TGI Friday! Our weekly round-up of recently published research study abstracts and related items | 7 September 2012


The return of TGI Friday! Recently published research study abstracts which haven’t made the headlines will be published here every Friday.


From The European Journal of Clinical Investigation, published online on 1 September 2012

Exercise and chronic fatigue syndrome: maximize function, minimize post-exertional malaise

Lily Chu, Fred Friedberg, Ken Friedman,Nereida Littrell, Staci Stevens, Ros Vallings.

As board members of the International Association for Chronic Fatigue Syndrome/ Myalgic Encephalomyelitis, we agree with Van Cauwenbergh et al.’s view [1] that exercise treatment should be carefully tailored to each individual with chronic fatigue syndrome (CFS) and have recently published a Primer directed at physicians [2]. Although a time-contingent approach may work for a percentage of patients, we recommend that any exercise be prescribed to maximize function while minimizing post-exertional malaise. A significant number of patients who exercise according to a set schedule despite increasing symptoms may suffer temporary setbacks and sometimes prolonged disability.

The full letter can be purchased HERE.

This is in response to this study published in May:

Eur J Clin Invest. 2012 May 25. doi: 10.1111/j.1365-2362.2012.02701.x. [Epub ahead of print]

How to exercise people with chronic fatigue syndrome: evidence-based practice guidelines.

Van Cauwenbergh D, De Kooning M, Ickmans K, Nijs J.

Chronic Pain and Chronic Fatigue Research Group (CHROPIVER), Department of Human Physiology, Faculty of Physical Education & Physiotherapy, Vrije Universiteit Brussel, Belgium Chronic Pain and Chronic Fatigue Research Group (CHROPIVER), Division of Musculoskeletal Physiotherapy, Department of Health Care Sciences, Artesis University College Antwerp, Belgium Department of Physical Medicine and Physiotherapy, University Hospital Brussels, Brussels,
Belgium.

Abstract

BACKGROUND  Despite the large number of studies emphasizing the effectiveness of graded exercise therapy (GET) and cognitive behavioural therapy (CBT) for people with chronic fatigue syndrome (CFS), clinicians are left wondering how exactly to apply exercise therapy to their patients with CFS. The aim of this literature review is to identify the appropriate exercise modalities (i.e. exercise duration, mode, number of treatment sessions, session length, duration
of treatment, exercise intensity and whether or not to apply home exercise program) for people with CFS.

MATERIALS AND METHODS  All studies that were identified through electronic databases (PubMed and PEDro) were assessed for methodological quality by using selection criteria (Delphi score).

RESULTS  In this literature review, 12 studies fulfilled all study requirements. One study had a low methodological quality. The parameters used in the GET and CBT interventions were divided into subgroups: (i) time or symptom contingent, (ii) exercise frequency and (iii) exercise modality.

CONCLUSION  The lack of uniformity in outcome measures and CFS diagnostic criteria make it difficult to compare the findings across studies. Based on the available evidence, exercise therapy for people with CFS should be aerobic and must comprise of 10-11 sessions spread over a period of 4-5 months. A time-contingent approach is preferred over a symptom-contingent way of exercising. In addition, people with CFS can perform home exercises five times a week with an initial duration of 5-15 min per exercise session. The exercise duration can be gradually increased up to 30 min.


From Clinical and Vaccine Immunology, published ahead of print 11 July 2012.

No Evidence for Xenotropic Murine Leukemia-Related Virus Infection in Sweden Using Internally Controlled Multiepitope Suspension Array Serology

Jonas Blomberg (a), Fredrik Blomberg(a), Anna Sjösten (a), Ali Sheikholvaezin (a), Agnes Bölin-Wiener(a), Amal Elfaitouri (a), Sanna Hessel (a), Carl-Gerhard Gottfries (b), Olof Zachrisson (b), Christiba Ohrmalm (a,c), Magnus Jobs (a.d) and Rüdiger Pipkorn (e).

