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Longitudinal investigation of natural killer cells and cytokines in CFS/ME

SOC

Senior Member
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There are reference ranges, for CD56 I believe. Don't know about CD56CD16. I had some CD56 test results recently, with a control level indicated:

NK phenotyping
CD56dim 98.1% (control 92.4%)


Please someone correct me if I'm wrong, but I've concluded that if I have 98.1% dim I must have only 1.9% bright, as the total refers to dim+bright.

Jenny
FWIW, my bright/dim combinations don't add up to 100%. They must be percentages of some larger total, but what total I have no idea.

CD8 bright 6.4%
CD8 dim 19.3%
CD3+CD8 bright 6.3%
CD3+CD8 dim 4.4%
CD3-CD8 bright 0.0%
CD3-CD8 dim 14.7%
CD3+CD8 bright CD56+ 0%
CD3-CD8 bright CD56+ 1.5%
CD3+CD8 dim CD56+ 0%
CD3-CD8 dim CD56+ 9.5%

CD3+CD56+CD8+ 0%
CD3-CD56+CD8- 3.7%
CD3-CD56+CD8+ 11.1%
CD3-CD56+CD11a+ 14.6%
 

alex3619

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They might not work for everyone, but considering some of the alternatives out there, the side effect and risk profile of SSRIs are quite benign, and IMO at least worth a try, especially if you have comorbid depression or anxiety.

EDIT: it might be that the reduced NKCA seen i ME/CFS is more pronounced than what is seen in other disorders, in which case it could still be a valuable biomarker.
Hi Adreno, the only drug that came close to killing me was an SSRI. First dose. Microdose. I took a minimal dose tab, scraped a bit off the side, took it. Within minutes I was out cold. I only woke up four days later (though I dimly recal several episodes of brief consciousness).

With regard to biomarkers, I agree with Staines: combining different biomarkers will increase specificity a lot.

Bye, Alex
 

Hope123

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It's off-topic for the thread but since people are talking about it: some ME/CFS specialists caution use of SSRIs in ME/CFS even for treating depression as it can cause some serious side effects and they suggest very low doses to start with. I think if SSRIs, TCAs, and similar classes of drugs were truly effective for ME/CFS, we would see more cases of people getting better from them. Many people with ME/CFS have been on these drugs over the years [in fact, some were misdiagnosed with only depression initially] and yet I'm not hearing any success stories. The drugs may help with co-morbid depression.

Also, would like to point out that I disagree with the Maes abstract where it states the fatigue of depression and ME/CFS are the same. Definitely not when it comes to exercise/ exertion. People with only depression often feel better post-exercise and increased physical activity may be part of treatment for depression; people with ME/CFS feel much worse. Where I can agree with the abstract is that inflammation of the brain via ME/CFS potentially can cause depression but it may be different from the depression people without ME/CFS have although on the surface, perhaps it can look the same. That is, we probably don't know enough yet to distinguish between different versions of depression and there is a lot we don't know about the immune system still.
 

August59

Daughters High School Graduation
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I had some positive effects with Cymbalta (which is technically a SNRI), but I quit taking it for financial reasons. I don't think it would be as much of an advantage now as my home life if is extremely stressffull and Cymbalta cancause anxiety and I already have it very badly. When I was going to Hunter Hopkins Center they always started anyone that needed an SSRI on Zoloft as it had the lowest side effects with PWC. If they could tolerate, but needed something different then they may change. They did however start very low and went up slow because of our tendency to react strongly minimal dose changes.

Sorry, I am just adding to the thread hijacking and will be glad to move it to another if mod feels that it would be appropriate
 

hixxy

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I don't know how much of this has already been posted on this thread earlier or on another thread. I heard the following bits of information from someone who attended a presentation in Melbourne last weekend by the lead researcher Sonya Marshall-Gradisnik on this study.

