B cells in the immune systems of people with CFS

Posted on 03/12/2015 by wames

Research abstract

Limited immunological changes have been previously reported in B cell phenotype in Chronic Fatigue Syndrome (CFS) patients, so there is no clear established role of B cells in the pathophysiology of CFS patients.

The aim of this study was to evaluate B cells subsets including naive, memory naive, memory switched, memory non-switched, double negative, transitional, plasmablasts, HLA-DR+, plasma and regulatory B cells (Breg) in CFS patients compared with non-fatigued controls.

B cell activation markers (CD81, CD21) and surface receptors (CD79a/b, IgM, IgD, IgA, IgE) were also examined in CFS patients compared with non-fatigued controls. 46 CFS patients (age=50.00 ± 2.00 years) and 34 non-fatigued controls (age=49.00 ± 2.16 years) participated in the study.

The percentage of BCR IgM+ B cells was significantly increased in the CFS group compared with non-fatigued controls (p=0.037). Similarly, there was a significant decrease in the CD1d+ B cells in the CFS group compared with nonfatigued controls (p=0.046). No additional differences in B cell phenotypes, activation markers and surface receptors were found in the CFS patients compared with the non-fatigued control group.

The differences observed in the B cell phenotype of CFS patients compared with non-fatigued controls may explain some of the disturbances in the immune homeostasis, however whether this is causal or the consequence of immunological imbalances previously reported in CFS patients requires further investigation.

Characterisation of B cell Subsets and Receptors in Chronic Fatigue Syndrome Patients by S Ramos, E Brenu, T Nuyen, J Ng, D Staines and D Marshall-Gradisnik in J Clin Cell Immunol 2015, 6:1 [Published date: January 26, 2015]

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The nature of fatigue in CFS

Posted on 03/11/2015 by wames

Research abstract

In this article, we report the findings of our study on the nature of fatigue in patients diagnosed with chronic fatigue syndrome.

Using ethnoscience as a design, we conducted a series of unstructured interviews and card sorts to learn more about how people with chronic fatigue syndrome describe fatigue. Participants (N = 14) described three distinct domains: tiredness, fatigue, and exhaustion.

Most participants experienced tiredness prior to diagnosis, fatigue during daily life, and exhaustion after overexertion. We also discuss participants’ ability to adapt to a variety of stressors and prevent shifts to exhaustion, and relate our findings to stress theory and other current research.

Primary strategies that promoted adaptation to stressors included pacing and extended rest periods. These findings can aid health care professionals in detecting impending shifts between tiredness, fatigue, and exhaustion and in improving adaptive strategies, thereby improving quality of life.

The Nature of Fatigue in Chronic Fatigue Syndrome by K  Olson, O Zimka, E Stein in Qual Health Res. 2015 Feb 26. pii [Epub ahead of print]

 

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Reduced cytokine levels may lead to neurological problems in CFS/ME

Posted on 03/09/2015 by wames

Research abstract

Objectives: Previous research has provided evidence for dysregulation
in peripheral cytokines in patients with Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME). To date only one study has examined cytokines in cerebrospinal fluid (CSF) samples of CFS/ME patients. The purpose of this pilot study was to examine the role of cytokines in CSF of CFS/ME patients.

Methods: CSF was collected from 18 CFS/ME patients and 5 healthy controls. The CSF samples were examined for the expression of 27 cytokines [interleukin (IL)-1β, IL-1ra, IL-2, IL-4, IL-6, IL-7, IL-8, IL-9, IL-10, IL-12p70, IL-13, IL-15, IL-17, basic FGF, eotaxin, G-CSF, GM-CSF, IFN-γ, IP-10, MCP-1 (MCAF), MIP-1α, MIP-1β, PDGF-BB, RANTES, TNF-α and VEGF] using the bio-plex human cytokine 27-plex assay.

Results: Of the 27 cytokines examined, only IL-10 was significantly reduced in the CFS/ME patients in comparison to the controls.

Conclusions: This preliminary investigation suggests that perturbations in inflammatory cytokines in the CSF of CFS/ME patients may contribute to the neurological discrepancies observed in CFS/ME.

Cytokines in the Cerebrospinal Fluids of Patients with Chronic Fatigue Syndrome/Myalgic Encephalomyelitis, by D Peterson, EW Brenu, G Gottschalk, S Ramos, T Ngyuen, D Staines, S Marshall-Gradisnik, in Mediators of Inflammation Vol 2015 , Article ID 929720, 4 pages

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Claire Jones, Welsh harpist with ME

Posted on 03/06/2015 by wames

Claire Jones, former Royal harpist from Pembrokeshire, talks about her experience of ME and road to recovery through homeopathy, chiropractic treatment, nutrition and psychological therapies.