(a) Section of Clinical Microbiology, Department of Medical Sciences, Uppsala University, Uppsala, Sweden
(b) Gottfries Clinic AB, Mölndal, Sweden
(c) National Veterinary Institute, Ultuna, Uppsala, Sweden
(d) Högskolan Dalarna, Falun, Sweden
(e) Deutsches Krebsforschungszentrum, Heidelberg, Germany

ABSTRACT

Many syndromes have a large number of differential diagnoses, a situation which calls for multiplex diagnostic systems. Myalgic encephalomyelitis (ME), also named chronic fatigue syndrome (CFS), is a common disease of unknown etiology.

A mouse retrovirus, xenotropic murine leukemia-related virus (XMRV), was found in ME/CFS patients and blood donors, but this was not corroborated. However, the paucity of serological investigations on XMRV in humans prompted us to develop a serological assay which cover many aspects of XMRV antigenicity.
It is a novel suspension array method, using a multiplex IgG assay with nine recombinant proteins from the env and gag genes of XMRV and 38 peptides based on known epitopes of vertebrate gammaretroviruses.

IgG antibodies were sought in 520 blood donors and 85 ME/CFS patients and in positive- and negative-control sera from animals. We found no differences in seroreactivity between blood donors and ME/CFS patients for any of the antigens. This did not support an association between ME/CFS and XMRV infection.

The multiplex serological system had several advantages: (i) biotinylated protein G allowed us to run both human and animal sera, which is essential because of a lack of XMRV-positive humans; (ii) a novel quality control was a pan-peptide positive-control rabbit serum; and (iii) synthetic XMRV Gag peptides with degenerate positions covering most of the variation of murine leukemia-like viruses did not give higher background than nondegenerate analogs. The principle may be used for creation of variant tolerant peptide serologies. Thus, our system allows rational large-scale serological assays with built-in quality control.


From Brain, Behaviour and Immunity, 26 May 2012: e-published ahead of print on 29 December 2011.

Genetic associations of fatigue and other symptom domains of the acute sickness response to infection.

Piraino B, Vollmer-Conna U, Lloyd AR.
Inflammation and Infection Research Centre, School of Medical Sciences, University of New South Wales, Australia.

Abstract

The acute sickness response to infection is a conserved set of changes in physiology and behaviour, featuring fever, fatigue, musculo-skeletal pain, disturbed mood, and cognitive difficulties.

The manifestations differ somewhat between individuals, including those infected with pathogens which do not have genetic variability – suggesting host determinants.

Principal components analysis (PCA) was applied to acute phase, self-report symptom data from subjects in the Dubbo Infection Outcomes Study (n=296) to
empirically derive indices of fatigue, pain, neurocognitive difficulties, and mood disturbance, as well as overall illness severity.

Associations were sought with functional single nucleotide polymorphisms (SNPs) in the cytokine genes, interleukin (IL)-6, tumour necrosis factor (TNF)-α, interferon (IFN)-γ, and IL-10.

The summed individual symptom indices correlated with overall severity and also with functional status. The relative contribution of individual symptom domains to the overall illness was stable over time within
subjects, but varied between subjects with the same infection.

The T allele of the IFN-γ +874 T/A SNP was associated with increased fatigue (p=0.0003; OR: 3.3). The C allele of the IL-10 -592 C/A SNP exerted a protective effect on neurocognitive difficulties (p=0.017; OR: 0.52); while the A allele for the IL-10 -592 SNP was associated with increased mood disturbance (p=0.044; OR: 1.83), as was the G allele of the IL-6 -174 G/C SNP (p=0.051; OR: 1.83). The acute sickness response
has discrete symptom domains including fatigue, which have unique genetic associations. These data provide novel insights into the pathophysiology of fatigue states.


From Current Rheumatology Reports 2012 Aug 31. [Epub ahead of print]

Role of Functional Brain Imaging in Understanding Rheumatic Pain.

