Publications (18)111.98 Total impact
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Article: Impact of statin discontinuation on mortality in patients with rheumatoid arthritis: a population-based study.
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ABSTRACT: To evaluate the impact of statin discontinuation on cardiovascular disease (CVD) mortality and all-cause mortality in a population-based cohort of patients with rheumatoid arthritis (RA). We conducted a population-based longitudinal study of RA patients with incident statin use followed from 1996 to 2006 using administrative health data. Statin discontinuation was defined as persistent nonuse for ≥3 months during the therapy course. Primary outcomes were mortality from all CVDs (CVD mortality) and secondary outcomes were deaths from all causes (all-cause mortality). Cox proportional hazards models with statin discontinuation as a time-dependent variable were used and multivariable models were adjusted for age, sex, comorbidities, and risk factors for mortality, and proxy indicators of RA severity. Over 16,144 person-years of followup in the cohort of 4,102 incident statin users, we documented 198 deaths due to CVD and 467 deaths overall. Adjusted hazard ratios for the association of statin discontinuation with death were 1.60 (95% confidence interval [95% CI] 1.15-2.23) for CVD mortality and 1.79 (95% CI 1.46-2.20) for all-cause mortality. The association between statin discontinuation and mortality outcomes was not modified by timing of the first statin prescription, age, and sex (P values for interaction ≥0.29). These population-based data indicate that statin discontinuation in patients with RA is associated with an increased risk of death from CVD and all causes. Findings provide support for the importance of compliance with therapy in RA patients who are prescribed statins.Arthritis care & research. 03/2012; 64(6):809-16. -
Article: Are either or both hyperuricemia and xanthine oxidase directly toxic to the vasculature? A critical appraisal.
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ABSTRACT: Basic research and clinical studies have implicated a role for hyperuricemia and for xanthine oxidoreductase (XOR), the enzyme that generates uric acid (UA), in not only gout but also vascular diseases. At present, asymptomatic hyperuricemia (i.e., in the absence of gout, urate nephrolithiasis, or tumor lysis syndrome) is not an indication for therapy. With the rise over the past several decades in prevalence of both gout and hyperuricemia, clarifying the potential adverse effects of hyperuricemia (in patients with and without gout) is of public health importance. UA is not simply an inert end-product of purine metabolism in humans, but rather has potential antioxidant, pro-oxidant, and pro-inflammatory effects. However controversy remains as to which, if any, of these effects are of clinical relevance in development and complications of human vascular diseases in gout and asymptomatic hyperuricemia. Clearly, not all individuals with hyperuricemia develop gout, and studies to date have also been unable to clarify in which subjects hyperuricemia may have detrimental effects on the vasculature. Further, studies of urate-lowering therapy with XOR inhibition or uricosuric agents have not been able to definitively identify whether any such effects may be mediated by UA versus XO. Adequately sized, prospective randomized clinical trials of sufficient duration, and employing appropriate biomarkers, now appear critical to resolve the putative toxic roles of UA and XO in the human arterial circulation. © 2011 American College of Rheumatology.Arthritis & Rheumatism 09/2011; 64(2):327-38. · 7.87 Impact Factor -
Article: Statin discontinuation and risk of acute myocardial infarction in patients with rheumatoid arthritis: a population-based cohort study.
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ABSTRACT: Screening for cardiovascular risk factors and treating hyperlipidaemia with statins are recommended to reduce the increased cardiovascular risk in individuals with rheumatoid arthritis (RA). However, poor compliance with statins may limit their therapeutic benefit. Our objective was to evaluate the impact of statin discontinuation on risk of acute myocardial infarction (AMI) among RA patients. The authors conducted a population-based cohort study of RA patients with incident statin use followed from May 1996 to March 2006 using administrative health data. Primary exposure was statin discontinuation for ≥ 3 months at any time during therapy course. The authors used Cox's proportional hazards models and modelled statin discontinuation as a time-dependent variable, while adjusting for age, sex, comorbidities, use of other medications influencing cardiac risk, and proxy indicators of RA severity. During 15 669 person-years of follow-up in 4102 incident-statin users with RA, the authors identified 264 AMI events. Statin discontinuation was associated with 67% increased risk of AMI (adjusted HR 1.67; 95% CI 1.24 to 2.25). There was a 2% increase in risk of AMI with each 1-month increase in the duration of discontinuation (adjusted HR 1.02; 95% CI 1.01 to 1.03). These associations were not modified by timing of first statin prescription, prior AMI status, sex and age (p values for interactions >0.17). These population-based data indicate that RA patients who discontinue statins have increased risk of AMI. Findings emphasise the need to raise awareness, among health professionals and people with RA, of the importance of compliance with statin therapy in RA.Annals of the rheumatic diseases 03/2011; 70(6):1020-4. · 8.11 Impact Factor -
Article: American College of Rheumatology/European League Against Rheumatism provisional definition of remission in rheumatoid arthritis for clinical trials.
