BREAKING NEWS: ‘Chronic fatigue syndrome eased by cancer drug’, New Scientist, 19 October 2011

From the ‘New Scientist’, 19 October 2011 (story by Andy Coghlan)

An anti-cancer drug could hold the key to treating chronic fatigue syndrome (CFS). Symptoms of the disease eased in 10 of 15 patients given rituximab, an anti-lymphoma drug.

Rituximab works by destroying white blood cells that make antibodies, called B cells. The results of the trial therefore strongly suggest that these white blood cells might be involved in causing CFS – a disorder also known as myalgic encephalomyelitis (ME) and one that has so far defied explanation.

The research was jointly led by Øystein Fluge and Olav Mella at the Haukeland University Hospital in Bergen, Norway. Their team discovered by accident that rituximab might work against CFS after seeing symptoms ease in a patient who had both lymphoma and CFS.

“We think it affects all symptoms [of CFS], so it must touch the central pathological mechanism causing the disease,” Fluge says.

Two of the 15 people in the trial appear to have completely recovered since they first received the drug three years ago. “Those two are both back at work,” Mella says.

Dramatic results

“It’s the most encouraging drug result so far in the history of this disease,” according to Charles Shepherd, medical adviser to the UK ME Association. “Although it’s a small trial, it’s produced dramatic results.”

The researchers say that following two doses of the drug being given in the first two weeks of the trial, there was a lag of three to eight months before symptoms began to subside. They say this delayed response tallies with the idea that CFS is caused by autoantibodies – antibodies, made by B cells, that mistakenly attack the body’s own tissues.

Rituximab is itself an antibody designed to target and destroy B cells. Mella says that all the B cells are gone within two weeks or so of the treatment, but autoantibodies typically survive in the body for another two or three months. “Washing out these antibodies is the most probable explanation for the time lag in benefits,” he says.

The researchers found no trace of XMRV, a mouse leukaemia virus once implicated as a possible cause of CFS. The virus has now been virtually eliminated as a possible cause.

Blind alley

“We looked as hard as we could for it, by several methods, but the search was negative,” Fluge says. “We think suggestions it was XMRV [causing CFS] have turned out to be a blind alley, caused by contamination of samples.”

Last month, one of the authors of the 2009 paper that implicated XMRV retracted his data from that study after acknowledging that the virus was present through contamination.

“XMRV is dead, a sad and disappointing story that raised a lot of false hopes for patients,” says Shepherd. He adds that it is important not to raise hopes again by over-hyping the rituximab results. “We’re still a long way from making this drug more widely available, but if someone wants to mount a UK trial, we’d look at that,” he said.

Encouraged by the extended remission of two of the people in the trial, the Norwegian researchers are now checking whether further, periodic doses of rituximab could permanently keep the symptoms of CFS at bay. Mella says it is possible that the five who saw no benefits from the trial might have done so eventually if they had received further doses.

To read the full report in PLoSONE, click HERE

English language translation of report on Norwegian TV tonight – photo of the two researchers.

European ME Alliance reaction to the news.

European ME Alliance report an apology from Norway’s Directorate of Public Health for the treatment of people with M.E.

20 thoughts on “BREAKING NEWS: ‘Chronic fatigue syndrome eased by cancer drug’, New Scientist, 19 October 2011”

  1. A poorly written article.

    Firstly, the paper in question supports the human gamma retrovirus hypothesis for ME because MLVs infect B cells.

    Secondly, none of the assay in this paper could have detected a human gamma retroviruses as they were all optimised to detect VP62 clone, which does not exist in nature.

    There are inherent dangers with such a treatment if the cause is HGRVs, as once the treatment is stopped levels of the viruses will return.

  2. Has no-one noticed that the TV2 article has a serious typo stating:

    “The two doctors say the results indicate that CFS is in fact a somatic decease.”

    🙁

  3. What I meant is they are saying that CFS IS a somatic disease instead of saying it is NOT a somatic disease…this must be corrected…!!!

