Dudley Group of Hospitals NHS Foundation Trust

Dudley, United Kingdom

Dudley Group of Hospitals NHS Foundation Trust

Dudley, United Kingdom
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Herbison P.,University of Otago | Doyle T.C.H.,Dunedin Hospital | Treharne G.J.,University of Otago | Treharne G.J.,Dudley Group of Hospitals NHS Foundation Trust
Rheumatology | Year: 2010

Objectives: To investigate correlates of fatigue among individuals with RA and OA, including mood, sleep, disease activity and radiographic damage. Methods: Fatigue was assessed using the Multidimensional Assessment of Fatigue-Global Fatigue Index (MAF-GFI) in 103 patients with RA and 103 with OA. Sleep disturbance and pain were assessed using a visual analogue scale anxiety and depression using the Hospital Anxiety and Depression scale and disability using the HAQ. In the RA cohort, the disease activity score-28 joint count (DAS-28) and the Van der Heijde modified Sharp score were calculated, and in the OA cohort, the Kellgren-Lawrence score and the WOMAC score calculated. Results: The MAF-GFI scores were higher in the OA cohort (P = 0.02). This was not significant after controlling for disability (P = 0.59). OA participants reported greater pain, disability, depression and sleeplessness than those with RA (all P<0.01). The strongest correlates of fatigue in the RA cohort were depression (P<0.001) and anxiety (P<0.001). There was no significant association with pain (P = 0.43), DAS-28 (P = 0.07), HAQ (P = 0.10) or Sharp score (P = 0.78). In OA, the correlates of fatigue were older age (P = 0.02), sleep disturbance (P = 0.03), depression (P = 0.04), disability (P = 0.04) and lower CRP (P = 0.001). Conclusions: Fatigue is common and severe in both RA and OA. In RA, fatigue had no significant association with pain, disease activity, disability or erosions, but was associated with depression and anxiety. The disparity in correlates indicates that generalizing the experience of fatigue between OA and RA is not appropriate. Fatigue is an important domain in the assessment of disease impact. © The Author 2009. Published by Oxford University Press on behalf of the British Society for Rheumatology.

Protogerou A.,National and Kapodistrian University of Athens | Zampeli E.,National and Kapodistrian University of Athens | Tentolouris N.,National and Kapodistrian University of Athens | Makrilakis K.,National and Kapodistrian University of Athens | And 3 more authors.
Annals of the Rheumatic Diseases | Year: 2012

Objective: Rheumatoid arthritis (RA) is associated with increased coronary artery disease (CAD) and subclinical carotid atheromatosis, reportedly to equal diabetes mellitus (DM). The presence of atheromatic plaques in femoral arteries of RA patients without DM was compared with with DM patients. Methods: Femoral plaques were recorded in 30 (17 men, age 43.0±12 years, disease duration 9.9±7.1 years) and 60 older RA patients (27 men, age 63.0±7.1 years, disease duration 11.4±7.9 years) matched 1:1 for age, gender and disease duration with DM types 1 and 2 patients, respectively. All were asymptomatic and free of CAD. Results: The number of femoral plaques per patient in either RA subgroup was comparable with DM (0.64±0.82 vs 0.77±0.89 in total respective populations, p=0.340); percentages of patients with femoral plaques were also comparable (RA vs DM type 1 20% and 13%, respectively; RA vs DM type 2 58% and 66%, respectively). Hypertension and dyslipidaemia were significantly more frequent in both DM groups than RA groups. Conclusions: Subclinical femoral atheromatosis in RA is analogous to DM, further confirming the territorial unrestricted acceleration of the atheromatic process in these patients. Cardiovascular risk stratification based on both carotid and femoral plaque detection in RA should be addressed prospectively.

Young S.P.,University of Birmingham | Kapoor S.R.,University of Birmingham | Kapoor S.R.,Sandwell and West Birmingham Hospitals NHS Trust | Viant M.R.,University of Birmingham | And 7 more authors.
Arthritis and Rheumatism | Year: 2013

Objective Inflammatory arthritis is associated with systemic manifestations including alterations in metabolism. We used nuclear magnetic resonance (NMR) spectroscopy-based metabolomics to assess metabolic fingerprints in serum from patients with established rheumatoid arthritis (RA) and those with early arthritis. Methods Serum samples were collected from newly presenting patients with established RA who were naive for disease-modifying antirheumatic drugs, matched healthy controls, and 2 groups of patients with synovitis of ≤3 months' duration whose outcomes were determined at clinical followup. Serum metabolomic profiles were assessed using 1-dimensional 1H-NMR spectroscopy. Discriminating metabolites were identified, and the relationships between metabolomic profiles and clinical variables including outcomes were examined. Results The serum metabolic fingerprint in established RA was clearly distinct from that of healthy controls. In early arthritis, we were able to stratify the patients according to the level of current inflammation, with C-reactive protein correlating with metabolic differences in 2 separate groups (P < 0.001). Lactate and lipids were important discriminators of inflammatory burden in both early arthritis patient groups. The sensitivities and specificities of models to predict the development of either RA or persistent arthritis in patients with early arthritis were low. Conclusion The metabolic fingerprint reflects inflammatory disease activity in patients with synovitis, demonstrating that underlying inflammatory processes drive significant changes in metabolism that can be measured in the peripheral blood. The identification of metabolic alterations may provide insights into disease mechanisms operating in patients with inflammatory arthritis. © 2013 The Authors. Arthritis & Rheumatism is published by Wiley Periodicals, Inc. on behalf of the American College of Rheumatology.

