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      Silent Burdens in Disease: Fatigue and Depression in SLE

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          Abstract

          At a time when health is being recognized as more than just avoiding death, age and comorbidity are becoming increasingly important aspects of chronic disease. Systemic Lupus Erythematous (SLE) is probably one of the best paradigms of modern chronic disease, sitting at the crossroads of numerous somatic health problems, immune activation, depression, pain, and fatigue. One hundred forty-eight female participants were enrolled in the present study: 50 diagnosed with SLE, 45 with major depressive disorder (MDD), and 53 age-matched controls. Statistically significant lower scores in quality-of-life dimensions related to physical impairment were found in SLE. Patients with MDD presented significant levels of pain, reduced physical summary component (PSC), and general health scores different from healthy controls. Fatigue was reported in 90% of women with SLE and 77.8% of the MDD patients in contrast with 39.6% in the control group. Significant correlations were seen among fatigue severity, age, and educational level in SLE. From our own previous work and more recent work on the association of immune activation and depression, unexplained fatigue in SLE may signify an early sign of immune activation flare-up. The search for cytokine markers should perhaps be extended to fatigue in SLE.

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          The development and initial validation of the Systemic Lupus International Collaborating Clinics/American College of Rheumatology damage index for systemic lupus erythematosus.

          To develop and perform an initial validation of a damage index for systemic lupus erythematosus (SLE). A list of items considered to reflect damage in SLE was generated through a nominal group process. A consensus as to which items to be included in an index was reached, together with rules for ascertainment. Each center submitted 2 assessments, 5 years apart, on 2 patients with active and 2 with inactive disease, of whom 1 had increased damage and the other had stable disease. Analysis of variance was used to test the factors physician, time, amount of damage, and activity status. Nineteen physicians completed the damage index on 42 case scenarios. The analysis revealed that the damage index could identify changes in damage seen in patients with both active and inactive disease. Patients who had active disease at both time points had a higher increase in damage. There was good agreement among the physicians on the assessment of damage in these patients. This damage index for SLE records damage occurring in patients with SLE regardless of its cause. The index was demonstrated to have content, face, criterion, and discriminant validity.
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            Depression and sickness behavior are Janus-faced responses to shared inflammatory pathways

            It is of considerable translational importance whether depression is a form or a consequence of sickness behavior. Sickness behavior is a behavioral complex induced by infections and immune trauma and mediated by pro-inflammatory cytokines. It is an adaptive response that enhances recovery by conserving energy to combat acute inflammation. There are considerable phenomenological similarities between sickness behavior and depression, for example, behavioral inhibition, anorexia and weight loss, and melancholic (anhedonia), physio-somatic (fatigue, hyperalgesia, malaise), anxiety and neurocognitive symptoms. In clinical depression, however, a transition occurs to sensitization of immuno-inflammatory pathways, progressive damage by oxidative and nitrosative stress to lipids, proteins, and DNA, and autoimmune responses directed against self-epitopes. The latter mechanisms are the substrate of a neuroprogressive process, whereby multiple depressive episodes cause neural tissue damage and consequent functional and cognitive sequelae. Thus, shared immuno-inflammatory pathways underpin the physiology of sickness behavior and the pathophysiology of clinical depression explaining their partially overlapping phenomenology. Inflammation may provoke a Janus-faced response with a good, acute side, generating protective inflammation through sickness behavior and a bad, chronic side, for example, clinical depression, a lifelong disorder with positive feedback loops between (neuro)inflammation and (neuro)degenerative processes following less well defined triggers.
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              Comparisons of the costs and quality of norms for the SF-36 health survey collected by mail versus telephone interview: results from a national survey.

              Many health status surveys have been designed for mail, telephone, or in-person administration. However, with rare exception, investigators have not studied the effect the survey mode of administration has on the way respondents assess their health and other important parameters (such as response rates, nonresponse bias, and data quality), which can affect the generalizability of results. Using a national sampling frame of noninstitutionalized adults from the General Social Survey, we randomly assigned adults to a mail survey (80%) or a computer-assisted telephone survey (20%). The surveys were designed to provide national norms for the SF-36 Health Survey. Total data collection costs per case for the telephone survey ($47.86) were 77% higher than that for the mail survey ($27.07). A significantly higher response rate was achieved among respondents randomly assigned to the mail (79.2%) than telephone survey (68.9%). Nonresponse bias was evident in both modes but, with the exception of age, was not differential between modes. The rate of missing responses was higher for mail than telephone respondents (1.59 vs. 0.49 missing items). Health ratings based on the SF-36 scales were less favorable, and reports of chronic conditions were more frequent, for mail than telephone respondents. Results are discussed in light of the trade-offs involved in choosing a survey methodology for health status assessment applications. Norms for mail and telephone versions of the SF-36 survey are provided for use in interpreting individual and group scores.
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                Author and article information

                Journal
                Autoimmune Dis
                Autoimmune Dis
                AD
                Autoimmune Diseases
                Hindawi Publishing Corporation
                2090-0422
                2090-0430
                2014
                28 January 2014
                : 2014
                : 790724
                Affiliations
                1Department of Clinical Neurosciences and Mental Health, Faculty of Medicine, University of Porto, 4200-319 Porto, Portugal
                2Rheumatology Department, São João Hospital, 4200-319 Porto, Portugal
                3IBMC/GABBA, University of Porto, 4150-180 Porto, Portugal
                Author notes
                *M. Figueiredo-Braga: mmfb@ 123456med.up.pt

                Academic Editor: Juan-Manuel Anaya

                Article
                10.1155/2014/790724
                3926392
                24592329
                b7b9739f-0a93-4855-90a0-c0e2cf9b0492
                Copyright © 2014 R. Fonseca et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 22 September 2013
                : 7 November 2013
                : 13 November 2013
                Categories
                Research Article

                Immunology
                Immunology

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