scholarly journals Depression as a risk factor for the development of rheumatoid arthritis: a population-based cohort study

RMD Open ◽  
2018 ◽  
Vol 4 (2) ◽  
pp. e000670 ◽  
Author(s):  
Isabelle A Vallerand ◽  
Ryan T Lewinson ◽  
Alexandra D Frolkis ◽  
Mark W Lowerison ◽  
Gilaad G Kaplan ◽  
...  

ObjectivesMajor depressive disorder (MDD) is associated with increased levels of systemic proinflammatory cytokines, including tumour necrosis factor alpha. As these cytokines are pathogenic in autoimmune diseases such as rheumatoid arthritis (RA), our aim was to explore on a population-level whether MDD increases the risk of developing RA.MethodsA retrospective cohort study was conducted using The Health Improvement Network (THIN) database (from 1986 to 2012). Observation time was recorded for both the MDD and referent cohorts until patients developed RA or were censored. Cox proportional hazards models were used to determine the risk of developing RA among patients with MDD, accounting for age, sex, medical comorbidities, smoking, body mass index and antidepressant use.ResultsA cohort of 403 932 patients with MDD and a referent cohort of 5 339 399 patients without MDD were identified in THIN. Cox proportional hazards models revealed a 31% increased risk of developing RA among those with MDD in an unadjusted model (HR=1.31, 95% CI 1.25 to 1.36, p<0.0001). When adjusting for all covariates, the risk remained significantly increased among those with MDD (HR=1.38, 95% CI 1.31 to 1.46, p<0.0001). Antidepressant use demonstrated a confounding effect that was protective on the association between MDD and RA.ConclusionMDD increased the risk of developing RA by 38%, and antidepressants may decrease this risk in these patients. Future research is necessary to confirm the underlying mechanism of MDD on the pathogenesis of RA.

BMJ Open ◽  
2019 ◽  
Vol 9 (3) ◽  
pp. e025124 ◽  
Author(s):  
Takako Fujita ◽  
Akira Babazono ◽  
Yumi Harano ◽  
Peng Jiang

ObjectiveWe sought to examine the effect of smoking cessation on subsequent development of depressive disorders.DesignThis was a retrospective cohort study.MethodsWe used administrative claim and health check data from fiscal years 2010 to 2014, obtained from the largest health insurance association in Fukuoka, Japan. Study participants were between 30 and 69 years old. The end-point outcome was incidence of depressive disorders. Survival analysis and Cox proportional hazards models were conducted. The evaluated potential confounders were sex, age, standard monthly income and psychiatric medical history.ResultsThe final number of participants was 87 255, with 7841 in the smoking cessation group and 79 414 in the smoking group. The result of survival analysis showed no significant difference in depressive disorders between the two groups. The results of Cox proportional hazards models showed no significant difference by multivariate analysis between participants, including users of smoking cessation medication (HR 1.04, 95% Cl 0.89 to 1.22) and excluding medication use (HR 0.97, 95% Cl 0.82 to 1.15).ConclusionsThe present study showed that there were no significant differences with respect to having depressive disorders between smoking cessation and smoking groups. We also showed that smoking cessation was not related to incidence of depressive disorders among participants, including and excluding users of smoking cessation medication, after adjusting for potential confounders. Although the results have some limitations because of the nature of the study design, our findings will provide helpful information to smokers, health professionals and policy makers for improving smoking cessation.


2019 ◽  
Vol 105 (3) ◽  
pp. e597-e609 ◽  
Author(s):  
Lihua Hu ◽  
Guiping Hu ◽  
Benjamin Ping Xu ◽  
Lingjuan Zhu ◽  
Wei Zhou ◽  
...  

