Paid work is associated with improved health-related quality of life in patients with rheumatoid arthritis

Numerous patients with rheumatoid arthritis (RA) end their working career due to consequences of the disease. No publication has reported whether there is an independent association between patients' health-related quality of life (HRQOL) and employment status. The objective of the study was to investigate the association of paid work and HRQOL in patients with RA whilst controlling for demographics and disease severity. This was a cross-sectional study. Three hundred and ten patients were consecutively recruited from two Norwegians hospitals when commencing disease modifying anti-rheumatic drug treatment. Data on demographics, employment status, disease activity (DAS28-3), physical functioning, pain, tiredness, and HRQOL (SF-36) were collected. HRQOL were compared between 123 patients working full- or part-time and 187 patients not working due to disability pension, retirement, being students or “home workers”. The regression analyses showed an independent positive association between paid work and the physical (p = 001) and the mental component (p = 012) of the SF-36 when controlling for demographics and disease severity. Paid work was statistically significantly associated with better HRQOL in patients with RA. The positive association of performing paid work and HRQOL imply that health care providers should thoroughly evaluate the possibilities for the patients to continue with paid work

Chronic non-specific low back pain - sub-groups or a single mechanism?

Copyright 2008 Wand and O'Connell; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Background: Low back pain is a substantial health problem and has subsequently attracted a considerable amount of research. Clinical trials evaluating the efficacy of a variety of interventions for chronic non-specific low back pain indicate limited effectiveness for most commonly applied interventions and approaches. Discussion: Many clinicians challenge the results of clinical trials as they feel that this lack of effectiveness is at odds with their clinical experience of managing patients with back pain. A common explanation for this discrepancy is the perceived heterogeneity of patients with chronic non-specific low back pain. It is felt that the effects of treatment may be diluted by the application of a single intervention to a complex, heterogeneous group with diverse treatment needs. This argument presupposes that current treatment is effective when applied to the correct patient. An alternative perspective is that the clinical trials are correct and current treatments have limited efficacy. Preoccupation with sub-grouping may stifle engagement with this view and it is important that the sub-grouping paradigm is closely examined. This paper argues that there are numerous problems with the sub-grouping approach and that it may not be an important reason for the disappointing results of clinical trials. We propose instead that current treatment may be ineffective because it has been misdirected. Recent evidence that demonstrates changes within the brain in chronic low back pain sufferers raises the possibility that persistent back pain may be a problem of cortical reorganisation and degeneration. This perspective offers interesting insights into the chronic low back pain experience and suggests alternative models of intervention. Summary: The disappointing results of clinical research are commonly explained by the failure of researchers to adequately attend to sub-grouping of the chronic non-specific low back pain population. Alternatively, current approaches may be ineffective and clinicians and researchers may need to radically rethink the nature of the problem and how it should best be managed

Prognostic factors for joint destruction in rheumatoid arthritis:A prospective longitudinal study of 318 patients

Objective. To quantify articular damage and to investigate prognostic factors for joint damage progression in rheumatoid arthritis (RA). Methods. RA patients satisfying the 1987 American College of Rheumatology criteria and with disease duration under 5 years were sampled from the EURIDISS longitudinal cohort study in Norway, The Netherlands, and France. Hand radiographs were assessed at baseline and at 2 to 3 year followup using Sharp score modified by van der Heijde. Assessment of erosion and joint space narrowing, performed in sequential order by a single reader blinded to patients' characteristics, had high intraobserver reproducibility (intraclass correlation coefficient 0.98-0.99). Baseline prognostic factors were analyzed in a multivariate linear regression model. Results. A total of 318 patients with RA aged 52.4 years (70.4% were female) and with a mean 2 years' disease duration at baseline were followed over 30 months. Median (quartiles) baseline and followup modified Sharp scores were 3 (0-11) and 9 (1-27), respectively, with 35.8% and then 22.3% of patients with no radiological damage. Controlling for age, sex, and country, the final joint damage was predicted by baseline modified Sharp score, rheumatoid factor positivity, time from disease diagnosis, patient global health assessment, and erythrocyte sedimentation rate, and by followup duration, explaining 76.8% of the outcome variance. Conclusion. This multinational study confirmed the prognostic role in RA of a set of features previously identified in smaller cohorts. It indicates which disease characteristics should be focused on in the early years of RA to identify patients at higher risk of developing severe disease and who are candidates for aggressive therapy

Predictors of depressive symptoms in persons with diabetic peripheral neuropathy: a longitudinal study

The aim of the study was to determine whether diabetic peripheral neuropathy (DPN) is a risk factor for depressive symptoms and examine the potential mechanisms for this relationship. This longitudinal study (9 and 18 month followup) of 338 DPN patients (mean age 61 years; 71% male; 73% type 2 diabetes) examined the temporal relationships between DPN severity (mean±SD; neuropathy disability score [NDS], 7.4±2.2; mean vibration perception threshold, 41.5±9.5 V), DPN somatic experiences (symptoms and foot ulceration), DPN psychosocial consequences (restrictions in activities of daily living [ADL] and social selfperception)and the Hospital Anxiety and Depression subscale measuring depressive symptoms (HADS-D; mean 4.9±3.7). Controlling for baseline HADS-D and demographic/disease variables, NDS at baseline significantly predicted increased HADS-D over 18 months. This association was mediated by baseline unsteadiness, which was significantly associated with increased HADS-D. Baseline ADL restrictions significantly predicted increased HADS-D and partly mediated the association between baseline unsteadiness and change in HADS-D. Increased pain, unsteadiness and ADL restrictions from baseline to 9 months each significantly predicted increased HADS-D over 18 months. Change in social self-perception from baseline to 9 months significantly predicted increased HADS-D and partly mediated the relationships of change in unsteadiness and ADL restrictions with change in HADS-D. These results confirm that neuropathy is a risk factor for depressive symptoms because it generates pain and unsteadiness. Unsteadiness is the symptom with the strongest association with depression,and is linked to depressive symptoms by perceptions of diminished self-worth as a result of inability to perform social roles

Mechanisms, impact and management of pain in rheumatoid arthritis

© 2014 Macmillan Publishers Limited. All rights reserved. People with rheumatoid arthritis (RA) identify pain as their most important symptom, one that often persists despite optimal control of inflammatory disease. RA pain arises from multiple mechanisms, involving inflammation, peripheral and central pain processing and, with disease progression, structural change within the joint. Consequently, RA pain has a wide range of characteristics-constant or intermittent, localized or widespread-and is often associated with psychological distress and fatigue. Dominant pain mechanisms in an individual are identified by critical evaluation of clinical symptoms and signs, and by laboratory and imaging tests. Understanding these mechanisms is essential for effective management, although evidence from preclinical models should be interpreted with caution. A range of pharmacological analgesic and immunomodulatory agents, psychological interventions and surgery may help manage RA pain. Pain contributes importantly to the clinical assessment of inflammatory disease activity, and noninflammatory components of RA pain should be considered when gauging eligibility for or response to biologic agents. Further randomized controlled trials are required to determine the optimal usage of analgesics in RA, and novel agents with greater efficacy and lower propensity for adverse events are urgently needed. Meanwhile, targeted use of existing treatments could reduce pain in people with RA