Inflammatory proteins are altered in chronic fatigue syndrome – a systematic review and meta-analysis, 2019, Strawbridge et al

Andy

Andy

Retired committee member
Highlights

• 42 studies meta-analysed, testing 20 proteins between patients with CFS and controls
• Patients had higher levels of 5 cytokines than controls (TNF, IL-2, IL-4, TGFb, CRP)
• Group differences were not significant for 12 proteins
• Results are heterogeneous but provide some support for an inflammatory role in CFS

Abstract
Immune dysfunction has been posited as a key element in the aetiology of chronic fatigue syndrome (CFS) since the illness was first conceived. However, systematic reviews have yet to quantitatively synthesise inflammatory biomarkers across the literature.

We undertook a systematic review and meta-analysis to quantify available data on circulating inflammatory proteins, examining studies recruiting patients with a CFS diagnosis and a non-affected control group.

Results were meta-analysed from 42 studies. Patients with CFS had significantly elevated tumour necrosis factor (ES = 0.274, p < 0.001), interleukin-2 (ES = 0.203, p = 0.006), interleukin-4 (ES = 0.373, p = 0.004), transforming growth factor-β (ES = 0.967, p < 0.001) and c-reactive protein (ES = 0.622, p = 0.019). 12 proteins did not differ between groups.

These data provide some support for an inflammatory component in CFS, although inconsistency of results indicates that inflammation is unlikely to be a primary feature in all those suffering from this disorder. It is hoped that further work will elucidate whether there are subgroups of patients with clinically-relevant inflammatory dysfunction, and whether inflammatory cytokines may provide a prognostic biomarker or moderate treatment effects.
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Paywall, https://www.sciencedirect.com/science/article/pii/S0149763419306128
Sci hub, not available
 
I'm a bit wary of this paper given where the authors are based

Rebecca Strawbridge, Maria-Laura Sartor,Fraser Scott, Anthony J.Cleare
Department of Psychological Medicine, Institute of Psychiatry, Psychology & Neuroscience, King’s College London, London, UK
 
No, yet ironic that non friends are talking about subgroups, which is where imho we all need to be heading.

Call me cynical, but the devil is in the detail and how they or their colleagues try to use it, perhaps to justify a PACE II.

Interesting that (from Trish's link) Marshall-Gradisnik et al arrive at the same kind of conclusion about inconsistency. I think its a valid observation.
https://link.springer.com/epdf/10.1186/s12883-019-1433-0?author_access_token=oGS8oSoB3ng5QwDUI7WPpm_BpE1tBhCbnbw3BuzI2RMOtEHGGPflRKBejc-Tt4mMSRHueZ2ixKhPcRX2xe9aSWwCAuS4omU-152hpfkHB_xL2KNMMlmd2WtbYSUUZl5DNjECpef8z-gRthYbVTQV4g==
it is recommended that the aforementioned limitations of the studies be addressed, and a standardised protocol, including consistent use of case definitions and selection of homogenous CFS/ME/SEIDpopulations that can be stratified, be developed for further evaluation into determining whether cytokines play a role in the aetiology of CFS/ME/SEID.
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They (Aussies) are talking about case definitions and homogenous CFS/ME/SEID populations which I believe translates as criteria and cohorts. Again IMHO this is subtyping and is where we have to be heading, all the more so after EDS/CCI became such a hot topic. And while mitochondria are a bone of contention inflammatory markers would surely be another approach worth persuing in parallel, particularly if we are envisaging multiple subtypes, the more methods for discerning differences the better.
 
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Merged thread

Didn't see this previously posted:

"Neurosci Biobehav Rev. 2019 Dec;107:69-83. doi: 10.1016/j.neubiorev.2019.08.011. Epub 2019 Aug 26.
Inflammatory proteins are altered in chronic fatigue syndrome-A systematic review and meta-analysis.
Strawbridge R1, Sartor ML2, Scott F2, Cleare AJ2.
Author information
1
Department of Psychological Medicine, Institute of Psychiatry, Psychology & Neuroscience, King's College London, London, UK. Electronic address: Becci.strawbridge@kcl.ac.uk.
2
Department of Psychological Medicine, Institute of Psychiatry, Psychology & Neuroscience, King's College London, London, UK.

Abstract
Immune dysfunction has been posited as a key element in the aetiology of chronic fatigue syndrome (CFS) since the illness was first conceived. However, systematic reviews have yet to quantitatively synthesise inflammatory biomarkers across the literature. We undertook a systematic review and meta-analysis to quantify available data on circulating inflammatory proteins, examining studies recruiting patients with a CFS diagnosis and a non-affected control group. Results were meta-analysed from 42 studies.

Patients with CFS had significantly elevated tumour necrosis factor (ES = 0.274, p < 0.001), interleukin-2 (ES = 0.203, p = 0.006), interleukin-4 (ES = 0.373, p = 0.004), transforming growth factor-β (ES = 0.967, p < 0.001) and c-reactive protein (ES = 0.622, p = 0.019). 12 proteins did not differ between groups.

These data provide some support for an inflammatory component in CFS, although inconsistency of results indicates that inflammation is unlikely to be a primary feature in all those suffering from this disorder. It is hoped that further work will elucidate whether there are subgroups of patients with clinically-relevant inflammatory dysfunction, and whether inflammatory cytokines may provide a prognostic biomarker or moderate treatment effects."

https://www.ncbi.nlm.nih.gov/pubmed/31465778
 
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Scihub link, https://sci-hub.se/10.1016/j.neubiorev.2019.08.011

Most studies utilised the CDC diagnostic criteria for CFS (Bennett et al., 1997; Borish et al., 1998; Buchwald et al., 1997; Cannon et al., 1999; Chao et al., 1991; Cheney et al., 1989; Giloteaux et al., 2016; Hardcastle et al., 2015; Jammes et al., 2009; Kennedy et al., 2004; Lattie et al., 2012; Macdonald et al., 1996; Maes et al., 2012; Montoya et al., 2017; Nakamura et al., 2010, 2013; Nater et al., 2008; Neu et al., 2014; Peterson et al., 1994; Raison et al., 2009; Robinson et al., 2010; Scully et al., 2010; Smylie et al., 2013; Spence et al., 2008; Straus et al., 1989; Sulheim et al., 2014; White et al., 2004, 2010; Wyller et al., 2015), while others used the ICD criteria (Broderick et al., 2010, 2013) or the Canadian criteria (Lidbury et al., 2017) and some used multiple diagnostic criteria (Ford et al., 2016 ; Hornig et al., 2017 ; Khaiboullina et al., 2015 ; Landi et al., 2016 ; Nagy-Szakal et al., 2017 ; Nakatomi et al., 2014 ; Russell et al., 2016).
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so I make that the majority of the studies used in the review, and therefore the results of this review, should be considered iffy on grounds of the selection criteria used.
 
King's college (and Anthony Cleare who is presumably AJ Cleare) are BPSers. I think they do this work to show they are looking at biology, but, sigh, there is nothing much there despite the protests of patients.

It may not apply here, not read the paper, but the problem with studies of immune dysfunction has always been that while it goes wrong in most patients, in some it goes up in others it goes down and there is no consistency. It is like the control of the immune system is wrong rather than any individual bit.

Then we have the problem that things are worse for us in PEM - that is when I get inflammatory symptoms - but then it goes back to normal.
 
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