Invest in ME/Prof Jonathan Edwards statement on UK Rituximab trial, 30 July

[Legendrew]

Apologies if this has been asked before, or the topic has been covered, I havent managed to read all of the posts on this thread (or understand all of them either ). Professor Edwards, I just wondered what your or anyone else's thoughts re those of us who respond to antibiotics (various ones including rifampicin, plus tetracyclines, macrolides) eg herxing/die-off reactions, followed by improvements. Although they have not been a cure as such, they have definitely helped for sure.

Unfortunately, the improvements either peter off or the side effects from the drugs usually become intolerable. I know that abx have immunomodulatory & anti-inflammatory actions too, but my question is, is it possible that any improvements from the antibiotics could be attributed to infected B-cells being killed off? ps. treatment was based on positive test results to various infections eg lyme, bartonella, chlamydia pneumoniae. thanks.

Funnily enough a week after the vaccination that initially triggered my illness off I had to take a course of antibiotics as my doctor thought my swollen glands were due to a bacterial infection (looking back I assume it was the initial triggering of the ME symptoms) and they made me so ill along with everything else! I had to stop taking them after 3 days due to spontaneous nosebleeds, lightheadedness, nausea and muscle aches/bruising around my joints. It's hard to distinguish which of these were caused by the antibiotic and which were triggered by the onset of ME but suffice to say i'm very wary of them now - I'm currently taking some topical ones for a mild ear infection but even that worried me!

I would have thought they would cause more distress than help to many due to the upset stomach they can often cause - especially considering many ME patients (myself included) have IBS type symptoms to start with along with more extreme reactions to medications in terms of side effects.

 

[froufox]

Hi Legendrew, thanks for sharing. Yes as you say its difficult to work out what is causing what sometimes. My ME was triggered by vaccines too - Hep B in my case...it was following my 4th jab/booster that I caught a viral ear infection, which led onto ME...I never recovered and that was 20yrs ago! I only tried abx the last few yrs since testing positive to various infections eg lyme, cpn and I have to say that they have been the most helpful treatment overall that Ive tried, though as I said the side effects became difficult to tolerate so I decided to stop. Though the fact that I experienced significant improvement does seem to suggest that I have various chronic infections....I dont know if this means the infections are at the root of the illness or as Prof Edwards says maybe as a result of immune dysregulation. I know that vaccines can trigger immune dysfunction and i wonder if either they are contaminated themselves, or disturb the body's ecology, and/or reactivate dormant infections? Who knows. There is some research that suggests that the Hep B vaccine in particular, can trigger demyelinating diseases via molecular mimicry.

 

[Graham]

Hi there! I'm the friend that Bob mentioned that was on steroids - prednisolone (or prednisone in the US), a cortiscosteroid. I went down with ME in 1999 after an infection following a sinus operation, then went down with PolyMyalgic Rheumatica in 2005 (inflammation of the arteries and veins). On 10 mg a day, I am pretty much as I was with ME before getting PMR: I can wean off, very very slowly (half a mg a month) but by the time I hit 7.5mg my energies are at dropping fast.

I have looked online a lot about this, and the picture is very mixed, but it does appear that I am in a small but significant minority. I did read an account by one doctor in the US who found that a low dose of 5 to 10 mg helped a proportion of his patients, but I cannot find the link any more.

It seems to me that there are two possibilities. The first, as suggested most recently by Stephen Holgate, and by many many good researchers before him, is that there may well be many different subsets within the broad label of ME, some may have an adrenal problem, but it may be dangerous to generalise. The second is that I haven't got ME at all but an adrenal problem: we all know how reluctant doctors are to test properly for adrenal insufficiency - they assert that the standard test is sufficient.

My sister, in Canada, wonders what my ME specialist makes of it. I just laugh. The only way to get a referral around here to a specialist is to cross their palms with large quantities of silver. An ME specialist diagnoses you, passes you back to a GP who then decides that there is no treatment or medication that is appropriate.

Cynical - moi?

 

[lansbergen]

http://www.cfids-cab.org/cfs-inform/Cytokines/visser.etal01.txt
http://www.ncbi.nlm.nih.gov/pubmed/11585638
LPS-induced IL-10 production in whole blood cultures from chronic fatigue syndrome patients is increased but supersensitive to inhibition by dexamethasone.