Abstract Background In addition to the controversy regarding the association of hyperuricemia with mortality, uncertainty also remains regarding the association between low serum uric acid (SUA) and mortality. We aimed to assess the relationship between SUA and all-cause and cause-specific mortality. Methods This cohort study included 9118 US adults from the National Health and Nutrition Examination Survey (1999-2002). Multivariable Cox proportional hazards models were used to evaluate the relationship between SUA and mortality. Our analysis included the use of a generalized additive model and smooth curve fitting (penalized spline method), and 2-piecewise Cox proportional hazards models, to address the nonlinearity between SUA and mortality. Results During a median follow-up of 5.83 years, 448 all-cause deaths occurred, with 100 cardiovascular disease (CVD) deaths, 118 cancer deaths, and 37 respiratory disease deaths. Compared with the reference group, there was an increased risk of all-cause, CVD, cancer, and respiratory disease mortality for participants in the first and third tertiles of SUA. We further found a nonlinear and U-shaped association between SUA and mortality. The inflection point for the curve was found at a SUA level of 5.7 mg/dL. The hazard ratios (95% confidence intervals) for all-cause mortality were 0.80 (0.65-0.97) and 1.24 (1.10-1.40) to the left and right of the inflection point, respectively. This U-shaped association was observed in both sexes; the inflection point for SUA was 6 mg/dL in males and 4 mg/dL in females. Conclusion Both low and high SUA levels were associated with increased all-cause and cause-specific mortality, supporting a U-shaped association between SUA and mortality.


2009 ◽  
Vol 27 (15_suppl) ◽  
pp. 9625-9625
Author(s):  
J. A. Berlin ◽  
P. J. Bowers ◽  
S. Rao ◽  
S. Sun ◽  
K. Liu ◽  
...  

9625 Background: When cancer patients (pts) with chemotherapy-induced anemia (CIA) respond to erythropoietic-stimulating agents (ESA), hemoglobin (Hb) typically increases within 4–8 weeks. This exploratory analysis examined whether mortality differs depending on Hb response after 4 or 8 weeks of epoetin alfa (EPO) treatment or depending on transfusion. Methods: Pt-level data were analyzed from 31 randomized studies (7,215 pts) of epoetin alfa vs non-EPO (15 studies) or placebo (16 studies) in pts with CIA. A landmark analysis was used; Hb change was set at a specific time (4 and 8 weeks) and subsequent survival was examined separately for EPO and placebo. Pts were categorized as “Hb increased” (>0.5 g/dL), “Hb decreased” (>0.5 g/dL), or “Hb stable” (within ±0.5 g/dL) compared to baseline. Hb stable was compared to other Hb change categories with Cox proportional hazards models, stratified by study and adjusted for potential confounders. Results: The hazard ratio (HR) for Hb decreased versus Hb stable at 4 weeks was 1.44 for EPO (95% CI: 1.04, 1.99), indicating worse survival for pts with a decline in Hb. This association was weaker for placebo (HR: 1.12; 95% CI: 0.74, 1.67). Increased risk with declining Hb in EPO-treated pts was most pronounced in studies that maintained Hb ≥12 g/dL or treated pts for >12–16 weeks (1,876 pts). Patterns were similar using the 8-week landmark. In both EPO-treated and placebo pts, transfusion increased the rate of on-study death ∼3.5 fold (treating transfusion as a time-dependent variable). Conclusions: These exploratory findings suggest that both decreased Hb after 4 or 8 weeks of EPO treatment and transfusion are associated with increased risk of death. In spite of adjustment for other prognostic factors, it is likely that this association reflects poorer underlying prognosis of pts whose Hb fails to respond. ESAs should be discontinued in the absence of a Hb response. [Table: see text]


2011 ◽  
Vol 27 (suppl 3) ◽  
pp. s336-s344 ◽  
Author(s):  
James Macinko ◽  
Vitor Camargos ◽  
Josélia O. A. Firmo ◽  
Maria Fernanda Lima-Costa

We use data from a population-based cohort of elderly Brazilians to assess predictors of hospitalizations during ten years of follow-up. Participants were 1,448 persons aged 60 years and over at baseline (1997). The outcome was self-reported number of hospitalizations per year. Slightly more than a fifth (23%) experienced no hospitalizations during the 10 year follow-up. About 30% had 1-2 events, 31% had between 3 and 7 events, and about 18% had 8 or more events during this time. Results of multivariable hurdle and Cox proportional hazards models showed that the risk of hospitalization was positively associated with male sex, increased age, chronic conditions, and visits to the doctors in the previous 12 months. Underweight was a predictor of any hospitalization, while obesity was an inconsistent predictor of hospitalization.


