Rituximab 'causes impaired immune function, Griffith study says'

R

Russell Fleming

Senior Member (Voting Rights)
Drug hoped to treat CFS causes impaired immune function, Griffith study says

March 27, 2018

Reports that a drug used to treat autoimmune diseases and cancer could also treat Chronic Fatigue Syndrome (CFS) have been refuted by a new Griffith University study.

To be published in BMC Pharmacology and Toxicology, the study by Griffith’s National Centre for Neuroimmunology and Emerging Diseases (NCNED) concluded that the use of Rituximab in CFS patients could incur problems with their immune cells and is not beneficial as a potential treatment.

The Natural Killer (NK) cells have vital functions in fighting viruses, bacteria and tumours.

“We found that these functions were significantly impaired when exposed to Rituximab in CFS patients,” says Scientific Co-Director of NCNED, Professor Sonya Marshall-Gradisnik.

CFS – sometimes known as ME (myalgic encephalomyelitis) – is a complex illness characterised by impaired memory and concentration, metabolic, cardiac, gut and immune dysfunction and debilitating muscle pain and fatigue on exertion (also known as neuroimmune exhaustion).

It is estimated that the prevalence rate of CFS/ME worldwide is between 1 and 2 per cent.

Related to the ion channels
The Gold Coast NCNED team has discovered the illness is related to problems in the ion channels that allow calcium into the body’s cells. Calcium is required by almost every cell in the human body and is vital in helping the immune system destroy a virus or infection.

The team has proven that patients with CFS/ME have lower levels of calcium coming into their cells, that their cells store less calcium and that this is the basis of their illness.

Professor Don Staines, Clinical Co-Director of NCNED, says: “These results are important as NK cells are already known to have impaired function in CFS patients, suggesting certain doses of Rituximab may not be beneficial for the treatment of this condition.”

“Undertaking an initial study has enabled us to secure additional research funding from the national competitive grants process from the Mason Foundation where we can now undertake a larger study using this drug in vitro to validate our novel findings,” says Professor Staines.

First author for these world-first scientific findings was PhD student, Ms Natalie Eaton. She will be presenting the study at an NCNED-sponsored conference later this year. The focus of the conference will be promoting greater understanding of pathology and pharmacothereapeutics for CFS, through a Research, Innovation, Discovery, Learning and Education (RIDLE) model.
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The team has proven that patients with CFS/ME have lower levels of calcium coming into their cells, that their cells store less calcium and that this is the basis of their illness.
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Nope, definitely not a hyped result at all, Griffiths University wouldn't do that.... :laugh:
 
Isn't it suppose to "impair" the immune system? I understood this was it's method of action, to take out one type of immune cell which was suspected of being faulty and force them to be replaced with new ones, which would presumably not be defective.

I'm struggling to see the point of this report, even assuming..........
 
It is not clear whether they looked at NK cells from patients treated with rituximab, in which case one wonders who did the trial, or NK cells in culture, which almost certainly tells us nothing.

I am afraid that if there was any doubt about the fact that this group do not have a clue, there is none now. What on earth do they think they are up to? Who cares what rituximab does to NK cells now? Of what possible relevance could it have to anything?
 
Jonathan Edwards said:
It is not clear whether they looked at NK cells from patients treated with rituximab, in which case one wonders who did the trial, or NK cells in culture, which almost certainly tells us nothing.
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It would most certainly have to be the latter. They recruited in the past for studies involving in vitro drug testing but as far as I'm aware haven't recruited for an actual in vivo trial of any kind.
 
Given that Ritximab has been shown not to be effective in a large double blind trial, I'm not sure what their point is. Though, as I understand it, Ritximab wipes out B cells, not NK cells, which seem to be the target of their research.

This team seems to have a very effective PR machine and to get lots of funding, and make claims of finding cause and biomarker. But have they actually published anything useful?
 
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I dont see the point of this study except to try and undermine ritux and the possible subset it may help - findings are still to be had. Are they boosting their own theories?

It wouldnt be surprising if ritux did affect NK cells? But that doesn't mean much even if correct and last I heard the NK cell findings were not able to be replicated anyway? I think I saw this at IiME and that NK cells are too difficult as a marker. You hear of some having decreased function and some having increased function. Which also does not mean causation.

Calcium channel blockers Griffiths are keen to try, you hear some go well on these and some don't but I haven't heard of them curing people anecdotally.

Excuse my ranting but I have watched them make many assertions with no proof or replications from elsewhere or researchers seemingly keen to replicate their findings. I also thought that Marshall-Gradsnik background was in sports medicine and muscle function? I could have that wrong.

They certainly are very good at PR and gaining funding.
 
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hixxy said:
I googled very briefly after seeing this media release and noticed this different publication about NK cells and Rituximab below.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5024429/
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I think I have seen this paper before and cannot work out what it is trying to tell us. The effect of rituximab on NK cells has nothing to do with the fact that NK cells mediate B cell killing as far as I can see. Since rituximab is a human antibody there is no obvious reason why it should do anything special to NK cells, which do not express CD20. The problem is that all you need is for there to be a low level of contamination of the NK sample with B cells or CD20+ T cells and you would see odd things happening.
 
hixxy said:
It would most certainly have to be the latter. They recruited in the past for studies involving in vitro drug testing but as far as I'm aware haven't recruited for an actual in vivo trial of any kind.
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I think probably yes. The only caveat is that there was a physician in Queensland who was using rituximab in ME but I don't think he was working with Griffith.
 
Jonathan Edwards said:
I am afraid that if there was any doubt about the fact that this group do not have a clue, there is none now.
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Thank you! I know nothing about hard research except for what is explained to me here and other ME organizations but I knew these "researchers" have been on to nothing from the get-go. And one of the most important clues to is the silence of the researchers here in the US about their "marker" research.

And just to clarify, Rituximab will not help anyone with ME. There is no SUBSET that can be helped. They don't have ME and were misdiagnosed.

Everything they are doing at Griffiths, their marker research going on for years is a sham and their disqualifying Rituximab as an ME drug the way they have is a joke. It is an invalid drug for us because it does not work on true ME or CFS or SEID. There IS NO SUBSET, just patients misdiagnosed with ME or CFS or SEID. That's what a criteria without a true marker will get you, people that are misdiagnosed. Maybe they had CANCER!
 
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