Is there any way I can be treated with rituximab privately?

[gregh286]

Yea its what makes this such a complex condition.
Some have sleep issues and some can do 12-15 hours dead as a stone.

 

[snowathlete]

Sleep problems started as one of my earliest symptoms and has remained dreadful. It's a major issue for me, just one major aspect of the disease, which I look forward to getting better along with everything else.

 

[BurnA]

And yes - it also sounded unlikely to me that none have responded, but I do trust the doctor who told me this. And thinking about it, surely if people had travelled to America and got treatment and it had worked, we would know about it.

I can across this on the Richmond and Kingston ME group website

The ME Association’s ‘Question Time’, held at Tiffin School in Kingston on 3 October, was a grand success. With an all-star top table of leading experts in the field — Dr Amolak Bansal, Dr Charles Shepherd, Jane Colby and Sue Luscombe — it was well attended; we counted 108 people in the hall, of whom 21 were members of the Richmond and Kingston ME Group.



Rituximab:In response to a question on progress in the use of Rituximab as a possible treatment for ME, Dr Bansal said that he would be attending a meeting next week to discuss this. The Norwegian studies show benefit, but none of the British people with ME who went to the USA for Rituximab treatment have benefited, despite high expectations. We need a double blind trial. It is best to combine Rituximab with antivirals and endocrine drugs. The Norwegian group had a specific cause of ME, and also we don’t have good anti-viral agents. Dr Shepherd said that the Norwegians are doing a Phase 3 trial, results are expected in 2018. The UK ME Research Collaborative have identified the timeline. The Norwegian success won’t wash in the UK, so we will need our own Phase 3 trial to persuade the Medical Research Council. Thus we are looking at 2022 before the drug could become available in the UK. Dr Bansal said that the USA are planning a randomised controlled trial but this has not yet got past their National Institute of Health. He feels that Rituximab is not curative because ME is a perpetuated disease, and hence the need to combine it with anti-virals.

I am curious if this is the source for the story that none of the British people who travelled to the US have responed to rtx.
Also, it states that all the patients in the Norwegian trial has a specific cause of ME - what does that mean ?

 

[Riley]

Also, it states that all the patients in the Norwegian trial has a specific cause of ME - what does that mean ?

I think he is suggesting that the Norwegian cohort in which success has been had has some specific cause of M.E. that is uniquely suited to treatment with Rituximab.

I don't believe there is any evidence to support that assertion.

 

[Ellkaye]

Sounds messy.
wild goose chase and injustice to patients to keep their hopes up.
How very disappointing. I feel for the many non-responders whose dr's were brainwashed by the literature of cytokines/chemokines by big name hollywood chilly pepper papers,and different types of severe arthritic/moldy ME papers from Scandinavia and elsewhere which just isnt ME even if they rose from their beds. Did they have PEM?
I m not saying it is a total no go. For example I take viread+raltegravir now 3days or 4days/week only. I wonder if I should top up/replace with rituximab. For now I feel I dont need it but who knows perhaps in the future yes,or catecorically quite simply no n never Need an expert to answer me.One who knows about ME firstly who diagnosed/s it during all their career preferably,who knows about RV's,reduced days as per iccarre,immune modulators et cetera and combination treatments to activate the immune system.
The sickest ones are in desperate need of help.
Dr's n patients right across the board n globe must gather n sit down n talk n discuss.

 

[Jonathan Edwards]

I can across this on the Richmond and Kingston ME group website
"The ME Association’s ‘Question Time’, held at Tiffin School in Kingston on 3 October, was a grand success. With an all-star top table of leading experts in the field — Dr Amolak Bansal, Dr Charles Shepherd, Jane Colby and Sue Luscombe — it was well attended; we counted 108 people in the hall, of whom 21 were members of the Richmond and Kingston ME Group.

Rituximab:In response to a question on progress in the use of Rituximab as a possible treatment for ME, Dr Bansal said that he would be attending a meeting next week to discuss this. The Norwegian studies show benefit, but none of the British people with ME who went to the USA for Rituximab treatment have benefited, despite high expectations. We need a double blind trial. It is best to combine Rituximab with antivirals and endocrine drugs. The Norwegian group had a specific cause of ME, and also we don’t have good anti-viral agents. Dr Shepherd said that the Norwegians are doing a Phase 3 trial, results are expected in 2018. The UK ME Research Collaborative have identified the timeline. The Norwegian success won’t wash in the UK, so we will need our own Phase 3 trial to persuade the Medical Research Council. Thus we are looking at 2022 before the drug could become available in the UK. Dr Bansal said that the USA are planning a randomised controlled trial but this has not yet got past their National Institute of Health. He feels that Rituximab is not curative because ME is a perpetuated disease, and hence the need to combine it with anti-virals."

