My Rituximab experience with RA and ME

[Nielk]

I received a copy of my latest blood work. This included a full T subset test.

Abnormalities show the following:

CD19, % and ABS is 0 - I didn't hear from the doctor yet but, I am assuming that this is very good? I think that this means my b cells are depleted?

CD8, % is 37 and ABS is 811 - both of these show higher than normal. I don't know what that means.

Everything else is in the normal range.

 

[heapsreal]

I received a copy of my latest blood work. This included a full T subset test.

Abnormalities show the following:

CD19, % and ABS is 0 - I didn't hear from the doctor yet but, I am assuming that this is very good? I think that this means my b cells are depleted?

CD8, % is 37 and ABS is 811 - both of these show higher than normal. I don't know what that means.

Everything else is in the normal range.

so do the improvement suppose to occur when b-cells come back.

if b cells are a resivoir for ebv, then should should start to see cd8 possibly come down over time?

 

[Nielk]

so do the improvement suppose to occur when b-cells come back.

if b cells are a resivoir for ebv, then should should start to see cd8 possibly come down over time?

I don't know the answers. I don't even know what CD8 is.

 

[heapsreal]

I don't know the answers. I don't even know what CD8 is.

cd8 is a t cell thats commonly elevated in ebv/cmv. This is what i mostly followed when using antivirals with corresponding improvement in my elevated cd8 ??

 

[deleder2k]

Why are we talking about EBV? Do you have an ongoing EBV infection @Nielk ?

 

[heapsreal]

Why are we talking about EBV? Do you have an ongoing EBV infection @Nielk ?

One theory of why rituximab works in cfs/me is that it depletes the B-cells which are said to be a resivoir for ebv?

 

[Nielk]

Why are we talking about EBV? Do you have an ongoing EBV infection @Nielk ?

I don't have a current infection but high titers for past infection with ebv.

 

[Bob]

so do the improvement suppose to occur when b-cells come back.

Any improvements should start once the levels of auto-antibodies starts to decline. This will happen gradually after the B cells have been depleted. (Antibodies are created by B Cells.) So depletion of the B cells is the first step, and then improvements will hopefully follow.

 

[Nielk]

Any improvements should start once the auto-antibodies levels start to decline. This will happen gradually after the B cells have been depleted. (Antibodies are created by B Cells.) So depletion of the B cells is the first step, and then improvements will hopefully follow.

Thanks Bob. I'm ready and waiting!

 

[deleder2k]

One theory of why rituximab works in cfs/me is that it depletes the B-cells which are said to be a resivoir for ebv?

Hm.. who's behind that theory?

 

[Valentijn]

Hm.. who's behind that theory?

Science. EBV infects B cells indefinitely. Rituximab kills off B cells. ME/CFS is acknowledged even by the hardcore psychobabblers to frequently be triggered by EBV infection.

And then there's logic. Killing off the B cells infected with the virus results in new B cells without the virus. Losing the virus may result in patient improvement.

 

[Jonathan Edwards]

These results are fine. CD19 should be zero. T cells are of no great interest. We do not bother to measure them.

The Norwegians were not thinking in terms of EBV when they tried rituximab and I cannot see it would make any sense to theorise about EBV here be honest. For all other autoimmune diseases the improvement is assumed to be due to fall in autoantibodies, as Bob points out. The Norwegian responses fitted with the same time scale as with other autoimmune disorders. If it was due to clearing EBV people should get better in a week!

 

[Nielk]

These results are fine. CD19 should be zero. T cells are of no great interest. We do not bother to measure them.

The Norwegians were not thinking in terms of EBV when they tried rituximab and I cannot see it would make any sense to theorise about EBV here be honest. For all other autoimmune diseases the improvement is assumed to be due to fall in autoantibodies, as Bob points out. The Norwegian responses fitted with the same time scale as with other autoimmune disorders. If it was due to clearing EBV people should get better in a week!

Thank you as always for your reply and input. It is priceless.

 

[heapsreal]

These results are fine. CD19 should be zero. T cells are of no great interest. We do not bother to measure them.

The Norwegians were not thinking in terms of EBV when they tried rituximab and I cannot see it would make any sense to theorise about EBV here be honest. For all other autoimmune diseases the improvement is assumed to be due to fall in autoantibodies, as Bob points out. The Norwegian responses fitted with the same time scale as with other autoimmune disorders. If it was due to clearing EBV people should get better in a week!

My understanding ebv is in other tissue and nervous system also, maybe cause of relapses. Ithink this is wwhy Dr kogelnek was also looking into antivirals with rituximab,

I know the standard school of thought is that ebv is nothing to worry about but it does seem to be a trigger in other autoimmune diseases. There is small pockets of ms people finding improvements with antivirals.

With low nk function and the role of nk cells to fight viral infected cells, I don't see any reason why herpes viruses are overlooked as a possible cause and or Co infection. Active herpes viruses are a common finding in many cfsme patients and proven by many cfsme docs.

it's not for everyone but there has been a significantly high success rate with antivirals in cfsme that a connection with b cells as a resivoir for herpes viruses is worth looking into further.

I guess this is why a combo of antivirals and rituximab was of interest to a few research docs.

 

[DanME]

I think, (like Dr. Edwards said) the main theory, why Retuximab works is through the depletion of Autoantibodies as in other autoimmune diseases. The depletion of EBV is probably not the mechanism of action.

Herpes viruses are not overlooked in ME/CFS in current research. Dr. Scheibenbogen in Berlin published a very nice paper on the possible deficiency to fight early stages of EBV in ME patients. One theorised way could be, that the immune system is constantly confronted with early EBV proteins and starts to confuse them with similar body proteins. Thus triggering an autoimmune disease with an unknown target.