She advises people with ME to listen to their bodies and calls for better services. Her 4th solo album Journey reflects her journey through ME.

BBC Radi0 Wales: Eleri Sion 2nd March 2015 [interview begins 1h 36 – online until end of March]

Daily Mail article: I feared for career says Royal harpist Claire Jones hit by ME [scroll down]

Wales online: Former royal harpist Claire Jones on her ME fight

Times: ‘It’s a real illness and a physical one’: Claire Jones’s struggle with ME

Videos on You Tube

Claire Jones website

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Disturbed sleep is key symptom in CFS

Posted on 03/05/2015 by wames

Research abstract

Objectives:
Sleep disturbances are common in chronic fatigue syndrome (CFS), and one of the key symptom complaints, yet it has been neglected by previous qualitative research. The aim was to explore the specific role of sleep in patients’ experience of their illness.

Design:
A qualitative semi-structured interview format facilitated a detailed and open exploration of sleep, and the extent to which its management and problems were linked to the lived experience of CFS.

Methods:
Eleven semi-structured interviews were conducted with individuals with CFS. Data were transcribed verbatim and analysed thematically, to explore and describe patients’ experience of their sleep, and its impact on their condition.

Results:
Sleep emerged as a key aspect of the illness experience, and its management and effect on daytime functioning was a central pre-occupation for all 11 participants; all of them saw sleep as playing a critical role in their illness through either maintaining or exacerbating existing symptoms.

Exploration of individual experiences presented three overarching themes: (1) sleep pattern variability over illness course and from day to day; (2) effect of sleep on daytime functioning; and (3) attempts at coping and sleep management.

Conclusions:
Each patient with CFS has a unique experience of sleep. Despite the differing narratives regarding the role of sleep in CFS, all participants held the belief that sleep is a vital process for health and well-being which has had a direct bearing on the course and progression of their CFS. Also, every participant regarded their sleep as in some way ‘broken’ and in need of management/repair. Patients’ insights demonstrate sleep-specific influences on their CFS, and the impact of disturbed sleep should be a consideration for clinical and research work.

The experience of sleep in chronic fatigue syndrome: A qualitative interview study with patients, by Zoe M. Gotts, Julia L. Newton, Jason G. Ellis and Vincent Deary in British Journal of Health Psychology [first published online: 26 Feb 2015]

Funded by
* Action for ME
* ME Research UK
* ME Association Ramsay Research Fund

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Distinct stages found in ME/CFS

Posted on 02/28/2015 by wames

Research abstract

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is an unexplained incapacitating illness that may affect up to 4 million people in the United States alone.

There are no validated laboratory tests for diagnosis or management despite global efforts to find biomarkers of disease. We considered the possibility that inability to identify such biomarkers reflected variations in diagnostic criteria and laboratory methods as well as the timing of sample collection during the course of the illness.

Accordingly, we leveraged two large, multicenter cohort studies of ME/CFS to assess the relationship of immune signatures with diagnosis, illness duration, and other clinical variables. Controls were frequency-matched on key variables known to affect immune status, including season of sampling and geographic site, in addition to age and sex.

We report here distinct alterations in plasma immune signatures early in the course of ME/CFS (n = 52) relative to healthy controls (n = 348) that are not present in subjects with longer duration of illness (n = 246).

Analyses based on disease duration revealed that early ME/CFS cases had a prominent activation of both pro- and anti-inflammatory cytokines as well as dissociation of intercytokine regulatory networks.

We found a stronger correlation of cytokine alterations with illness duration than with measures of illness severity, suggesting that the immunopathology of ME/CFS is not static. These findings have critical implications for discovery of interventional strategies and early diagnosis of ME/CFS.

Distinct plasma immune signatures in ME/CFS are present early in the course of illness, by Mady Hornig, José G. Montoya, Nancy G. Klimas, Susan Levine, Donna Felsenstein, Lucinda Bateman, Daniel L. Peterson, C. Gunnar Gottschalk, Andrew F. Schultz, Xiaoyu Che, Meredith L. Eddy, Anthony L. Komaroff, W. Ian Lipkin in Science Advances 27 Feb 2015: Vol. 1 no. 1  e1400121

Scientists discover robust evidence that Chronic Fatigue Syndrome is a biological illness (Columbia University)

BBC report: Distinct stages to chronic fatigue syndrome identified

The clock was (is) ticking: major study suggests ME/CFS is hit and run disorder, by Cort Johnson (Health Rising)

You tube video: Mady Hornig, MD, Associate Professor of Epidemiology and Director of Translational Research at the Center for Infection and Immunity discusses the impact that the latest findings may have on ME/CFS diagnosis and treatment

 

 

 

 

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MRI shows differences between CFS and depression

Posted on 02/27/2015 by wames

Research article:

White matter (WM) involvement in chronic fatigue syndrome (CFS) was assessed using voxel-based regressions of brain MRI against CFS severity scores and CFS duration in 25 subjects with CFS and 25 normal controls (NCs).