  4. @fluffyspit
    I don’t want to embarrass you – but a somatic disease is a physical disease (related to the body and not of the mind), and so the TV2 article is correct. I think you have confused it with “somatoform” which describes a mental illness.

    I admit I had to double check.

    Anyway, good news all around – I wonder if this will make the main press?

    1. My apologies for my mistake…I should have Googled the word Somatic…I did indeed mistake it for the term Somatoform. So sorry…thank you for pointing out the mistake…I have them often 🙂

  5. The above article contains some typically disappointing observations from Dr Charles Shepherd.
    He does a disservice to the M.E, community by misrepresenting the facts with regards to the XMRV story.
    Whilst an error made by the Silverman lab has led to a partial retraction of Lombardi et al.,the rest of the paper still stands and the basic hypothesis, that a human retrovirus (of murine origin) is associated with this illness, is still entirely credible.
    The Norwegian Rituximab study supports and is consistent with that notion.

  6. @fluffyspit
    FYI: Somatic means and illness of the body, not the mind. (you might be confusing this with psychosomatic!)

  7. I think it is time to let the the XMRV thing die, keeping going on about it only adds to the mindset of others that people with ME have a mental problem and not a physical one and are desperate to cline to anything to prove themselves not mental. I think this research could be something that could lead to a better understanding of what is happening in the the bodies of people with ME, we must not be so narrow minded, I’m ill and have been for 15+ years and I welcome all studies and I thank the doctors above PLEASE can this be studied more. For now XMRV is dead let it drop and lets move onto something positive I was just as disappointed as others over XMRV hope was raised but is has proved not to be so we need to move on there is so much more to this illness and the affects it has on the body than just how it starts, lots of virus have already been show to course it so we know that is a fact, what we need to understand is why the body reacts in such a wide and sever way, this study looks very hopeful
    Also we need to be a bit more grateful to all these researchers who are working so hard on our behave to help us I thank them and want each to know that I really do appreciate the work they do.
    I would happily volunteer if a study was started hear????

    1. There is no scientific reason to let human gammaretrovirus research die. The simple truth is that we do not know the host range of the viruses that Lombardi et al, discovered and Lo et al. confirmed. The gag sequences were polytropic in both papers, but without the full length clone we cannot say they are xenotropic. There is a very good chance some will be, but they are not the same xenotropic virus as discovered in relation to prostate cancer.

      All assays, including those in this paper, that have used the VP62 clone to optimise their PCR to are invalidated as VP62 has never been found in nature. It does not matter if they claim the assay could detect MLV viruses, when the assay have not been optimised for HGRVs.

      Therefore we have a string of papers that are no longer relevant to this field and 2 positive HGRVs studies that found ME/cfs patients to be infected. That is why it is unscientific and clearly emotive to say XMRV is dead. The viruses are HGRVs and the research is only now starting. Next task is a full length clone of the viurses that Dr Mikvoits and Dr Ruscetti discovered.

  8. @ Tabatha: Just because one specific strain of a whole family of retroviruses has been shown to be problematic, doesn’t preclude the rest from playing a role …… you forget that Alter/Lo demonstrated this.

    Is that really sufficient reason to give up on the most compelling line of investigation into this illness that we have seen to date?

    Whilst the Rituximab study doesn’t say anything about causation, the one thing that it does help to demonstrate is the true biomedical nature of the illness. If anything, it strengthens the case for believing that there is a pathogen involved and that the B cells are infected !

    Clearly you are saying that treatment trials with Rituximab are a good idea, even though it’s beneficial effects are only transient. What was/is your opinion about trialling antiretrovirals?

    1. XMRV in prostate cancer is still a solid finding. This is why everyone is still conducting studies. Not one scientist has stopped their research, they have only made statements that they have.

  9. Hi, if you’re real Tabatha then you must be young.
    And blind and foolish—to fall into the trap of “let’s ignore the virology” which is being constantly set by those who want to.
    Just like it is with M.S.
    “Let’s forget it.”
    How wonderful that will be–not–if it’s allowed to happen.