Jones AK, Huneke NT, Lloyd DM, Brown CA, Watson A.

Human Pain Research Group, School of Translational Medicine, University of Manchester, Clinical Sciences Building, Salford Royal NHS Foundation Trust, Salford, M6 8HD, UK.

Abstract

Rheumatic pain and, in particular, rheumatoid arthritis, osteoarthritis and fibromyalgia, are common and debilitating chronic pain syndromes. Recently, human functional neuroimaging, for example EEG, fMRI, and PET has begun to reveal some of the crucial central nervous system mechanisms underlying these diseases.

The purpose of this review is to summarise current knowledge on the brain mechanisms of rheumatic pain revealed by functional neuroimaging techniques.

The evidence suggests that two mechanisms may be largely responsiblefor the clinical pain associated with these rheumatic diseases:abnormalities in the medial pain system and/or central nervous system sensitisation and inhibition.

If we can understand how functioning of the central nociceptive system becomes altered, even in the absence of peripheral nociceptive input, by using functional neuroimaging techniques, in the future we may be able to develop improved, more effective treatments for patients with chronic rheumatic pain.


From the University of South Australia’s School of Pharmacy and Medical Sciences

STUDY VOLUNTEERS NEEDED

Healthy Subjects and Patients with Chronic Fatigue Syndrome

We are seeking volunteers to participate in a research study investigating the levels of carnitines and fatty acids (important compounds for energy production) in patients with chronic fatigue syndrome.

The study consists of two parts: Part A (a single blood sample) and Part B (breath testing). Volunteers can choose to take part in Part A only or both Part A and Part B of the study.

Blood samples can be collected at your local IMVS collection centre. Breath testing will be conducted at the University of South Australia, City East Campus.

Study participants will be reimbursed ($20 for Part A and $100 for Part B) for out-of-pocket expenses, inconvenience and time involved.

For more information, please contact Dr Stephanie Reuter Lange via email (stephanie.reuterlange@unisa.edu.au) or call +61 8 8302 1872.

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From Brain, Behaviour and Immunity, 26 May 2012. E-published ahead of print on 29 December 2011.

Genetic associations of fatigue and other symptom domains of the acute sickness response to infection.

Piraino B, Vollmer-Conna U, Lloyd AR.

Inflammation and Infection Research Centre, School of Medical Sciences, University of New South Wales, Australia.

Abstract

The acute sickness response to infection is a conserved set of changes in physiology and behaviour, featuring fever, fatigue, musculo-skeletal pain, disturbed mood, and cognitive difficulties. The manifestations differ somewhat between individuals, including those infected with pathogens which do not have genetic variability–suggesting host determinants.

Principal components analysis (PCA) was applied to acute phase, self-report symptom data from subjects in the Dubbo Infection Outcomes Study (n=296) to empirically derive indices of fatigue, pain, neurocognitive difficulties, and mood disturbance, as well as overall illness severity.

Associations were sought with functional single nucleotide polymorphisms (SNPs) in the cytokine genes, interleukin (IL)-6, tumour necrosis factor (TNF)-α, interferon (IFN)-γ, and IL-10. The summed individual symptom indices correlated with overall severity and also with functional status. The relative contribution of individual symptom domains to the overall illness was stable over time within subjects, but varied between subjects with the same infection.

The T allele of the IFN-γ +874 T/A SNP was associated with increased fatigue (p=0.0003; OR: 3.3). The C allele of the IL-10 -592 C/A SNP exerted a protective effect on neurocognitive difficulties (p=0.017; OR: 0.52); while the A allele for the IL-10 -592 SNP was associated with increased mood disturbance (p=0.044; OR: 1.83), as was the G allele of the IL-6 -174 G/C SNP (p=0.051; OR: 1.83).

The acute sickness response has discrete symptom domains including fatigue, which have unique genetic associations. These data provide novel insights into the pathophysiology of fatigue states.


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