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Systematic review of digital and non-digital non-pharmacological interventions that target quality of life and psychological outcomes in adults with systemic lupus erythematosus.

ABSTRACT:

Background

Patients with systemic lupus erythematous (SLE) experience psychological comorbidities and impaired quality of life (QOL). We conducted a systematic review to examine the efficacy of non-pharmacological interventions for improving psychological outcomes and/or QOL in patients with SLE. To expand on a previous systematic review in this area and enhance our understanding of efficacious interventions for this population, our search included quasi-experimental and experimental studies of interventions delivered or supported by remote methods (including digitally) or in person.

Methods

A comprehensive literature search was conducted with a research librarian using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines and was registered before data extraction on the international prospective register of systematic reviews PROSPERO Web site (CRD42020154962). The search included controlled-vocabulary and title/abstract terms related to non-pharmacological interventions for SLE published through October 2019 in MEDLINE (Ovid), Cochrane Library databases (Wiley), Embase (Elsevier), CINAHL (EBSCO), PsycINFO (EBSCO), Web of Science (Clarivate), ACM Digital (Association of Computer Machinery), and IEEE Xplore. Studies were synthesized using a systematic narrative synthesis framework. Risk of bias was assessed.

Results

Twenty-three studies were included: 21 randomized controlled trials and two quasi-experimental studies. Non-pharmacological diet, physical activity, psychological, and course-based interventions improved QOL and psychological outcomes, and were delivered in traditional settings (e.g., hospital) or remotely. No studies assessing digital non-pharmacological interventions were identified in our search. Quality assessments showed serious risk of bias for the two quasi-experimental studies, and high risk of bias in a subset of experimental studies.

Conclusions

Non-pharmacological interventions benefit patients with SLE. Future research should include more representative samples in rigorous evaluations and consider ways to incorporate digital technologies to increase accessibility.

SUBMITTER: Chang A

PROVIDER: S-EPMC8122052 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:The mitochondrion supplies energy to the cell and regulates apoptosis. Unlike other mammalian organelles, mitochondria are formed by binary fission and cannot be directly produced by the cell. They contain numerous copies of a compact circular genome that encodes RNA molecules and proteins involved in mitochondrial oxidative phosphorylation. Whereas, mitochondrial DNA (mtDNA) activates the innate immune system if present in the cytosol or the extracellular milieu, it is also the target of circulating autoantibodies in systemic lupus erythematosus (SLE). However, it is not known whether mitochondrial RNA is also recognized by autoantibodies in SLE. In the present study, we evaluated the presence of autoantibodies targeting mitochondrial RNA (AmtRNA) in SLE. We quantified AmtRNA in an inducible model of murine SLE. The AmtRNA were also determined in SLE patients and healthy volunteers. AmtRNA titers were measured in both our induced model of murine SLE and in human SLE, and biostatistical analyses were performed to determine whether the presence and/or levels of AmtRNA were associated with clinical features expressed by SLE patients. Both IgG and IgM classes of AmtRNA were increased in SLE patients (n = 86) compared to healthy controls (n = 30) (p < 0.0001 and p = 0.0493, respectively). AmtRNA IgG levels correlated with anti-mtDNA-IgG titers (r s = 0.54, p < 0.0001) as well as with both IgG and IgM against β-2-glycoprotein I (anti-β2GPI; r s = 0.22, p = 0.05), and AmtRNA-IgG antibodies were present at higher levels when patients were positive for autoantibodies to double-stranded-genomic DNA (p < 0.0001). AmtRNA-IgG were able to specifically discriminate SLE patients from healthy controls, and were negatively associated with plaque formation (p = 0.04) and lupus nephritis (p = 0.03). Conversely, AmtRNA-IgM titers correlated with those of anti-β2GPI-IgM (r s = 0.48, p < 0.0001). AmtRNA-IgM were higher when patients were positive for anticardiolipin antibodies (aCL-IgG: p = 0.01; aCL-IgM: p = 0.002), but AmtRNA-IgM were not associated with any of the clinical manifestations assessed. These findings identify mtRNA as a novel mitochondrial antigen target in SLE, and support the concept that mitochondria may provide an important source of circulating autoantigens in SLE.