I am curious if this is the source for the story that none of the British people who travelled to the US have responed to rtx.
Also, it states that all the patients in the Norwegian trial has a specific cause of ME - what does that mean ?

That looks a fairly garbled account of the situation, although the overall message is not far off track.

As I understand it most ME patients who have travelled to USA for rituximab (and there are very few) have done so through Dr Bansal and none that he knows of have responded usefully. Dr Bansal has mentioned this to me on a number of occasions. But I do not think we have any evidence for Norwegian patients having a specific cause for their ME - we cannot have because nobody has any information on a cause. What may be true, however, is that the Norwegian patients have a different pattern of disease since they were mostly recruited through a neurologist.

Dr Bansal is keen on anti-virals but I doubt he would have said 'it is best to combine rituximab with antivirals' since we have no evidence for that. Moreover, if we do not have good anti-viral agents there seems even less point.

I am not sure what it means that the CMRC have identified a timeline. A number of people have felt that a rituximab trial in the UK was worth getting going for some years but the problem is in getting a suitable design. It is also not true to say that the Norwegian trial will not wash in the UK. It will do fine if it shows a clear benefit from rituximab. There are rules about having multiple trials for drug licensing and separately there are 'non-rules' (i.e. chaos) on which NICE basis decision on NHS funding. But as new situations come along these have to be adjusted. Further trials are needed for scientific purposes like getting the right dose and identifying responder subgroups but I am personally not convinced that a parallel large phase III trial in the UK is the best way to spend money. Normally during drug development there is one major phase III efficacy study backed up by dose-response or other studies that are capable of confirming efficacy and also producing other information - but they do not need to be on the same scale.

 

[Ellkaye]

Then again I was 50% originally.Maybe the arv's would have worked quicker with rituximab i dont know but I think not n perhaps it s an unnecessary question.

I took more normal arv doses at the start(s) of them, perhaps I should ve taken less as I do now.

That said it did take 18 months to get me (upward curve) to 95% and also to find out the 3or4days/week protocol on both arv's is stable n effective enough now so even if I was mild the arv s didnt find it so easy to work n settle to the current low dose until they managed to settle down the body through their mechanism at the normal dose perhaps (though the most raltegravir I ever took was 35%-45% adherence just like now(couldnt tolerate it daily it was really potent though I tried so that was/is my upper limit).It is the Viread I took daily 100% but now also only needed at 45%-50% adherence too.

Perhaps I could ve taken less(viread) before too I dont know.Or maybe doing so would ve not been aggressive enough for it to be given a chance to stick later in the immune system memory at a reduced days dose.

Feel quite happy now with three of four days of both per week so both at a reduced stable dose now after all that. In essence it just felt that i just had to find the correct number of days AND to create the right setting for my body to have a good response. If rituximab can help there VERY GENTLY then great.If not then maybe it is not the right med. I am no expert. Or maybe an initial normal dose of arv s is just as good n then reduced or pulsed in with another arv.
With good cancer type multivitamins for good measure n to keep the peace in the important gut.

I m going to research use of rituximab in HIV in iccarre patients or those on arv s daily. I m keeping an open mind. But for now I still need a lot of convincing about the necessity n effectiveness of rituximab but I cant exclude it.
Clinicians in practice are weary of it I believe.

Has anyone done white blood cell cd3/4/8 counts before n after rituximab? It does not wipe those out do it?
I confuse all these markers.

I really have no idea if a gently does it arv approach is better right from the beginning or not.Perhaps depends how sick u are n how well u can tolerate all these meds.Or with antibiotics to target the gut firstly? Or some other kick starting immune system remedy..Regenerating blood cells,blood transplants? Then arv s?

Overmedication with arv's can be an issue though so that's one thing to be aware of.

Just adding my two pennies worth to the corpus of discussion and of clinical data,accepted or not. I feel for the sickest ones who have been ill too long n for who treatment effectiveness will be more complex,financially too.

All decisions must obviously be taken with your brave gamechanging common sense curious brave sensible doctors who have decades of experience with true ME as defined by Melvin Ramsey.There are enough of those doctors around.

 

[heapsreal]

Maybe dr kogelneck is on track when he mentioned valcyte with rtx a couple years back. I'm guess dr montoya would be thinking alongthe same lines as they worked with each other in other cfs research .

 

[Ellkaye]

That looks a fairly garbled account of the situation, although the overall message is not far off track.

