EBV Test Interpretation- Quest Diagnostics

[Jonathan Edwards]

@Jonathan Edwards I have to respectfully disagree with you as I was diagnosed with viral re-activation of EBV by one of the top CFS treatment centers in the US (OMI) and they are very up to date on the most current research.

I had high IgM and EA yet it has been 2.5 years since I had mono. My diagnosis was based on real science and not on a hand-out that I got on the internet. I have been on an anti-viral for three weeks and honestly have already felt some improvement.

Please know I am posting this with the upmost respect to you to further dialogue and all of this is very helpful to me in my treatment journey.

Also wanted to add there were many viruses that I had high IgG but NOT IgM and was told they were inactive and only showed past infection (unlike the EBV.)

I am not sure we disagree Gingergrrl. You had a high IgM titre and specifically for EBV, with high EAD. That begins to look like enough evidence to think that you are still actively reacting to EBV. To be sure I think you would need evidence of free virus. However, I do not know enough about the risk/benefit of antivirals for EBV to comment on the treatment, which may be reasonable in the context.

I am not saying that some people with CFS symptoms may not in fact have what I might have to call ME7, which is effectively an EBV infection that never comes under control. Delayed recovery from EBV is well recognised and if anything it is so well recognised that maybe it should not even be lumped under ME but just called protracted EBV infection. (Reactivation sounds the wrong word for people who never actually get better in between.) What I am arguing for is being precise and cautious about test interpretation. Otherwise people with ME2 or ME5 may get treated for ME7 and end up with an unfortunate and unnecessary adverse reaction. My original suggestion to aussie777 was that an IgM titre was needed and also a doctor who knew how to interpret it. It sounds as if you have got that sorted.

 

[Gingergrrl]

@Jonathan Edwards Thank you for your reply and it makes a lot of sense. If there is an ME7 (using your classification) then I believe I would be in that overall group. However, just to clarify, I do consider mine a re-activation b/c I had a period of about 10 months where I believed I had fully recovered from mono/EBV (although blood tests may have shown differently- I do not know b/c I was not re-tested at that time.)

I got severe mono/EBV in March & April 2012 (confirmed by blood test) in which I had high fever for three weeks straight, liver tests off the charts, dehydration requiring IV's at the ER, abcess on my tonsil, etc, etc. It was the sickest I had been in my life. By the end of April I believed I was better and went back to work full-time while simultaneously planning my wedding. I had normal energy levels and no symptoms.

In Jan 2013, I started to get unexplained autonomic and cardiac issues (and at different times diagnosed with IST and POTS and put on a beta blocker.) All year I got sicker and sicker but continued to work full time through Oct when I first took medical leave. I was then diagnosed with Hashimoto's Disease and began thyroid treatment but my symptoms continued to worsen with severe, debilitating fatigue and what I now know to be PEM (I did not have the proper terms or diagnosis at that point.) I returned to work for Dec 2013-Feb 2014 but was so ill I went back on medical leave in March 2014 and have been out ever since.

My endocrinologist and later a naturopath both felt I had CFS (b/c of the earlier mono/EBV) and my ND tested me for EBV IgG, IgM & EA which were all positive. I began natural anti-virals and all kinds of supplements. It was not until going to OMI in July 2014 that I was told beyond a shadow of a doubt that I had ME/CFS and viral-reactivation of EBV along with NK functioning of 5 and MTHFR mutations (and all kinds of autonomic issues.) I was started on Famvir and can honestly say that in three weeks of Famvir, I feel some improvement.

Would this fit with your ME7 category (since I did have normal functioning of 10 months in between mono and CFS starting?)

 

[Jonathan Edwards]

Would this fit with your ME7 category (since I did have normal functioning of 10 months in between mono and CFS starting?)

Now things are getting complicated. I agree this would have to be a re-activational ME7. But it looks to me as if you might be ME4 after all! But then I never said that all these MEs had to be separate. (I think I said they could overlap and feed off each other.) So this seems to be an ME4.7 case (or ME7.4?). Maybe the EBV facilitated the autoimmune thyroid process and that allowed a reactivation. Or is the chicken the egg? I would be interested to know how things work out. Dr Kogelnik isa good person to be handling this I think!

