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

[Leopardtail]

From what I recall in the research, it's something like 95% of ME/CFS patients have NMH and/or POTS. So not just "many" but rather nearly all of us.

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.

Most ME/CFS patients actually have NMH, not POTS. But POTS is better understood and easier to say, hence a lot of people with NMH talk about their "POTS" when it's not what they actually have. But that's a somewhat irrelevant matter of terminology, despite doctors often liking to shut down if a patient uses a technically incorrect term at any point

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.

OI can and has left me bedbound for weeks at a time. Being forced to lie down all day is painful, frustrating, and really really boring. It's well worth trying a reasonable treatment based on trustworthy test results, when that treatment can cause a drastic increase in quality of life.

Indeed, requiring that we KNOW the cause and KNOW exactly how the treatment will and won't effect us is a rather extreme requirement which I don't think is present in any other illness or even idiopathic and uncomplicated cases of OI. And it's that mindset which is leaving us untested and untreated for extremely debilitating symptoms.

Treating my OI has made the biggest difference to my symptoms thus far, and I only wish I was able to do it with active assistance and oversight from a local doctor.

Given @Jonathan Edwards context here, I do understand his point. If the OI is caused by low blood volume, we need to know whether that results from Aldosterone deficient, ADH deficit, or some form of other polyuria. If it's not blood volume we need to establish whether it's of Nervous origin.

What we actually need is a NICE (or other national) guideline that states "if an ME patient shows symptoms of OI, then the GP should first test as follows" based upon that results the next action should be: In other words a proper structured pathway for diagnosis.

As he also states for each 'root cause' we need to know what level of which treatment is right for an ME patient. Julia Newton has made a good start on that one, but more work is needed. That however requires the MRC and NHS (here) to stop wasting money testing infective treatments and focus some finance on what does have a chance of working.

 

[Leopardtail]

Very interesting. I have delayed OI (not recognised by my local cardiologist but would get me a diagnosis and treatment in the US). I'm not sure whether to work harder at getting an NHS diagnosis and to seek drug treatment for it, even though it's probably my most limiting symptom. I'm concerned that masking it might hide any improvement I'm getting from things I'm trying that could address the fundamental immune problems, and that using steroids etc. might cause long-term harm, as well as interfering with immune therapies. On the other hand, Prof Newton has just shown that having OI is related to early mortality. Tough one.

Please clarify this "delayed OI" - I am confused!!!

 

[Valentijn]

I'm concerned that masking it might hide any improvement I'm getting from things I'm trying that could address the fundamental immune problems, and that using steroids etc. might cause long-term harm, as well as interfering with immune therapies. On the other hand, Prof Newton has just shown that having OI is related to early mortality. Tough one.

Regarding masking symptoms, my experience has been that I get a short boost in my PEM threshhold when first starting OI treatments, which then fades away. Probably due to having been forced to lie down so much, building up a bit of an energy reserve in the process, and then burning through it once I can get up and do things again. So I can still use PEM as a good indicator of progress. Also, the drugs I've taken (first Strattera then Yohimbe) have short half-lives and their effects on OI wear off quite quickly when stopping them.

Though I do agree that we need to be very careful about what we're taking to avoid likely interactions or additional problems. Hence my preference for an NRI over the SNRIs which doctors prefer, since I recall very clearly how badly an SSRI affected me And when later trying an ADRA2A antagonist, based on research showing overexpression of it in ME patients, and the ability of it to cause my low norepinephrine levels, I went for the drug (well, tree bark) which very specifically affects only ADRA2A, ADRA2B, and ADRA2C, even though there are medications with similar action which I would have a much easier time getting if I didn't mind a dozen or so nasty side effects.

 

[Valentijn]

Please clarify this "delayed OI" - I am confused!!!

Neurally Mediated Hypotension (NMH) won't always hit immediately when standing up, especially in milder cases or during a good spell. It can take 30 minutes or more to hit, then causing blood pressure and/or pulse pressure to drop to the point where we're having serious problems staying upright. Unfortunately the TTT is typically used to detect OI problems with a faster onset, and might not have a long enough duration to detect NMH.

 

[alex3619]

Sorry if this is a silly question, but I haven't been awake for long! If the NK cells have the same cell surface markers in blood and in isolation, doesn't this suggest that something in the blood is attracted to the markers and consequently reduces the cell function?

I am not sure about this. Maybe. We do not know they have the same cell surface markers in both though. That is something that needs to be tested. It may be that removed from the blood the cell surface marker expression changes.
What is likely is that something is inducing a functional change ... but via what pathway? I don't currently know enough about this to even vaguely speculate more than I have. It could be NK cell specific, or something more general that just impacts NK cells more.

