What causes chronic fatigue syndrome?
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ABSTRACT:
SUBMITTER: White PD
PROVIDER: S-EPMC524091 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:Here report ME/CFS-related plasma proteome analysis using untargeted ultra-performance liquid chromatography – tandem mass spectrometry (UPLC-MS/MS). We identified differing profiles between ME/CFS patients, as well as ME/CFS subgroups based on their IBS co-morbidity status, and controls. In addition, we identify a set of proteins that may predict ME/CFS status.
2020-07-07 | PXD016622 | Pride
Project description:Human genome-wide Affymetrix GeneChip arrays were used to compare the levels of gene expression in the peripheral blood mononuclear cells (PMBCs) of male patients with post-viral chronic fatigue (n=8) and male healthy control subjects (n=7). Patients and healthy subjects differed significantly in the level of expression of 366 genes. Analysis of the differentially expressed genes indicated functional implications in immune modulation, oxidative stress and apoptosis. Prototype biomarkers were identified on the basis of differential levels of gene expression and possible biological significance. Differential expression of key genes identified in this study offer an insight into the possible mechanism of chronic fatigue following infection. The representative biomarkers identified in this research appear promising as potential biomarkers for diagnosis and treatment. Keywords: comparison between two groups of samples
2009-01-27 | GSE14577 | GEO
Project description:Chronic Fatigue Syndrome (CFS), also known as myalgic encephalomyelitis, is a complex multifactorial disease that is characterized by the persistent presence of fatigue and other particular symptoms for a minimum of 6 months. Symptoms fail to dissipate after sufficient rest and have major effects on the daily functioning of CFS sufferers. CFS is a multi-system disease with a heterogeneous patient population showing a wide variety of functional disabilities and its biological basis remains poorly understood. Stable alterations in gene function in the immune system have been reported in several studies of CFS. Epigenetic modifications have been implicated in long-term effects on gene function, however, to our knowledge, genome-wide epigenetic modifications associated with CFS have not been explored. We examined the DNA methylome in peripheral blood mononuclear cells isolated from CFS patients and healthy controls using the Illumina HumanMethylation450 BeadChip array, controlling for invariant probes and probes overlapping polymorphic sequences.
2014-08-12 | GSE59489 | GEO
Project description:Chronic Fatigue Syndrome (CFS), also known as myalgic encephalomyelitis, is a complex multifactorial disease that is characterized by the persistent presence of fatigue and other particular symptoms for a minimum of 6 months. Symptoms fail to dissipate after sufficient rest and have major effects on the daily functioning of CFS sufferers. CFS is a multi-system disease with a heterogeneous patient population showing a wide variety of functional disabilities and its biological basis remains poorly understood. Stable alterations in gene function in the immune system have been reported in several studies of CFS. Epigenetic modifications have been implicated in long-term effects on gene function, however, to our knowledge, genome-wide epigenetic modifications associated with CFS have not been explored. We examined the DNA methylome in peripheral blood mononuclear cells isolated from CFS patients and healthy controls using the Illumina HumanMethylation450 BeadChip array, controlling for invariant probes and probes overlapping polymorphic sequences. Genomic DNA from 24 peripheral blood mononuclear cells (PBMC) samples (12 CFS, 12 controls) were bisulfite-converted and hybridised to the Illumina Infinium HumanMethylation450 BeadChip. GenomeStudio files were generated and the data was analyzed using the Illumina Methylation Analyzer R package.
2014-08-12 | E-GEOD-59489 | biostudies-arrayexpress
Project description:BACKGROUND:Orthostatic intolerance (OI) is a significant problem for those with chronic fatigue syndrome (CFS). We aimed to characterize orthostatic intolerance in CFS and to study the effects of exercise on OI. METHODS:CFS (n?=?39) and control (n?=?25) subjects had recumbent and standing symptoms assessed using the 20-point, anchored, ordinal Gracely Box Scale before and after submaximal exercise. The change in heart rate (?HR???30 bpm) identified Postural Orthostatic Tachycardia Syndrome (POTS) before and after exercise, and the transient, exercise-induced postural tachycardia Stress Test Activated Reversible Tachycardia (START) phenotype only after exercise. RESULTS:Dizziness and lightheadedness were found in 41% of recumbent CFS subjects and in 72% of standing CFS subjects. Orthostatic tachycardia did not account for OI symptoms in CFS. ROC analysis with a threshold???2/20 on the Gracely Box Scale stratified CFS subjects into three groups: No OI (symptoms?<?2), Postural OI (only standing symptoms???2), and Persistent OI (recumbent and standing symptoms???2). CONCLUSIONS:Dizziness and Lightheadedness symptoms while recumbent are an underreported finding in CFS and should be measured when doing a clinical evaluation to diagnose orthostatic intolerance. POTS was found in 6 and START was found in 10 CFS subjects. Persistent OI had symptoms while recumbent and standing, highest symptom severity, and lability in symptoms after exercise. Trial registration The trial was registered at the following: https://clinicaltrials.gov/ct2/show/NCT03567811.
