patients with mild to inactive RA (0.021; 95% CI 0.019, 0.023) than in moderate to severe RA (0.003; 95% CI 0.001, 0.006). The overall progression rate during biologic treatment was 0.008 (95% CI 0.005, 0.011); for patients with moderate to severe RA, the rate was 0.001 (95% CI ?0.005, 0.003).Conclusion
Age and comorbidity are important predictors of the rate of loss of functional status, and have a stronger effect on HAQ progression than does biologic treatment. There is little difference in progression rates among biologics. Patients with more severe RA progress less than those with less severe RA, a possible function of regression to the mean.10.
The risk of congestive heart failure in rheumatoid arthritis: A population‐based study over 46 years
Paulo J. Nicola Hilal Maradit‐Kremers Vronique L. Roger Steven J. Jacobsen Cynthia S. Crowson Karla V. Ballman Sherine E. Gabriel 《Arthritis \u0026amp; Rheumatology》2005,52(2):412-420
Objective
It is hypothesized that the systemic inflammation associated with rheumatoid arthritis (RA) promotes an increased risk of cardiovascular (CV) morbidity and mortality. We examined the risk and determinants of congestive heart failure (CHF) in patients with RA.Methods
We assembled a population‐based, retrospective incidence cohort from among all individuals living in Rochester, Minnesota, in whom RA (defined according to the American College of Rheumatology 1987 criteria) was first diagnosed between 1955 and 1995, and an age‐ and sex‐matched non‐RA cohort. After excluding patients in whom CHF occurred before the RA index date, all subjects were followed up until either death, incident CHF (defined according to the Framingham Heart Study criteria), migration from the county, or until January 1, 2001. Detailed information from the complete medical records (including all inpatient and outpatient care provided by all local providers) regarding RA, ischemic heart disease, and traditional CV risk factors was collected. Cox models were used to estimate the effect of RA on the development of CHF, adjusting for CV risk factors and/or ischemic heart disease.Results
The study population included 575 patients with RA and 583 subjects without RA. The CHF incidence rates were 1.99 and 1.16 cases per 100 person‐years in patients with RA and in non‐RA subjects, respectively (rate ratio 1.7, 95% confidence interval [95% CI] 1.3–2.1). After 30 years of followup, the cumulative incidence of CHF was 34.0% in patients with RA and 25.2% in non‐RA subjects (P< 0.001). RA conferred a significant excess risk of CHF (hazard ratio [HR] 1.87, 95% CI 1.47–2.39) after adjusting for demographics, ischemic heart disease, and CV risk factors. The risk was higher among patients with RA who were rheumatoid factor (RF) positive (HR 2.59, 95% CI 1.95–3.43) than among those who were RF negative (HR 1.28, 95% CI 0.93–1.78).Conclusion
Compared with persons without RA, patients with RA have twice the risk of developing CHF. This excess risk is not explained by traditional CV risk factors and/or clinical ischemic heart disease.11.
D. Saadoun B. Wechsler K. Desseaux D. Le Thi Huong Z. Amoura M. Resche‐Rigon P. Cacoub 《Arthritis \u0026amp; Rheumatology》2010,62(9):2806-2812
Objective
To report the long‐term mortality in patients with Behçet's disease (BD).Methods
A cohort of 817 patients fulfilling the international criteria for BD from a single center in France were analyzed for causes of death, the standardized mortality ratio (SMR), and the factors associated with mortality.Results
Among the 817 patients with BD, 41 (5%) died after a median followup of 7.7 years, of whom 95.1% were male. The mean ± SD age at death was 34.8 ± 11.9 years. Main causes of death included major vessel disease (mainly, arterial aneurysm and Budd‐Chiari syndrome) (43.9%), cancer and malignant hemopathy (14.6%), central nervous system involvement (12.2%), and sepsis (12.2%). The mortality rate at 1 year and 5 years was 1.2% and 3.3%, respectively. There was an increased mortality among patients ages 15–24 years (SMR 2.99, 95% confidence interval [95% CI] 1.54–5.39) and those ages 25–34 years (SMR 2.90, 95% CI 1.80–4.49) as compared with age‐and sex‐matched healthy controls. The mortality decreased in patients older than age 35 years (SMR 1.23, 95% CI 0.75–1.92). In multivariate analyses, male sex (hazard ratio [HR] 4.94, 95% CI 1.53–16.43), arterial involvement (HR 2.51, 95% CI 1.07–5.90), and a high number of BD flares (HR 2.37, 95% CI 1.09–5.14) were independently associated with the risk of mortality.Conclusion
The overall mortality in our BD cohort was 5% after a median followup of 7.7 years. Male sex, arterial involvement, and the number of flares were associated with mortality in BD.12.