    Jane

  10. I agree with Tabatha that XMRV is over! Studies all over the world by good researchers have piled up the evidence against XMRV. Lots of money has been spent trying to replicate the results of Lombardi/Mikovits. I admit that the involvement of Wessley in one of the early negative studies made me distrustful of that study but i don’t understand why every other researcher either can’t or doesn’t want to find XMRV/HGRV. Also, where is there any proof of ‘HGRV’ in people with ME? Alter and Lo found probably also found contamination as an experiment carried out (in Coffin’s lab) by putting 1% of 1 mouse cell into a PCR reaction produced the exact same phylogenetic tree as Alter/Lo’s work.

    Why is it when someone posts a comment that is critical of the XMRV theory their very reality (as an ME sufferer?)is called into question. This has happened to me and i’ve noticed it on numerous blog comments or forum postings. Probably it is just evidence of the depths of paranoia some of us have sunk. Futhermore, i find some of the comments janehill made towards tabatha to be patronising and think an apology is warranted.

    1. The viruses discovered in Lombardi et al. are not VP62/XMRV. All the 00 papers used VP62 to optimise their assay to and therefore could never have detected a human gammaretroviruses. All that research is now invalidated.

      There is still not one published replication study of Lombardi et al. So you are incorrect about that.

      There is also no evidence of contamination in Lombardi et al. or Lo et al. and the findings were the same. Polytropic gag sequences.

      None of the HGRVs have ever been found in mice, so you are also incorrect there.

      Why is it that people who write justified criticism of research that has nothing to say about HGRVs science is called into question? I think it is just evidence of the depths of paranoia some of us have sunk.

  11. I’ve just added an interesting new snippet to the main story – the apology from the Norwegian Directorate of Public Health.

    An apology from a government department to PWME! That must be unprecedented anywhere.

  12. Dr Montoya of Stanford has previously said it is his dream that those doctors who do not believe will apologise to ME patients; and now we have this brilliant, respectful reaction from Norwegian Health Department. It truly is heartwarming when doctors/politicians behave humanely and respectfully towards people with our illness – this is as it should be and as it always should have been.

    Sadly, we will be a long time waiting to get an apology from the dolts who run the show here. The UK media has not even picked up on this story!!!

    And no matter how this particular research pans out, they still owe us an apology for what they have subjected us to for the last 20/30 years.

  13. Amazingly pleased to hear this. Had been to see my GP this morning as, after being diagnosed with ME 4 years ago, we are now querying whether I have Behcets Disease (in which the immune system attacks the body), due to new symptoms. I told him I am convinced whatever I have is strongly related to my massively over-reacting immune system. I had dreadful urticaria 10 years ago for which I was eventually put on cyclosporin to ‘knock my immune system on the head’. Despite being told I would feel dreadful I felt fantastic on it and that was before I was ‘ill’.The urticaria is back with a vengeance, along with the whole raft of ME symptoms. I am hoping the consultant I am being referred to will agree to a trial to see if depressing my immune system by whatever means, might give me my life (and possibly nursing career) back. I am actually, excitedly, holding my breath for once!!!

  14. I’m with Tabatha and nah on this one. I have severe ME, an underactive thyroid and have just been diagnosed with rheumatoid arthritis. Personally I’m excited about the possibility of treating the ME and RA with one drug (if I could tolerate it).

    Everything I have read about the results of this trial makes sense to me. It’s seems to have got closer to the crux of the matter than any other trial so far. If XMRV is involved then I think it’s as one of a number of potential triggers and not the cause.

    With other autoimmune diseases triggers can be viruses, traumatic life events etc. After the death of my brother my ME went from being just a handful of vague symptoms to full blown and at the same time my thyroid went from being borderline to requiring treatment.

    With plenty of evidence of immune dysfunction from a number of other studies this to me looks very promising indeed.

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