John H.,Dudley Group of Hospitals NHS Foundation Trust | John H.,University of Birmingham | Toms T.E.,Dudley Group of Hospitals NHS Foundation Trust | Toms T.E.,University of Manchester | And 2 more authors.
Current Opinion in Cardiology | Year: 2011

PURPOSE OF REVIEW: This review examines current evidence to address the question whether rheumatoid arthritis (RA) is a coronary heart disease equivalent, similar to type 2 diabetes mellitus (DM2). RECENT FINDINGS: Cross-sectional and longitudinal epidemiological studies show a two-fold higher risk of cardiovascular disease (CVD) in patients with RA, and the magnitude of this increased risk is comparable to the risk associated with DM2. However, the mechanisms responsible for this appear to be different in the two conditions, with RA-related CVD being attributed to 'high-grade' systemic inflammation as well as classical CVD risk factors. Several classical risk factors are affected by RA or its medications, and there are some paradoxical associations between obesity or lipid abnormalities and CVD death in RA. SUMMARY: Management of RA-related CVD is likely to require both aggressive control of inflammation and systematic screening and management of classical CVD risk factors. It remains unknown whether primary prevention strategies applied successfully in DM2 would be equally easy to implement and demonstrate similar benefits in people with RA. © 2011 Lippincott Williams & Wilkins, Inc.

John H.,Dudley Group of Hospitals NHS Foundation Trust | John H.,University of Manchester | Carroll D.,University of Manchester | Kitas G.D.,Dudley Group of Hospitals NHS Foundation Trust
Rheumatology | Year: 2011

Patient education is an integral component of the management of chronic diseases. Education programmes designed for people with RA have historically aimed to improve their arthritis symptoms and outcomes. Novel educational material is required to address significant comorbidities, particularly cardiovascular disease (CVD) associated with RA. We appraise the components of education programmes incorporated in disease management in people with RA and programmes used for CVD prevention in the general population, including their design and delivery, use of behaviour theory, evaluation and long-term efficacy. We then integrate the findings in order to inform the development of educational material specifically addressing CVD in RA. This approach may be useful for other major comorbidities of RA as well as other musculoskeletal conditions. © The Author 2011. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved.

Kitas G.D.,Dudley Group of Hospitals NHS Foundation Trust | Kitas G.D.,University of Manchester | Gabrie S.E.,Mayo Medical School
Annals of the Rheumatic Diseases | Year: 2011

Rheumatoid arthritis is associated with an increased risk for cardiovascular events, such as myocardial infarction and stroke. Epidemiological evidence suggests that classic cardiovascular risk factors, such as hypertension, dyslipidaemia, insulin resistance and body composition alterations are important but not sufficient to explain all of the excess risk. High-grade systemic inflammation and its interplay with classic risk factors may also contribute. Some associations between classic risk factors and cardiovascular risk in people with rheumatoid arthritis appear counterintuitive but may be explained on the basis of biological alterations. More research is necessary to uncover the exact mechanisms responsible for this phenomenon, develop accurate systems used to identify patients at high risk, design and assess prevention strategies specific to this population of patients.

Yuksel S.,Bogazici University | Ayvazyan L.,Yerevan State Medical University | Gasparyan A.Y.,Dudley Group of Hospitals NHS Foundation Trust
Open Cardiovascular Medicine Journal | Year: 2010

Numerous inflammatory and innate immune pathways are involved in atherogenesis. Elaboration of clinical models of inflammation-induced atherogenesis may further advance our knowledge of multiple inflammatory pathways implicated in atherogenesis and provide a useful tool for cardiovascular prevention. Familial Mediterranean fever (FMF) is a chronic inflammatory disorder with profiles of inflammatory markers close to that seen in the general population. In a few recent studies, it has been shown that endothelial dysfunction, increased atherosclerotic burden and activation of platelets accompany attack-free periods of FMF. Colchicine is proved to be useful in suppression of inflammation in FMF. Preliminary basic and clinical studies suggest that this relatively safe drug may be useful for cardiovascular protection in patients with FMF and in the general population. Multinational prospective studies are warranted to further elaborate clinical model of inflammation-induced atherosclerosis associated with FMF. © Yüksel et al.

