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Can ME/CFS patients in the UK choose who they go to see on the NHS?

Leopardtail

Senior Member
Messages
1,151
Location
England
How can you distinguish between this and people truly not getting a cold?

Okay this question made little sense. How can you distinguish between a healthy immune system, and one that doesn't react appropriately, giving the illusion of never getting infections?
Professor Edwards may correct me here, but it's very hard to do without comprehensive tests. That is why both items were combined into one option. Once we have more data that may change.

E.g. if everybody else in the house has a cold, you don't but your fatigue goes through the roof, that's a possible indicator. Positive response to anti-biotics is an indicator.
E.g. if everybody else in the house has a cold, you feel exactly the same would gives us different clues.
E.g. was able to work it out due to: rise in blood sugar, tiny amounts of very elastic mucous, slight rise in body temperature. It took me weeks though and required close observation.

For now, my mind is on 'symptom recording' kept as simple as possible so that we can start tracking what symptoms go together. The hope is that once we can correlate symptoms.

In short, if I could separate those two events symptomatically, I would do so.. Right now both would be 'lack of infectious symptoms' at a time when others were infected.
A useful exercise would be to correlate the symptoms with lab work so we can identify which is happening how often.

I know from personal experience that the two things are horrendously hard to split apart, hence my reluctance to assume anything. This stuff is like banging your head against a brick wall isn't it? :bang-head:

Most obvious question, do you understand the nature of the problem? I suspect you do but wanted to check I am not missing the point....
 

Leopardtail

Senior Member
Messages
1,151
Location
England
Dear Sasha,
The problem is that most drugs that target the immune system have pretty terrible side effects. Several are carcinogenic. Of the people who received oral cyclophosphamide in the early years I think 40% developed bladder cancer. Azathioprine causes skin and mouth cancer - not often but I stopped using it when a dear patient of mine got mouth cancer - very luckily it could be removed. Steroids cause bone collapse and heart disease. Most of the drugs also increase risk of serious infections, some of them fatal and untreatable. And although some of these drugs do help for autoimmune conditions like rheumatoid arthritis most are no longer used because they do not do enough good to justify the harm. They are still used in conditions that have a high mortality if not treated, like lupus but not much else. Methotrexate may be reasonably safe and it does help RA but it very rarely produces remission and often produces nausea.

Things suddenly changed when the new specific biologic drugs came along. They still have problems but they have much more realistic risk/benefit ratios. At first sight none of these are relevant to ME, since there seem to be no autoantibodies and no signs of high TNF or IL-6 like a very high CRP. So far it looks as if rituximab might be useful after all but from what I have heard TNF blockers are not showing much benefit. There is an IL-17 inhibitor that has been tried for RA and not done very well that might possibly work in ME since Mady Hornig has found IL-17 levels up in early disease. But that would be a new research venture.
I shared you concerns about immune system meds, and know most doctors are understandably wary of them. Do you have any view on the prospect of intervening with external causes and thus indirectly resurrecting normal immune function? E.g. levels of melatonin, methylation issues, etc etc.... ?
 

Jonathan Edwards

"Gibberish"
Messages
5,256
@Jonathan Edwards, given the problems we all agree on with having ME and trying to get the NHS to make some progress with us, can I ask what you would do if you were a long-time sick, severely ill PWME (given your inside knowledge of how the NHS works and how clinicians within it think)?

And whether there's anything that patients (either individually or as a group) can do to improve the situation?

Is our only option, as you see it, to wait for the outcome of RCTs or the establishment of an agreed biomarker?

Plan A: Well, if I was tomorrow struck down with ME, after 6 months and one day (or less) I would persuade my friend Samantha to give me some rituximab - but then I had always wanted to have an excuse to try some. When we first started using it Jo Cambridge and I joked that everyone should get a shot at fifty because it would definitely cure old age. And recommending it to someone else is different.

