The draft scope for the NICE guideline on ME/CFS is now out for consultation, June 2018

Hi Peter - it's 'orthostatic intolerance'.

 

OI was discussed at the last stakeholder meeting and I thought it was agreed that it was within the scope to consider addressing it.

OI is a symptom, identified by a clinical history. There seem to be various tests like tilt table that document changes in blood pressure and pulse rate but I doubt we know what to do about these or even whether they are causative. You cannot predict treatments just from theory. They need proper trials.

 

The list looks pretty reasonable to me, except when it gets to the exercise bit.
I don't think it is cruel to provide GPs with backup about not prescribing potentially dangerous drugs that we have no reason to think are beneficial.

 

That's good to hear.

I agree it's a difficult area. People can have negative tilt-test results and yet have all the symptoms of OI, and in the US, I gather that people like Peter Rowe would treat them regardless. But NICE appears to have some guidance for orthostatic hypotension (or at least to approve the European Federation of Neurological Societies' guideline, if I'm reading this correctly), and I think that some of that guidance would be based on trials of the various treatments. (I've read accounts of trials of various interventions in that area.)

 

I have been reading (as much as I'm able) all your responses and it is overwhelming for me.

I do not have enough cognitive function to be able to read everything and process it all. So I don't know the scope of PACE.

I do know my ME has only gotten worse. I would like to know if there is a good source to point my PCP to. I have a follow up appt soon and would like to ask him to read studies and updates on ME before I go.

Anyone have a good answer? Or am I just too naive...and uneducated.... sick.

 

As I see it 'OI' is a symptom - orthostatic intolerance - not a cause of a symptom. It can have various causes, some related to haemodynamics and some maybe not. I am not impressed by people getting treated without proper evidence, as you know!

Hmm, yes. But this is specifically orthostatic hypotension due to autonomic failure, which they explain is rare - and so trials are hard to do. Moreover, it is not clear that the trials were blinded and the improvement in quality of life was pretty unimpressive even if blood pressure went up. I suspect this has slipped through because midodrine is licensed for this so there has to be a guideline and since it is for a rare complication of diabetes or rarer systemic diseases affecting the autonomic nervous system and trials are hard to do they may be flexible.

There is no good reason to think that because people in this rare group get some improvement in physiological measures that midodrine is any use for OI in ME. It needs testing. There are lots of people with ME and we are told many have OI so doing a trial would be easy. Why have physicians who use midodrine not done that? Why has the manufacturer not set up a trial to get a license in ME? I suspect the answer is that few people with ME actually have a low enough blood pressure to be held responsible for OI. In which case midodrine does not make a lot of sense theoretically, let alone in terms of evidence.

 

Thank you for your reply.

People with ME are surely lucky to have some advocates who are well versed in political strategies, who know how committees work and how they can be manoeuvred with the best of intentions. The VIRAS approach (and my personal approach) has been to base arguments on the fundamental principals of science and research. This comes from my long-standing belief that these are and always have been, 100% on the side of patients. PWME have nothing to fear from good science and research, but they have every reason to mistrust political sophistry. That is not to say that the latter has anything inherently wrong with it, but it can easily be used wrongly, which IMO genuine science and research cannot.

You repeatedly imply that the VIRAS comments will annoy the NICE committee, but you do not explain why they would find them annoying, nor why NICE would not welcome challenging comments and questions, as any serious and sincere scientist or researcher would. If anything, you seem to take a dimmer view of the committee than VIRAS, at least we give them the benefit of the doubt, that they will take on board legitimate concerns, rather than throwing their toys out of the pram like a lot of brats. You have yet to point out any inaccuracies in our comments, or why the NICE remarks which we challenge are actually correct and should remain unaltered.

It seems from your remarks that getting rid of, or keeping GET and CBT in the NICE guideline is hanging in the balance. IMO it is much worse than that. Research into these ‘treatments’ dominates clinical trials. If NICE proceed on the basis that patients with ‘fatigue’ are legitimate ‘ME/CFS’ participants in research, then the literature search for clinical trials, can only reach one conclusion. GET and CBT are the only evidence based treatments for PWME. In fact in keeping with their claim to produce ‘evidence-based’ guidelines, NICE will have no alternative but to recommend them as treatments for ‘mildly’ to ‘moderately’ affected patients.