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ABSTRACT: Remission in rheumatoid arthritis (RA) is an increasingly attainable goal, but there is no widely used definition of remission that is stringent but achievable and could be applied uniformly as an outcome measure in clinical trials. This work was undertaken to develop such a definition. A committee consisting of members of the American College of Rheumatology, the European League Against Rheumatism, and the Outcome Measures in Rheumatology Initiative met to guide the process and review prespecified analyses from RA clinical trials. The committee requested a stringent definition (little, if any, active disease) and decided to use core set measures including, as a minimum, joint counts and levels of an acute-phase reactant to define remission. Members were surveyed to select the level of each core set measure that would be consistent with remission. Candidate definitions of remission were tested, including those that constituted a number of individual measures of remission (Boolean approach) as well as definitions using disease activity indexes. To select a definition of remission, trial data were analyzed to examine the added contribution of patient-reported outcomes and the ability of candidate measures to predict later good radiographic and functional outcomes. Survey results for the definition of remission suggested indexes at published thresholds and a count of core set measures, with each measure scored as 1 or less (e.g., tender and swollen joint counts, C-reactive protein [CRP] level, and global assessments on a 0-10 scale). Analyses suggested the need to include a patient-reported measure. Examination of 2-year followup data suggested that many candidate definitions performed comparably in terms of predicting later good radiographic and functional outcomes, although 28-joint Disease Activity Score-based measures of remission did not predict good radiographic outcomes as well as the other candidate definitions did. Given these and other considerations, we propose that a patient's RA can be defined as being in remission based on one of two definitions: (a) when scores on the tender joint count, swollen joint count, CRP (in mg/dl), and patient global assessment (0-10 scale) are all ≤ 1, or (b) when the score on the Simplified Disease Activity Index is ≤ 3.3. We propose two new definitions of remission, both of which can be uniformly applied and widely used in RA clinical trials. We recommend that one of these be selected as an outcome measure in each trial and that the results on both be reported for each trial.Arthritis & Rheumatism 03/2011; 63(3):573-86. · 7.87 Impact Factor -
Article: Serum uric acid levels and the risk of type 2 diabetes: a prospective study.
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ABSTRACT: To evaluate the impact of serum uric acid levels on the future risk of developing type 2 diabetes independent of other factors. We used prospective data from the Framingham Heart Study original (n=4883) and offspring (n=4292) cohorts to examine the association between serum uric acid levels and the incidence of diabetes. We used Cox proportional hazards models to estimate the relative risk of incident diabetes adjusting for age, sex, physical activity, alcohol consumption, smoking, hypertension, body mass index, and blood levels of glucose, cholesterol, creatinine, and triglycerides. We identified 641 incident cases of diabetes in the original cohort and 497 cases in the offspring cohort. The incidence rates of diabetes per 1000 person-years for serum uric acid levels <5.0, 5.0-5.9, 6.0-6.9, 7.0-7.9 and ≥8.0 mg/dL were 3.3, 6.1, 8.7, 11.5, and 15.9, respectively, in the original cohort; and 2.9, 5.0, 6.6, 8.7, and 10.9, respectively, in the offspring cohort (P-values for trends <.001). Multivariable relative risks per mg/dL increase in serum uric acid levels were 1.20 (95% confidence interval; 1.11-1.28) for the original cohort and 1.15 (95% confidence interval; 1.06-1.23) for the offspring cohort. These prospective data from 2 generations of the Framingham Heart Study provide evidence that individuals with higher serum uric acid; including younger adults, are at a higher future risk of type 2 diabetes independent of other known risk factors. These data expand on cross-sectional associations between hyperuricemia and the metabolic syndrome, and extend the link to the future risk of type 2 diabetes.The American journal of medicine 10/2010; 123(10):957-61. · 4.47 Impact Factor -
Article: Epidemiology of gout in women: Fifty-two-year followup of a prospective cohort.