Lone N. Troelsen Peter Garred Hans Ole Madsen Sren Jacobsen 《Arthritis \u0026amp; Rheumatology》2007,56(1):21-29
Objective
Patients with rheumatoid arthritis (RA) have excess morbidity and mortality due to ischemic heart disease. It has been suggested that high serum levels of mannose‐binding lectin (MBL) and agalactosyl IgG (IgG‐G0) are associated with increased inflammation in RA. MBL also enhances inflammation‐mediated tissue injury during postischemic reperfusion. This study was undertaken to examine whether these factors are associated with increased risk of ischemic heart disease in RA.Methods
MBL alleles were genotyped in 229 Danish patients with RA. In addition, serum levels of MBL and IgG‐G0 were measured. Incidences of ischemic heart disease, myocardial infarction, and death due to ischemic heart disease after the diagnosis of RA were assessed in a prospective study.Results
During a median followup of 9.5 years, ischemic heart disease was diagnosed in 8 of 27 patients with genetically determined high serum levels of MBL, as compared with 24 of the remaining 192 patients (data not available on 10 patients). After correction for other known risk factors, the hazard ratio (HR) was 3.6 (95% confidence interval [95% CI] 1.4–9.2). The corrected HR for myocardial infarction was 9.0 (95% CI 2.2–36.4). High serum levels of MBL also conferred an increased risk of death due to ischemic heart disease (age‐ and sex‐adjusted HR 10.5, 95% CI 2.7–41.3). However, further analyses showed that these associations were present only in patients with high serum levels of IgG‐G0.Conclusion
Genetically determined high serum levels of MBL and high serum levels of IgG‐G0 are associated with increased risk of ischemic heart disease, myocardial infarction, and premature death in patients with RA.13.
Kevin Haynes Timothy Beukelman Jeffrey R. Curtis Craig Newcomb Lisa J. Herrinton David J. Graham Daniel H. Solomon Marie R. Griffin Lang Chen Liyan Liu Kenneth G. Saag James D. Lewis 《Arthritis \u0026amp; Rheumatology》2013,65(1):48-58
Objective
To compare the incidence of cancer following tumor necrosis factor α (TNFα) inhibitor therapy to that with commonly used alternative therapies across multiple immune‐mediated diseases.Methods
The Safety Assessment of Biological Therapeutics study used data from 4 sources: national Medicaid and Medicare databases, Tennessee Medicaid, pharmacy benefits plans for Medicare beneficiaries in New Jersey and Pennsylvania, and Kaiser Permanente Northern California. Propensity score–adjusted hazard ratios (HRs) and 95% confidence intervals (95% CIs) were computed to estimate the relative rates of cancer, comparing those treated with TNFα inhibitors to those treated with alternative disease‐modifying therapies. The cancer‐finding algorithm had a positive predictive value ranging from 31% for any leukemia to 89% for female breast cancer.Results
We included 29,555 patients with rheumatoid arthritis (RA) (13,102 person‐years), 6,357 patients with inflammatory bowel disease (1,508 person‐years), 1,298 patients with psoriasis (371 person‐years), and 2,498 patients with psoriatic arthritis (618 person‐years). The incidence of any solid cancer was not elevated in RA (HR 0.80 [95% CI 0.59–1.08]), inflammatory bowel disease (HR 1.42 [95% CI 0.47–4.26]), psoriasis (HR 0.58 [95% CI 0.10–3.31]), or psoriatic arthritis (HR 0.74 [95% CI 0.20–2.76]) during TNFα inhibitor therapy compared to disease‐specific alternative therapy. Among RA patients, the incidence of any of the 10 most common cancers in the US and of nonmelanoma skin cancer was not increased with TNFα inhibitor therapy compared to treatment with comparator drugs.Conclusion
Short‐term cancer risk was not elevated among patients treated with TNFα inhibitor therapy relative to commonly used therapies for immune‐ mediated chronic inflammatory diseases in this study.14.
