The clinical value of cytokines in chronic fatigue syndrome.

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J Transl Med. 2019 Jun 28;17(1):213. doi: 10.1186/s12967-019-1948-6.
The clinical value of cytokines in chronic fatigue syndrome.
Yang T1, Yang Y2, Wang D2, Li C2, Qu Y2, Guo J2, Shi T2, Bo W2, Sun Z3, Asakawa T4,5.
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Abstract
Chronic fatigue syndrome (CFS) is a heterogeneous disorder with uncertain pathogenesis. Without effective therapy, CFS is characterized by disabling fatigue, depression, memory loss, and somatic discomfort. This comprehensive and impartial review aimed to assess the available evidence and examined the potential clinical value of using cytokines for the monitoring of CFS and as targets for the treatment of CFS. Inflammatory reactions and immune modulation are considered to contribute to the pathophysiology of CFS, and it is well documented that cytokines present in both blood and cerebrospinal fluid (CSF) are closely associated with the progression and severity of CFS.

However, pathophysiological and methodological limitations prevent using circulating cytokines as independent diagnostic indices. Moreover, there is no evidence to support the use of CSF cytokines as independent diagnostic indices. Nevertheless, a comprehensive evaluation of changes in circulating and CSF cytokines may improve clinical understanding of the pathophysiology of patients with CFS, aiding in the establishment of an appropriate diagnosis.

Importantly, the available evidence does not support the value of cytokines as therapeutic targets. We believe that an improved understanding of cytokine-related mechanisms will be helpful to explore new cytokine-related therapeutic targets.

KEYWORDS:
Chronic fatigue syndrome; Cytokine; Immune modulation; Individual diagnosis; Inflammatory reaction
PMID: 31253154 DOI: 10.1186/s12967-019-1948-6

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I agree there's no current clinical value. That's not to say that there can't one day be research value, once measurements grow more accurate.

Worth pointing to this new study on Sjogrens that even though patients have much higher cytokines than non-patients, in some cases higher cytokine levels correlated with patients feeling less fatigued.

https://forums.phoenixrising.me/thr...lammatory-cytokines-a-validation-study.76838/

It's as though once you've got the sickness, the cytokines might work to make you feel better.
 
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Diwi9

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It's sad to see that we have so little understanding of the operations of cytokines in 2019. If anyone had taken serious interest in this illness 30 years ago, perhaps this medical blackhole would be explainable. What does fatigue really mean? Or for that matter, pain? Anyone in medicine who believes they can explain this to a ME/CFS patient understands neither. It would be wonderful if the NIH was not just compartmentalized and lobbied on the basis of illnesses, but actually pursued mechanisms. Fatigue is not one thing, neither is pain...and neither can be adequately explained or treated medically at this point in time...seems like an area that should involve major interest on a national level given the lack of productivity...but alas, until there is a potential patent...there is no motivation.
 

S-VV

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The absolute state of 2019 cytokine research.

They cant even use consistent criteria when selecting participants.

Tgf-beta has been known for a long time. Il-8 as well. The "usual" proinflammatory cytokines don't appear to be elevated in me/CFS. If only it were so easy.

The only consistent results have been obtained when doing Gene expression analysis. These reveal a crearly pro-inflammatory picture.

Maybe it's time to look at paracrine prostaglandings/leukotrienes.
 

ljimbo423

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The only consistent results have been obtained when doing Gene expression analysis. These reveal a crearly pro-inflammatory picture.
This is a really good point and I'm jealous that I didn't think of it!:)
Here is a screenshot of that gene expression analysis. It clearly shows a pro-inflammatory gene expression in CFS at the 14 minute mark-

1562015109041.png

 

cigana

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The absolute state of 2019 cytokine research.

They cant even use consistent criteria when selecting participants.

Tgf-beta has been known for a long time. Il-8 as well. The "usual" proinflammatory cytokines don't appear to be elevated in me/CFS. If only it were so easy.

The only consistent results have been obtained when doing Gene expression analysis. These reveal a crearly pro-inflammatory picture.

Maybe it's time to look at paracrine prostaglandings/leukotrienes.
Anecdotal: my prostaglandins are consistently elevated.
 

cigana

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Here too, but it´s dangerous enough.

For three times I got very good effects from 50mg doxycyline.
Once I got excellent results (practically instant cure) from high dose amoxicillin, though that was not maintained. I'm working now on the theory the inflammation is caused by spinal issues. It's early days but some minor improvements from spinal manipulation have very similar effects to those pharmaceuticals (albeit at lower "power").
 

nandixon

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I'm working now on the theory the inflammation is caused by spinal issues.
It's certainly very suspicious. (Relatedly, see this post for the use of IVIG for antiinflammatory purposes in spinal cord injury: https://forums.phoenixrising.me/threads/had-an-appointment-with-dr-bolognese.76680/#post-2213465)

I'm suspicious too that chronic injury or irritation to the spinal cord (and/or brainstem) might also be one cause of various elevated antibody and/or autoantibody titers that some ME/CFS people see as well, as this is also known in acute spinal cord injury.

The role of more subtle spinal cord issues in causing or perpetuating detrimental systemic (as opposed to local) inflammatory and immunological processes has perhaps been very greatly underappreciated by the medical profession.
 

pattismith

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