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ABSTRACT: Despite the recent doubling of the incidence of gout among women and its substantial prevalence particularly in the aging female population, the risk factors for gout among women remain unknown. We undertook this study to evaluate purported risk factors for incident gout among women and to compare them with those among men. Using prospective data from the Framingham Heart Study, we examined over a 52-year period (1950-2002) the relationship between purported risk factors and the incidence of gout in 2,476 women and 1,951 men. We documented 304 incident cases of gout, 104 of them among women. The incidence rates of gout for women per 1,000 person-years according to serum uric acid levels of <5.0, 5.0-5.9, 6.0-6.9, 7.0-7.9, and > or = 8.0 mg/dl were 0.8, 2.5, 4.2, 13.1, and 27.3, respectively (P for trend < 0.0001). The magnitude of this association was lower than that among men (P for interaction = 0.0002). Multivariate relative risks conferred by increasing age (per 5 years), obesity (body mass index > or = 30 kg/m(2)), alcohol intake (> or = 7 ounces of pure alcohol/week), hypertension, and diuretic use were 1.24, 2.74, 3.10, 1.82, and 2.39, respectively (all P < 0.05), for women. These prospective data with long-term followup provide evidence that higher levels of serum uric acid increase the risk of gout in a graded manner among women, but the rate of increase is lower than that among men. Increasing age, obesity, alcohol consumption, hypertension, and diuretic use were associated with the risk of incident gout among women.Arthritis & Rheumatism 04/2010; 62(4):1069-76. · 7.87 Impact Factor -
Article: Uric acid and insulin sensitivity and risk of incident hypertension.
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ABSTRACT: Uric acid, insulin sensitivity, and endothelial dysfunction may be important in the development of hypertension. Corresponding circulating biomarkers are associated with risk of hypertension, but because these factors may be interrelated, whether they independently affect risk is unknown. In 1496 women aged 32 to 52 years without hypertension at baseline, we prospectively analyzed the associations between fasting plasma levels of uric acid, insulin, triglycerides, the insulin sensitivity index, and 2 biomarkers associated with endothelial dysfunction (homocysteine and soluble intercellular adhesion molecule-1) and the odds of incident hypertension. Odds ratios were adjusted for standard risk factors and then for all biomarkers plus estimated glomerular filtration rate and total cholesterol level. Population-attributable risk was estimated for biomarkers significantly associated with hypertension. All the biomarkers were associated with incident hypertension after adjustment for standard hypertension risk factors. However, after simultaneously controlling for all the biomarkers, estimated glomerular filtration rate, and total cholesterol level, only uric acid and insulin levels were independently associated with incident hypertension. Comparing the highest and lowest quartiles of uric acid levels, the odds ratio was 1.89 (95% confidence interval, 1.26-2.82). A similar comparison yielded an odds ratio of 2.03 (95% confidence interval, 1.35-3.05) for insulin levels. Using an estimated basal incidence rate of 14.6 per 1000 annually, 30.8% of all hypertension occurring in young women annually is associated with uric acid levels of 3.4 mg/dL or greater (to convert to micromoles per liter, multiply by 59.485). For insulin levels of 2.9 microIU/mL or greater (to convert to picomoles per liter, multiply by 6.945), this proportion is 24.2%. Differences in uric acid and insulin levels robustly and substantially affect the risk of hypertension in young women. Measuring these biomarkers in clinical practice may identify higher-risk individuals.Archives of internal medicine 02/2009; 169(2):155-62. · 11.46 Impact Factor -
Article: Fructose and vitamin C intake do not influence risk for developing hypertension.