 

[Gingergrrl]

I apologize I have not read through the full other thread on the different ME's. Does ME4 mean that someone has autoimmune thyroid issues like me? Also, I am seeing Dr. Kaufman (not Kogelnick) at OMI although both are ME/CFS heroes in my book!

 

[SOC]

I must respectfully disagree with Dr Edwards.
From Labtestsonoline:

If a person has positive VCA-IgG and EA-D IgG tests, then it is highly likely that he has a current or recent EBV infection.

Care must be taken when interpreting results of EBV antibody testing. The signs and symptoms as well as the medical history of the person tested must be taken into account.

Some signs and symptoms associated with mono include:

• Fatigue
• Fever
• Sore throat
• Swollen lymph glands
• Enlarged spleen and/or liver (sometimes)

Most ME patients have these symptoms of mono.

Reactivation of the virus is rarely a health concern unless the person is significantly and persistently immune compromised, as may happen in those who have HIV/AIDS or organ transplant recipients.

Many (most, all?) ME patients are persistently immune compromised -- a situation where reactivation is much more likely. This point is largely ignored by doctors who do not fully understand ME.

It is also my understanding that IgM antibodies do not persist long after the early phases of infection, so it would not be expected to see IgM antibodies in a chronic infection.

 

[Jonathan Edwards]

I apologize I have not read through the full other thread on the different ME's. Does ME4 mean that someone has autoimmune thyroid issues like me? Also, I am seeing Dr. Kaufman (not Kogelnick) at OMI although both are ME/CFS heroes in my book!

I defined ME4 as due to effects of antithyroid antibodies that are independent of any effect on thyroxine level - which I guess is the reason why so many people with Hashimoto's disease do not lose several of their symptoms when they take thyroxine.

 

[Ema]

I realise that what I am saying is not popular with all.

It's not a matter of popular or not popular. It's a matter of antiquated (I only believe what I was taught in medical school or have read in certain journals) vs progressive thought (I am willing to be open minded and consider evidence from all sources, including clinical and anecdotal experience, and use my judgment to give the evidence the weight it deserves).

Science was always meant to be constantly revised as we learned how new information can be fit into our existing models. Models were always meant to be discarded when they had outlived their usefulness. But this isn't happening and it is a VERY BIG problem in medicine today.

Medical science should be the very epitome of flowing, creative research directions and yet it seems to attract some of the most staid practitioners who are afraid to do anything that they haven't been doing for the past 100 years.

However, I prefer to base my thoughts on the work of people who have worked in government or university funded institutions and produced peer reviewed scientific papers, like my mother did, than on the opinions of commercial practitioners expressed on websites and handouts for patients, which are designed to sell to the patient what they want to hear.

That's fine in theory as a personal opinion on which to base your own care. Everyone will have a different tolerance for "experimental" theories.

We have to use the tests we have and interpret them to the best of our abilities. This is true for all testing, not just EBV.

We cannot bemoan the lack of perfect tests and then allow people to sit in purgatory without ANY treatment because we don't have all (or even many) of the answers to a most complicated problem yet. As long as people are informed, they should be able to make these kind of decisions for themselves along with their doctors.

At some point, it has to be *enough* to trust the research that has been done by those such as Lerner and Montoya in this area. And they say that people with an elevated EBV-EA IgG titer often have a reactivated form of the virus and often improve with antiviral treatment. Their experience and research is worth quite a lot in my opinion and should not be disregarded because it is not always funded by a (rarely unbiased) government or a university. It is often published in peer reviewed journals though.

Not to mention, recent research is warning us all of the dangers of relying solely on so-called evidence based medicine. It's just not making people well the way it should be or actually saving us money as a society. In fact, we are sicker than ever and only the insurance companies are rich. Basing one's entire treatment philosophy on this premise seems naive at best. Especially considering the lag of nearly two decades on average for research to make it's way into common clinical practice.

http://protomag.com/statics/MGH_SP10_Evidence_F5.pdf

http://forums.phoenixrising.me/inde...-trials-and-selective-publication-free.30887/

I think it is worth thinking this through because I see a very real danger here. The key problem, as highlighted on PR, is that many doctors think 'ME' is not an illness, but a false belief. How you can falsely believe you have pain I don't know, but if the ME community does have false beliefs about infections then it's just too easy for doctors to assume that is all there is to it - false beliefs encouraged by quacks.

