19 research outputs found

    Clinical phenotypes of depressed patients with evidence of inflammation and somatic symptoms.

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    Funder: MQ: Transforming Mental Health; Grant(s): MQDS17\40, MQDS17/40Whether depressed patients with evidence of inflammation are more appropriate candidates for immunotherapies is being tested in several clinical trials, which are selecting patients based on elevated C-reactive protein (CRP) and inflammation-related symptoms. However, studies of the clinical and phenotypic profile of depressed patients with elevated CRP are relatively scarce. We have investigated detailed clinical characteristics of 84 depressed patients, grouped as those with (CRP≥3 mg/L) and without (CRP<3 mg/L) inflammation. All patients met the International Classification of Diseases 10th Revision criteria for current depressive episode and had somatic symptoms of depression. We report that depressed patients with inflammation are more likely to be older (P=0.04), have higher body mass index (P<0.01), and be on non-selective serotonin reuptake inhibitor anti-depressants (P=0.04). After adjusting for potential confounders, the inflammation group had higher depression severity (adjusted mean difference, 8.82; 95% CI, 3.91-13.72), somatic symptoms (adjusted mean difference, 3.25; 95% CI, 1.58-4.92), state anxiety (adjusted mean difference, 9.25; 95% CI, 3.82-14.67), perceived stress (adjusted mean difference, 4.58; 95% CI, 1.98-7.18), and fatigue (adjusted mean difference, 9.71; 95% CI, 3.09-6.33), but not anhedonia. The inflamed group also had poorer quality of life (adjusted mean difference, -0.18; 95% CI, -0.32-0.05). At individual depressive symptom level, the inflammation group had increased guilty feelings (adjusted odds ratio [OR], 7.28; 95% CI, 2.09-31.17), pessimism (adjusted OR, 5.38; 95% CI, 1.53-22.73), concentration difficulties (adjusted OR, 4.56; 95% CI, 1.32-19.02), and indecisiveness (adjusted OR, 4.21; 95% CI, 1.15-18.54). Our findings highlight the clinical features associated with inflammation in depressed patients with somatic symptoms, including poor quality of life, supporting the need for intervention targeting this group. These results could also aid patient and outcome selection in future clinical trials testing immunotherapies in depression. Replication of these findings in larger samples is required.This work was funded by a Wellcome Trust fellowship to GMK (grant code: 201486/Z/16/Z). GMK also acknowledges funding support from Cambridgeshire and Peterborough NHS Foundation Trust R&D Department (Grant code: G101481), the BMA Foundation (J Moulton grant 2019); the MQ: Transforming Mental Health (grant code: MQDS17/40); and the Medical Research Council UK (grant codes: MC_PC_17213 and MR/S037675/1). The BMA Foundation J Moulton grant supports ÉMF and the MRC grant MC_PC_17213 supports JTP. NK is supported by the International Max Planck Research School of Translational Psychiatry (IMPRS-TP). The funding sources had no role in study design; collection, analysis, and interpretation of data; writing of the report; and the decision to submit the paper for publication

    Depression in patients with spondyloarthritis:prevalence, incidence, risk factors, mechanisms and management

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    Depression is a major neuropsychiatric disorder common in patients with rheumatological conditions including spondyloarthritis (SpA). It is associated with higher disease activity, functional impairment, poor treatment response and quality of life in patients with musculoskeletal disorders. Using ankylosing spondylitis (AS) and psoriatic arthritis (PsA) as examples, we have reviewed the evidence regarding the burden, risk factors, potential mechanisms and clinical management of depression in spondyloarthritis. The prevalence of depression is higher in patients with AS and PsA compared with the general population, with evidence of moderate/severe depression in about 15% of patients with AS or PsA. Mild depression is even more common and estimated to be present in about 40% of patients with AS. In addition to conventional risk factors such as stressful life events and socioeconomic deprivation, increased risk of depression in SpA may be associated with disease-related factors, such as disease activity, poor quality of life, fatigue, and sleep disturbances. Emerging evidence implicates inflammation in the aetiology of depression, which could also be a shared mechanism for depression and chronic inflammatory conditions such as AS and PsA. It is imperative for clinicians to actively assess and treat depression in SpA, as this could improve treatment adherence, quality of life, and overall long-term clinical and occupational outcomes. The use of validated tools can aid recognition and management of depression in rheumatology clinics. Management of depression in SpA, especially when to refer to specialist mental health services, are discussed

    Depression in patients with spondyloarthritis: prevalence, incidence, risk factors, mechanisms and management

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    Funder: MQ: Transforming Mental Health; FundRef: https://doi.org/10.13039/501100008162; Grant(s): MQDS17/40Funder: cambridge trust; FundRef: https://doi.org/10.13039/501100003343Depression is a major neuropsychiatric disorder common in patients with rheumatological conditions including spondyloarthritis (SpA). It is associated with higher disease activity, functional impairment, poor treatment response and quality of life in patients with musculoskeletal disorders. Using ankylosing spondylitis (AS) and psoriatic arthritis (PsA) as examples, we have reviewed the evidence regarding the burden, risk factors, potential mechanisms and clinical management of depression in spondyloarthritis. The prevalence of depression is higher in patients with AS and PsA compared with the general population, with evidence of moderate/severe depression in about 15% of patients with AS or PsA. Mild depression is even more common and estimated to be present in about 40% of patients with AS. In addition to conventional risk factors such as stressful life events and socioeconomic deprivation, increased risk of depression in SpA may be associated with disease-related factors, such as disease activity, poor quality of life, fatigue, and sleep disturbances. Emerging evidence implicates inflammation in the aetiology of depression, which could also be a shared mechanism for depression and chronic inflammatory conditions such as AS and PsA. It is imperative for clinicians to actively assess and treat depression in SpA, as this could improve treatment adherence, quality of life, and overall long-term clinical and occupational outcomes. The use of validated tools can aid recognition and management of depression in rheumatology clinics. Management of depression in SpA, especially when to refer to specialist mental health services, are discussed

    Neurocognitive Performance in Depressed Patients with low-grade inflammation and somatic symptoms.

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    BACKGROUND: The link between inflammation and depression has been investigated extensively. Cognitive dysfunction in depression is an unmet treatment need. A better understanding of possible links between inflammation and cognition in people with depression may help to identify new treatment targets. METHODS: We report findings from a study comparing a range of cognitive functions between 80 depressed patients with (C-reactive protein ≥3 ​mg/L; n ​= ​37) and without (CRP<3 ​mg/L; n ​= ​43) evidence of inflammation. All participants met the International Classification of Diseases 10th Revision criteria for current depressive episode and had somatic symptoms of depression. All participants completed cognitive testing and clinical assessment and were screened for acute infection. RESULTS: Patients with evidence of inflammation, compared to those without, had slower psychomotor speed as measured by symbol coding task (mean difference ​= ​0.06, 95% CI ​= ​0.003-0.11) and slower reaction time, as measured by a simple movement time task (mean difference ​= ​26.56, 95% CI ​= ​-48.92 to -4.20). These effects were fully explained after controlling for age, sex, and body mass index. Measures of emotional processing, memory, and planning were comparable between two groups. CONCLUSIONS: Certain cognitive domains, particularly processing speed and reaction time may be more affected in depressed patients with evidence of low-grade inflammation and somatic symptoms. Further studies with larger samples are required for a clearer understanding of the association between inflammation and cognitive dysfunction in depression
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