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ABSTRACT: Higher uric acid levels are associated with an increased risk for developing hypertension. Higher intake of fructose increases plasma uric acid levels and higher intake of vitamin C reduces uric acid levels, but whether these nutrients are independently associated with the risk for developing hypertension is unknown. We studied this question by analyzing data from participants of three large and independent prospective cohorts: Nurses' Health Study 1 (n = 88,540), Nurses' Health Study 2 (n = 97,315), and the Health Professionals Follow-up Study (n = 37,375). Relative risks and 95% confidence intervals for incident hypertension were computed according to quintiles of fructose intake and categories of vitamin C intake using multivariable Cox proportional hazards regression. Fructose intake was not associated with the risk for developing hypertension; the multivariable relative risks (95% confidence intervals) for the highest compared with the lowest quintile of fructose intake were 1.02 (0.99 to 1.06) in Nurses' Health Study 1, 1.03 (0.98 to 1.08) in Nurses' Health Study 2, and 0.99 (0.93 to 1.05) in Heath Professionals Follow-up Study. Regarding vitamin C, the relative risks for individuals who consumed > or =1500 mg/d compared with those who consumed <250 mg/d were 0.89 (0.83 to 0.96) in Nurses' Health Study 1, 1.02 (0.91 to 1.14) in Nurses' Health Study 2, and 1.06 (0.97 to 1.15) in Health Professionals Follow-up Study. In conclusion, fructose and vitamin C intake do not substantially influence the risk for developing hypertension.Journal of the American Society of Nephrology 01/2009; 20(4):863-71. · 9.66 Impact Factor -
Article: Gout and the risk of Parkinson's disease: a cohort study.
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ABSTRACT: Several studies have suggested that higher serum uric acid levels lead to a lower risk of Parkinson's disease (PD) because uric acid exerts antioxidant effects on neurons. Our objective was to examine the relationship between gout and the risk of PD in persons age > or = 65 years. We conducted a population-based cohort study using the British Columbia Linked Health Database and PharmaCare data (i.e., prescription drug data for those age > or = 65 years). We compared incidence rates of PD between 11,258 gout patients and 56,199 controls matched on age, sex, date of gout diagnosis, and length of medical record. Cox proportional hazards models were used to estimate the relative risk (RR) of PD, adjusting for age, sex, prior comorbid conditions, and use of diuretics and nonsteroidal antiinflammatory drugs. Over an 8-year median followup, we identified 1,182 new cases of PD. Compared with individuals without gout, the multivariate RR of PD among those with gout was 0.70 (95% confidence interval [95% CI] 0.59-0.83). In subgroup analyses, the inverse association was similarly present in both sexes and was evident among those who did not use diuretics (RR 0.66, 95% CI 0.54-0.81), but not among diuretic users (RR 0.80, 95% CI 0.58-1.10, P for interaction 0.35). Our population-based data provide evidence for a protective effect of gout on the risk of PD and support the purported protective role of uric acid.Arthritis & Rheumatism 11/2008; 59(11):1549-54. · 7.87 Impact Factor -
Article: Menopause, postmenopausal hormone use and serum uric acid levels in US women--the Third National Health and Nutrition Examination Survey.
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ABSTRACT: Despite the substantial prevalence of gout in the ageing female population, female hormonal influence has not been comprehensively examined. We evaluated and quantified the potential independent association between menopause, postmenopausal hormone use and serum uric acid levels in a nationally representative sample of women. Using data from 7662 women aged 20 years and older in the Third National Health and Nutrition Examination Survey (1988 to 1994), we examined the relation between menopause, postmenopausal hormone use and serum uric acid levels. We used multivariate linear regression to adjust for other risk factors for hyperuricaemia such as dietary factors, age, adiposity, alcohol use, renal function, hypertension and diuretic use. Menopause was associated with higher serum uric acid levels. After adjusting for covariates, serum uric acid levels among women with natural menopause and surgical menopause were greater than premenopausal women by 0.34 mg/dl (95% confidence interval [CI], 0.19 to 0.49) and 0.36 mg/dl (95% CI, 0.14 to 0.57), respectively. Current postmenopausal hormone use was associated with a lower serum uric acid level among postmenopausal women (multivariate difference, 0.24 mg/dl [95% CI, 0.11 to 0.36]). The serum uric acid levels increased with increasing age categories (crude difference between 20 to 29 years and 70 years and over = 1.03 mg/dl, p for trend < 0.001), but this increase was not present after adjusting for other covariates (p for trend = 0.66). These findings from a nationally representative sample of US women indicate that menopause is independently associated with higher serum uric acid levels, whereas postmenopausal hormone use is associated with lower uric acid levels among postmenopausal women. The age-associated increase in serum uric acid levels in women may be explained by menopause and other age-related factors.Arthritis research & therapy 10/2008; 10(5):R116. · 4.27 Impact Factor -
Article: Hyperlipidaemia, statin use and the risk of developing rheumatoid arthritis.