2021 ◽  
pp. jrheum.201248
Author(s):  
Markus Bredemeier ◽  
Roberto Ranza ◽  
Adriana Maria Kakehasi ◽  
Aline Ranzolin ◽  
Inês Guimarães da Silveira ◽  
...  

Objective To evaluate the safety of the methotrexate (MTX)-leflunomide (LEF) combination in rheumatoid arthritis (RA), comparing it with other therapeutic schemes involving conventional synthetic (cs-) and biologic (b-) disease modifying anti-rheumatic drugs (DMARDs) or JAK inhibitors (JAKi). Methods RA patients starting the first treatment course with a csDMARD (without previous use of biologic or JAKi) or first bDMARD/JAKi were followed-up in a registry-based, multicentric cohort study in Brazil (BiobadaBrasil). The primary outcome was the incidence of serious adverse events (SAEs); secondary outcomes included serious infections. Multivariate Cox proportional hazards models and propensity score matched analysis (PSMA) were used for statistical comparisons. Results In total, 1671 patients (5349 patient-years [PY]) were enrolled; 452 patients (1537 PY) received MTX plus LEF. The overall incidence of SAEs was 5.6/100 PY. The hazard of SAEs for MTX plus LEF was not higher than for MTX or LEF (adjusted hazard ratio: 1.00, 95% CI, 0.76 to 1.31, P=0.984). The MTX-LEF combo presented a lower hazard of SAEs (0.56, 0.36 to 0.88, P=0.011) and infectious SAEs (0.48, 0.25 to 0.94, P=0.031) than bDMARDs/JAKi with MTX or LEF. MTX plus LEF presented lower hazard of SAEs than MTX plus SSZ (0.33, 0.16 to 0.65, P=0.002). Analysis using PSMA confirmed the results obtained with traditional multivariate Cox analysis. Conclusion In our study, MTX plus LEF presented a relatively good overall safety profile in comparison to MTX plus SSZ and schemes involving advanced therapies in RA.


2021 ◽  
Vol 10 (6) ◽  
Author(s):  
Bin Yan ◽  
Ruohan Li ◽  
Jiamei Li ◽  
Xuting Jin ◽  
Fan Gao ◽  
...  

Background Previous studies have suggested that sleep timing is associated with cardiovascular risk factors. However, there is no evidence on the relationship between sleep timing and congestive heart failure (CHF). We aimed to examine this relationship in this study. Methods and Results We recruited 4765 participants (2207 men; mean age, 63.6±11.0 years) from the SHHS (Sleep Heart Health Study) database in this multicenter prospective cohort study. Follow‐up was conducted until the first CHF diagnosis between baseline and the final censoring date. Sleep timing (bedtimes and wake‐up times on weekdays and weekends) was based on a self‐reported questionnaire. Cox proportional hazard models were constructed to investigate the association between sleep timing and CHF. During the mean follow‐up period of 11 years, 519 cases of CHF (10.9%) were reported. The multivariable Cox proportional hazards models revealed that participants with weekday bedtimes >12:00  am (hazard ratio [HR], 1.56; 95% CI, 1.15–2.11; P =0.004) and from 11:01  pm to 12:00  am (HR, 1.25; 95% CI, 1.00–1.56; P =0.047) had an increased risk of CHF compared with those with bedtimes from 10:01  pm to 11:00  pm . After stratified analysis, the association was intensified in participants with a self‐reported sleep duration of 6 to 8 hours. Furthermore, wake‐up times >8:00  am on weekdays (HR, 1.53; 95% CI, 1.07–2.17; P =0.018) were associated with a higher risk of incident CHF than wake‐up times ≤6:00  am . Conclusions Delayed bedtimes (>11:00  pm ) and wake‐up times (>8:00  am ) on weekdays were associated with an increased risk of CHF.