As I understand it most ME patients who have travelled to USA for rituximab (and there are very few) have done so through Dr Bansal and none that he knows of have responded usefully. Dr Bansal has mentioned this to me on a number of occasions. But I do not think we have any evidence for Norwegian patients having a specific cause for their ME - we cannot have because nobody has any information on a cause. What may be true, however, is that the Norwegian patients have a different pattern of disease since they were mostly recruited through a neurologist.

Dr Bansal is keen on anti-virals but I doubt he would have said 'it is best to combine rituximab with antivirals' since we have no evidence for that. Moreover, if we do not have good anti-viral agents there seems even less point.

I am not sure what it means that the CMRC have identified a timeline. A number of people have felt that a rituximab trial in the UK was worth getting going for some years but the problem is in getting a suitable design. It is also not true to say that the Norwegian trial will not wash in the UK. It will do fine if it shows a clear benefit from rituximab. There are rules about having multiple trials for drug licensing and separately there are 'non-rules' (i.e. chaos) on which NICE basis decision on NHS funding. But as new situations come along these have to be adjusted. Further trials are needed for scientific purposes like getting the right dose and identifying responder subgroups but I am personally not convinced that a parallel large phase III trial in the UK is the best way to spend money. Normally during drug development there is one major phase III efficacy study backed up by dose-response or other studies that are capable of confirming efficacy and also producing other information - but they do not need to be on the same scale.

How about running an arv trial in ME patients with low immunodeficient cd3/4/8's ? And/or who are positive on the mikovits/ruscetti sffv antibody test? And/or who match positive to their original unaltered hgrv dna contamination free isolates?

 

[Ellkaye]

Maybe dr kogelneck is on track when he mentioned valcyte with rtx a couple years back. I'm guess dr montoya would be thinking alongthe same lines as they worked with each other in other cfs research .

You need experienced wise astute ME clinicians in there.
Why isnt Montoya more vocal about the hgrv positives Lipkin found in his patients?
All I see is paralysis n fear.
AV's like valgan vala acycl etc just havent stood the definitive test of time

Aaaand the baaaand plays on n on n on

 

[heapsreal]

You need experienced wise astute ME clinicians in there.
Why isnt Montoya more vocal about the hgrv positives Lipkin found in his patients?
All I see is paralysis n fear.
AV's like valgan vala acycl etc just havent stood the definitive test of time

Aaaand the baaaand plays on n on n on

I think they believe theres an infectious role in cfsme . The exact role i guess they dont know but herpes viruses like ebv cmv hhv6 reactivating is a sign of something else causing immune dysfunction .

Right or wrong RV research has been tarnished . Money for more research is needed, has been since day dot, with the band playing on.

Theres alot going on behind the scenes that most of us dont know.

 

[Ellkaye]

I think they believe theres an infectious role in cfsme . The exact role i guess they dont know but herpes viruses like ebv cmv hhv6 reactivating is a sign of something else causing immune dysfunction .

Right or wrong RV research has been tarnished . Money for more research is needed, has been since day dot, with the band playing on.

Theres alot going on behind the scenes that most of us dont know.

They sure tarnished xmrv silvermann. But thankfully by doing so they polished xmrvMikovits' hgrv which came to the fore as the real and only common pathogen here. So that's really positive.

 

[Ellkaye]

There is an open label phase 2 trial with cyclophosphamide currently in progress. There are threads which discuss it, you should look there. Similar story to rtx, patients were observed to respond during cancer treatment.
Its a lot more potent than rtx though.

is this taken orally ??

Thanks for that info, which is very interesting.

Recently I read through most of the threads on this rituximab sub-forum, specifically looking for people who had tried rituximab, to try to gauge the response rate.

Out of the 12 people I found on these forums who were treated with rituximab, only one person so far has responded (@Rebecca2z, but she certainly responded very well — see this thread). Though of this 12, there are two people who only recently started rituximab, so it is too early to tell. And there were also three people who stopped posting, so their status is unknown.

But we can say that out of the 7 people for which we have the full data, only 1 has responded to rituximab.

I understand that Rebecca's ME/CFS appeared as a result of chronic Epstein-Barr virus infection, some 30 years ago. So Rebecca's ME/CFS appears to have been EBV-triggered (remember that EBV chronically infects B cells).





It's conceivable that in Norway, there may have been an epidemic of ME/CFS caused by a particular pathogen, creating a specific subset of ME/CFS patients that respond well to rituximab.

There was in fact a large outbreak of giardiasis in Bergen, Norway in 2004 (giardiasis = intestinal infection with the parasite Giardia lamblia), and it was found that 5% of patients who came down with giardiasis in Bergen went on to develop ME/CFS. So Giardia lamblia appears to be a trigger of ME/CFS. (They also found a 39% prevalence rate for IBS in these Bergen giardiasis cases, 6 years later).

