Pediatric chronic fatigue syndrome: current perspectives

Crawley, Esther

doi:10.2147/phmt.s126253

Cited by 24 publications

(24 citation statements)

References 76 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A recent review by the EUROpean Myalgic Encephalomyelitis Network (EUROMENE) epidemiology working group notes that population prevalence could reach numbers up to 5% depending on the diagnostic criteria applied and geographic locations explored. 14 In addition, reports of the disease onset at early ages (adolescent and pediatric cases) 15 reflect an increasing magnitude of the sanitary problem, social impact, and economic burden associated with ME/CFS, mainly deriving from a deficient knowledge of ME/CFS pathophysiology and lack of treatment (other than palliative). ME/CFS etiology has been linked to a variety of potential triggering factors.…”

Section: Introductionmentioning

confidence: 99%

Epigenetic Components of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Uncover Potential Transposable Element Activation

Almenar-Pérez

Ovejero

Sánchez-Fito

et al. 2019

Clinical Therapeutics

View full text Add to dashboard Cite

Purpose: Studies to determine epigenetic changes associated with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) remain scarce; however, current evidence clearly shows that methylation patterns of genomic DNA and noncoding RNA profiles of immune cells differ between patients and healthy subjects, suggesting an active role of these epigenetic mechanisms in the disease. The present study compares and contrasts the available ME/CFS epigenetic data in an effort to evidence overlapping pathways capable of explaining at least some of the dysfunctional immune parameters linked to this disease. Methods: A systematic search of the literature evaluating the ME/CFS epigenome landscape was performed following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses criteria. Differential DNA methylation and noncoding RNA differential expression patterns associated with ME/CFS were used to screen for the presence of transposable elements using the Dfam browser, a search program nurtured with the Repbase repetitive sequence database and the RepeatMasker annotation tool. Findings: Unexpectedly, particular associations of transposable elements and ME/CFS epigenetic hallmarks were uncovered. A model for the disease emerged involving transcriptional induction of endogenous dormant transposons and structured cellular RNA interactions, triggering the activation of the innate immune system without a concomitant active infection. Implications: Repetitive sequence filters (ie, RepeatMasker) should be avoided when analyzing transcriptomic data to assess the potential participation of repetitive sequences ("junk repetitive DNA"), representing >45% of the human genome, in the onset and evolution of ME/CFS. In addition, transposable element screenings aimed at designing cost-effective, focused empirical assays that can confirm or disprove the suspected involvement of transposon transcriptional activation in this disease, following the pilot strategy presented here, will require databases gathering large ME/CFS epigenetic datasets.

show abstract

Section: Introductionmentioning

confidence: 99%

Epigenetic Components of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Uncover Potential Transposable Element Activation

Almenar-Pérez

Ovejero

Sánchez-Fito

et al. 2019

Clinical Therapeutics

View full text Add to dashboard Cite

show abstract

“…CFS, also often described as myalgic encephalomyelitis, is characterized not only by severe and prolonged fatigue drastically impairing life quality, and much more attention has been paid in the past year than ever ( 1 – 6 ). CFS is observed even in children and adolescents ( 7 ). CFS is induced by impairment of neuronal–endocrine–immune interactions with various symptoms including circadian rhythm abnormalities ( 8 , 9 ).…”

Section: Introductionmentioning

confidence: 99%

Glial Activation and Expression of the Serotonin Transporter in Chronic Fatigue Syndrome

et al. 2018

View full text Add to dashboard Cite

Fatigue is commonly reported in a variety of illnesses and has major impact on quality of life. Chronic fatigue syndrome (CFS) is a debilitating syndrome of unknown etiology. The clinical symptoms include problems in neuroendocrine, autonomic, and immune systems. It is becoming clear that the brain is the central regulator of CFS. For example, neuroinflammation, especially induced by activation of microglia and astrocytes, may play a prominent role in the development of CFS, though little is known about molecular mechanisms. Many possible causes of CFS have been proposed. However, in this mini-review, we summarize evidence for a role for microglia and astrocytes in the onset and the maintenance of immunologically induced CFS. In a model using virus mimicking synthetic double-stranded RNA, infection causes sequential signaling such as increased blood brain barrier (BBB) permeability, microglia/macrophage activation through Toll-like receptor 3 (TLR3) signaling, secretion of IL-1β, upregulation of the serotonin transporter (5-HTT) in astrocytes, reducing extracellular serotonin (5-HT) levels and hence reduced activation of 5-HT1A receptor subtype. Hopefully, drug discovery targeting these pathways may be effective for CFS therapy.

show abstract

“…Although possibly underestimated, the global prevalence for FM has been set at 2-8% and at 0.23-0.41 for ME/CFS with predominant ratios of females over males [13][14][15][16][17]. In addition, increasing numbers of patients being affected at early ages [18] highlights the considerable and raising needs for appropriate healthcare programs and the stepping demands for alleviation of associated economic/social burdens.…”

Section: Introductionmentioning

confidence: 99%

Impact of Polypharmacy on Candidate Biomarker miRNomes for the Diagnosis of Fibromyalgia and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Striking back on Treatments

Almenar-Pérez

Sánchez-Fito

Ovejero

et al. 2019

Preprint

View full text Add to dashboard Cite

Fibromyalgia (FM) and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) are diseases of unknown etiology presenting complex and often overlapping symptomatology. Despite promising advances on the study of miRNomes of these diseases, no validated molecular diagnostic biomarker yet exists. Since FM and ME/CFS patient treatments commonly include polypharmacy it is of concern that biomarker miRNAs are masked by drug interactions. Aiming at discriminating between drug-effects and true disease-associated differential miRNA expression, we evaluated the potential impact of commonly prescribed drugs on disease miRNomes, as reported by the literature. By using the web search tools SM2miR, Pharmaco-miR and repoDB, we found a list of commonly prescribed drugs that impact on FM and ME/CFS miRNomes and therefore could be interfering in the process of biomarker discovery. On another end, disease-associated miRNomes may incline patient´s response to treatment and toxicity. Here, we explored treatments for diseases in general that could be affected by FM and ME/CFS miRNomes finding a long list of them, including treatments for lymphoma, a type of cancer affecting ME/CFS patients at a higher rate than healthy population. We conclude that FM and ME/CFS miRNomes could help refine pharmacogenomic/pharmacoepigenomic analysis to elevate future personalized medicine and precision medicine programs in the clinic.

show abstract

Pediatric chronic fatigue syndrome: current perspectives

Cited by 24 publications

References 76 publications

Epigenetic Components of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Uncover Potential Transposable Element Activation

Epigenetic Components of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Uncover Potential Transposable Element Activation

Glial Activation and Expression of the Serotonin Transporter in Chronic Fatigue Syndrome

Impact of Polypharmacy on Candidate Biomarker miRNomes for the Diagnosis of Fibromyalgia and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Striking back on Treatments

Contact Info

Product

Resources

About