The effectiveness of psychological interventions for fatigue in cancer survivors: systematic review of randomised controlled trials.

BACKGROUND: Fatigue is a common symptom in cancer patients that can persist beyond the curative treatment phase. This systematic review evaluated the effectiveness of psychological interventions for cancer-related fatigue in post-treatment cancer survivors. METHODS: We searched relevant online databases and sources of grey literature. Randomised controlled trials (RCTs) evaluating psychological interventions in adult cancer patients after the completion of treatment, with fatigue as an outcome measure, were included. Two review authors extracted data independently from the selected studies and assessed the methodological quality using the Cochrane Collaboration Risk of Bias Tool. RESULTS: Thirty-three psychological interventions were identified. The sample size of the included studies varied between 28 and 409, with 4525 participants overall. Twenty-three of the included studies reported a significant effect of the interventions on reducing fatigue in cancer survivors. Most interventions focused on psychoeducation, mindfulness, cognitive or behaviour therapy-oriented strategies. However, studies differed widely in terms of measurement tools used to assess fatigue, mode, duration and frequency of the intervention delivery. CONCLUSIONS: This review showed some tentative support for psychological interventions for fatigue after cancer treatment. However, as the RCTs were heterogeneous in nature and the number of high-quality studies was limited, definitive conclusions are not yet possible. With the growing need for stage-specific research in cancer, this review sought to inform current practice and to summarise the existing evidence base of randomised controlled trials in the area. SYSTEMATIC REVIEW REGISTRATION: PROSPERO registration number: CRD42014015219.

The role of perceived and actual disease status in adjustment to rheumatoid arthritis.

OBJECTIVES: To examine the role and relative impact of illness perceptions, coping strategies and clinical disease indicators on adjustment in patients with rheumatoid arthritis. METHOD: Participants were 75 women with rheumatoid arthritis. The Illness Perception Questionnaire (IPQ), the COPE questionnaire and the Arthritis Impact Measurement Scale (AIMS) were administered during a semistructured interview. Disease status was indicated by physician ratings of joint involvement and by the laboratory indices of erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). RESULTS: Statistically significant correlations (P<0.01) were in the expected direction. Various aspects of adjustment (good physical function, low pain and depression) were associated with perceptions of low illness identity, high control/cure, more serious illness consequences and long illness timeline. Low disease activity was related to good physical function. Depression was associated with high use of coping by denial and with less frequent use of five COPE strategies: active coping, planning, seeking instrumental social support, positive reinterpretation and growth, and acceptance. In hierarchical regression analysis, disease status explained variance in physical function (15%). Illness perceptions accounted for variance in all three adjustment outcomes, ranging from 22 to 27%. Coping variables did not add to the explanation of variance on adjustment. CONCLUSIONS: Illness perceptions have significant implications for adaptation to illness and they outweigh the impact of medical disease status on depression, physical function and pain. Health interventions based on understanding and modifying perceptions of illness may prove useful in facilitating patient well-being.

Agonist-induced endocytosis and recycling of the gonadotropin-releasing hormone receptor: effect of beta-arrestin on internalization kinetics.

This study examined the dynamics of endocytotic and recycling events associated with the GnRH receptor, a unique G protein-coupled receptor (GPCR) without the intracellular carboxyl-terminal tail, after agonist stimulation, and investigated the role of beta-arrestin in this process. Subcellular location of fluorescently labeled epitope-tagged GnRH receptors stably expressed in HEK 293 cells was monitored by confocal microscopy, and the receptor/ligand internalization process was quantified using radioligand binding and ELISA. Agonist stimulation resulted in reversible receptor redistribution from the plasma membrane into the cytoplasmic compartment, and colocalization of internalized GnRH receptors with transferrin receptors was observed. Internalization experiments for the GnRH receptor and another GPCR possessing a carboxy-terminal tail, the TRH receptor, showed that the rate of internalization for the GnRH receptor was much slower than for the TRH receptor when expressed in both HEK 293 and COS-7 cells. TRH receptor internalization could be substantially increased by coexpression with beta-arrestin in COS-7 cells, while GnRH receptor internalization was not affected by coexpression with beta-arrestin in either cell type. Coexpression of the GnRH receptor with the dominant negative beta-arrestin (319-418) mutant did not affect its ability to internalize, and activated GnRH receptors did not induce time-dependent redistribution of beta-arrestin/green fluorescent protein to the plasma membrane. However, the beta-arrestin mutant impaired the internalization of the TRH receptor, and activated TRH receptors induced the beta-arrestin/green fluorescent protein translocation. This study demonstrates that, despite having no intracellular carboxy-terminal tail, the GnRH receptor undergoes agonist-stimulated internalization displaying distinctive characteristics described for other GPCRs that internalize via a clathrin-dependent mechanism and recycle through an acidified endosomal compartment. However, our data indicate that the GnRH receptor may utilize a beta-arrestin-independent endocytotic pathway.