Leonid Padyukov Camilla Silva Patrik Stolt Lars Alfredsson Lars Klareskog 《Arthritis \u0026amp; Rheumatology》2004,50(10):3085-3092
Objective
The main genetic risk factor for rheumatoid arthritis (RA) is the shared epitope (SE) of HLA–DR, while smoking is an important environmental risk factor. We studied a potential gene–environment interaction between SE genes and smoking in the etiology of the 2 major subgroups of RA: rheumatoid factor (RF)–seropositive and RF‐seronegative disease.Methods
A population‐based case–control study involving incident cases of RF‐seropositive and RF‐seronegative RA (858 cases and 1,048 controls) was performed in Sweden. Cases and controls were classified according to their cigarette smoking status and HLA–DRB1 genotypes. The relative risk of developing RA was calculated for different gene/smoking combinations and was compared with the relative risk in never smokers without SE genes.Results
The relative risk of RF‐seropositive RA was 2.8 (95% confidence interval [95% CI] 1.6–4.8) in never smokers with SE genes, 2.4 (95% CI 1.3–4.6) in current smokers without SE genes, and 7.5 (95% CI 4.2–13.1) in current smokers with SE genes. Smokers carrying double SE genes displayed a relative risk of RF‐seropositive RA of 15.7 (95% CI 7.2–34.2). The interaction between smoking and SE genes was significant, as measured by the attributable proportion due to interaction, which was 0.4 (95% CI 0.2–0.7) for smoking and any SE, and 0.6 (95% CI 0.4–0.9) for smoking and a double SE. Neither smoking nor SE genes nor the combination of these factors increased the risk of developing RF‐seronegative RA.Conclusion
The disease risk of RF‐seropositive RA associated with one of the classic genetic risk factors for immune‐mediated diseases (the SE of HLA–DR) is strongly influenced by the presence of an environmental factor (smoking) in the population at risk.15.
Wilbert B. van den Hout Zuzana de Jong Marten Munneke Johanna M. W. Hazes Ferdinand C. Breedveld Theodora P. M. Vliet Vlieland 《Arthritis care & research》2005,53(1):39-47
Objective
To estimate the cost utility and cost effectiveness of long‐term, high‐intensity exercise classes compared with usual care in rheumatoid arthritis (RA) patients.Methods
RA patients (n = 300) were randomly assigned to either exercise classes or UC; followup lasted for 2 years. Outcome measures were quality‐adjusted life years (QALYs) according to the EuroQol (EQ‐5D), Short Form 6D (SF‐6D), and a transformed visual analog scale (VAS) rating personal health; functional ability according to the Health Assessment Questionnaire (HAQ) and McMaster Toronto Arthritis Patient Preference Interview (MACTAR); and societal costs.Results
QALYs in both randomization groups were similar according to the EQ‐5D and SF‐6D, but were in favor of usual care according to the VAS (annual difference 0.037 QALY; 95% confidence interval [95% CI] 0.002, 0.069). Functional ability was similar according to the HAQ, but in favor of the exercise classes according to the MACTAR (annual difference 2.9 QALY; 95% CI 0.9, 4.9). Annual medical costs of the exercise program were estimated at €780 per participating patient (€1 ≈ $1.05). The increase per patient in total medical costs of physical therapy was estimated at €430 (95% CI €318, 577), and the increase in total societal costs at €602 (95% CI €?490, 1,664). For societal willingness‐to‐pay equal to €50,000 per QALY, usual care had better cost utility than exercise classes, and significantly so according to the VAS.Conclusion
From a societal perspective and without taking possible preventive health effects into account, long‐term, high‐intensity exercise classes provide insufficient improvement in the valuation of health to justify the additional costs.16.