As well as voxel-based morphometry, a novel voxel-based quantitative analysis of T1- and T2-weighted spin-echo (T1w and T2w) MRI signal level was performed.

Severity scores included the Bell CFS disability scale and scores based on the 10 most common CFS symptoms.

Hospital Anxiety and Depression Scale (HADS) depression and anxiety scores were included as nuisance covariates.

By relaxing the threshold for cluster formation, we showed that the T1w signal is elevated with increasing CFS severity in the ventrolateral thalamus, internal capsule and prefrontal WM.

Earlier reports of WM volume losses and neuroinflammation in the midbrain, together with the upregulated prefrontal myelination suggested here, are consistent with the midbrain changes being associated with impaired nerve conduction which stimulates a plastic response on the cortical side of the thalamic relay in the same circuits.

The T2w signal versus CFS duration and comparison of T2w signal in the CFS group with the NC group revealed changes in the right middle temporal lobe WM, where impaired communication can affect cognitive function.

Adjustment for depression markedly strengthened cluster statistics and increased cluster size in both T1w severity regressions, but adjustment for anxiety less so.

Thus, depression and anxiety are statistical confounders here, meaning that they contribute variance to the T1w signal in prefrontal WM but this does not correlate  with the co-located variance from CFS severity.

MRI regressions with depression itself only detected associations with WM volume, also located in prefrontal WM.

We propose that impaired reciprocal brain–body and brain–brain communication through the midbrain provokes peripheral and central responses which contribute to CFS symptoms.

Although anxiety, depression and CFS may share biological features, the present evidence indicates that CFS is a distinct disorder.

Evidence in chronic fatigue syndrome for severity-dependent upregulation of prefrontal myelination that is independent of anxiety and depression, by Leighton R. Barnden, Benjamin Crouch, Richard Kwiatek, Richard Burnet and Peter Del Fante in NMR in Biomedicine Vol 28 Issue 3, pages 404–413, March 2015 [Article first published online: 22 FEB 2015]

 

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Reconditioning programme for CFS

Posted on 02/23/2015 by wames

Research abstract:

AIM: Physical exercise can be part of treatment in patients with chronic fatigue syndrome (CFS), where the aim would be to improve strength and endurance through increasing physical exercise (intensity and time) without aggravating symptomatology. The present study examines the effectiveness of a reconditioning programme (focusing on strength, endurance, balance and proprioception) for achieving maximum functional capacity according to the clinical status of CFS patients.

METHODS: Sixty-eight patients with CFS were randomly assigned to two groups: a control group (CG) comprising 22 patients and an active group (AG) of 46 patients, the latter being invited to take part in a functional reconditioning programme based on 12 weeks of laboratory training followed by a further 12-week home training period. Functional assessments were as follows: before (I) and after (II) the laboratory training and after (III) the home training.

RESULTS: In the AG, 22 patients (67%) completed the intervention (laboratory) stage and 20 finished the whole protocol (61%). Patients in the AG showed improved static and dynamic balance, as well as significantly greater maximum strength (F=7.059, p<0.05). Differences in resistance strength were also observed, with the AG showing a 19.9% improvement between functional assessments I and II (p=0.04). We don’t found changes in the CG.

CONCLUSION: A physical exercise programme of this kind might offer CFS patients the opportunity to improve their strength, balance and quality of life, there being only a very small risk of relapse and none of the adverse effects of other treatments.

Physical effects of a reconditioning programme in a group of chronic fatigue syndrome patients, by E Guillamó et al in  Journal of Sports Medicine and Physical Fitness, 18 February 2015 (published ahead of print).

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Measuring substantial reductions in activity

Posted on 02/20/2015 by wames

Research abstract

The case definitions for Myalgic Encephalomyelitis/chronic fatigue syndrome (ME/CFS), ME, and CFS each include a disability criterion requiring substantial reductions in activity in order to meet diagnostic criteria. Difficulties have been encountered in defining and operationalizing the substantial reduction disability criterion within these various illness definitions.

The present study sought to relate measures of past and current activities in several domains including the SF-36, an objective measure of activity (e.g., actigraphy), a self-reported quality of life scale, and measures of symptom severity.

Results of the study revealed that current work activities had the highest number of significant associations with domains such as the SF-36 subscales, actigraphy, and symptom scores. As an example, higher self-reported levels of current work activity were associated with better health. This suggests that current work related activities may provide a useful domain for helping operationalize the construct of substantial reductions in activity.