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ABSTRACT: To evaluate whether statins are associated with a protective effect on the development of rheumatoid arthritis (RA). A nested case-control study was conducted using data from the General Practice Research Database. A study population consisting of three groups of subjects aged 40-89 years was identified: (1) patients exposed to a statin or other lipid-lowering agent (LLA); (2) patients with a diagnosis of hyperlipidaemia in the absence of lipid-lowering drug treatment and (3) a random sample of 25 000 individuals with no diagnosis of hyperlipidaemia nor a prescription for a LLA. From this population incident cases of RA and up to four controls for each case were identified, matched on age, sex, general practice, number of years of recorded history in the database and index date. The independent effects of hyperlipidaemia and statins on the development of RA were evaluated using conditional logistic regression. 313 cases of RA and 1252 matched controls were identified. Compared with patients with untreated hyperlipidaemia, or hyperlipidaemia treated with LLA other than statins, the adjusted odds ratio for patients with no hyperlipidaemia was 0.68 (95% CI 0.50 to 0.91). When those with hyperlipidaemia who received statins were compared with those with hyperlipidaemia who did not use statins (ie, untreated hyperlipidaemia patients or those treated with non-statin LLA) the OR was 0.59 (95% CI 0.37 to 0.96). These data provide evidence to support the hypothesis that statins may be protective against the development of RA in patients with hyperlipidaemia.Annals of the rheumatic diseases 08/2008; 68(4):546-51. · 8.11 Impact Factor -
Article: Vitamin C intake and serum uric acid concentration in men.
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ABSTRACT: We examined associations between vitamin C intake and serum uric acid in men in a population-based study. We included 1387 men without hypertension and with body mass index (BMI) < 30 kg/m(2) in the Health Professional Follow-up Study. Dietary intake was assessed with a semiquantitative food frequency questionnaire validated for use in this population. Serum uric acid concentrations were measured. Greater intakes of total vitamin C were significantly associated with lower serum uric acid concentrations, after adjustment for smoking, BMI, ethnicity, blood pressure, presence of gout, use of aspirin, and intake of energy, alcohol, dairy protein, fructose, meat, seafood and coffee. An inverse dose-response association was observed through vitamin C intake of 400-500 mg/day, and then reached a plateau. Adjusted mean uric acid concentrations across total vitamin C intake categories (< 90, 90-249, 250-499, 500-999, or > or = 1000 mg/day) were 6.4, 6.1, 6.0, 5.7, and 5.7 mg/dl, respectively (p for trend < 0.001). Greater vitamin C intake was associated with lower prevalence of hyperuricemia (serum uric acid > 6 mg/dl). Multivariate odds ratios for hyperuricemia across total vitamin C intake categories were 1 (reference), 0.58, 0.57, 0.38, and 0.34 (95% CI 0.20-0.58; P for trend < 0.001). When we used dietary data, which were assessed 4-8 years before blood collection, as predictors, we observed similar inverse associations between vitamin C intake and uric acid. These population-based data indicate that vitamin C intake in men is inversely associated with serum uric acid concentrations. These findings support a potential role of vitamin C in the prevention of hyperuricemia and gout.The Journal of Rheumatology 05/2008; 35(9):1853-8. · 3.69 Impact Factor -
Article: Estimates of the prevalence of arthritis and other rheumatic conditions in the United States. Part II.
