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      Use of the painDETECT tool in rheumatoid arthritis suggests neuropathic and sensitization components in pain reporting

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          Abstract

          Rheumatoid arthritis (RA) is an inflammatory autoimmune condition typified by systemic inflammation targeted toward synovial joints. Inhibition of proinflammatory networks by disease-modifying antirheumatic drugs, eg, methotrexate and biologic therapies, including tumor necrosis factor-α inhibitors, often leads to suppression of disease activity observed at the clinical level. However, despite the era of widespread use of disease-modifying treatments, there remain significant groups of patients who continue to experience pain. Our study formulated a pain assessment tool in the arthritis clinic to assess feasibility of measurements including the visual analog scale (VAS) and painDETECT to assess multimodal features of pain in people with established RA (n=100). Clinical measures of disease activity (Disease Activity Score in 28 Joints [DAS28]) were also recorded. Our data showed that despite the majority of subjects on at least one disease-modifying agent, the majority of patients reported severe pain (54%) by VAS, despite well-controlled clinical disease, with mean DAS28 2.07±0.9. Using the painDETECT questionnaire, 67% of patients had unlikely neuropathic pain. A significant proportion of subjects (28%) had possible neuropathic pain and 5% had features of likely neuropathic pain by painDETECT scoring. We found a positive correlation between VAS and painDETECT ( R 2=0.757). Of note, the group who had likely or probable neuropathic pain also showed significantly increased pain reporting by VAS ( P<0.01). Subjects who were clinically obese (body mass index >30) also had statistically higher proportions of pain reporting (VAS 89.0±0.7 mm) compared with subjects who had a normal body mass index (VAS 45.2±21.8 mm), P<0.05. Our findings suggest that multimodal features of pain perception exist in RA, including neuropathic and sensitization elements, perhaps explaining why a subgroup of people with RA continue to experience ongoing pain, despite their apparent suppression of inflammation.

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          Most cited references 28

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          Remission in rheumatoid arthritis: agreement of the disease activity score (DAS28) with the ARA preliminary remission criteria.

          To determine which cut-off point in the RA disease activity score (DAS28) corresponds to fulfilment of the ARA criteria for clinical remission. The disease activity of patients included in the Nijmegen RA inception cohort was systematically assessed every 3 months. For all visits, a modification of the ARA preliminary criteria for clinical remission was applied and the DAS28 was calculated. Receiver operating characteristic analysis was used to determine the cut-off point with maximum sensitivity and specificity in DAS28 corresponding with fulfilment of the modified ARA criteria. Three hundred and seventy-eight patients contributed 4378 visits. In 6.5% of the visits four of the five items and in 1.5% all five items of the modified ARA criteria were fulfilled. The optimal cut-off point for the DAS28 that corresponds to fulfilment of the modified ARA criteria was determined to be 2.66. DAS28 <2.6 corresponds to fulfilment of the preliminary ARA criteria for clinical remission in RA.
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            The Disease Activity Score and the EULAR response criteria.

            The Disease Activity Score (DAS), its modified version the DAS28, and the DAS-based European League Against Rheumatism (EULAR) response criteria are well-known measures of disease activity in rheumatoid arthritis (RA). The DAS is a clinical index of RA disease activity that combines information from swollen joints, tender joints, the acute phase response, and general health. The EULAR response criteria classify individual patients as non-, moderate, or good responders, depending on the extent of change and the level of disease activity reached. The DAS, DAS28, and EULAR response criteria have been validated extensively. For daily practice, it has been shown that a tight control strategy, including measurement of disease activity using the DAS and planned adjustment of antirheumatic medication, is an effective strategy for RA. This article summarizes the development and validation of the DAS and DAS28 and their use in clinical trials and practice for the clinician.
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              The role of the central nervous system in the generation and maintenance of chronic pain in rheumatoid arthritis, osteoarthritis and fibromyalgia

              Pain is a key component of most rheumatologic diseases. In fibromyalgia, the importance of central nervous system pain mechanisms (for example, loss of descending analgesic activity and central sensitization) is well documented. A few studies have also noted alterations in central pain processing in osteoarthritis, and some data, including the observation of widespread pain sensitivity, suggest that central pain-processing defects may alter the pain response in rheumatoid arthritis patients. When central pain is identified, different classes of analgesics (for example, serotonin-norepinephrine reuptake inhibitors, α2δ ligands) may be more effective than drugs that treat peripheral or nociceptive pain (for example, nonsteroidal anti-inflammatory drugs and opioids).
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                Author and article information

                Journal
                J Pain Res
                J Pain Res
                Journal of Pain Research
                Journal of Pain Research
                Dove Medical Press
                1178-7090
                2014
                14 October 2014
                : 7
                : 579-588
                Affiliations
                Infection and Immunity Research Institute, St George’s, University of London, London, UK
                Author notes
                Correspondence: Nidhi Sofat, Infection and Immunity Research Institute, St George’s, University of London, Cranmer Terrace, London SW17 ORE, UK, Email nsofat@ 123456sgul.ac.uk

                *These authors contributed equally to this work

                Article
                jpr-7-579
                10.2147/JPR.S69011
                4207578
                © 2014 Ahmed et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

                The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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                Original Research

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