Could the increased IL-10 production be a result of B10 cells involvement ?

http://arthritis-research.com/content/15/S1/S1

Review
IL-10-producing regulatory B cells (B10 cells) in autoimmune disease

Ioannis Kalampokis, Ayumi Yoshizaki and Thomas F Tedder*

 

[voner]

A very reasonable analysis but I am more optimistic. I have looked through a lot of claimed markers and have a hundred more to look at but the majority of them I would drop in the wastebin on two counts - the data are presented in a way that does not look reliable and the story they are designed to support is based on some old chestnut that does not make sense in the bigger perspective. I may not be Usain Bolt but most of these look like the Hillbilly County Junior Team. In contrast there are maybe four or five groups who look like serious medal contenders and Dr Light may well be one of them. I am not going to be the one who finds the biomarker but I am interested in encouraging support for those who may be on the right track. We do not need anything very dramatic-sounding or highly specific, just something that seems to fit with the implications of Fluge and Mella's study and takes things a step forward.

But the next step is not convincing the medical community. That takes 15 years. And they usually get it half wrong. All you need is to convince a few people to help put in place an experiment that gives the pay off. So we showed that rituximab worked for RA long before the 'medical community' had any idea what was going on. If finding a biomarker gets us to discovering who with ME will really benefit from rituximab then we do not need anybody to take an interest in the biomarker first. We just need to get on and make use of it. Once it has been shown to be useful then the medical community will use it, just as they use rituximab for RA. I fully realise that anyone can play this game and end up chasing moonbeams. All I can say is that over a period of thirty years I think I learnt to tell moonbeams from 24 carat ingots. There are certain ways of telling. If the Norwegian study can be confirmed we know there is gold in this particular hill. All I can see at the moment are some glints but I feel reasonably confident after mining for 15 years on the RA field that I know which people know what they should be looking for.

Prof. Edwards,

Thank you for your enlightening replies about the subject of biomarkers. Prospecting for gold is actually done in with a very similar mindset. The analogy works for me.

I think what confused me is that when us patients meet with researchers and organizations like CFIDS of America (One of the major ME Associations in the United States), They keep hammering the point that the researchers need to find biomarkers. But the biomarkers that these researchers were talking about are biomarkers that will proclaim this is a real disease and biomarkers that will separate different patient groups into subsets.

You seem to be looking at it from the standpoint of that there are patients we can treat successfully and there's a biomarker that will help us identify them And hopefully we can also use that to further flesh out the story of what is happening is within these patients.

When I used to look for gold, what you're doing right now was the part of the gold prospecting process I think I enjoyed the most. This was in the days before the Internet was prominent. I would do research and pinpoint areas that had clues that indicated there might be gold. I would haunt libraries, County assessor offices looking at records, Pour through old journals and ancient records and all sorts of oddball locations and talk to all sorts of people. Many of the people I would talk to would live in the middle of nowhere and not really like being Sociable, But I always found the give-and-take with these folks to be entertaining, and sometimes enlightening. I would Hunt & poke into every corner I could think of, and then within the given time frame put together a plan and try it out.

I would consult with talk and to other people who do the similar jobs as I did, and I was always amazed at how the vast majority of them just did not do this pondering, early phase of work. Most would doggedly stick to the model they were using without ever questioning it even though it wasn't working very well. Many would run down along avenues that just were obviously not pragmatic and needlessly spend Their funders money. I guess they just did not have it in them to step back and wonder "what's going on here and why".

Of course, that's what a lot of us chronically sick people spend our days wondering, "what's going on here and why".

anyway, thanks for the Discussion.

 

[Dolphin]

Also, I am under the impression that Rituximab is an expensive drug and especially since it has to be given by infusion - so I am surprised this would be considered cheaper - what would be more expensive options? Or is there different pricing/cost of Rituximab in different countries?

I recall reading that the drug itself cost the NHS a price less than £1000 (I can't remember exact figure - high 3 figures). There would then be extra infusion costs. However, this is in the range of costs that not a tiny number might even be able to pay for privately.

I then recall hearing a figure of $70,000 being quoted for the US. These are in two different ball parks, even if the $70,000 for the US is presumably for more than one infusion.

Anyone know anything more?

 

[rosie26]

Whatever causes, starts the ball rolling with ME, seems to make us extremely vulnerable, to viruses (flu etc), these viruses seem to finish the job and ultimately knock us down completely into the chasm of full on ME.