The very real danger here is pandering to the lowest common denominator. I cannot change how uneducated, short-sighted doctors who have not picked up a medical journal since the day they graduated from medical school view ME/CFS. There will always be bad, uninformed doctors out there and there will always be quacks. Both of these extremes hurt patient outcomes. It's our task to figure out how to sit in the middle of the spectrum and keep both sides honest.

I am not suggesting that all these EBV titres mean nothing. But what I think is likely is that they mean something more complicated than 'reactivated infection'.

Of course they mean something more complicated. That's what all these doctors and researchers are trying to find. But in the meanwhile, "suggestive of a chronic or reactivated infection" and "predictive of treatment success with antivirals" is the best we've got.

Somebody said that virus might not be found because it hides away in tissues. But in simple terms EBV infection hidden away in tissues is what all normal people have. It only becomes a 'reactivated' infection, if the virus starts being exported and gets into tissues other than B cells and causes symptoms directly - in which case you should find it there. If it is actually causing a sore throat, for instance, my guess is that you should find virus in saliva. Note that even normal people maybe have a bit of 'reactivation' with EBV in the saliva some of the time, because when I got mono at 18 my girlfriend was perfectly fine.

Or maybe the EBV induced damage to the B cells is what is responsible for the symptoms...because the immune response is compromised overall. Maybe some people get lymphoma...and other people get ME/CFS.

So why don't we try and think of a more subtle reason for linking these tests to some of the real causes that cause real MEs.

Great idea...but let's not stop treating patients that present with certain clinical symptoms in the meanwhile.

OK, so that is speculation, but I am going to suggest a test of the two theories. How many people with ME on PR are aware of having infected another person with EBV through close contact? This would not happen very often because something like 80% of the population are infected as infants and nobody knows about it. You would probably have to get pretty close to a teenager or young adult who had not had childhood infection - hence the old name of 'the kissing disease'. But has a case of infection of another person by a person with ME (more than 6 months after an initial infective episode) been documented?

I agree, it would not happen very often that someone would get a new EBV infection from someone with ME/CFS because most everyone is exposed at an early age. Most people should be able to fight off a reactivation because they have a healthy immune system. It would be rare, as is ME/CFS, to find two people together that were both susceptible though I am sure that it has happened.

We also shouldn't forget that other herpes viruses can also cause a mono like illness. I, for one, couldn't say whether or not it is EBV or high CMV titers that are causing my symptoms.

 

[heapsreal]

Let's not forget the Dubbo study showing 10% of people who got ebv mono went on to develop cfs. 2 other infections were also studied I think qfever and maybe parvo virus but can't be certain, these also had similar % of people going on to develop cfs/post viral issues.

 

[Gingergrrl]

I defined ME4 as due to effects of antithyroid antibodies that are independent of any effect on thyroxine level - which I guess is the reason why so many people with Hashimoto's disease do not lose several of their symptoms when they take thyroxine.

@Jonathan Edwards, I have never taken Thyroxine and take Armour Thyroid. My TSH levels are perfect now (around 1.0) with a very tiny micro dose of Armour (7.5 mg each morning.) That is why my endocrinologist felt that while I did have Hashimoto's (high levels of both antibodies and elevated TSH prior to Armour) he also felt that the severity of my unremitting fatigue and autonomic dysfunction/tachycardia were due to something beyond Hashimoto's. He suspected CFS even though he did not know how to treat it. He did not feel that Hashimoto's was a sub-type of CFS but rather that I have two distinct things. I do believe that the EBV could have set off the Hashimoto's although that I cannot prove!

The rest I am quoting from @Ema

Science was always meant to be constantly revised as we learned how new information can be fit into our existing models. Models were always meant to be discarded when they had outlived their usefulness. But this isn't happening and it is a VERY BIG problem in medicine today. Medical science should be the very epitome of flowing, creative research directions and yet it seems to attract some of the most staid practitioners who are afraid to do anything that they haven't been doing for the past 100 years.

That is very true and well said!

