Chronic Fatigue Exhibits Heterogeneous Autoimmunity Characteristics Which Reflect Etiology (Danilenko et al, 2022)

Consul

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Abstract

Abstract: Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is considered to be associated with post-viral complications and mental stress, but the role of autoimmunity also remains promising. A comparison of autoimmune profiles in chronic fatigue of different origin may bring insights on the pathogenesis of this disease. Thirty-three patients with CFS/ME were divided into three subgroups. The first group included Herpesviridae carriers (group V), the second group included stress-related causes of chronic fatigue (distress, group D), and the third group included idiopathic CFS/ME (group I). Were evaluated thirty-six neural and visceral autoantigens with the ELISA ELI-test (Biomarker, Russia) and compared to 20 healthy donors, either without any fatigue (group H), or “healthy but tired” (group HTd) with episodes of fatigue related to job burnout not fitting the CFS/ME criteria. β2-glycoprotein-I autoantibodies were increased in CFS/ME patients, but not in healthy participants, that alludes the link between CFS/ME and antiphospholipid syndrome (APS) earlier suspected by Berg et al. (1999). In CFS/ME patients, an increase in levels of autoantibodies towards the non-specific components of tissue debris (double-stranded DNA, collagen) was shown. Both CFS and HTd subgroups had elevated level of autoantibodies against serotonin receptors, glial fibrillary acidic protein and protein S100. Only group V showed an elevation in the autoantibodies towards voltage-gated calcium channels, and only group D had elevated levels of dopamine-, glutamate- and GABA-receptor autoantibodies, as well as NF200-protein autoantibodies. Therefore, increased autoimmune reactions to the multiple neural antigens and to adrenal
medullar antigen, but not to other tissue-specific somatic ones were revealed. An increase in autoantibody levels towards some neural and non-tissue-specific antigens strongly correlated with a CFS/ME diagnosis. Autoimmune reactions were described in all subtypes of the clinically significant chronic fatigue. Visceral complaints in CFS/ME patients may be secondary to the neuroendocrine involvement and autoimmune dysautonomia. CFS may be closely interrelated with antiphospholipid syndrome, that requires further study.


The study (pdf):
https://mdpi-res.com/d_attachment/p...thophysiology-29-00016.pdf?version=1653483756
 

Wishful

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I can't judge the quality of the study, and I'm suspicious of the use of genuine fatigue as a factor, but at least it sounds like interesting research.
 

Consul

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I can't judge the quality of the study, and I'm suspicious of the use of genuine fatigue as a factor, but at least it sounds like interesting research.
Yes looks very interresting and im also unsure about the quality.

Here is a quote from the study
It is especially interesting that, in our study, the elevated levels of autoantibodies to β2-glycoprotein-I correlated most significantly with CFS/ME diagnosis. This particular autoantigen is also known as an antiphospholipid syndrome (APS) marker [37]. As early as 1999, a hypothesis was introduced considering CFS/ME as a form of mild chronic APS, confirmed by some similarities of hemostasis/antihemostasis system status in these two entities [38]. Our data can probably draw new attention to this old concept, being for a long time out of the scope of attention in CFS/ME studies.
In the paper they mention Scheibenbogens 2018 pilot study on immunoadsorption with good short term results. Has anyone followed up on this, and did they try removing the aabs mentioned in this study also, and particularly the one mentioned in the quote?
 

pattismith

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@MonkeyMan

this interesting study divides ME/CFS patients according to possible causality, this might improve the quality of the research.

Abstract

Abstract:

Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is considered to be associated with post-viral complications and mental stress, but the role of autoimmunity also remains promising.

A comparison of autoimmune profiles in chronic fatigue of different origin may bring insights on the pathogenesis of this disease.

Thirty-three patients with CFS/ME were divided into three subgroups.

The first group included Herpesviridae carriers (group V),
the second group included stress-related causes of chronic fatigue (distress, group D),
and the third group included idiopathic CFS/ME (group I).

Were evaluated thirty-six neural and visceral autoantigens with the ELISA ELI-test (Biomarker, Russia) and compared to 20 healthy donors, either without any fatigue (group H), or “healthy but tired” (group HTd) with episodes of fatigue related to job burnout not fitting the CFS/ME criteria.

β2-glycoprotein-I autoantibodies were increased in CFS/ME patients, but not in healthy participants, that alludes the link between CFS/ME and antiphospholipid syndrome (APS) earlier suspected by Berg et al. (1999).

In CFS/ME patients, an increase in levels of autoantibodies towards the non-specific components of tissue debris (double-stranded DNA, collagen) was shown.

Both CFS and HTd subgroups had elevated level of autoantibodies against serotonin receptors, glial fibrillary acidic protein and protein S100.

Only group V showed an elevation in the autoantibodies towards voltage-gated calcium channels, and only group D had elevated levels of dopamine-, glutamate- and GABA-receptor autoantibodies, as well as NF200-protein autoantibodies. Therefore, increased autoimmune reactions to the multiple neural antigens and to adrenalme dullar antigen, but not to other tissue-specific somatic ones were revealed.

An increase in autoantibody levels towards some neural and non-tissue-specific antigens strongly correlated with a CFS/ME diagnosis.

Autoimmune reactions were described in all subtypes of the clinically significant chronic fatigue.

Visceral complaints in CFS/ME patients may be secondary to the neuroendocrine involvement and autoimmune dysautonomia.

CFS may be closely interrelated with antiphospholipid syndrome, that requires further study.