2017 ◽  
Vol 44 (6) ◽  
pp. 732-739 ◽  
Author(s):  
Elena Myasoedova ◽  
Sherine E. Gabriel ◽  
Eric L. Matteson ◽  
John M. Davis ◽  
Terry M. Therneau ◽  
...  

Objective.To assess trends in cardiovascular (CV) mortality in patients with incident rheumatoid arthritis (RA) in 2000–07 versus the previous decades, compared with non-RA subjects.Methods.The study population consisted of Olmsted County, Minnesota, USA residents with incident RA (age ≥ 18 yrs, 1987 American College of Rheumatology criteria was met in 1980–2007) and non-RA subjects from the same underlying population with similar age, sex, and calendar year of index. All subjects were followed until death, migration, or December 31, 2014. Followup was truncated for comparability. Aalen-Johansen methods were used to estimate CV mortality rates, adjusting for competing risk of other causes. Cox proportional hazards models were used to compare CV mortality by decade.Results.The study included 813 patients with RA and 813 non-RA subjects (mean age 55.9 yrs; 68% women for both groups). Patients with incident RA in 2000–07 had markedly lower 10-year overall CV mortality (2.7%, 95% CI 0.6–4.9%) and coronary heart disease (CHD) mortality (1.1%, 95% CI 0.0–2.7%) than patients diagnosed in 1990–99 (7.1%, 95% CI 3.9–10.1% and 4.5%, 95% CI 1.9–7.1%, respectively; HR for overall CV death: 0.43, 95% CI 0.19–0.94; CHD death: HR 0.21, 95% CI 0.05–0.95). This improvement in CV mortality persisted after accounting for CV risk factors. Ten-year overall CV mortality and CHD mortality in 2000–07 RA incidence cohort was similar to non-RA subjects (p = 0.95 and p = 0.79, respectively).Conclusion.Our findings suggest significantly improved overall CV mortality, particularly CHD mortality, in patients with RA in recent years. Further studies are needed to examine the reasons for this improvement.


2015 ◽  
Vol 35 (5) ◽  
pp. 566-575 ◽  
Author(s):  
Fenfen Peng ◽  
Xi Xia ◽  
Feng He ◽  
Zhijian Li ◽  
Fengxian Huang ◽  
...  

Objective To explore the effect of glycated hemoglobin (HbA1c) and albumin-corrected glycated serum proteins (Alb-GSP) on the mortality of diabetic patients receiving continuous peritoneal dialysis (PD). Methods In this single-center retrospective cohort study, incident diabetic PD patients from January 1, 2006, to December 31, 2010, were recruited, and followed up until December 31, 2011. The effect of HbA1c and Alb-GSP on mortality was evaluated by Cox proportional hazards models. Results A total of 200 patients (60% male, mean age 60.3 ± 10.6 years) with a mean follow-up of 29.0 months (range: 4.3 - 71.5 months) were recruited. Sixty-four patients died during the follow-up period, of whom 21 died of cardiovascular disease (CVD). Mean values for HbA1c, GSP and Alb-GSP were 6.7% (range: 4.1 - 12.5%), 202 μmol/L (range: 69 - 459 μmol/L), and 5.78 μmol/g (range: 2.16 - 14.98 μmol/g), respectively. The concentrations of GSP and Alb-GSP were closely correlated with HbA1c ( r = 0.41, p < 0.001 and r = 0.45, p < 0.001, respectively). In multivariate Cox proportional hazards models, patients with HbA1c ≥8% were associated with increased risk of all-cause mortality (hazard ratio [HR] = 2.29, 95% confidence interval [CI]: 1.06 - 4.96, p = 0.04), but no increased mortality in patients with 6.0% ≤ HbA1c ≤ 7.9%. Patients with Alb-GSP ≤ 4.50 μmol/g had increased all-cause and non-cardiovascular mortality (HR = 2.42, 95% CI: 1.13 - 5.19, p = 0.02; and HR = 2.98, 95% CI: 1.05 - 8.48, p = 0.04 respectively). Conclusions Increased HbA1c and decreased Alb-GSP may be associated with poorer survival in diabetic PD patients, with a non-significant trend observed for poorer survival with the highest level of Alb-GSP.