At some point, it has to be *enough* to trust the research that has been done by those such as Lerner and Montoya in this area. And they say that people with an elevated EBV-EA IgG titer often have a reactivated form of the virus and often improve with antiviral treatment. Their experience and research is worth quite a lot in my opinion and should not be disregarded because it is not always funded by a (rarely unbiased) government or a university. It is often published in peer reviewed journals though.

I agree and it was the research of Lerner, Montoya, and those at OMI that led me to feel comfortable to try an anti-viral for EBV. I would not have tried it in the absence of testing but once my tests (from Feb through July 2014) all confirmed active EBV, and this was the sickest I had been since actually having mono, I knew that I needed to try something. All of the current studies pointed to an anti-viral. And while I am still quite impaired and do not believe there is a "Cure", there have been many days since starting Famvir that I have felt as much as a 20% improvement to pre-Famvir and my family notices it, too, and I have only been on it for three weeks!

 

[Jonathan Edwards]

@Jonathan Edwards, I have never taken Thyroxine and take Armour Thyroid. My TSH levels are perfect now (around 1.0) with a very tiny micro dose of Armour (7.5 mg each morning.) That is why my endocrinologist felt that while I did have Hashimoto's (high levels of both antibodies and elevated TSH prior to Armour) he also felt that the severity of my unremitting fatigue and autonomic dysfunction/tachycardia were due to something beyond Hashimoto's. He suspected CFS even though he did not know how to treat it. He did not feel that Hashimoto's was a sub-type of CFS but rather that I have two distinct things. I do believe that the EBV could have set off the Hashimoto's although that I cannot prove!

That is interesting. As far as I know endocrinologists are very well aware that patients often continue to feel unwell after thyroid replacement but it is universally put down to 'taking a bit of time for the physiology to adjust'. I have over the years heard so many patients say that they still went on feeling unwell even years after taking a thyroid replacement and also patients having 'flu-like illness' when the Hashimoto's first appears that are clearly not due to low hormone levels (this is also recognised by the endocrinologist but ignored) that I came to think that the autoantibodies must be making people feel unwell quite apart from the effect on thyroid levels. And as I mentioned on another thread this is known to be the case in Graves's disease, where antibodies produce a number of problems quite serpate from the effect on the gland.

So I am not surprised that your physician thought there must be 'something more' and it would be reasonable to categorise it as CFS, but I think the cause is something endocrinologists have been staring in the face for decades - what I call ME4.

Just to clarify, when I said thyroxine I meant T4 in any form (or in fact T3 would do). Armour thyroid is a tissue extract that contains a mixture of T4 and T3 as I understand it, just not purified.

 

[Jonathan Edwards]

Dear SOC,
I did see that sentence on the Labtestonline site, but I think we have to read the whole thing in context. This is obviously a very condensed account designed to be relevant for common, simple situations and I don't think that is what we are needing. Most people having these tests done have had a very recent 'mono' like illness and the question is whether it is EBV infection or something else. So for these people it will be true that a positive result for EA and the other antigens will indicate a current or recent EBV infection.

But we need to take into account Bayes' theorem, which says that likelihoods are very dependent on what you already know or assume. If a person is known to have had EBV infection 2 years ago then the interpretation of the result is very different. I agree that CFS patients have symptoms like mono but we still have to reassess the statistical interpretation. IgG secreting plasma cells usually continue to produce IgG for at least 1-5 years. There are exceptions but this seems to be true for antibodies to common infections. So an infection 2 years ago could account for IgG EA. I think that this test was originally introduced in the hope that it would only be positive immediately after infection but the papers I have looked at suggest that since 1990 that has been regarded as not reliably so. The Holtorf/Lerner site Ema flagged up gives 12 references since 1990 and these are all for viral isolation or IgM EA. It doesn't look to me that anyone would take IgG EA as reliable in the last 15 years. The Labtestonline site just says 'recent' and that does not give us a firm answer.

