TGI Friday! Our weekly round-up of recently published research abstracts | 22 January 2016

From Fatigue: Biomedicine, Health & Behavior. Published online, 19 January 2016.

Case definitions integrating empiric and consensus perspectives

Leonard A. Jason(a*), Stephanie McManimen(a), Madison Sunnquist(a), Abigail Brown(a), Jacob Furst(a), Julia L. Newton(b) & Elin Bolle Strand( c)
a) Center for Community Research, DePaul University, Chicago, IL, USA
b) Institute for Ageing and Health, Newcastle University, Newcastle upon Tyne, UK
c) Oslo University Hospital, Oslo, Norway

Abstract

BACKGROUND

There has been considerable controversy regarding how to name and define the illnesses known as myalgic encephalomyelitis (ME) and chronic fatigue syndrome (CFS). The Institute of Medicine (IOM) report has proposed new clinical criteria and a new name for this
illness, but aspects of these recommendations have been scrutinized by patients and scientists.

PURPOSE

It is possible that both empiric and consensus approaches could be used to help settle some of these diagnostic challenges. Using patient samples collected in the USA, Great Britain, and Norway (N = 556), the current study attempted to categorize patients using more general as well as more restricted case definitions.

RESULTS

Overall, the outcomes suggest that there might be four groupings of patients, with the broadest category involving those with chronic fatigue (N = 62), defined by six or more months of fatigue which cannot be explained by medical or psychiatric conditions.

A second category involves those patients who have chronic fatigue that can be explained by a medical or psychiatric condition (N = 47).

A third category involves more specific criteria that have been posited both by the IOM report, Canadian Clinical Case criteria, ME-ICC criteria and a more empiric approach.

These efforts have specified domains of substantial reductions of activity, post-exertional malaise, neurocognitive impairment, and sleep dysfunction (N = 346). Patients with these characteristics were more functionally impaired than those meeting just chronic fatigue criteria, p  < .05. Finally, those meeting even more restrictive ME criteria proposed by Ramsay, identified a smaller and even more impaired group, p < .05. CONCLUSION It is important that scientists world-wide develop consensus on how to identify and classify patients using clinical and research criteria, and ultimately develop subtypes within such categories.


From Molecular Psychiatry, February 2016 (To access full paper click HERE)

Cytokine network analysis of cerebrospinal fluid in myalgic encephalomyelitis/chronic fatigue syndrome

M Hornig(1,2), G Gottschalk(3), DL Peterson(3), KK Knox(4,5), AF Schultz(1), ML Eddy(1), X Che(1) and WI Lipkin(1,2,6)
1) Center for Infection and Immunity, Columbia University Mailman School of Public Health, New York, NY, USA;
2) Department of Epidemiology, Columbia University Mailman School of Public Health, New York, NY, USA;
3) Sierra Internal Medicine at Incline Village, Incline Village, NV, USA;
4) Coppe Healthcare Solutions, Waukesha, WI, USA;
5) Simmaron Research, Incline Village, NV, USA and
6)Departments of Pathology and Neurology, College of Physicians and Surgeons, Columbia University, New York, NY, USA. Correspondence: Dr M Hornig, Center for Infection and Immunity, Columbia University Mailman School of Public Health, 722 West 168th Street, Room 1706, New York, NY 10032, USA.
E-mail: mh2092@cumc.columbia.edu

Abstract

Myalgic encephalomyelitis/chronic fatigue syndrome is an unexplained debilitating disorder that is frequently associated with cognitive and motor dysfunction. We analyzed cerebrospinal fluid from 32 cases, 40 subjects with multiple sclerosis and 19 normal subjects frequency-matched for age and sex using a 51-plex cytokine assay.

Group-specific differences were found for the majority of analytes with an increase in cases of CCL11 (eotaxin), a chemokine involved in eosinophil recruitment. Network analysis revealed an inverse relationship between interleukin 1 receptor antagonist and colony-stimulating factor 1, colony-stimulating factor 2 and interleukin 17F, without effects on interleukin 1α or interleukin 1β, suggesting a disturbance in interleukin 1 signaling.

Our results indicate a markedly disturbed immune signature in the cerebrospinal fluid of cases that is consistent with immune activation in the central nervous system, and a shift toward an allergic or T helper type-2 pattern associated with autoimmunity.


From the Journal of Translational Medicine, 20 January 2016. (open access)

Mitochondrial DNA variants correlate with symptoms in myalgic encephalomyelitis/chronic fatigue syndrome

Paul Billing-Ross(1†), Arnaud Germain(2†), Kaixiong Ye(3), Alon Keinan(3), Zhenglong Gu(1) and Maureen R. Hanson(2*)
* Corresponding author: Maureen R Hanson mrh5@cornell.edu
† Equal contributors
1) Division of Nutritional Sciences, Cornell University, Ithaca 14853, NY, USA
2) Department of Molecular Biology and Genetics, Cornell University, Ithaca 14853, NY, USA
3) Department of Biological Statistics and Computational Biology, Cornell University, Ithaca 14853, NY, USA

Abstract

BACKGROUND

Mitochondrial dysfunction has been hypothesized to occur in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), a disease characterized by fatigue, cognitive difficulties, pain, malaise, and exercise intolerance. We investigated whether haplogroup, single nucleotide polymorphisms (SNPs), or heteroplasmy of mitochondrial DNA (mtDNA) were associated with health status and/or symptoms.

METHODS

Illumina sequencing of PCR-amplified mtDNA was performed to analyze sequence and extent of heteroplasmy of mtDNAs of 193 cases and 196 age- and gender-matched controls from DNA samples collected by the Chronic Fatigue Initiative. Association testing was carried out to examine possible correlations of mitochondrial sequences with case/control status and symptom constellation and severity as reported by subjects on Short Form-36 and DePaul Symptom Questionnaires.

RESULTS

No ME/CFS subject exhibited known disease-causing mtDNA mutations. Extent of heteroplasmy was low in all subjects. Although no association between mtDNA SNPs and ME/CFS vs. healthy status was observed, haplogroups J, U and H as well as eight SNPs in ME/CFS cases were significantly associated with individual symptoms, symptom clusters, or symptom severity.

CONCLUSIONS

Analysis of mitochondrial genomes in ME/CFS cases indicates that individuals of a certain haplogroup or carrying specific SNPs are more likely to exhibit certain neurological, inflammatory, and/or gastrointestinal symptoms. No increase in susceptibility to ME/CFS of individuals carrying particular mitochondrial genomes or SNPs was observed.


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