Yvonne M. Golightly Stephen W. Marshall Virginia B. Kraus Jordan B. Renner Andrs Villaveces Carri Casteel Joanne M. Jordan 《Arthritis \u0026amp; Rheumatology》2011,63(8):2276-2283
Objective
To explore the ability of osteoarthritis (OA)–related biomarkers to predict incident radiographic knee OA in a large sample of African American and Caucasian men and women.Methods
Baseline levels of serum cartilage oligomeric matrix protein (COMP), hyaluronan (HA), high‐sensitivity C‐reactive protein (hsCRP), and keratan sulfate (KS) and baseline and followup radiographs were available for 353 knees without baseline osteophyte formation and for 446 knees without baseline joint space narrowing (JSN). Cox models estimated the hazard ratio (HR) and 95% confidence interval (95% CI) for incident knee OA for a 1‐unit increase in the ln of each biomarker, with adjustment for age, race, sex, body mass index, and knee OA of the contralateral limb. Report of chronic knee symptoms was explored as a modifier of the association.Results
The hazard of incident knee osteophytes (HR 2.16 [95% CI 1.39–3.37]) and incident JSN (HR 1.82 [95% CI 1.15–2.89]) increased with higher baseline ln(COMP) levels. The hazard of incident knee JSN increased with higher ln(HA) levels (HR 1.46 [95% CI 1.14–1.87]). Baseline ln(hsCRP) and ln(KS) did not predict incident knee outcomes. HRs per unit increase in ln(COMP), ln(HA), and ln(KS) were higher among knees with chronic symptoms than among those without symptoms.Conclusion
Higher baseline ln(COMP) and ln(HA) levels were associated with incident knee OA over an average followup period of 6.3 years. These results represent detection of a molecular stage of OA prior to radiographic manifestations. Further exploration is needed to determine how chronic knee symptoms modify the biomarker–incident knee OA association.17.
Jrmie Sellam Houria Hendel‐Chavez Stphanie Rouanet Karim Abbed Bernard Combe Xavier Le Loët Jacques Tebib Jean Sibilia Yassine Taoufik Maxime Dougados Xavier Mariette 《Arthritis \u0026amp; Rheumatology》2011,63(4):933-938
Objective
To examine whether serum B cell markers can predict response to rituximab, a B cell–depleting monoclonal antibody, in patients with refractory rheumatoid arthritis (RA).Methods
This rituximab re‐treatment dose study (SMART [eSsai MAbthera sur la dose de Re‐Traitement]) involved 208 patients with refractory RA. Serum markers of B cell activation (anti–cyclic citrullinated peptide [anti‐CCP] antibodies, rheumatoid factor [RF], serum IgG, IgA, and IgM levels, serum κ and λ free light chains, and serum BAFF) were assessed before the first rituximab cycle (1,000 mg on days 1 and 15). Univariate and multivariate analyses were performed to identify factors associated with a European League Against Rheumatism (EULAR) response at 24 weeks.Results
There were 149 responders (72%). Two baseline factors were associated with a EULAR response at 24 weeks in multivariate analysis: the presence of anti‐CCP antibodies or RF (odds ratio 3.5 [95% confidence interval 1.6–7.6]) and a serum IgG concentration above normal (odds ratio 2.11 [95% confidence interval 1.02–4.33]), with synergy between them (odds ratio 6.0 [95% confidence interval 2.2–16.2]).Conclusion
The presence of RF or anti‐CCP antibodies and elevated IgG are 2 simple biomarkers that can be used routinely before therapy to predict response to rituximab in patients with refractory RA.18.
