The impact of disease activity, pain, disability and treatments on fatigue in established rheumatoid arthritis
Department of Rheumatology, King's College London School of Medicine, Weston Education Centre, London SE5 9RJ, UK. Clinical Rheumatology
(Impact Factor: 1.77).
11/2011; 31(4):717-22. DOI: 10.1007/s10067-011-1887-y
We investigate a range of clinical factors and anti-rheumatic treatments, for their degree of association with rheumatoid arthritis (RA) fatigue in 557 patients. A range of clinical measures concerning disability, pain and disease activity together with drug history were recorded as part of routine clinical visits. Fatigue was measured using the Functional Assessment of Chronic Illness Therapy (FACIT-F) questionnaire. Spearman's correlation (p < 0.05) evaluated FACIT-F against the other clinical measures. Mean FACIT-F was compared between the treatment groups. Multivariate linear regression analysis investigated association between the clinical measures and FACIT-F in more detail. Correlation (p < 0.05) with FACIT-F was the strongest for Health Assessment Questionnaire (HAQ) (r = −0.68), patient global (r = −0.64) and pain (r = −0.62) visual analogue scores. In multivariate models, DAS28, HAQ and pain explained variability in fatigue the best (R
2 = 0.54). Further analyses, looking at the sub components of DAS28, show that fatigue is mainly associated with tender joint counts and pain rather than swollen joint counts or erythrocyte sedimentation rate. RA fatigue levels were not significantly different between patients on no treatment, disease modifying anti-rheumatic drugs or biologics. Fatigue in established RA is not specifically influenced by the type of treatment used but is associated with tender joint counts, pain and disability. This finding is in contrast to recent trials in early RA that suggest biologics are better than traditional disease modifying anti-rheumatic drugs for fatigue. This difference in result may be because the origins of fatigue are not the same in early compared with established RA.
Available from: Teresa M Ward
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To examine the association between parent/proxy- and child-reported fatigue and disease activity in children with polyarticular, extended oligoarticular, and persistent oligoarticular juvenile idiopathic arthritis (JIA).
We enrolled a cross-sectional cohort of 309 children recruited from the Seattle Children's Hospital rheumatology clinic from 2009-2011. Parents and children completed the PedsQL Multidimensional Fatigue Scales. The parent/proxy, child, and/or physician provided additional disease activity data at each clinic visit, including active joint count, pain, and the Childhood Health Assessment Questionnaire (C-HAQ). Disease activity was dichotomized as active or inactive using the American College of Rheumatology provisional criteria for clinically inactive disease. The Juvenile Arthritis Disease Activity Score (JADAS) was also calculated. Linear regression was used to examine the associations between fatigue and disease activity.
Associations among fatigue, clinically inactive disease, and the JADAS were not statistically significant after controlling for pain. In the multivariable models of fatigue, the C-HAQ and parent/child-reported disease activity were significantly associated with fatigue; however, only the C-HAQ remained significantly associated after adjustment for pain. The C-HAQ and parent/child-reported disease activity explained 17% and 30% of the variance in fatigue for the parent/proxy- and child-reported multivariable models, respectively.
In this cohort, functional ability, as measured by the C-HAQ, was significantly associated with fatigue. Child- and parent/proxy-reported pain were important confounders of the relationship between fatigue and disease activity. Routinely incorporating pain and fatigue into interventional and observational trials of JIA will enable better delineation of the relationships between these variables.
Available from: rsp.ima-press.net
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ABSTRACT: A growing number of reports indicate that anti-inflammatory actions of fish oil (FO) are beneficial against systemic lupus erythematosus (SLE). However, the majority of pre-clinical studies were performed using 5-20% FO, which is higher than the clinically relevant dose for lupus patients. The present study was performed in order to determine the effective low dose of FDA-approved concentrated FO (Lovaza®) compared to the commonly used FO-18/12 (18-Eicosapentaenoic acid [EPA]/12-Docosahexaenoic acid [DHA]). We examined the dose-dependent response of Lovaza® (1% and 4%) on an SLE mouse strain (NZBxNZW)F1 and compared the same with 1% and 4% placebo, as well as 4% FO-18/12, maintaining standard chow as the control. Results show for the first time that 1% Lovaza® extends maximal lifespan (517 d) and 4% Lovaza® significantly extends both the median (502 d) and maximal (600 d) life span of (NZBxNZW)F1 mice. In contrast, FO-18/12 extends only median lifespan (410 d) compared to standard chow diet (301 d). Additionally, 4% Lovaza® significantly decreased anti-dsDNA antibodies, reduced glomerulonephritis and attenuated lipopolysaccharide-induced pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) in splenocytes compared to placebo. 4% Lovaza® was also shown to reduce the expression of inflammatory cytokines, including IL-1β, IL-6 and TNF-α, while increasing renal anti-oxidant enzymes in comparison to placebo. Notably, NFκB activation and p65 nuclear translocation were lowered by 4% Lovaza® compared to placebo. These data indicate that 1% Lovaza® is beneficial, but 4% Lovaza® is more effective in suppressing glomerulonephritis and extending life span of SLE-prone short-lived mice, possibly via reducing inflammation signaling and modulating oxidative stress.
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