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      Enhanced reactivity to pain in patients with rheumatoid arthritis

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          Abstract

          Introduction

          Maladaptive physiological responses to stress appear to play a role in chronic inflammatory diseases such as rheumatoid arthritis (RA). However, relatively little stress research in RA patients has involved the study of pain, the most commonly reported and most impairing stressor in RA. In the present study, we compared psychophysical and physiological responses to standardized noxious stimulation in 19 RA patients and 21 healthy controls.

          Methods

          Participants underwent a single psychophysical testing session in which responses to a variety of painful stimuli were recorded, and blood samples were taken at multiple time points to evaluate the reactivity of cortisol, interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) to the experience of acute pain.

          Results

          The findings suggest that RA patients display a fairly general hyperalgesia to mechanical and thermal stimuli across several body sites. In addition, while serum cortisol levels did not differ at baseline or following pain testing in patients relative to controls, the RA patients tended to show elevations in serum IL-6 and demonstrated enhanced pain-reactivity of serum levels of TNF-α compared with the healthy controls ( P < 0.05).

          Conclusions

          These findings highlight the importance of pain as a stressor in RA patients and add to a small body of literature documenting amplified responses to pain in RA. Future studies of the pathophysiology of RA would benefit from the consideration of acute pain levels when comparing RA patients with other groups, and future trials of analgesic interventions in RA patients may benefit from evaluating the effects of such interventions on inflammatory activity.

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          Most cited references61

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          The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis.

          The revised criteria for the classification of rheumatoid arthritis (RA) were formulated from a computerized analysis of 262 contemporary, consecutively studied patients with RA and 262 control subjects with rheumatic diseases other than RA (non-RA). The new criteria are as follows: 1) morning stiffness in and around joints lasting at least 1 hour before maximal improvement; 2) soft tissue swelling (arthritis) of 3 or more joint areas observed by a physician; 3) swelling (arthritis) of the proximal interphalangeal, metacarpophalangeal, or wrist joints; 4) symmetric swelling (arthritis); 5) rheumatoid nodules; 6) the presence of rheumatoid factor; and 7) radiographic erosions and/or periarticular osteopenia in hand and/or wrist joints. Criteria 1 through 4 must have been present for at least 6 weeks. Rheumatoid arthritis is defined by the presence of 4 or more criteria, and no further qualifications (classic, definite, or probable) or list of exclusions are required. In addition, a "classification tree" schema is presented which performs equally as well as the traditional (4 of 7) format. The new criteria demonstrated 91-94% sensitivity and 89% specificity for RA when compared with non-RA rheumatic disease control subjects.
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            Pathophysiology of peripheral neuropathic pain: immune cells and molecules.

            Damage to the peripheral nervous system often leads to chronic neuropathic pain characterized by spontaneous pain and an exaggerated response to painful and/or innocuous stimuli. This pain condition is extremely debilitating and usually difficult to treat. Although inflammatory and neuropathic pain syndromes are often considered distinct entities, emerging evidence belies this strict dichotomy. Inflammation is a well-characterized phenomenon, which involves a cascade of different immune cell types, such as mast cells, neutrophils, macrophages, and T lymphocytes. In addition, these cells release numerous compounds that contribute to pain. Recent evidence suggests that immune cells play a role in neuropathic pain in the periphery. In this review we identify the different immune cell types that contribute to neuropathic pain in the periphery and release factors that are crucial in this particular condition.
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              Characteristics and prediction of early pain after laparoscopic cholecystectomy.

              Small-scale studies have suggested a large inter-individual variation in early postoperative pain after laparoscopic cholecystectomy, emphasizing the need for improved analgesic treatment and valid predictors. We investigated prospectively the association between a preoperative nociceptive stimulus by ice water (cold pressor test), neuroticism, dyspepsia, patient history of biliary symptoms, intraoperative factors, and demographic information in 150 consecutive patients undergoing uncomplicated laparoscopic cholecystectomy for their influence on early postoperative pain. During the first postoperative week patients registered overall pain, incisional, visceral, and shoulder pain on a visual analogue scale and verbal rating scale, and daily analgesic requirements were noted. Throughout the first postoperative week overall pain showed a pronounced inter-individual variability. Incisional pain dominated in incidence and intensity compared with visceral pain, which in turn dominated over shoulder pain. In a multivariate analysis model, preoperative neuroticism, sensitivity to cold pressor-induced pain, and age were identified as independent risk factors for early postoperative pain. Our results suggest that future analgesic studies after laparoscopic cholecystectomy should focus on reduction of incisional pain.
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                Author and article information

                Journal
                Arthritis Res Ther
                Arthritis Research & Therapy
                BioMed Central
                1478-6354
                1478-6362
                2009
                4 May 2009
                : 11
                : 3
                : R61
                Affiliations
                [1 ]Department of Anesthesiology, Harvard Medical School, Brigham & Women's Hospital, 850 Boylston Street, Suite 302, Chestnut Hill, MA 02467, USA
                [2 ]Department of Psychiatry, Johns Hopkins University School of Medicine, 600 N. Wolfe Street, Baltimore, MD 21287, USA
                [3 ]Division of Rheumatology, Johns Hopkins University School of Medicine, 5200 Eastern Avenue, MFL Suite 4100, Baltimore, MD 21224, USA
                [4 ]Johns Hopkins University School of Nursing, 525 N. Wolfe Street, Baltimore, MD 21287, USA
                Article
                ar2684
                10.1186/ar2684
                2714104
                19413909
                b7433c54-e386-4b40-8c12-903e77a682e8
                Copyright © 2009 Edwards et al.; 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.

                History
                : 16 February 2009
                : 1 April 2009
                : 17 April 2009
                : 4 May 2009
                Categories
                Research Article

                Orthopedics
                Orthopedics

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