1. The team is moving from Bond University to a Griffith University (teaching hospital attached)
2. The last study only included those in South east QLD. There are intentions (no formal plans) to include other hospitals, in order to expand future studies
3. They are looking at trying to incorporate as many bed-bound and house-bound PWCs as possible in future studies. (The studies in the past have only been of those who have been well enough to attend the facilities)
4. They are hinting at a Rituximab pilot.
5. They will be mostly exploring ME/CFS as an autoimmune disease.

I heard these bits of information 3rd party, so I can't really confirm any of it.
 

Chris

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Many thanks--a great find, as others have said. I am interested in the "seasonal" aspect--I have always been worse in late fall and winter, and then improved somewhat as spring and summer come round. This year I have increased my Vit D supplementation, and have used a UV lamp too. Will soon get my Vit D retested (it was bottom of the normal range, despite taking over 1,000 IU daily); have also been taking AHCC pulsed, and more recently most of Terry Wahls' stuff--and am slowly improving, though exercise tolerance seems to be the last thing to really move upwards--sleep and general feeling are leading the pack.
Best, Chris
 
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The thing about SSRIs is that they have been shown to have properties that should be very advantageous in ME/CFS, including:

- being neuroprotective/increasing neurogenesis
- being anti-inflammatory
- reducing autoimmunity
- normalizing the HPA axis, at least partially
- improving NKCA
- decreasing pain
The list of drugs with properties that should be advantageous in ME/CFS is very long. The list of drugs that actually have substantial effects are much smaller.

The funny thing is, when seretonic activity was measured by various groups of psychiatrists, they found that seretonic activity was either normal increased in those who were not currently taking psychotropic medicine. Two groups hypothesised that elevated serotonic activity could lead to increased sensations of fatigue.

Increased brain serotonin function in men with chronic fatigue syndrome
http://www.bmj.com/content/315/7101/164.full


Neuroendocrine assessment of serotonin (5-HT) function in chronic fatigue syndrome.
http://www.ncbi.nlm.nih.gov/pubmed/7788624

Contrasting neuroendocrine responses in depression and chronic fatigue syndrome.
http://www.ncbi.nlm.nih.gov/pubmed/8550954
These data confirm that depression is associated with hypercotisolaemia and reduced central 5-HT neurotransmission and suggest that CFS may be associated with hypocortisolaemia and increased 5-HT function. The opposing responses in CFS and depression may be related to reversed patterns of behavioural dysfunction seen in these conditions. These findings attest to biological distinctions between these disorders.
The above was also a study involving S. Wessely.
 

Valentijn

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My platelet serotonin measured quite a bit below normal, but taking anything that affects it (5HTP, Amitriptyline) makes my pain and OI quite a bit worse. Which is unfortunate, because I was able to read a few novels again while taking 5HTP over the past week, and it was a lot easier to think clearly. Though I felt too sedated to want to do any actual thinking :p
 

August59

Daughters High School Graduation
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What I thought was also interesting in this study was the continuous change all the way through the 12 months. I would hope that maybe they will go back and try to pull samples at 24 and even 36 months to see if there is a point of drastic change or if possibly there is ever a point of stabilzation. It does appear though that there will probably be test taken to find out at what stage an individual is in and treat accordingly. This probably why people are getting such various effects even when taking the same treatment
 

Jenny

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FWIW, my bright/dim combinations don't add up to 100%. They must be percentages of some larger total, but what total I have no idea.

CD8 bright 6.4%
CD8 dim 19.3%
CD3+CD8 bright 6.3%
CD3+CD8 dim 4.4%
CD3-CD8 bright 0.0%
CD3-CD8 dim 14.7%
CD3+CD8 bright CD56+ 0%
CD3-CD8 bright CD56+ 1.5%
CD3+CD8 dim CD56+ 0%
CD3-CD8 dim CD56+ 9.5%

CD3+CD56+CD8+ 0%
CD3-CD56+CD8- 3.7%
CD3-CD56+CD8+ 11.1%
CD3-CD56+CD11a+ 14.6%
Curiouser and curiouser!