Plan B: I would log on to a self-help ME website and bash people over the head (verbally) until by arguing and arguing we had worked out what was really going on and the logical way to treat it. And I would not let people get away with claiming stuff that was not backed up by solid evidence. I would listen with interest and think of the possibilities opened up but I would be ruthlessly logical (a bit like Socrates). If I did not have the knowledge to have an opinion of my own on a particular technical issue I would challenge everyone who claimed they did until I had sussed out who knew what they were talking about and who was dealing in horse manure. I would do that because that is what I did on a Friday night for RA for about five years. We had hardly done any new experiments of our own prior to the day we decided to try treating people. We just argued about stuff that was already known. And most of that five years was about learning not to be afraid to question things and try arguing a case. In short, I would do exactly what we are doing now. That is our best hope, I think. And if some bright researcher turns up something new that changes the game, we all know about it by teatime because people are keeping an eye out.

For instance you made me think about anti-IL-17. Maybe that should be pursued. My friend Pierre Miossec knows all about it and studied it in RA. Maybe Dr Hornig has already twigged? I will do a little exploring. So you are not powerless, doing nothing. You have a direct line to something happening. And I bet it's not just me that listens in here. I bet those researchers across the continents have a peek at PR now and again even if they keep Schtum. I know for a fact their patients do and give them stick as a result!

So, in other words, I doubt searching for a better option on the NHS at the moment will get very far, but that doesn't mean that it will be another ten years before anything happens.
 

Leopardtail

Senior Member
Messages
1,151
Location
England
Plan A: Well, if I was tomorrow struck down with ME, after 6 months and one day (or less) I would persuade my friend Samantha to give me some rituximab - but then I had always wanted to have an excuse to try some. When we first started using it Jo Cambridge and I joked that everyone should get a shot at fifty because it would definitely cure old age. And recommending it to someone else is different.

Plan B: I would log on to a self-help ME website and bash people over the head (verbally) until by arguing and arguing we had worked out what was really going on and the logical way to treat it. And I would not let people get away with claiming stuff that was not backed up by solid evidence. I would listen with interest and think of the possibilities opened up but I would be ruthlessly logical (a bit like Socrates). If I did not have the knowledge to have an opinion of my own on a particular technical issue I would challenge everyone who claimed they did until I had sussed out who knew what they were talking about and who was dealing in horse manure. I would do that because that is what I did on a Friday night for RA for about five years. We had hardly done any new experiments of our own prior to the day we decided to try treating people. We just argued about stuff that was already known. And most of that five years was about learning not to be afraid to question things and try arguing a case. In short, I would do exactly what we are doing now. That is our best hope, I think. And if some bright researcher turns up something new that changes the game, we all know about it by teatime because people are keeping an eye out.

For instance you made me think about anti-IL-17. Maybe that should be pursued. My friend Pierre Miossec knows all about it and studied it in RA. Maybe Dr Hornig has already twigged? I will do a little exploring. So you are not powerless, doing nothing. You have a direct line to something happening. And I bet it's not just me that listens in here. I bet those researchers across the continents have a peek at PR now and again even if they keep Schtum. I know for a fact their patients do and give them stick as a result!

So, in other words, I doubt searching for a better option on the NHS at the moment will get very far, but that doesn't mean that it will be another ten years before anything happens.
Jonathan,

we do not have consistent presentation of symptoms. The overall pattern shows some similarity (e.g. something in every system) but vast variation in the detail. Would you do that search before, or after preparing a really detailed outline of your symptoms?

In other words would you engage first then thinking about your symptoms or vice-versa?
 

Leopardtail

Senior Member
Messages
1,151
Location
England
How can you distinguish between this and people truly not getting a cold?

Okay this question made little sense. How can you distinguish between a healthy immune system, and one that doesn't react appropriately, giving the illusion of never getting infections?
@A.B.
Thanks for challenging all this, it will produce a much better result....

Would the question itself be clearer if it were:
  • I get infections and/or show few symptoms of infection?
I don't think that's quite right, but am sure we can polish it....


Does anybody know a ME patients with more allergic symptoms who might want to weight in on the original post??
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
I think we can show infectious symptoms without an infection. What we call infectious symptoms are typically immune mediated. If hormones or other factors were inducing symptoms, then how could we tell them apart from a real infection? Only with specific infectious symptoms and lab findings would you be sure.