It certainly seems to me that there is some over reaction going on in ME, absurd amounts. Outrageous sensitivities to noise, temperature, visual sensory, exertion PEM which requires absurd amounts of rest to try and recover from. Inflammation intensifies and rages at slightest amount exertion causing stomach problems, headaches, sinusitis, facial bone pain, muscle ache and pain, joint discomfort, glands ache and in severe ME there is also the unbearable poisonous feeling circulating in the blood vessels. Multitudes of symptoms to deal with in a very weakened state.

btw, I was given Prednisone in the first year of ME, I had to stop taking it immediately. I found it utterly intolerable.

I noticed someone else mentioned Interferon, I pondered this one a lot in the first years of my ME, perhaps another sign of the over reaction. ? What ever causes ME may make the immune system think a flu virus is a catastrophic fatal danger and over react. ?

In the Severe years, ME feels like it is trying to kill you. It keeps hitting hard.

 

[Firestormm]

Thanks for the reply

...
I am thinking that in ME we should expect people responding to rituximab to show some B cell or antibody changes. That I think is important to pursue in lots of different approaches. As far as I know there is little evidence for permanent structural damage in ME so that should not be so much of an issue.

So does it then follow, from what you said, and speaking plainly, that people with a diagnosis of ME, should display B-cell abnormalities prior to being treated with Rituximab? And is this something you can test for and better define your cohort - thus perhaps leading to an improved response rate?

Or, given the random nature of generation (of which I understand very little), are antibodies always likely to be present? Could they be present one day and not the next? And how might this be allowed for with any test to determine suitability?

I realise that part of what I am asking is perhaps what is missing and not known in ME; but perhaps Norway were able to observe pre and post treatment changes from their initial work and have been better able to account for this in their current trial.

 

[Marco]

Apologies if this has been asked before, or the topic has been covered, I havent managed to read all of the posts on this thread (or understand all of them either ). Professor Edwards, I just wondered what your or anyone else's thoughts re those of us who respond to antibiotics (various ones including rifampicin, plus tetracyclines, macrolides) eg herxing/die-off reactions, followed by improvements. Although they have not been a cure as such, they have definitely helped for sure.

Unfortunately, the improvements either peter out or the side effects from the drugs usually become intolerable. I know that abx have immunomodulatory & anti-inflammatory actions too, but my question is, is it possible that any improvements from the antibiotics could be attributed to infected B-cells being killed off? ps. treatment was based on positive test results to various infections eg lyme, bartonella, chlamydia pneumoniae. thanks.

For what its worth many compounds have physiological effects beyond and often unrelated to their original purpose and assumed therapeutic pathway (e.g. SSRI anti-depressants typically take a few weeks to work while serotonin levels rise almost immediately suggesting their anti-depressant effects may be due to other actions).

When I was looking for existing drugs that might target 'neuroinflammation' I found that Doxycycline (and other tetracycline antibiotics such as Minocycline) has been shown to reduce glutamate excitotoxicity and may be effective in treating pain via inhibitory effects on TNF-alpha. Similarly beta lactam type antibiotics (which include penicillin derived antibiotics) activate the EAAT2 glutamate transporter protein and in an animal model one such antibiotic, ceftriaxone, increased glutamate re-uptake thereby reducing excitotoxicity and providing neuroprotection.

The EAAT2 glutamate transporter has been implicated in neurodegenerative diseases such as Alzheimer’s disease, Huntington’s disease, amyotrophic lateral sclerosis (ALS) and in relapsing/remitting MS.

Not that this is necessarily relevant to any improvements you experienced. These antibiotics may have other very different documented physiological effects which a different search might have turned up.

Difficult to say when many drug effects are 'messy'.

 

[Ecoclimber]

I thought this was interestng as the rearch is still conintuing.

https://www.ncbi.nlm.nih.gov/pubmed/21383843
PLoS One. 2011 Feb 23;6(2):e17287. doi: 10.1371/journal.pone.0017287.
Distinct cerebrospinal fluid proteomes differentiate post-treatment lyme disease from chronic fatigue syndrome.
Schutzer SE, Angel TE, Liu T, Schepmoes AA, Clauss TR, Adkins JN, Camp DG, Holland BK, Bergquist J, Coyle PK, Smith RD, Fallon BA, Natelson BH.
Schutzer, Natelson et.al came up with a biomraker that distinguish between chronic fatigue and Lyme disease. The procedure is not userful as a bio-marker because of the lumbar puntucre procedure.

You are have theLght gound breaking stury on the Dorsal Root Ganglia. They
proposes that a varicella-zoster infection of the dorsal root ganglia or other peripheral ganglia could readily account for a number of factors in CFS the acute onset, the wide variety of symptoms, the high misery/low fatality index and the post-exertional relapse found.