The strongest argument against these trials is that they include people who only have fatigue and were therefore not researching M.E. or CFS. Because I am doing my own analysis of the PACE Trial, I have not read the doubtless, marvellous work of Matthees and Wilshire, but I have seen some summaries and charts. My sense is that whilst they raise serious issues about the conduct and analysis of the research, they have not demolished all the findings.

Furthermore, even if the PACE Trial was withdrawn or downgraded, GET and CBT would still stand-out as the treatments of choice based on published clinical trials. It would be a moral victory for patients if NICE stated in its guideline that the PACE Trial was biased and represented ‘very poor quality’ evidence, but that would not expunge GET and CBT from its recommendations. If anyone doubts this, please ask yourself this question: “how did GET and CBT get into the first NICE guideline?” It was published 3.5 years before the PACE Trial was published. Even without the PACE trial there are now even more clinical trials using those ‘interventions’.

In modern times, I acknowledge that political sophistry probably has more weight and influence than a scientific approach, but VIRAS will leave that to others who know what they are doing, and we will stick to what we know. I remember only too well what happened when Action for ME tried their clumsy hand at that game, they helped to get ethical approval for the PACE Trial and sold out the patients.

PS. VIRAS were represented at the Stakeholder meetings

 

I thought most people on the butt end of your comments about 'deliberate strategies' etc. annoying to be honest, Peter.
I have given the arguments for not annoying people.
I am not sure what political sophistry has to do with it.

 

http://occupyme.net/2018/07/16/how-to-represent/#comments

This is a recent blog from Jenny Spotila on how to represent patients. Written under 5 headings. For anyone who can't read the whole, there is a summary near the end.

Well worth reading for anyone who will be representing a group of patients at a committee meeting.

 

It looks as though my googling has been inadequate, along with my reading of the literature!

But we're still left with the fact that (according to survey data) most PWME have OI, and that it's a potentially treatable symptom.

Shouldn't any OI patient be investigated to get to the bottom (if possible) of the nature of their OI? Not just tilt-testing but other cardio tests and autonomic testing? And then be treated accordingly? Or is the evidence-base rubbish there too? (A genuine question - it's a big area and I've only read a few papers and can't remember whether they addressed the issues you raised.)

Your other point raises a question I've been thinking a lot about lately and I'll start a fresh thread on it.

 

Yes, they should, if there is good reason on the history to think there is a cardiovascular cause. But the tests will only be interpretable if someone has done the systematic research to show what findings are genuinely significant. The midodrine studies seemed to show that keeping the blood pressure up did not necessarily have any effect on feeling less dizzy, even in the autonomic cases.

I don't know how good the evidence for mechanisms of OI in ME is but if studies have been done by clinicians who collect patients of particular interest to them in tertiary referral clinics it is unlikely to tell us much useful. Disease mechanisms need to be studied in unselected representative cases.

 

I think you make a good point Adrian. I add these remarks. One is that M.E. was 'diagnosed' by a criteria which according to Williams had not been validated, and certainly when compared with the ICC looks very shaky. The claim that there was no difference by criteria cannot be verified because they left this out of the data-set, though I agree that the individual diagnostic charts look similar. Also, an overriding problem with the data, is that there was far too much improvement across the board in the PACE Trial. M.E. and CFS are chronic. A small percentage of those diagnosed, recover and others improve over time - not the levels seen in one year. Whether SMC was a valid control group is debatable and debated. The trial manuals specifically precluded SMC doctors from providing any advice included within the treatment arms. It is clear that White et al were eager to imply that SMC was a 'treatment' by calling it a 'comparison group' - I believe that I am correct in saying that the phrase 'control group' does not appear anywhere in the Lancet report.

Whilst it is a strong argument that there was response bias which I have actually been writing about for years, it is insufficient. Considerable actual improvements occurred which are not explained by that, and IMO it is more significant that these changes occurred across the groups suggesting a lot of misdiagnosed participants.

 

I am interested that you think that there is improvement that is not explained by subjective bias. Do we have good reason to think that? And if it occurs across all four arms then presumably it is not due to CBT or GET. So we still have no evidence that CBT or GET are useful in 'non-ME' fatigue.

 

Could you please elaborate what you mean by ''actual improvements'', and how these occurred in PACE?

 

But glucocorticoides?
Also what is suggested is not to check for iron, B12 and folate deficiency, OI and infections ("unless indicated" - sorry, I have met too many doctors to know that most doctors will read that as "do nothing").
Well, ok.