For example, I used to get a lot of what I called false flu. Flu-like symptoms, no sneezing, typically after eating lots of omega-6 polyunsaturated fat. Such fats induce series 2 eicosanoids, hormones that can trigger immune responses.
 

Leopardtail

Senior Member
Messages
1,151
Location
England
I think we can show infectious symptoms without an infection. What we call infectious symptoms are typically immune mediated. If hormones or other factors were inducing symptoms, then how could we tell them apart from a real infection? Only with specific infectious symptoms and lab findings would you be sure.

For example, I used to get a lot of what I called false flu. Flu-like symptoms, no sneezing, typically after eating lots of omega-6 polyunsaturated fat. Such fats induce series 2 eicosanoids, hormones that can trigger immune responses.
Good point...

That crossed my mind too.... Some symptoms seem more unique (e.g. green mucous due to immune cells). Pain is completely useless as a symptom. This is all part of the stuff we need to tease out isn't it?

I also produce bugger all in the way of Eiconsanoids with infection.

For now thought its the symptomatic presentations I am after.... the changes that occur distinct to normal ME symptoms with the (hypothesised) infection. e.g. my wife gets sick and I see certain changes, substitute family member, husband etc as applies.

Just by way of facetious theory testing... could it be that you WERE infected and the fats permitted the immune response?

Keep the thoughts coming please Alex....
 

Leopardtail

Senior Member
Messages
1,151
Location
England
Sorry but I don't feel my symptoms are primariliy immune mediated at least not in the traditional sense.

I also agree that this discussion should be on another thread.
it is going to be split off.. the immune research vs the NHS stuff....
 

Leopardtail

Senior Member
Messages
1,151
Location
England
Sorry but I don't feel my symptoms are primarily immune mediated at least not in the traditional sense.

I also agree that this discussion should be on another thread.
No probs, was not thinking so much immune mediated, as immune symptoms irrespective of cause.....
 

NK17

Senior Member
Messages
592
If I remember correctly Mady Hornig and Ian Lipkin have been talking about a quite clear different picture between PWME who have been sick less than 3 years and PWME who have been ill longer.

I think that our immune system derangement is central and probably reflects the chronicity of the disease. An allergic type response might be the first immunological alert and then we move toward a dysfunctional hypo and hyper alert toward a specific groups/families of pathogens ( by the way NK cells are very much implicated in host immune response against herpes viruses and human papilloma viruses).

For what is worth I can report that it's been several years now that my blood tests show 0 eosinophils, while when I was younger I had clear "allergic" manifestations (eczema etc.).

Something or more than a something has been derailing and hacking my immune system ;).

My homeostatic equilibrium is a memory of the long and lost past.

I agree wholeheartedly with @Jonathan Edwards and since I'm already deep on the Plan A2 path, I'm seriously considering to move on to Plan B.

Can't wait to hear that the norwegian have finally started their Phase III rituximab trial, that Dr. Cambridge and colleagues have their super tight clinical trial protocol ready and are recruiting patients from reputable ME clinics/doctors and that Dr. Kogelnik and Prof. Davis are marching toward a replication study here in the US, armed with some much needed and non refutable genetic/genomics data from their deep sequencing genome wide studies.
 

Jonathan Edwards

"Gibberish"
Messages
5,256
It can show specific blood pressure reactions to orthostatic challenge, which can give relevant specialists a good idea of what to try for treatment. Additional testing can also then be ordered to find a more proximate cause of the OI, such as norepinephrine levels, blood volume, certain auto-antibodies, diabetes insipidus, etc etc.

With appropriate followup testing, it should be somewhat straightforward to decide on effective treatments to try. I think it's also a bit ridiculous to completely withhold treatment for a severely disabling symptom on the excuse that it might cause unexpected problems.

OK, but this discussion is for real, Valentijn. If it is 'straightforward to decide on effective treatments to try' then the 'relevant specialists' you quote as having a good idea what to use must presumably have validated their policy sufficiently to have written up the evidence in such a way that I can get it out and read it. I can then ring up (I am serious) the rheumatologists in Sasha and Justy's local hospitals (they all know who I am) and suggest they follow the well documented and reasonably safe policy suggested. They are used to following what I suggest so there should be no problem.