You are have peope who are predisposition, upon receiving the HINI flu, all there hyprocretin wipes away.
his article indicates that a pathogen H1N1 or an influenza vaccination is a cause of an autoimmune disease. It could be a subset of ME patients or it could lead to a dead end but I thought it would be worth exploring before posting a thread on it. It could be controversial.
http://forums.phoenixrising.me/inde...e-cause-of-m-e-c-f-s.21737/page-4#post-341425

Research had found that narcolepsy is an autoimmune disease that destroys the neuropeptide Hypocretin located in the Hypothalamus within the brain. Hypocretin and/or receptors OXi1 and Oxi2 control the entire body's asleep and awake state as well as circadian rhythms. Furthermore, it down regulates the HPA Axis, muscle... olfactory, inability to adjust to temperature extremes, severe insomnia, brain fog and memory issues, POTS, blood pressure volume, cardiovascular issues basically the human homeostasis...Occam's razor!

It is caused by a gene mutation through an exposure to an influenza pathogen. This can be passed on genetically to other generations. Not every one that has this mutated gene develops this condition but 90% of the people who do have narcolepsy vs. controls have this gene mutation in the HLA ( Human Leukocyte Antigen) It is near the same location as a mutated gene expression for MS!

What if the immune system targets this pathogen but also mistakes proteins in the brain that regulate sleep/awake cycles as a pathogen and take them out as well? Research has shown that this is what exactly occurs in narcoleptic patients?

Dr. I would be interested in yout feeback? Would this make a possible challnge for you, to took outside the box.? Who knows, maybe chronic illensses and diseases are conncted in somewau.

Eco

 

[Snow Leopard]

I think what confused me is that when us patients meet with researchers and organizations like CFIDS of America (One of the major ME Associations in the United States), They keep hammering the point that the researchers need to find biomarkers. But the biomarkers that these researchers were talking about are biomarkers that will proclaim this is a real disease and biomarkers that will separate different patient groups into subsets.

It is really about following leads. Yes, we would like to find biomarkers, but how? You need some leads to follow and this is one of those leads. As I said on a previous thread, when Maria was just starting her crowd funding campaign, this drug is not necessarily the end solution, but rather a potential clue, at least in the long run. If these studies (Mela/Fluge and Edwards) demonstrate an effect, then it sends a message out there "please explain". It will bring a lot of new people into the field and perhaps we will no longer be in the catch-22 funding situation. (eg scientists don't spend a lot of effort applying for grants that will be knocked back and funding agencies say they can't fund more as they need more high quality proposals). Perhaps in time ME/CFS will no longer be funded a magnitude of order lower than every other disease category in the NIH and NHMRC (Aus.) lists, when comparing societal disease burden (DALYs)...........

 

[froufox]

Hi Marco, thanks yes I completely agree about the multiple, and also perhaps unknown actions of some antibiotics/drugs in general, and that some of the improvements I experienced may well, at least partly, be explained by that. However, would that also explain herxing/die-off reactions too? I mean once the inflammation pathways are under control, I wonder if that could lead to some kind of normalisation of the immune response, which in turn allows it to fight off whatever pathogens we are harbouring?? Also just to add to that, I have responded to anti-virals aswell in the past eg famvir....again short-term improvements that did not last, but very definite improvements in functionality/energy. Ive also have also had some quite dramatic improvements at times from other pathogen killing treatments eg drugs/herbs for worms/parasites. Again, all temporary. So, all the evidence seems to suggest, at least in my case multiple pathogens, whether that is due to either a dysregulated or a suppressed immune system, I don't know, but with all the horrific symptoms that Rosie26 describes so well eg a constant feeling of being poisoned.

Re steroids, I also took hydrocortisone for 6 months (averaging 15mg)) and although I never really felt worse as such whilst I was on it, although not much better either, it was clear to me that my body became dependent on it pretty quickly, no doubt due to an alreadyhypersensitive and dysfunctional HPA axis....I'd already been struggling with severe adrenal dysfunction for yrs prior to that. It felt like the h/c interfered with that delicate feedback mechanism that was already right on the edge in my case. When I weaned off the h/c, my adrenals tanked pretty badly and my cortisol levels nosedived and I also experienced a big exacerbation in inflammation. I have never really been the same since (that was 7yrs ago), although my adrenals/HPA axis are thankfully a bit stronger these days.

For what its worth many compounds have physiological effects beyond and often unrelated to their original purpose and assumed therapeutic pathway (e.g. SSRI anti-depressants typically take a few weeks to work while serotonin levels rise almost immediately suggesting their anti-depressant effects may be due to other actions).

