Rituximab 'causes impaired immune function, Griffith study says'

[Andy]

For what it's worth.

Abstract
Background

A recent in vitro pilot investigation reported Rituximab significantly reduced natural killer (NK) cell cytotoxicity in healthy donors. Chronic fatigue syndrome/Myalgic encephalomyelitis (CFS/ME) is a debilitating disorder of unknown etiology. A consistent finding is a significant reduction in NK cell cytotoxicity. Rituximab has been reported having questionable potential therapeutic benefits for the treatment of CFS/ME, however, the potential effects of Rituximab on NK cell cytotoxicity in CFS/ME patients are yet to be determined.

Methods
A total of eight CFS/ME patients (48.63 ± 15.69 years) and nine non-fatigued controls (NFC) (37.56 ± 11.06 years) were included using the Fukuda case definition. Apoptotic function, lytic proteins and degranulation markers were measured on isolated NK cells using flow cytometry following overnight incubation with Rituximab at 10 μg/ml and 100 μg/ml.

Results
There was a significant reduction in NK cell lysis between CFS/ME patients and NFC following incubation with Rituximab at 100 μg/ml at 12.5:1 and 6.25:1 effecter-target (E:T) ratios (p < 0.05). However, there was no significant difference for NFC following incubation with Rituximab at 10 μg/ml and 100 μg/ml.

There was no significant difference between CFS/ME patients and NFC for granzyme A and granzyme B prior to incubation with Rituximab and following overnight incubation with Rituximab at 10 μg/ml. There was a significant decrease in granzyme B in CFS/ME patients compared to NFC with 100 μg/ml of Rituximab prior to K562 cells stimulation (p < 0.05).

There was a significant increase in CD107a (p < 0.05) and CD107b expression (p < 0.01) in NFC after stimulation with K562 cells prior to incubation with Rituximab. There was a significant increase in CD107b expression between CFS/ME patients and NFC prior to incubation with Rituximab and without stimulation of K562 cells (p < 0.01). Importantly, there was a significant increase in CD107b following overnight incubation with 100 μg/ml of Rituximab in NFC prior to K562 cells stimulation (p < 0.01).

Conclusion
This study reports significant decreases in NK cell lysis and a significant increase in NK cell degranulation following Rituximab incubation in vitro in CFS/ME patients, suggesting Rituximab may be toxic for NK cells. Caution should be observed in clinical trials until further investigations in a safe and controlled in vitro setting are completed.

https://bmcpharmacoltoxicol.biomedcentral.com/articles/10.1186/s40360-018-0203-8

 

[Marky]

Why would they study this Literally makes no sense at all, unless they wanted to make some badly founded assumptions on their calcium channel theory of course..

 

[ivorin]

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!

Hi Melanie, I am currently on IVIG and am being considered for Ritux after that. Is there any reason you are so adamant about RTX not being helpful to a subset of CFS patients? Was there something else published other than the outcome of the big trial being a fail? I haven't been tuned in as I'm half dead and just trying to make it till I see if I respond to IVIG. Thanks!