Except that I don't think somehow I will be doing that. If these policies are not written up it is no use for Sasha or Justy to hope to get them on the NHS because nobody knows what they are! In the old days it was standard for my medical colleagues to claim they knew when to use this treatment and when to use that because they had the 'clinical experience' needed. They did all sorts of fancy tests despite the fact that nobody was quite sure why. Then about twenty years ago their bluff was called and it became embarrassing when older colleagues made such claims. Studies had shown that you need hard data.

So I am still waiting to see the instructions that would allow me to pick up that telephone for Sasha. I am absolutely ready to do that.
 

Sasha

Fine, thank you
Messages
17,863
Location
UK
I can then ring up (I am serious) the rheumatologists in Sasha and Justy's local hospitals (they all know who I am) and suggest they follow the well documented and reasonably safe policy suggested. They are used to following what I suggest so there should be no problem.

Outstanding! And of course you're right, they do know who you are. I had a consultation with my local rheumatology guy because of concerns (which he laid to rest) that I had some symptoms possibly suggesting RA or Sjogren's and was talking about the Norwegian Rituximab trial without a glimmer, until I mentioned that you were advising the UK trial, and then he said that of course he knew who you were and got all interested.

So I am still waiting to see the instructions that would allow me to pick up that telephone for Sasha. I am absolutely ready to do that.

Thank you! I very much appreciate that. Let's hope that we get some well-evidenced treatment sooner or later.

I also appreciate the work-out you're giving us on our ideas. Constructive discussion like this is hugely useful.
 

Marco

Grrrrrrr!
Messages
2,386
Location
Near Cognac, France
So I am still waiting to see the instructions that would allow me to pick up that telephone for Sasha. I am absolutely ready to do that.

Not being facetious but maybe a first port of call would be to talk to these folks :

Autonomic Neuropathy Is Treatable

There are substantial data from diabetic patients taking Carvedilol that support
the results of this case study. With non-invasive, independent, simultaneous,
quantitative measures of parasympathetic and sympathetic activity, CAN can
be detected, identified earlier, treated specifically based on the patient’s
individual physiology, and monitored. This results in improved outcomes, a
better quality of life, and preserved longevity through a reduction in morbidity
and mortality

http://wadepage.org/files/file/REDUCING RISKS/Autonomic Neuropathy.pdf
 
Messages
15,786
I can then ring up (I am serious) the rheumatologists in Sasha and Justy's local hospitals (they all know who I am) and suggest they follow the well documented and reasonably safe policy suggested. They are used to following what I suggest so there should be no problem.
According to http://www.nhs.uk/Conditions/Blood-pressure-(low)/Pages/Diagnosis.aspx :
Your GP or practice nurse will usually be able to diagnose low blood pressure very easily. However, determining the reason for low blood pressure can often be more difficult.

If you have an underlying condition causing low blood pressure, it is likely you will have other symptoms as well. You should discuss these with your GP, who may recommend further tests.

Further tests may include blood tests to check for anaemia and measurements taken of your hormone levels or blood sugar (glucose) level, or an electrocardiogram (ECG) to detect any irregularities in your heart rhythm.
And regarding treatment:
Treating underlying conditions
If your GP suspects your low blood pressure is being caused by an underlying health condition, you may be referred to hospital for further tests and treatment.

For example, if your low blood pressure is related to hormone problems (see causes of low blood pressure for more information), you may be referred to a specialist called an endocrinologist who may prescribe hormone replacement medication.

Medication for low blood pressure
Very few people are prescribed medication for low blood pressure. The symptoms of hypotension can usually be treated by making the above changes to your lifestyle and, in particular, by increasing your fluid and salt intake.

If medication is necessary, it will usually be medicines to expand the volume of your blood or to constrict (narrow) your arteries. By increasing your blood, or decreasing your arteries, your blood pressure will increase because there will be more blood flowing through a smaller space.
It's not particularly detailed, but the sentiment is there: verify the symptom, then run some more tests and/or try some treatments. The Tilt Table Test isn't specifically mentioned, but many hospitals have one and presumably they're using them to diagnose autonomic dysfunction.