| S-EPMC6547462 | biostudies-literature
Project description:More than 2 million people in the United States have myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). We performed targeted, broad-spectrum metabolomics to gain insights into the biology of CFS. We studied a total of 84 subjects using these methods. Forty-five subjects (n = 22 men and 23 women) met diagnostic criteria for ME/CFS by Institute of Medicine, Canadian, and Fukuda criteria. Thirty-nine subjects (n = 18 men and 21 women) were age- and sex-matched normal controls. Males with CFS were 53 (±2.8) y old (mean ± SEM; range, 21-67 y). Females were 52 (±2.5) y old (range, 20-67 y). The Karnofsky performance scores were 62 (±3.2) for males and 54 (±3.3) for females. We targeted 612 metabolites in plasma from 63 biochemical pathways by hydrophilic interaction liquid chromatography, electrospray ionization, and tandem mass spectrometry in a single-injection method. Patients with CFS showed abnormalities in 20 metabolic pathways. Eighty percent of the diagnostic metabolites were decreased, consistent with a hypometabolic syndrome. Pathway abnormalities included sphingolipid, phospholipid, purine, cholesterol, microbiome, pyrroline-5-carboxylate, riboflavin, branch chain amino acid, peroxisomal, and mitochondrial metabolism. Area under the receiver operator characteristic curve analysis showed diagnostic accuracies of 94% [95% confidence interval (CI), 84-100%] in males using eight metabolites and 96% (95% CI, 86-100%) in females using 13 metabolites. Our data show that despite the heterogeneity of factors leading to CFS, the cellular metabolic response in patients was homogeneous, statistically robust, and chemically similar to the evolutionarily conserved persistence response to environmental stress known as dauer.
| S-EPMC5027464 | biostudies-literature
Project description:We have conducted a double-blind study to assess the possible involvement of the human herpesviruses (HHVs) HHV6, HHV7, Epstein-Barr virus (EBV), and cytomegalovirus in chronic fatigue syndrome (CFS) patients compared to age-, race-, and gender-matched controls. The CFS patient population was composed of rigorously screened civilian and Persian Gulf War veterans meeting the Centers for Disease Control and Prevention's CFS case definition criteria. Healthy control civilian and veteran populations had no evidence of CFS or any other exclusionary medical or psychiatric condition. Patient peripheral blood mononuclear cells were analyzed by PCR for the presence of these HHVs. Using two-tailed Fisher's exact test analyses, we were unable to ascertain any statistically significant differences between the CFS patient and control populations in terms of the detection of one or more of these viruses. This observation was upheld when the CFS populations were further stratified with regard to the presence or absence of major axis I psychopathology and patient self-reported gradual versus acute onset of disease. In tandem, we performed serological analyses of serum anti-EBV and anti-HHV6 antibody titers and found no significant differences between the CFS and control patients.
| S-EPMC95690 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2023-12-22 | GSE251792 | GEO
Project description:Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a complex disease of unknown etiology. Multiple studies point to disruptions in immune functioning in ME/CFS patients as well as specific genetic polymorphisms and alterations of the DNA methylome in lymphocytes. However, potential interactions between DNA methylation and genetic background in relation to ME/CFS have not been examined. In this study we explored this association by characterizing the epigenetic (~480 thousand CpG loci) and genetic (~4.3 million SNPs) variation between cohorts of ME/CFS patients and healthy controls. We found significant associations of DNA methylation states in T-lymphocytes at several CpG loci and regions with ME/CFS phenotype. These methylation anomalies are in close proximity to genes involved with immune function and cellular metabolism. Finally, we found significant correlations of genotypes with methylation modifications associated with ME/CFS. The findings from this study highlight the role of epigenetic and genetic interactions in complex diseases, and suggest several genetic and epigenetic elements potentially involved in the mechanisms of disease in ME/CFS.
2020-08-25 | GSE156792 | GEO
Project description:RationaleRelationship dissatisfaction has been linked with worse health outcomes in many patient populations, though the mechanism(s) underlying this effect are unclear. Among patients with chronic fatigue syndrome (CFS) and their partners, there is evidence for a bi-directional association between poorer relationship satisfaction and the severity of CFS-related fatigue.ObjectiveHere, we hypothesized that relationship dissatisfaction negatively impacts fatigue severity through greater depression and less patient satisfaction about communication about symptoms to partners.MethodBaseline data were drawn from diagnosed CFS patients (N = 150) participating in a trial testing the efficacy of a stress management intervention. Data derived from fatigue severity (Fatigue Symptom Index, FSI), depression (Center for Epidemiologic Survey-Depression, CES-D), relationship quality (Dyadic Adjustment Scale, DAS) and communication satisfaction (Patient Symptom Disclosure Satisfaction, PSDS) questionnaires were used for bootstrapped indirect effect analyses using parallel mediation structural equation modeling in Mplus (v8). Age and BMI were entered as covariates.ResultsGreater relationship satisfaction predicted greater communication satisfaction (p < 0.01) and lower CES-D scores (p < 0.01), which in turn were each significantly related to greater fatigue severity (p < 0.05). Tests of the indirect paths indicated that relationship satisfaction had a significant effect on fatigue severity through both constructs, but primarily via depression. There was no direct association between relationship satisfaction and fatigue severity after the intermediate variables (depression, communication satisfaction) were included in the model.ConclusionResults highlight the importance of considering depression and communication-related factors when examining the effects of relationship satisfaction on CFS symptoms such as fatigue. Further mechanism-based, longitudinal research might identify relationship-related mediating variables that can be targeted therapeutically.
| S-EPMC8088125 | biostudies-literature