Young S.P.,University of Birmingham |
Kapoor S.R.,University of Birmingham |
Viant M.R.,University of Birmingham |
Byrne J.J.,University of Birmingham |
And 5 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.
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.
Douglas M.R.,University of Birmingham |
Douglas M.R.,Dudley Group of Hospitals NHS Foundation Trust
Expert Review of Neurotherapeutics | Year: 2013
Pharmacological and surgical treatments offer symptomatic benefits to patients with Parkinson's disease; however, as the condition progresses, patients experience gradual worsening in symptom control, with the development of a range of disabling complications. In addition, none of the currently available therapies have convincingly shown disease-modifying effects-either in slowing or reversing the disease. These problems have led to extensive research into the possible use of gene therapy as a treatment for Parkinson's disease. Several treatments have reached human clinical trial stages, providing important information on the risks and benefits of this novel therapeutic approach, and the tantalizing promise of improved control of this currently incurable neurodegenerative disorder. © 2013 Expert Reviews Ltd.
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.
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.