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ABSTRACT: To provide a single source for the best available estimates of the US prevalence of and number of individuals affected by osteoarthritis, polymyalgia rheumatica and giant cell arteritis, gout, fibromyalgia, and carpal tunnel syndrome, as well as the symptoms of neck and back pain. A companion article (part I) addresses additional conditions. The National Arthritis Data Workgroup reviewed published analyses from available national surveys, such as the National Health and Nutrition Examination Survey and the National Health Interview Survey. Because data based on national population samples are unavailable for most specific rheumatic conditions, we derived estimates from published studies of smaller, defined populations. For specific conditions, the best available prevalence estimates were applied to the corresponding 2005 US population estimates from the Census Bureau, to estimate the number affected with each condition. We estimated that among US adults, nearly 27 million have clinical osteoarthritis (up from the estimate of 21 million for 1995), 711,000 have polymyalgia rheumatica, 228,000 have giant cell arteritis, up to 3.0 million have had self-reported gout in the past year (up from the estimate of 2.1 million for 1995), 5.0 million have fibromyalgia, 4-10 million have carpal tunnel syndrome, 59 million have had low back pain in the past 3 months, and 30.1 million have had neck pain in the past 3 months. Estimates for many specific rheumatic conditions rely on a few, small studies of uncertain generalizability to the US population. This report provides the best available prevalence estimates for the US, but for most specific conditions more studies generalizable to the US or addressing understudied populations are needed.Arthritis & Rheumatism 02/2008; 58(1):26-35. · 7.87 Impact Factor -
Article: Plasma uric acid level and risk for incident hypertension among men.
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ABSTRACT: Several studies have found that uric acid (UA) level is associated with an increased risk for hypertension, but the association could be confounded by metabolic factors that were not included in these previous studies. UA level and risk for incident hypertension was examined prospectively among men who participated in the Health Professionals' Follow-up Study. From among men without hypertension at the time blood was collected, 750 participants who developed hypertension during the subsequent 8 yr and 750 age-matched controls were selected. In addition to adjustment for standard hypertension risk factors and renal function, adjustments controlled for fasting insulin, triglyceride, and cholesterol levels. The mean age of participants was 61 yr, and mean plasma UA level was 6.0 mg/dl (SD 1.25 mg/dl). The multivariable relative risk (RR) for a 1-SD increase in UA was 1.02 (95% confidence interval [CI]0.87 to 1.18); the RR comparing the highest with lowest quartile of UA was 1.08 (95% CI 0.71 to 1.63). The multivariable RR associated with a 1-SD increase in UA was 1.38 (95% CI 1.05 to 1.81) for men aged <60 yr and 0.90 (95% CI 0.74 to 1.10) for men >or=60 yr (P = 0.04 for interaction). However, further adjustment for fasting insulin, triglyceride, and cholesterol levels attenuated the results (RR for men <60 yr 1.24; 95% CI 0.93 to 1.66). In conclusion, no independent association between UA level and risk for incident hypertension was found among older men.Journal of the American Society of Nephrology 02/2007; 18(1):287-92. · 9.66 Impact Factor -
Article: Epidemiology of crystal arthropathy.
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ABSTRACT: Gout is an inflammatory arthritis mediated by the crystallization of uric acid within the joints and often is associated with hyperuricemia. Data suggest that the overall disease burden of gout remains substantial and may be increasing. Identifying and characterizing modifiable risk factors for gout is a major step in preventing and managing this painful condition. As more scientific data on the risk factors and comorbidities of gout become available, their integration into gout prevention and care strategies may become essential. This article reviews the relevant epidemiologic data, with a focus on recent progress and data on other crystal arthropathies.Rheumatic Disease Clinics of North America 06/2006; 32(2):255-73, v. · 3.02 Impact Factor -
Article: Epidemiology, risk factors, and lifestyle modifications for gout.