They even talk about underlying conditions, and don't suggest that it's inappropriate to test or treat for hypotension due to having an additional diagnosis or underlying cause. There is no rational reason to exclude ME/CFS patients from getting a treatable symptom treated, when non-ME/CFS patients can clearly expect to have the identical symptom tested for and treated.
 

Leopardtail

Senior Member
Messages
1,151
Location
England
I don't want to derail the thread by yakking on about my own circumstance but basically, my HR doesn't rise sufficiently in the first instance to be classified as OI but as I remain standing, it rises and rises until it's well over the normal HR of a healthy person who is standing still.

Symptomatically, I can remain upright for longer than a person with classic OI but am eventually forced to lie down. I spend a total of about five hours a day lying down, paced throughout the day. The rest of the time, I have to have my feet up, apart from short periods of walking or sitting normally. Acute infections can bring on more obvious OI symptoms such as lightheadedness and force me to crawl rather than walk to avoid passing out.

If you google on "delayed orthostatic intolerance" you'll find some references.
High heart rate would be POTS (a type of OI), if it falls or does not rise enough that would be another form of OI (orthostatic hypotension).
I suffered delayed OI myself now I know what it is....
 

Leopardtail

Senior Member
Messages
1,151
Location
England
OK, but this discussion is for real, Valentijn. If it is 'straightforward to decide on effective treatments to try' then the 'relevant specialists' you quote as having a good idea what to use must presumably have validated their policy sufficiently to have written up the evidence in such a way that I can get it out and read it. I can then ring up (I am serious) the rheumatologists in Sasha and Justy's local hospitals (they all know who I am) and suggest they follow the well documented and reasonably safe policy suggested. They are used to following what I suggest so there should be no problem.

Except that I don't think somehow I will be doing that. If these policies are not written up it is no use for Sasha or Justy to hope to get them on the NHS because nobody knows what they are! In the old days it was standard for my medical colleagues to claim they knew when to use this treatment and when to use that because they had the 'clinical experience' needed. They did all sorts of fancy tests despite the fact that nobody was quite sure why. Then about twenty years ago their bluff was called and it became embarrassing when older colleagues made such claims. Studies had shown that you need hard data.

So I am still waiting to see the instructions that would allow me to pick up that telephone for Sasha. I am absolutely ready to do that.
The three causes of OI that I know of are: POTS, NMH, OH - all of these will have separate NICE guidelines since they are well established diseases.
What are you looking for that you don't find there?

I did get investigation for OI so it can be done.
 

Jonathan Edwards

"Gibberish"
Messages
5,256
OK, I think I saw the paper Marco cited on a previous occasion. The authors recommend treatment on the basis of what seems logical to them - if A is up bring A down, if B is down bring B up. But they do not cite any formal evidence for this having been shown to be the right thing to do. This sort of 'flying by the seat of the pants' medicine is to my mind obsolete. This may be the best advice there is in this field, simply because there is nothing better, but I would not want to recommend something for the treatment of a member of my family on this sort of 'what ought to work' basis. They don't really deal with low blood pressure either.

The NHS and Mayo blurbs I had found in my own trawling and they really don't say much. I absolutely agree that PWME who also have anaemia or Addison's disease causing OI should have the necessary tests for ANOTHER cause for OI on top of ME. But we are working from the starting point that it seems that 95% of PWME have OI, which presumably means that MEs cause OI as well and that sort of OI we have no clue what to do about as far as I can see. There is of course nothing in the 'mainsteam' literature on treating ME-related OI because ME does not exist in the mainstream literature. I totally agree that that is a problem that needs addressing but until it is I cannot pick up the phone, can I?

From what I have read so far the distinction between POTS, NMH and OH is not very clear in the scientific literature and I don't think they are 'well established diseases'. They seem more like reasonably well demarcated physiological patterns or subgroups of patterns. That demarcation may help distinguish causal categories at one level but I am still very unclear what treatment for ME-related OI is well validated. Steroids come up on the Mayo site and I would not want to recommend those. So does Midodrine, but I do not think that is licensed in the UK and apparently the FDA wanted to withdraw the license in the US. I don't think I would want to take an alpha agonist.