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      Depressive symptoms, pain and disability for adolescent patients with juvenile idiopathic arthritis: results from the Childhood Arthritis Prospective Study

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          Abstract

          Objectives

          To determine if depressive symptoms assessed near diagnosis associate with future measures of pain, disability and disease for adolescent patients diagnosed with JIA.

          Methods

          Data were analysed from JIA patients aged 11–16 years recruited to the Childhood Arthritis Prospective Study, a UK-based inception cohort of childhood-onset arthritis. Depressive symptoms (using the Mood and Feelings Questionnaire; MFQ), active and limited joint count, disability score (Childhood Health Assessment Questionnaire), pain visual analogue scale and patient’s general evaluation visual analogue scale were collected. Associations between baseline measures (first visit to paediatric rheumatologist) were analysed using multiple linear regression. Linear mixed-effect models for change in the clinical measures of disease over 48 months were estimated including MFQ as an explanatory variable.

          Results

          Data from 102 patients were analysed. At baseline, median (IQR) age was 13.2 years (11.9–14.2 years) and 14.7% scored over the MFQ cut-off for major depressive disorder. At baseline, depressive symptoms significantly associated with all clinical measures of disease ( P ⩽ 0.01). High baseline depressive symptoms scores predicted worse pain ( P ⩽ 0.005) and disability ( P ⩽ 0.001) 12 months later but not active and limited joint counts.

          Conclusions

          Adolescent patients with JIA and depressive symptoms had more active joints, pain and disability at the time of their first specialist appointment. The associations between baseline depression and both pain and disability continued for at least one year, however, this was not the case for active joint count.

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          Most cited references32

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          Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk.

          We propose a model wherein chronic stress results in glucocorticoid receptor resistance (GCR) that, in turn, results in failure to down-regulate inflammatory response. Here we test the model in two viral-challenge studies. In study 1, we assessed stressful life events, GCR, and control variables including baseline antibody to the challenge virus, age, body mass index (BMI), season, race, sex, education, and virus type in 276 healthy adult volunteers. The volunteers were subsequently quarantined, exposed to one of two rhinoviruses, and followed for 5 d with nasal washes for viral isolation and assessment of signs/symptoms of a common cold. In study 2, we assessed the same control variables and GCR in 79 subjects who were subsequently exposed to a rhinovirus and monitored at baseline and for 5 d after viral challenge for the production of local (in nasal secretions) proinflammatory cytokines (IL-1β, TNF-α, and IL-6). Study 1: After covarying the control variables, those with recent exposure to a long-term threatening stressful experience demonstrated GCR; and those with GCR were at higher risk of subsequently developing a cold. Study 2: With the same controls used in study 1, greater GCR predicted the production of more local proinflammatory cytokines among infected subjects. These data provide support for a model suggesting that prolonged stressors result in GCR, which, in turn, interferes with appropriate regulation of inflammation. Because inflammation plays an important role in the onset and progression of a wide range of diseases, this model may have broad implications for understanding the role of stress in health.
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            The macrophage theory of depression.

            R.S. Smith (1991)
            Excessive secretion of macrophage monokines is proposed as the cause of depression. Monokines when given to volunteers can produce the symptoms necessary for the Diagnostic and Statistical Manual of Mental Disorders, Third Edition Revised (DSM-III-R) diagnosis of major depressive episode. Interleukin-1 (IL-1) can provoke the hormone abnormalities linked with depression. This theory provides an explanation for the significant association of depression with coronary heart disease, rheumatoid arthritis, stroke and other diseases where macrophage activation occurs. The 3:1 female/male incidence of depression ratio is accounted for by estrogen's ability to activate macrophages. The extraordinary low rate of depression in Japan is consistent with the suppressive effect of eicosapentanoic acid on macrophages. Fish oil is proposed as a prophylaxis against depression and omega-6 fat as a promoter. Infection, tissue damage, respiratory allergies and antigens found in food are some of the possible causes of macrophage activation triggering depression.
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              • Article: not found

              Relationships between cognitive emotion regulation strategies and depressive symptoms: A comparative study of five specific samples

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                Author and article information

                Journal
                Rheumatology (Oxford)
                Rheumatology (Oxford)
                brheum
                Rheumatology (Oxford, England)
                Oxford University Press
                1462-0324
                1462-0332
                August 2018
                25 April 2018
                25 April 2018
                : 57
                : 8
                : 1381-1389
                Affiliations
                [1 ]Arthritis Research UK Centre for Adolescent Rheumatology, University College London, London, UK
                [2 ]Arthritis Research UK Centre for Epidemiology, University of Manchester, Manchester, UK
                [3 ]Department of Academic Rheumatology, Faculty of Life Sciences & Medicine, London, UK
                [4 ]Psychology Department, Institute of Psychiatry Psychology and Neuroscience, Kings College London, London, UK
                [5 ]Department of Clinical Pharmacology, William Harvey Research Institute, Queen Mary University of London, London, UK
                [6 ]Child and Adolescent Psychological Services, University College London Hospital NHS Foundation Trust, London, UK
                [7 ]Paediatric Rheumatology, Institute Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK
                [8 ]Department of Rheumatology, Alder Hey Children’s Foundation NHS Trust Liverpool, Liverpool, UK
                [9 ]Department of Rheumatology, Royal Manchester Children’s Hospital, Manchester, UK
                [10 ]Department of Rheumatology, Royal Hospital for Children, Glasgow, UK
                [11 ]Paediatric Rheumatology, Royal Hospital for Sick Children, Edinburgh, UK
                [12 ]UCL GOS Institute of Child Health, University College London, London, UK
                Author notes

                Wendy Thomson and Yiannis Ioannou contributed equally to this study.

                Present address: UCB Celltech, 216 Bath Road, Slough SW1 3WE, UK.

                Correspondence to: Yiannis Ioannou, Arthritis Research UK Centre for Adolescent Rheumatology, University College London, Rayne Institute, 5 University Street, London, WC1E 6JF, UK. E-mail: y.ioannou@ 123456ucl.ac.uk
                Author information
                http://orcid.org/0000-0003-1714-9963
                http://orcid.org/0000-0002-1081-9170
                http://orcid.org/0000-0001-8242-9262
                Article
                key088
                10.1093/rheumatology/key088
                6055569
                29697850
                f2954510-c3bb-4662-9775-0d9e055d791c
                © The Author(s) 2018. Published by Oxford University Press on behalf of the British Society for Rheumatology.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 6 June 2017
                : 7 March 2018
                Page count
                Pages: 9
                Funding
                Funded by: Arthritis Research UK 10.13039/501100000341
                Award ID: 20542
                Funded by: Arthritis Research UK 10.13039/501100000341
                Award ID: 20542
                Funded by: Arthritis Research UK 10.13039/501100000341
                Award ID: 20164
                Funded by: Arthritis Research UK 10.13039/501100000341
                Funded by: Arthritis Research UK 10.13039/501100000341
                Award ID: 20385
                Funded by: Genomics at Manchester University
                Categories
                Clinical Science

                Rheumatology
                adolescent rheumatology,juvenile idiopathic arthritis,depression,pain,disability
                Rheumatology
                adolescent rheumatology, juvenile idiopathic arthritis, depression, pain, disability

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