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ABSTRACT: Gout affects more than 1% of adults in the USA, and it is the most common form of inflammatory arthritis among men. Accumulating data support an increase in the prevalence of gout that is potentially attributable to recent shifts in diet and lifestyle, improved medical care, and increased longevity. There are both nonmodifiable and modifiable risk factors for hyperuricemia and gout. Nonmodifiable risk factors include age and sex. Gout prevalence increases in direct association with age; the increased longevity of populations in industrialized nations may contribute to a higher prevalence of gout through the disorder's association with aging-related diseases such as metabolic syndrome and hypertension, and treatments for these diseases such as thiazide diuretics for hypertension. Although gout is considered to be primarily a male disease, there is a more equal sex distribution among elderly patients. Modifiable risk factors for gout include obesity, the use of certain medications, high purine intake, and consumption of purine-rich alcoholic beverages. The increasing prevalence of gout worldwide indicates that there is an urgent need for improved efforts to identify patients with hyperuricemia early in the disease process, before the clinical manifestations of gout become apparent.Arthritis research & therapy 02/2006; 8 Suppl 1:S2. · 4.27 Impact Factor -
Article: Comorbid depression is an independent risk factor for mortality in patients with rheumatoid arthritis.
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ABSTRACT: Whether comorbid depression increases mortality in patients with rheumatoid arthritis (RA) is unknown. Our objective was to determine whether the presence of depression predicted mortality in patients with RA. We followed 1290 consecutive outpatients with RA who met our stringent inclusion criteria during an 18-year observation period. Since 1981, demographic, clinic, and self-report data were collected and entered into a computer database at the time of each clinic visit. The comorbidity data were consistently recorded beginning in 1991. Our primary independent variable was the mean of the Arthritis Impact Measurement Scales (AIMS) depression scores during the first 4 years of entry into the clinic cohort (average 4-year depression). Data were analyzed using Cox proportional hazard models. After adjusting for covariates, the hazard ratio (HR) for each unit increase in the average 4-year depression score on mortality was 1.14 (p < 0.0001). Using only the data obtained from 1991 to 2003, the mortality risk was slightly increased (HR 1.35, p < 0.0001). To reduce residual confounding due to RA disease activity and/or comorbid medical conditions, we then excluded deaths during the first 2 years after study onset. With this method, the HR for the average 4-year depression remained significant (HR 1.35, p < 0.0001). Because an AIMS depression score > or = 4 is consistent with clinical depression, we analyzed the dataset using the average 4-year depression score as a dichotomous variable (score < 4 or > or = 4). The HR of clinical depression on mortality was 2.2 (95% CI 1.2- 3.9, p = 0.01). Depression increases the risk of mortality in RA. Our study highlights the importance of comorbid depression in patients with RA.The Journal of Rheumatology 07/2005; 32(6):1013-9. · 3.69 Impact Factor -
Article: Controlling for time-dependent confounding using marginal structural models
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ABSTRACT: Longitudinal studies in which exposures, confounders, and outcomes are measured repeatedly over time have the potential to allow causal inferences about the effects of exposure on outcome. There is particular interest in estimating the causal effects of medical treatments (or other interventions) in circumstances in which a randomized controlled trial is difficult or impossible. However, standard methods for estimating exposure effects in longitudinal studies are biased in the presence of time-dependent confounders affected by prior treatment. This article describes the use of marginal structural models (described by Robins, Hernán, and Brumback [2000]) to estimate exposure or treatment effects in the presence of time-dependent confounders affected by prior treatment. The method is based on deriving inverse-probability-of-treatment weights, which are then used in a pooled logistic regression model to estimate the causal effect of treatment on outcome. We demonstrate the use of marginal structural models to estimate the effect of methotrexate on mortality in persons suffering from rheumatoid arthritis. Copyright 2004 by StataCorp LP.Stata Journal 01/2004; 4(4):402-420. · 2.22 Impact Factor
Top co-authors
Top Journals
Institutions
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2010
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Arthritis Research Centre of Canada
Richmond, British Columbia, Canada -
University of Massachusetts Boston
Boston, MA, USA
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2009
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Partners HealthCare
Boston, MA, USA
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2007–2009
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Harvard University
- • Channing Laboratory
- • Department of Nutrition
Boston, MA, USA
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2008
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Massachusetts General Hospital
Boston, MA, USA -
University of British Columbia - Vancouver
Vancouver, British Columbia, Canada -
Erasmus MC
- Department of Immunology
Rotterdam, South Holland, Netherlands
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2006
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University of Alabama at Birmingham
- Division of Clinical Immunology and Rheumatology
Birmingham, AL, USA -
Vancouver General Hospital
Vancouver, British Columbia, Canada
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