Cooper S.C.,Sandwell General Hospital | Cooper S.C.,Dudley Group of Hospitals NHS Foundation Trust | Trudgill N.J.,Sandwell General Hospital
Cancer Causes and Control | Year: 2012

Esophageal adenocarcinoma (EAC) is five times more common among men. EAC tissue exhibits an increased concentration of androgen receptors. We previously reported lower EAC incidence following prostate cancer (PC), suggesting androgen deprivation therapy may reduce EAC incidence, but were unable to demonstrate reducing incidence of EAC with time (latency effect) that would support a cumulative effect of anti-androgen treatment. The Survival Epidemiology and End Results (SEER9) dataset from 1977-2004 was therefore examined to identify subjects with a first malignant primary of PC. Subjects were followed until second primary cancer diagnosis, death, or time period end. Age- and period-adjusted standardized incidence ratios (SIR) were calculated as an estimate of relative risk of an esophageal second malignant primary. Between 1977 and 2004, 343,538 subjects (following exclusion criteria) developed PC as a first primary malignant tumor, providing 2,014,337 years of follow-up. Subsequently 604 esophageal cancers developed, with 763 expected. The incidence of EAC fell following PC [SIR 0.83 (95 % CI 0.74-0.93)] with a latency effect identified with SIR 1.1 3 months to 1 year post-PC, SIR 0.85 1-5 years post-PC, and SIR 0.75 greater than five years post-PC. The incidence of esophageal squamous cell carcinoma (ESCC) after PC was also reduced [SIR, 0.79 (0.69-0.89)], with evidence of a latency effect also seen. There is a reduced risk of developing esophageal cancer, both EAC and ESCC, following PC. Androgen deprivation therapy may contribute, but changes in lifestyle following PC diagnosis and decrease in ESCC incidence are also plausible explanations. © 2012 Springer Science+Business Media B.V.

Treharne G.J.,University of Otago | Treharne G.J.,Dudley Group of Hospitals NHS Foundation Trust
International Journal of Clinical Rheumatology | Year: 2010

Fatigue is a common and disabling symptom in a number of rheumatic diseases, including rheumatoid arthritis, ankylosing spondylitis and osteoarthritis. Patients frequently rank fatigue as one of their most disabling symptoms, adversely affecting quality of life and employment opportunities. The aims of this article are to: first, define the concept of fatigue in rheumatic disease, its nature, prevalence and impact; second, describe questionnaires that have been validated as measures of fatigue among people with rheumatic diseases; third, outline the factors which have been identified as influencing fatigue, including disease activity/severity, disability, pain, sleep disturbance, mood, self-efficacy, illness perceptions and coping; and finally, synthesize the sparse evidence currently available regarding the best strategies for managing fatigue in rheumatic disease. Recent research has suggested that disease-modifying antirheumatic drugs and biologic therapies are effective in ameliorating fatigue in both rheumatoid arthritis and ankylosing spondylitis, but the mechanism by which they reduce fatigue is not clear. Tailored exercise and psychological interventions show promise. Further studies are needed to determine the best ways of managing the fatigue associated with rheumatic disease. The assessment of fatigue in rheumatology clinics should be part of standard practice. © 2010 Future Medicine Ltd.

John H.,Dudley Group of Hospitals NHS Foundation Trust | Kitas G.,Dudley Group of Hospitals NHS Foundation Trust
European Journal of Internal Medicine | Year: 2012

Cardiovascular disease (CVD) comorbidity is a significant issue for the inflammatory arthritides (IA). There is a wealth of mortality studies showing increased cardiovascular mortality in rheumatoid arthritis (RA) and the evidence suggests that the same is likely to be true of psoriatic arthritis (PsA) and ankylosing spondylitis (AS). CVD co-morbidity is due to ischaemic pathologies driven by accelerated atherosclerosis and relates to the increased prevalence and clustering of classical risk factors, which may also be affected by treatments for IA, and their interplay with novel risk factors, namely systemic inflammation. Currently we are unable to quantify the contribution that classical and novel risk factors make to an individuals' CVD risk and specific algorithms need to be developed and validated in RA, PsA and AS to facilitate clinical management. Furthermore, large clinical trials are required to assess the effect of lifestyle modifications, primary prevention strategies and effective immunosuppression on hard CVD endpoints. However, in the meantime, a pragmatic approach should be adopted towards CVD risk management. Consensus opinion has generated guidelines for the management of CVD risk in IA and we discuss the importance of assessing each individual for CVD risk and establishing a system for routine risk factor identification alongside a commitment to treat identified risk factors to specific targets. © 2012 European Federation of Internal Medicine.

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