Hilal Maradit‐Kremers Paulo J. Nicola Cynthia S. Crowson Karla V. Ballman Sherine E. Gabriel 《Arthritis \u0026amp; Rheumatology》2005,52(3):722-732
Objective
To determine whether systemic inflammation confers any additional risk for cardiovascular death among patients with rheumatoid arthritis (RA), after adjusting for traditional cardiovascular risk factors and comorbidities.Methods
Using the population‐based data resources of the Rochester Epidemiology Project, we assembled an incidence cohort of all Rochester, Minnesota residents ages ≥18 years who first fulfilled the American College of Rheumatology 1987 criteria for RA between January 1, 1955 and January 1, 1995. All subjects were followed up longitudinally through their complete (inpatient, outpatient) medical records, beginning at age 18 years and continuing until death, migration, or January 1, 2001. Detailed information on the occurrence of various cardiovascular risk factors (personal history of coronary heart disease [CHD], congestive heart failure, smoking, hypertension, dyslipidemia, body mass index [BMI], diabetes mellitus, menopausal status) as well as indicators of systemic inflammation and RA disease severity (rheumatoid factor [RF] seropositivity, erythrocyte sedimentation rate [ESR], joint swelling, radiographic changes, RA nodules, RA complications, RA treatments, disease duration) and comorbidities were collected on all subjects. Causes of death were ascertained from death certificates and medical records. Cox regression models were used to estimate the independent predictors of cardiovascular death.Results
This inception cohort comprised a total of 603 RA patients whose mean age was 58 years, of whom 73% were women. During a mean followup of 15 years, 354 patients died and cardiovascular disease was the primary cause of death in 176 patients. Personal history of CHD, smoking, hypertension, low BMI, and diabetes mellitus, as well as comorbidities, including peripheral vascular disease, cerebrovascular disease, chronic pulmonary disease, dementia, ulcers, malignancies, renal disease, liver disease, and history of alcoholism, were all significant risk factors for cardiovascular death (P < 0.01 for each). Multivariable Cox regression analyses, controlled for cardiovascular risk factors and comorbidities, revealed that the risk of cardiovascular death was significantly higher among RA patients with at least 3 ESR values of ≥60 mm/hour (hazard ratio [HR] 2.03, 95% confidence interval [95% CI] 1.45–2.83), RA vasculitis (HR 2.41, 95% CI 1.00–5.81), and RA lung disease (HR 2.32, 95% CI 1.11–4.84).Conclusion
These results indicate that markers of systemic inflammation confer a statistically significant additional risk for cardiovascular death among patients with RA, even after controlling for traditional cardiovascular risk factors and comorbidities.19.
S Parra B Coll G Aragons J Marsillach R Beltrn A Rull J Joven C Alonso‐Villaverde J Camps 《HIV medicine》2010,11(4):225-231
Objectives
HIV‐infected patients show an increased cardiovascular disease (CVD) risk resulting, essentially, from metabolic disturbances related to chronic infection and antiretroviral treatments. The aims of this study were: (1) to evaluate the agreement between the CVD risk estimated using the Framingham risk score (FRS) and the observed presence of subclinical atherosclerosis in HIV‐infected patients; (2) to investigate the relationships between CVD and plasma biomarkers of oxidation and inflammation.Methods
Atherosclerosis was evaluated in 187 HIV‐infected patients by measuring the carotid intima‐media thickness (CIMT). CVD risk was estimated using the FRS. We also measured the circulating levels of interleukin‐6, monocyte chemoattractant protein‐1 (MCP‐1) and oxidized low‐density lipoprotein (LDL), and paraoxonase‐1 activity and concentration.Results
There was a weak, albeit statistically significant, agreement between FRS and CIMT (κ=0.229, P<0.001). A high proportion of patients with an estimated low risk had subclinical atherosclerosis (n=66; 56.4%). In a multivariate analysis, the presence of subclinical atherosclerosis in this subgroup of patients was associated with age [odds ratio (OR) 1.285; 95% confidence interval (CI) 1.084–1.524; P=0.004], body mass index (OR 0.799; 95% CI 0.642–0.994; P=0.044), MCP‐1 (OR 1.027; 95% CI 1.004–1.050; P=0.020) and oxidized LDL (OR 1.026; 95% CI 1.001–1.051; P=0.041).Conclusion
FRS underestimated the presence of subclinical atherosclerosis in HIV‐infected patients. The increased CVD risk was related, in part, to the chronic oxidative stress and inflammatory status associated with this patient population.20.
Simon Tarp Else M. Bartels Henning Bliddal Daniel E. Furst Maarten Boers Bente Danneskiold‐Samse Mette Rasmussen Robin Christensen 《Arthritis \u0026amp; Rheumatology》2012,64(11):3511-3521