Measuring substantial reductions in activity, by Charles Schafer Meredyth Evans Leonard A. Jason, Suzanna So & Abigail Brown in Journal of Prevention & Intervention in the Community Volume 43,  Issue 1, 2015, pages 5-19 [Published online: 13 Jan 2015]

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Non-celiac gluten sensitivity co-exists with CFS and FM

Posted on 02/20/2015 by wames

Letter to editor:

We have closely read the article published by Isasi et al.1 in Reumatologia Clínica presenting a case of fibromyalgia (FM) and chronic fatigue syndrome (CFS) caused by non-celiac sensitivity to gluten (NGCD). We would like to comment our experience with this attractive topic regarding patients with FM/CFS, which I hope will contribute to an improved knowledge of this association.

The authors have reasonably ruled out celiac disease (CD) and have hypothesized that NGCD is the cause of FM and CFS in their patient; upon complete remission (CR) of symptoms, both digestive and musculoskeletal, with a gluten-free diet (GFD).

CFS is characterized by intense fatigue in addition to cognitive, autonomic, neuroendocrine, immunoallergic and musculoskeletal symptoms, newly appearing and inexplicable, lasting for at least 6 months.

In the criteria (C) from the most recent international consensus in 2011, gastrointestinal alterations were included (irritable bowel syndrome [IBS] as was sensitivity to foodstuff) as diagnostic criteria for CFS.2

This new classification allows us to consider NGCD as a comorbid condition (CC), which perpetuates CFS and not unleashes it. In our series of 200 patients affected by CFS attended at the Unidad del Camp de Tarragona (2011–2013), we found the following CC: 101 patients (50.5%) with FM, 38 patients (19%) with chronic autoimmune thyroiditis, 31 patients (15.5%) with NGCD and 27 patients (13.5%) with IBS.

At the onset of GFD, in addition to multidisciplinary treatment, most of our patients (up to 80%) had improvement of their intestinal symptoms (abdominal pain, diarrhea, flatulence, oral ulcers) and a very modest response to extra intestinal symptoms (fatigue, bone pain, alterations in concentration and depression) without reaching CR.

Therefore, we have supported the theory of overlap between FM/CFS and NGCD without concluding that the latter is its cause in this patient population, but may aggravate its symptoms. This term was probably employed for the first time in 1978 by Ellis and Linaker.

There is increasing evidence suggesting the existence of NGCD. This concept groups patients who do not comply with the criteria of CD but experiment intestinal symptoms and/or extra intestinal manifestations when consuming gluten. Recent studies haveproposed that FODMAP (fermented oligo, di, monosacharides and polyols) as components of the wheat causing symptoms of NGCD, in addition to gluten.3

Its prevalence is estimated to be 10 times greater than CD. In Table 1 we expose the diagnostic criteria used to define NGCD.4 The gold standard for its diagnosis would be a double blind intervention controlled with placebo, because taking gluten out of the diet could lead to a placebo effect that may explain the improvement or remission of symptoms.

In conclusion, we must take into account several considerations in the case presented by the authors. First, NGCD is a comorbid condition of FM/CFS, not the factor triggering it. Second, both FM and CFS are 2 chronic and complex diseases from the diagnostic and therapeutic standpoint, which require multidisciplinary management (adequate nutrition and dietary balance, symptom-based treatment, cognitive-conductual therapy and regulated gradual physical exercise) more than a simple GFD. Third, we believe that the case presented is a NGCD with extra intestinal affection (FM/CFS-like symptoms) more than FM/CFS per se.

References

  1. Isasi C, Tejerina E, Fernández-Puga N, Serrano-Vela JI.
    Fibromyalgia and chronic  fatigue syndrome caused by non-celiac gluten sensitivity. Reumatol Clin. 2014,
  2. Carruthers BM, van de Sande MI, de Meirleir KL, Klimas NG, Broderick G, Mitchell T, et al. Myalgic encephalomyelitis: international consensus criteria.
    J Intern Med.  2011;270:327–38.
  3. Gibson PR, Sheperd SJ. Food choice as a key management strategy for functional gastrointestinal symptoms. Am J Gastroenterol. 2012;107:657–66.
  4. Sapone A, Bai JC, Ciacci C, Dolinsek J, Green PH, Hadjivassiliou M, et al. Spectrum of gluten-related disorders: consensus on new nomenclature and classification.  BMC Med. 2012;10:13.

Response to: Fibromialgia y fatiga crónica causada por sensibilidad al gluten no celíaca [Fibromyalgia and Chronic Fatigue Syndrome Caused by Non-celiac Gluten Sensitivity], by Rami Qanneta, Ramon Fontova, Antoni Castel in Reumatol Clin. 2014

 

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