Autoantibody determination in chronic fatigue syndrome (CFS)

SWAlexander

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This is a google auto translation:

Chronic Fatigue Syndrome (CFS), also known as Myalgic Encephalomyelitis (ME), is a common and severe multisystem disease.
A defined cause could not be found so far. What is clear, however, is that dysregulation of the immune system, the hormone system, the autonomic nervous system and the cellular energy metabolism occurs in ME/CFS.

In about 2/3 of the cases ME/CFS is triggered by an infection. In addition to pathogens such as Epstein-Barr virus (EBV), herpesviruses, enteroviruses, influenza, dengue viruses, bacteria (borrelia, chlamydia, legionella, coxia) other triggers are possible. For example, a cervical spine trauma, operations, pregnancy, particularly physical exertion or psychological stress can be associated with the onset of the disease.
The main symptoms of ME/CFS are severe fatigue and exercise intolerance. This means a delayed (up to 48 hours) massive aggravation of the symptoms even after little physical or mental exertion (PEM = Post-Exertional Malaise). These symptoms can then last for days to weeks. In addition, most patients suffer from pain, flu-like symptoms and cognitive disorders such as concentration and memory problems, speech disorders, sensitivity to stimuli, irritable bowel disorders and pronounced sleep disorders. Susceptibility to infections and allergies have also been described. Further information can be found on the website of the German Society for ME/CFS eV (https://www.mecfs.de).

In connection with the SARS-CoV-2 coronavirus, it has also been observed that some of the patients develop symptoms weeks to months after the infection, which are referred to as "long-COVID" or "post-COVID-19 syndrome" and develop ME /CFS remember. These include above all fatigue, PEM and brain fog (cognitive dysfunction).

pathomechanism

The underlying pathomechanism in ME/CFS is not yet fully understood. Persistent immune dysregulation, characterized by changes in cytokine profiles and immunoglobulin levels (decreased or increased), T- and B-cell phenotype, and reduced natural killer cell function, has often been described. Furthermore, there is convincing evidence that ME/CFS has an autoimmune etiology in patients with a previous infection, as autoantibodies are also detectable.

ME/CFS is a diagnosis of exclusion

In order to make a suspected clinical diagnosis of CFS, an extensive clinical and laboratory diagnostic exclusion diagnosis must first be carried out. In addition, the Canadian Consensus Criteria (CCC) or the International Consensus Criteria (ICC) for ME/CFS must be met. The diagnosis of ME/CFS can only be made if the symptoms last longer than 6 months, as this differentiates the post-infectious fatigue. Other diseases associated with chronic fatigue must also be ruled out, such as autoimmune diseases, neurodegenerative diseases or cancer. Common comorbid conditions in CFS include fibromyalgia, irritable bowel syndrome, Hashimoto's thyroiditis, and endometriosis.

There are currently no specific laboratory parameters that can be used to reliably diagnose the presence of ME/CFS.

Neurotransmitter receptor autoantibodies are detectable in approximately 30% of patients with ME/CFS

Autoantibodies (AAb) against various antigens, including neurotransmitter receptors, have been identified by several groups in postinfectious ME/CFS. Neurotransmitter receptors belong to the group of G protein-coupled receptors (GPCR). GPCRs are localized in cell membranes and are responsible for the perception and transmission of extracellular stimuli into the interior of the cell. They thereby trigger biochemical signaling cascades in the cell. After binding to their respective receptors, AAb directed against GPCR can have both agonistic and antagonistic effects (Fig. 1).

Since they change the function of the target cells as a result of receptor binding, they are among the so-called functional AAbs. They belong to a regulatory network that is dysregulated in numerous diseases and thus involved in the pathogenesis of various autoimmune and non-autoimmune diseases.

AAbs against neurotransmitter receptors such as β-adrenergic receptors and muscarinic acetylcholine receptors (mAChR) also play a role in ME/CFS. As early as 2003 it could be shown that increased concentrations of AAk against mAChR can be detected and correlated with muscle weakness and neurocognitive disorders. In a study by Prof. Scheibenbogen's working group, significantly increased AAbs against β-adrenergic receptors and muscarinic acetylcholine receptors were found in some ME/CFS patients compared to healthy people.

Numerous AAk were also detected in long-COVID, including against various G protein-coupled receptors. Ongoing studies will show whether these GPCR-AAk are, for example, the cause of the persistence of the symptoms.

The tests for the quantitative determination of the AAb against β1/β2 adrenergic receptors and M3/M4 muscarinic acetylcholine receptors (mAChR) are available in our laboratory. Positive AAk results can be used to support the diagnosis of ME/CFS, but are not considered conclusive. Inconspicuous AAb findings, however, do not rule out the presence of ME/CFS, since only about 30% of patients have neurotransmitter receptor AAb (Fig. 2 a

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SWAlexander

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β-adrenergic receptors
There are nearly endless articles on β-adrenergic receptors and circulating catecholamines, are important regulators of cardiac function available. Though, so far very few connections was made to ME/CFS.
One more issue very rarely discussed or examined is TSH.
Yesterday finally, after pushing doctors for a Thyroid exam (possible Hashimoto) after constant fluctuating T3 (high) and T4 (normal), I had a sonogram.
Preliminary sonogram results:
Left thyroid enlarged with a 0.75 mm cyst filled with liquid.
Right side 0.75 mm cyst and 0.5 mm filled with liquid.
Further tests are necessary.
 

Violeta

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β-adrenergic receptors
There are nearly endless articles on β-adrenergic receptors and circulating catecholamines, are important regulators of cardiac function available. Though, so far very few connections was made to ME/CFS.
One more issue very rarely discussed or examined is TSH.
Yesterday finally, after pushing doctors for a Thyroid exam (possible Hashimoto) after constant fluctuating T3 (high) and T4 (normal), I had a sonogram.
Preliminary sonogram results:
Left thyroid enlarged with a 0.75 mm cyst filled with liquid.
Right side 0.75 mm cyst and 0.5 mm filled with liquid.
Further tests are necessary.
Have you had any further testing done?

Does it seem strange that T3 is in the high range? Did your doctor have an explanation for that?