 

[alex3619]

Neurally Mediated Hypotension (NMH) won't always hit immediately when standing up, especially in milder cases or during a good spell. It can take 30 minutes or more to hit, then causing blood pressure and/or pulse pressure to drop to the point where we're having serious problems staying upright. Unfortunately the TTT is typically used to detect OI problems with a faster onset, and might not have a long enough duration to detect NMH.

I see it as a threshold effect. The longer you stand, the lower the threshold (or that the factors pushing over the threshold are higher). If you have not had enough sleep, then its lower too. If you are in PEM, its probably lower. It all adds up.

 

[Marco]

So distilling the immune system variations out we have:

• apparent lack of infection either due to poor immune response preventing symptoms or excellent function preventing infection
• poor function causing long lasting infection
• infection causing symptomatic improvement
• infection causing marked increase in fatigue

Any more items folks?

@MeSci - what would you add on the 'allergic' end of the spectrum?
@Hip, @alex3619 , @Freddd do any of your have further ideas?

I find it highly unlikely that even the most isolated PWME wouldn't be exposed to at least a fair proportion of the regular bugs circulating around the general population. In respect of those who never seem to catch anything (like me - I can count the number of colds etc in 30 years on one hand) it suggests to me that they are probably catching and effectively dealing with minor infections - what is missing is the usual symptoms associated with the 'sickness response'.

Given that we spend every day feeling crappy it may not be that surprising that we don't notice additional symptoms that are effectively the same ones we experience every day. You could also speculate that something is triggering an ongoing sickness reponse in PWME in the absence of infection.

 

[Sasha]

Please clarify this "delayed OI" - I am confused!!!

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.

 

[Leopardtail]

Neurally Mediated Hypotension (NMH) won't always hit immediately when standing up, especially in milder cases or during a good spell. It can take 30 minutes or more to hit, then causing blood pressure and/or pulse pressure to drop to the point where we're having serious problems staying upright. Unfortunately the TTT is typically used to detect OI problems with a faster onset, and might not have a long enough duration to detect NMH.

With you now.... I get that too it can occur 10-15 mins after standing up. I am guessing it to be OI triggered by PEM. I do get immeidate OI if I stand up very rapidly though, something I have formed the habit of not doing.

 

[Leopardtail]

I find it highly unlikely that even the most isolated PWME wouldn't be exposed to at least a fair proportion of the regular bugs circulating around the general population. In respect of those who never seem to catch anything (like me - I can count the number of colds etc in 30 years on one hand) it suggests to me that they are probably catching and effectively dealing with minor infections - what is missing is the usual symptoms associated with the 'sickness response'.

Given that we spend every day feeling crappy it may not be that surprising that we don't notice additional symptoms that are effectively the same ones we experience every day. You could also speculate that something is triggering an ongoing sickness reponse in PWME in the absence of infection.

I think this is all covered in this point:

• apparent lack of infection either due to poor immune response preventing symptoms or excellent function preventing infection

By preventing infection at the end, I am wording for 'Joe Public' meaning that the immune system combats potential infection fast enough that in the eyes of most patients 'they don't get a cold'.

The first point that does not seem to be clear enough is that most symptoms of infection: discoloured mucous, running nose, sore throat, etc are not cuaed by the infection but by immune response.
To illustrate this first point: I got very ill and had blood sugar elevation in autumn/winter spring. No runny nose, no chesty cough, few of the normal 'diagnostic markers'. However anti-biotics helped for as long as I took them, however since my immune system was under-functioning problems resolves when the course stopped. Hence having the infection, and having symptoms of infection may not correlate. The blood sugar response to anti-biotics for example is known issue with insulin controlled diabetics but only occurs with a true infection, its a side-effect not of the drug, but the response to the drug.

The wording needs work, but is my intent clear now, or is there a further point I need to add?

 

[A.B.]

By preventing infection at the end, I am wording for 'Joe Public' meaning that the immune system combats potential infection fast enough that in the eyes of most patients 'they don't get a cold'.

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?

 

[Leopardtail]

How can you distinguish between this and people truly not getting a cold?

That point would cover people who actually do not get ill with an infection, for whatever reason.

The chances of you not getting a cold, not getting any infection are pretty remote. E.g. if you live with somebody who gets a cold virus, so do you. If you have a good immune system your body kills it, and you don't get the illness that goes with it.

What we can't tell apart (especially with ME) is whether you don't have the cold at all (because your immune system is working) or you have it but don't show clear symptoms (because your immune system is active enough to keep you alive, but not doing the things that produce symptoms).

Because our immune systems still work, but often don't work well, it makes dealing with infection or even working out if we have one a nightmare for doctor and patient alike. I can only tell because of slight changes in body temperature and changes in my blood sugars.

 

[Marco]

I think this is all covered in this point:

• apparent lack of infection either due to poor immune response preventing symptoms or excellent function preventing infection

By preventing infection at the end, I am wording for 'Joe Public' meaning that the immune system combats potential infection fast enough that in the eyes of most patients 'they don't get a cold'.