Hopefully somebody finds the epitop (the target) soon. That would explain the whole pathophysiology.

 

[heapsreal]

I think, (like Dr. Edwards said) the main theory, why Retuximab works is through the depletion of Autoantibodies as in other autoimmune diseases. The depletion of EBV is probably not the mechanism of action.

Herpes viruses are not overlooked in ME/CFS in current research. Dr. Scheibenbogen in Berlin published a very nice paper on the possible deficiency to fight early stages of EBV in ME patients. One theorised way could be, that the immune system is constantly confronted with early EBV proteins and starts to confuse them with similar body proteins. Thus triggering an autoimmune disease with an unknown target.

Hopefully somebody finds the epitop (the target) soon. That would explain the whole pathophysiology.

I guess im just think they need to research to see if there is a similar mechanisim, i say this because at the moment rituximab and antivirals both work for certain groups of cfs pts to some degree etc. Are we look at the same mechanisms, or similar pathways and can we get sustained and better more effective improvement by combining both therapies.

I just think its worth looking into. If it pans out to be very different then we have two obvious sub groups that can be treated and appropriate testing needs to be worked out to diagnose the right patient for the right treatment. Im not against cfs being an auto immune illness but theres alot of unanswered questions i would like to see answered eventually. I would also like to see ampligen put into this group and work out its mechanisms and if they share any sinilar pathways??

 

[Seven7]

@heapsreal Here is my theory: I am not autoimmune, but when the doctor gives me medicine like inmmune modulators and equillibrant she always says " we have to monitor and go low and slow so you dont develop autoimmunity. So obviously you can have CFS and not autoimmunity (like in my case) so I wonder if some have gotten there by medications or is it a natural progression of the disease. I just wonder the others getting tests like me what their story is.

Or Am I misinterpreting when you say autoimmunity, we are not talking about known tests markers???

 

[deleder2k]

@heapsreal Here is my theory: I am not autoimmune, but when the doctor gives me medicine like inmmune modulators and equillibrant she always says " we have to monitor and go low and slow so you dont develop autoimmunity. So obviously you can have CFS and not autoimmunity (like in my case) so I wonder if some have gotten there by medications or is it a natural progression of the disease. I just wonder the others getting tests like me what their story is.

Or Am I misinterpreting when you say autoimmunity, we are not talking about known tests markers???

How doyou know you're not autoimmune?

 

[NK17]

I'm too brain fogged to extrapolate right now, but I think that both @heapsreal and @DanielBR are right in talking about EBV as a triggering, or shall I say tipping factor, in a group of PWME.

They are right when they talk about the important study of Dr. Scheibenbogen at Charite in Berlin as well as the interest of Dr. Kogelnik here in the US to conduct a 4 arm study with both Valganciclovir and Rituximab (25% would get Rituxan only, 25% Rituxan+Valcyte, 25% Valcyte only and the remaining 25% placebo).

Ideally in the not too far future we'll also have Ampligen approved specifically for ME, but that is another long and twisted saga.

I hope to be alive and kicking to see all this treatments approved for ME.

The way I see this disease, that I've been living with for 3/4 of my life, is that it's a very serious neuro-immune disease that we are only now starting to pay attention to and because of the lagging of scientific interest in it we still don't see the forest, but the single trees. What I mean by saying that is that there might be subgroups, but we need to realize that being ME a chronic disease, just like lupus or MS, it's a continuum and we get to seek medical attention, when we can, at different times in the disease.

Our doctors have to realize that whatever organic damage we are now able to see (via MRI's etc.) it's only the tip of the iceberg.

I'm certain that my ME started with IM infectious mono (back in 1981) and then slowly took hold of my immune system, or dismantled whatever was left of it.

I got diagnosed only in 2011 and the window of opportunity for some treatments might be long gone.

This is just my personal story, but one that I've learned to recognize and share with many of my fellow sufferers.

 

[Kati]

I'm too brain fogged to extrapolate right now, but I think that both @heapsreal and @DanielBR are right in talking about EBV as a triggering, or shall I say tipping factor, in a group of PWME.

They are right when they talk about the important study of Dr. Scheibenbogen at Charite in Berlin as well as the interest of Dr. Kogelnik here in the US to conduct a 4 arm study with both Valganciclovir and Rituximab (25% would get Rituxan only, 25% Rituxan+Valcyte, 25% Valcyte only and the remaining 25% placebo).

Ideally in the not too far future we'll also have Ampligen approved specifically for ME, but that is another long and twisted saga.

I hope to be alive and kicking to see all this treatments approved for ME.

The way I see this disease, that I've been living with for 3/4 of my life, is that it's a very serious neuro-immune disease that we are only now starting to pay attention to and because of the lagging of scientific interest in it we still don't see the forest, but the single trees. What I mean by saying that is that there might be subgroups, but we need to realize that being ME a chronic disease, just like lupus or MS, it's a continuum and we get to seek medical attention, when we can, at different times in the disease.

Our doctors have to realize that whatever organic damage we are now able to see (via MRI's etc.) it's only the tip of the iceberg.

I'm certain that my ME started with IM infectious mono (back in 1981) and then slowly took hold of my immune system, or dismantled whatever was left of it.

I got diagnosed only in 2011 and the window of opportunity for some treatments might be long gone.

This is just my personal story, but one that I've learned to recognize and share with many of my fellow sufferers.

@NK17 I have been at it for just under 6 years now with 3 different rounds of treatments, to no avail. While early treatment and general attitude (pacing, resting, etc) is important, it may not change the course of the disease by much, at least so far. Regardless I feel hopeful that one day, we will get it figured out.