When I was looking for existing drugs that might target 'neuroinflammation' I found that Doxycycline (and other tetracycline antibiotics such as Minocycline) has been shown to reduce glutamate excitotoxicity and may be effective in treating pain via inhibitory effects on TNF-alpha. Similarly beta lactam type antibiotics (which include penicillin derived antibiotics) activate the EAAT2 glutamate transporter protein and in an animal model one such antibiotic, ceftriaxone, increased glutamate re-uptake thereby reducing excitotoxicity and providing neuroprotection.

The EAAT2 glutamate transporter has been implicated in neurodegenerative diseases such as Alzheimer’s disease, Huntington’s disease, amyotrophic lateral sclerosis (ALS) and in relapsing/remitting MS.

Not that this is necessarily relevant to any improvements you experienced. These antibiotics may have other very different documented physiological effects which a different search might have turned up.

Difficult to say when many drug effects are 'messy'.

 

[froufox]

Thanks lansbergen, thats interesting. Ive had IL-10 tested a few times, and its always been high, the last time a few months ago it was 101 (10-80).

Could the increased IL-10 production be a result of B10 cells involvement ?

http://arthritis-research.com/content/15/S1/S1

Review
IL-10-producing regulatory B cells (B10 cells) in autoimmune disease

Ioannis Kalampokis, Ayumi Yoshizaki and Thomas F Tedder*

 

[Jonathan Edwards]

I recall reading that the drug itself cost the NHS a price less than £1000 (I can't remember exact figure - high 3 figures). There would then be extra infusion costs. However, this is in the range of costs that not a tiny number might even be able to pay for privately. I then recall hearing a figure of $70,000 being quoted for the US. These are in two different ball parks, even if the $70,000 for the US is for more than one infusion.

A course of two Igm rituximab infusions, which tends to need repeating every 8-12 months, cost the NHS £4,000 not long ago. Infusion services tend to charge around £1,000 per infusion but this may more than cover local costs. So a course will cost the NHS around £6,000 now. Fluge and Mella used the oncologists' dose by body surface area rule and gave what on average would be about 1.5gm total so that would be £5,000 for the two infusion course. Once off patent (November 2013) the cost ought to come down but nobody knows whether it will in practice.

 

[Jonathan Edwards]

So does it then follow, from what you said, and speaking plainly, that people with a diagnosis of ME, should display B-cell abnormalities prior to being treated with Rituximab? And is this something you can test for and better define your cohort - thus perhaps leading to an improved response rate?
Or, given the random nature of generation (of which I understand very little), are antibodies always likely to be present? Could they be present one day and not the next? I realise that part of what I am asking is perhaps what is missing and not known in ME; but perhaps Norway were able to observe pre and post treatment changes from their initial work and have been better able to account for this in their current trial.

You have a habit of getting to the crux of the matter Firestormm. That is the line I personally think is worth following. If there are relevant antibodies they will not go up and down that much - maybe over months or years a bit but only in degree. other B cell markers may indeed be more temperamental. The problem as I see it is a more subtle one. To give an example: when we first started treating RA it was our impression that the best responses occurred in patients with moderate levels of rheumatoid factor antibodies (RF). It became fairly clear that patients with no antibodies did not respond much. It also looked as if patients with very high RF antibody levels did not get the best (or longest) responses because their disease was just too tough to get on top of. I am not sure that this latter point ever proved true in statistical analysis of the bigger studies but it seemed to hold up in our clinic. The point is that any given B cell misbehaviour marker might turn out to predict response to rituximab or it might mark 'the tip of a very big iceberg' in cases too tough to respond. It might be a negative predictor. There will be a small number of people with ME with high levels on one of any number of B cell markers (ANA for instance). The problem is making a sensible choice on how to try to validate the predictive value of markers and which ones. To say more would be to speak on behalf of a team of other people who will actually conduct a study and it is not for me to do that.

 

[Jonathan Edwards]

Research had found that narcolepsy is an autoimmune disease that destroys the neuropeptide Hypocretin located in the Hypothalamus within the brain. Hypocretin and/or receptors OXi1 and Oxi2 control the entire body's asleep and awake state as well as circadian rhythms.

It is caused by a gene mutation through an exposure to an influenza pathogen. This can be passed on genetically to other generations. Not every one that has this mutated gene develops this condition but 90% of the people who do have narcolepsy vs. controls have this gene mutation in the HLA ( Human Leukocyte Antigen) It is near the same location as a mutated gene expression for MS!