I'm not quite sure that's what I meant. I'm not suggesting either a poor immune response or an overly efficient one. I"m suggesting a pretty normal immune response (to occasional infections) but where many of the symptoms of sickness behaviour are experienced on an ongoing basis. Come to think of it I'm pretty 'snotty' with gritty eyes and a cough all the time - but I am a smoker.

 

[Leopardtail]

I'm not quite sure that's what I meant. I'm not suggesting either a poor immune response or an overly efficient one. I"m suggesting a pretty normal immune response (to occasional infections) but where many of the symptoms of sickness behaviour are experienced on an ongoing basis. Come to think of it I'm pretty 'snotty' with gritty eyes and a cough all the time - but I am a smoker.

Smiles, that was another thought I meant to include:
If one's normal symptoms mimic infection, that removes even more of the clues.
I for example had permanent 'flu level' muscular pain, very sore throat, tiredness - hence those symptoms are masked.
I am not able with any level of infection to produce much mucous and what I do produce is very 'elastic' hence doctors can't detect that symptom very well, although I know it - that is one example of where an immune symptom has gone.
I also don't get that sickly colour in my face, or discoloured mucous, both immune manifestations.

To explain the focus of my original question: I have spotted for different patterns of 'immune stuff' on the thread that can be spotted purely from symptoms. The wording of which clearly needs work. It's a work in progress.

Important thing @Marco , do you shown any immune pattern of symptoms that are not on that list?
(excluding the stuff your smoking causes?)

 

[MeSci]

So distilling the immune system variations out we have:

• apparent lack of infection either due to poor immune response preventing symptoms or excellent function preventing infection
• poor function causing long lasting infection
• infection causing symptomatic improvement
• infection causing marked increase in fatigue

Any more items folks?

@MeSci - what would you add on the 'allergic' end of the spectrum?
@Hip, @alex3619 , @Freddd do any of your have further ideas?

Sorry - I'm very busy. You can find my details on various issues by searching the forum. I have a big backlog of posts to catch up on and a lot else to do as well.

BTW a lot of these posts seem to be straying too far from the thread title and should perhaps be in the thread about different types of ME.

 

[Leopardtail]

I think that you are somewhat misconstruing and misrepresenting my position. Like most sufferers, I have multisystem symptomatology. I also read scientific papers and discussions on multiple potential causes, subgroups, etc.

What I am most interested in (as I think are we all) is how to address the fundamental cause(s) of the illness. This may differ in different people. I have addressed this in my main 'leaky gut' blogpost.

I currently find the leaky-gut/autoimmunity theory most compelling, at least for my own pattern of illness development and symptomatology, and it seems to fit well for many others too. Many of us have found that addressing the basis of this has brought about considerable improvement, although recovery is of course elusive. Others have not seen such improvements, and sometimes improvements cease after a promising start.

I remain open to all credible scientific evidence on this and other theories.

Smiles.. think we are in the same place just an issue of wording. The gut should (in its immunity role) eliminate or control substance animal, vegetable or mineral that should not be there and prevent their transit into the body and not react to normal food stuffs. I mean immunity in the larger sense of controlling all substances. What was primarily on my mind was that you seem to report a fair number of intolerance reactions to foods or supplements that I do no stuffer (possibly allergic style over-activity) where I use to suffer more immune system not working on organic invaders type stuff because I had those different issues.

Where you have leaky gut, some allergic stuff there - I used to have 'colds' that lasted six months. Hence as I tried to highlight to Professor Edwards it impact the research that is most applicable to each of us, the treatments that are best for us and the specialists more likely to help us. I focussed purely on immunity because that is the current dominant discourse on the thread.

I am aware though that like of all us you suffer a wide range of issues across systems - I was just trying to focus on one point at once, and deliberately chose you to bring your comments on the issue at hand precisely because your experience is often the polar opposite of mine and we need the Prof to form a balanced, fully rounded viewof our population..

Would like to hear your comments on my question re 'forms of immune issue' above...

 

[Leopardtail]

Sorry - I'm very busy. You can find my details on various issues by searching the forum. I have a big backlog of posts to catch up on and a lot else to do as well.

Not going hunting, but felt I should invite you to chip in....

 

[Sasha]

@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?

 

[Jonathan Edwards]

I think you mentioned earlier that response to Rituximab could be considered a biomarker. I'm still surprised that the consultants I've seen (an immunologist and an infectious disease specialist), both convinced that I have an immune system problem that's causing my ME, won't try an immune therapy on me to see if it works, but maybe that's my naivety about the risk/benefit ratio.

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.

 

[Sasha]

Thanks, @Jonathan Edwards - that's a very clear explanation of the considerable risks involved with immune system drugs (which I hadn't heard before).

That's interesting about biologic drugs. I hadn't know about these. For anyone else who hasn't, here's some info:

http://www.webmd.com/rheumatoid-arthritis/guide/biologics