Remember that it is at the Haukeland University Hospital in Bergen where Fluge and Mella are conducting their rituximab trials.

Thus it is quite conceivable that Fluge and Mella may be treating many patients whose ME/CFS was originally triggered by Giardia lamblia, or patients for whom Giardia lamblia plays a significant role in their disease, because these patients caught Giardia lamblia during the 2004 outbreak in Bergen.

Now I read that Giardia lamblia is linked to autoimmune diseases, particularly with neurological autoimmune processes such as multiple sclerosis, ALS (Lou Gehrig’s disease), and Parkinson’s disease (ref: here, but unsure of the validity of this source). So when Giardia lamblia triggers ME/CFS, this parasite may be precipitating an autoimmune-driven type of ME/CFS.

This may explain why rituximab works so well for ME/CFS patients in Bergen.

I thought ME was reached at as a diagnosis once everything else including primary autoimmune disease had been excluded.
Do people have multiple diagnoses...?

Also if u treat with rituximab i guess u wipe out the rv until it only returns again..?

Can rituximab responders please give us a list of their autoimmune diagnoses. ME plus.....plus.....plus
.....? And how fatigued were u b4 n after for your ME and also for your exhausting autoimmune ailments? How do u distinguish the different fatigues of your different ailments?

'Similar' is a very misleading word but a very powerful one indeed.

a bit like serving water for everyone to drink. Pleases n quenches everyone's thirst, but forgets their other tastes. But if water is the only thing going then obviously i m thirsty so i ll have it.

Thanks

 

[Ellkaye]

that said :


http://www.ncbi.nlm.nih.gov/pubmed/12848988

Autoimmun Rev. 2002 Dec;1(6):329-37.
HIV and autoimmunity.
Zandman-Goddard G1, Shoenfeld Y.
Author information

• 1Center for Autoimmune Diseases, Department of Medicine 'B', Sheba Medical Center, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Hashomer 52621, Israel.

did rituximab responders have autoimmune diseases before or after getting ME or both and old ones became worse and new ones appeared with ME on top to add some compassion to their fatigue states as diagnosed by misinformed doctors casually?

lots to consider, but yes, everyone deserves help, for their own disease, including those with ONLY pure ME

 

[Hip]

I thought ME was reached at as a diagnosis once everything else including primary autoimmune disease had been excluded.

What is a "primary autoimmune disease"? Did you get mixed up with primary immunodeficiency?

You don't need to exclude all other diseases before arriving at a diagnosis of ME/CFS. Many ME/CFS patients have more than one disease, including autoimmune diseases.

 

[Ellkaye]

What is a "primary autoimmune disease"? Did you get mixed up with primary immunodeficiency?

You don't need to exclude all other diseases before arriving at a diagnosis of ME/CFS. Many ME/CFS patients have more than one disease, including autoimmune diseases.

your reply says it all.............

So it would follow that those with autoimmune diseases can have ME ??

This is what has always been the problem.
Very sad state of affairs.

And all because of the fear of a RV.
Lots of water muddying.

ME is a SIMPLE disease.

it is not the complex collection of different diseases it has been made out to be.

 

[deleder2k]

@Ellkaye, I've attached a table that shows details from the 2015 Rituximab study. It includes whether patients had an infection upfront or not. From what I've heard and seen I think there is no reason to believe that the outbreak of Giardia in Bergen had something to do with the results of the study.

Cyclophosphamide is given IV.

 

[Ellkaye]

Wasnt suggesting any outbreak of anything had anything to do with anything.

Am just saying what many other diseases in the past declared/undeclared do some of these patients all have underpinning them to create their overall disease state?

What diseases would other dr's that saw them in the past say they have? Do researchers look into their medical records? Or self reported ?

 

[BurnA]

Were they diagnosed with Canadian Consensus Criteria or Fukuda?


What % of patients said they had ME ?


What were the other diseases they had declared?


Was viral evidence an inclusion ?

I am sorry but your posts are very difficult to follow and somewhat confusing. You may have picked something up wrong or misinterpreted something so now your questions seem a bit all over the place.
I suggest reading a lot of the threads on rtx as most of your questions will probably be answered there and if not maybe come back with a few specific questions.

 

[A.B.]

So what's the rationale behind B cell depletion plus antivirals?

The possibility that Rituximab works by eradicating some virus that lives in B cells has been discussed but Edwards and Fluge/Mella agree that the response pattern is consistent with autoimmunity and not consistent with elimination of B cell inhabiting viruses.