What if the immune system targets this pathogen but also mistakes proteins in the brain that regulate sleep/awake cycles as a pathogen and take them out as well? Research has shown that this is what exactly occurs in narcoleptic patients? Eco

Thanks for mentioning this. I was aware that narcolepsy was associated with the MHC DR1 haplotype (gene variation). I had not yet heard that this has been linked to an autoimmune response to hypocretin. I will read further. This would clearly be a good analogy for ME (or a subset) - an autoimmune reaction that simply presents as impairment of neurological function with no other standard signs of inflammatory disease. What I am unclear about is where the flu comes in, or maybe the adjuvant in the flu jab (which would be a quite different mechanism). The story sounds like the old molecular mimicry idea that all immunologists seem to believe in for no very good reason. Maybe this is the good reason at last, or maybe somebody has got a bit overenthusiastic in the storytelling in the journals or newspapers?

Fascinating, thanks.

 

[Ecoclimber]

The abstracts to the research are published here:

Hypocretin deficiency develops during onset of human narcolepsy with cataplexy.
https://www.ncbi.nlm.nih.gov/pubmed/23288981

Incidence of narcolepsy in Norwegian children and adolescents after vaccination against H1N1 influenza A.
https://www.ncbi.nlm.nih.gov/pubmed/23773727

Genetic association, seasonal infections and autoimmune basis of narcolepsy
https://www.ncbi.nlm.nih.gov/pubmed/23497937

A patient with both narcolepsy and multiple sclerosis in association with Pandemrix vaccination.
https://www.ncbi.nlm.nih.gov/pubmed/22841884

Finding could lead to new treatments, better understanding of other autoimmune diseases
https://news.stanford.edu/news/1999/august11/narcolepsy-811.html


Note: this would only apply to a subset of patients who have a predisposition to the specific gene. HLA-DQB1*0602

Thanks for your input!

 

[Dolphin]

I recall reading that the drug itself cost the NHS a price less than £1000 (I can't remember exact figure - high 3 figures). There would then be extra infusion costs. However, this is in the range of costs that not a tiny number might even be able to pay for privately. I then recall hearing a figure of $70,000 being quoted for the US. These are in two different ball parks, even if the $70,000 for the US is for more than one infusion.

A course of two Igm rituximab infusions, which tends to need repeating every 8-12 months, cost the NHS £4,000 not long ago. Infusion services tend to charge around £1,000 per infusion but this may more than cover local costs. So a course will cost the NHS around £6,000 now. Fluge and Mella used the oncologists' dose by body surface area rule and gave what on average would be about 1.5gm total so that would be £5,000 for the two infusion course. Once off patent (November 2013) the cost ought to come down but nobody knows whether it will in practice.

Cheers. I presume the figure I saw was for 1gm.
Those sorts of figures are still very different to the $70000 I have heard people mention for the US (anyone able to confirm/deny that figure).

 

[Kati]

I have been told the cost of one dose varies between 6000$ and 6700$ in the US. The cost of infusion in the US is definitely not 1000 £. Thankfully, patients have been able to get pharmaceutical fnancial assistance, so the cost to them patients is not 70 000$, much much less.

Dr Edwards would be best consulting Dr F, M and K as to what protocol to use. i don't feel it is up to patients to tell him what protocol they are on. It has put people like me in serious trouble in the past. There are groups of people, doctors and scientists preying on situations like these.

 

[Dolphin]

I have been told the cost of one dose varies between 6000$ and 6700$ in the US. The cost of infusion in the US is definitely not 1000 £.

More or less?

Thankfully, patients have been able to get pharmaceutical financial assistance, so the cost to them patients is not 70 000$, much much less.

Thanks for the reply.
Here is where I came across the $70,000 figure for the US. No idea why they were so far off:

http://www.whchronicle.com/tag/myalgic-encephalomyelitis/

CFS: One Disease and Its Costs

What would happen to health care if a million new patients with just one of many now incurable and largely untreated diseases flooded the system, relying on medicine that could cost $70,000? - See more at: http://www.whchronicle.com/tag/myalgic-encephalomyelitis/#sthash.llowcwII.dpuf

[..]

Neither is available except to a few patients in trials. And cost? Ampligen costs about $25,000 for a year of treatment, and Rituxan comes in at a whopping $70,000. - See more at: http://www.whchronicle.com/tag/myalgic-encephalomyelitis/#sthash.llowcwII.dpuf

Think they may have mentioned the $70,000 figure in one or more MECFS Alert videos