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      Postdialysis Fatigue: A Frequent and Debilitating Symptom

      1 , 1

      Seminars in Dialysis

      Wiley

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          Most cited references 35

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          The neuroimmune basis of fatigue.

          The exact nature and pathophysiology of fatigue remain largely elusive despite its high prevalence in physically ill patients. Studies on the relationship between the immune system and the central nervous system provide a new perspective on the mechanisms of fatigue. Inflammatory mediators that are released by activated innate immune cells at the periphery and in the central nervous system alter the metabolism and activity of neurotransmitters, generate neurotoxic compounds, decrease neurotrophic factors, and profoundly disturb the neuronal environment. The resulting alterations in fronto-striatal networks together with the activation of insula by inflammatory interoceptive stimuli underlie the many dimensions of fatigue including reduced incentive motivation, decreased behavioral flexibility, uncertainty about usefulness of actions, and awareness of fatigue. Published by Elsevier Ltd.
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            The association between fatigue and inflammatory marker levels in cancer patients: a quantitative review.

            Increased cytokine and neopterin levels may be responsible for cancer-related fatigue, the most common complaint among cancer patients. We quantitatively reviewed empirical findings on this topic, focusing on studies not using immunotherapy. PubMed, PsychINFO and BIOSIS were searched for articles published until July 2006. Studies remained unweighted or were weighted according to study quality and sample size. The correlation coefficient r was used for statistical analyses. Heterogeneity among the studies was examined using the I(2) index. Eighteen studies (1037 participants) of moderately high methodological quality were located and statistically analyzed. Most studies measured more than one inflammatory marker, resulting in a total of 58 correlation estimates. In 31 of these, we had to input a null correlation because results had been simply reported as nonsignificant and no further statistical information was available. General analyses based on weighting according to sample size showed a significantly positive correlation between fatigue and circulating levels of inflammatory markers (r=0.11, p<0.0001). Analyses of individual inflammatory markers revealed significantly positive correlations between fatigue and IL-6 (r=0.12, p=0.004), fatigue and IL-1 ra (r=0.24, p=0.0005), and fatigue and neopterin (r=0.22, p=0.0001). Fatigue did not correlate significantly with IL-1 beta (r=0.05, p=0.42) or TNF-alpha (r=0.04, p=0.34). Given its preliminary nature due to the limited available data, this quantitative review showed a positive association between cancer-related fatigue and circulating levels of IL-6, IL-1 ra and neopterin. Future studies examining the relationship between cancer related fatigue and inflammation would benefit from multiple rather than single blood sampling and from repeated daily ratings of the multidimensional nature of fatigue.
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              Examining the role of neuroinflammation in major depression.

              Recent findings have established a connection between inflammation and major depression and specifically the role of the hypothalamic-pituitary-adrenal (HPA) axis in depression. This article reviews clinical and experimental studies examining the role of the HPA axis, HPA hyperactivity (resulting in increased cortisol levels), as well as the proinflammatory cytokines tumor necrosis factor, C-reactive protein, and the interleukins, in depressed patients. Similarly this paper will review data supporting increased cytokine levels in depression and specifically differential effects in treatment-resistant patients, as well as potentially distinguishing in particular depression subtypes. Understanding the role of the immune system and inflammation in patients with major depression is essential in order to develop efficacious treatments potentially targeting inflammation in relation to the depression in order to reduce patient symptomatology and comorbidities.
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                Author and article information

                Journal
                Seminars in Dialysis
                Semin Dial
                Wiley
                08940959
                May 2016
                May 2016
                January 25 2016
                : 29
                : 3
                : 222-227
                Affiliations
                [1 ]Hemodialysis Service; Department of Urology and Nephrology; Catholic University; Rome Italy
                Article
                10.1111/sdi.12468
                © 2016
                Product
                Self URI (article page): http://doi.wiley.com/10.1111/sdi.12468

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