2016 ◽  
Vol 76 (2) ◽  
pp. 364-370 ◽  
Author(s):  
Jonas K Eriksson ◽  
Lennart Jacobsson ◽  
Karin Bengtsson ◽  
Johan Askling

AimsTo assess and compare the incidence of cardiovascular (CV) events, by CV phenotype, between patients with ankylosing spondylitis (AS), rheumatoid arthritis (RA) and the general population.MethodsUsing linkages of national and population-based registers, we identified one cohort of prevalent patients with AS (n=5358), one with RA (n=37 245) and one with matched general population subjects (n=25 006). These cohorts were identified in 2006 through 2011 and were followed in 31 December 2012, for first ever occurrence of acute coronary syndromes (ACS), deep venous thromboembolism, pulmonary embolism and stroke, respectively. For each outcome, we calculated incidence rates standardised to the age and sex distribution of the AS cohort, as well as relative risks using Cox proportional hazards models.ResultsBased on 69 ACS events during 20 251 person-years of follow-up of the patients with AS, and 966 events during 127 014 person-years in the RA cohort, the age/sex-adjusted relative risks for ACS compared with the general population was 1.3 (95% CI 1.0 to 1.7) for AS and 1.7 (1.4 to 2.0) for RA. For thromboembolic events, the corresponding risks were 1.4 (1.1 to 1.9) in AS and 1.8 (1.5 to 2.1) in RA. Finally, for stroke, the relative risks were 1.5 (1.1 to 2.0) in AS and 1.5 (1.2 to 1.8) in RA, compared with the general population.ConclusionsPrevalent patients with AS are at a 30%–50% increased risk of incident CV events. When compared with patients with RA, this level of increase was similar for stroke, but only half as high for ACS and thrombotic events.


2015 ◽  
Vol 42 (5) ◽  
pp. 835-840 ◽  
Author(s):  
Shaowei Wu ◽  
Eunyoung Cho ◽  
Wen-Qing Li ◽  
Jiali Han ◽  
Abrar A. Qureshi

Objective.Alcohol intake has been associated with an increased risk of psoriasis. However, the association between alcohol intake and risk of psoriatic arthritis (PsA) has been unclear. We evaluated the association between alcohol intake and risk of incident PsA in a large cohort of US women.Methods.Our present study included a total of 82,672 US women who provided repeated data on alcohol intake over the followup period (1991–2005). Self-reported PsA was validated using the Psoriatic Arthritis Screening and Evaluation (PASE) questionnaire. Cox proportional hazards models were used to estimate the age-adjusted and multivariate-adjusted HR and 95% CI for the PsA in association with alcohol intake.Results.We documented 141 incident PsA cases during 14 years (1,137,763 person-yrs) of followup. Compared to non-drinkers, the multivariate HR for PsA were 0.70 (95% CI 0.48–1.01) for 0.1–14.9 g/day, 1.43 (95% CI 0.67–3.08) for 15.0–29.9 g/day, and 4.45 (95% CI 2.07–9.59) for ≥ 30.0 g/day of cumulative average alcohol intake. Risk estimates were generally consistent when using updated alcohol intake and baseline alcohol intake in 1991 as the exposures, and when the analysis was restricted to those who developed psoriasis during the followup.Conclusion.Excessive alcohol intake was associated with an increased risk of incident PsA in a cohort of US women.


Sign in / Sign up

Export Citation Format

Share Document