As you say, at the bottom the Labtestonline site mentions reactivation occurring in immunocompromised individuals. The problem for me in the claim that ME patients are immune compromised is that the major research groups working on ME seem to be agreed that we simply do not know that. (And quite a lot of people on PR seem to get no problems with infection - something that researchers comment on as well.) When I chaired the IiME Research Colloquium I made a slide to put up at the end that started 'What do we already know'. It got a laugh from anaudience that included Dr Hornig, Dr Kogelnik, Dr Scheibenbogen, Dr Blomberg, Dr Newton, Dr Bansal, Dr Marshall-Gradisnik and several others and they all chimed out in unison 'nothing'. Nobody has a blood test that can be reliably predicted to even separate a population of ME patients from controls even on statistical grounds. I know
that because I am desperately trying to find one to help design a trial. I would not need Canadian Criteria if I could just do a blood test that said 'immune compromised'.

I am not arguing against the fact that there may be many physicians out there who know too little about MEs or are not interested. My viewpoint is based on what I have learnt from the most highly respected researchers in the field and it is them who say they cannot find virus present in ME. If I remember rightly both Dr Hornig and Dr Scheibenbogen, who have expert viral facilities deliberately went looking and did not find viruses.

The time course of IgM is not predictable (I know this from measuring these things with Dr Cambridge for the last 15 years) from one situation to another but we have a reasonable understanding of what stimulates its production. Whenever antigen is present freely exposed and not neutralised by IgG antibodies it will stimulate IgM producing B cells to turn into plasma cells and make IgM. If antigen continues to be around, as in rheumatoid arthritis, IgM production can go on life long. In infections it usually goes down because antigen is neutralised as soon as IgG is produced in bulk and IgM plasma cells do not live more than a few weeks. But if antigen contiues to be available IgM production should continue. Moreover, if there are danger signals either from infection or autoimmune mechanisms then IgM production can be stimulated in a non-specific way.

To be honest I do not think any of us, or indeed anyone else knows enough to be sure about any of this and that is the point I am wanting to make. We simply do not know enough to draw definite conclusions and that being the case we need to look at evidence critically - that is not an outdated approach to science, it is the only way to avoid producing a morass of uninterpretable half-truths. I am getting involved in these arguments because I am advising people wanting to set up drug trials that may involve significant risk to PWMEs. I need to know that facts are real facts, just as an airline pilot needs to know that the engineers have checked the landing gear and the radar equipment.

 

[Jonathan Edwards]

Dear Ema,
Can you refer me to papers by Montoya or Lerner showing the evidence for reactivated EBV infection in ME. Nothing about this was presented at the IiME conference as far as I am aware.

 

[Gingergrrl]

That is interesting. As far as I know endocrinologists are very well aware that patients often continue to feel unwell after thyroid replacement but it is universally put down to 'taking a bit of time for the physiology to adjust'. I have over the years heard so many patients say that they still went on feeling unwell even years after taking a thyroid replacement and also patients having 'flu-like illness' when the Hashimoto's first appears that are clearly not due to low hormone levels (this is also recognised by the endocrinologist but ignored) that I came to think that the autoantibodies must be making people feel unwell quite apart from the effect on thyroid levels.

So I am not surprised that your physician thought there must be 'something more' and it would be reasonable to categorise it as CFS, but I think the cause is something endocrinologists have been staring in the face for decades - what I call ME4.

@Jonathan Edwards I want to clarify that we are on the same page diagnostically b/c I can't tell from your last post. If you are trying to say that there is a sub-group that you have labeled as ME4 which have both ME/CFS and a separate, co-morbid diagnosis of Hashimoto's then I am in that group.

But if you are trying to say that ME4 just means that a person has Hashimoto's and NOT ME/CFS than I completely disagree with your hypothesis. There are of course individuals who have only Hashimoto's and even when they take medication and their TSH is perfect, they continue to have symptoms. This is explained well in books such as "Stop the Thyroid Madness" by Mary Shomon.

However, in my case, I did not improve even after my TSH was perfect b/c I also had undiagnosed ME/CFS triggered by having mono/EBV two years prior. I was having severe autonomic dysfunction and cardiac issues, soul crushing fatigue and PEM, and a whole list of stuff that could not be attributed to Hashimoto's alone. I desperately wanted to believe that it was all due to Hashimoto's and ended my medical leave and returned to work full-time for three more months only to get sicker and sicker.

Four doctors (an integrative psychiatrist, endo, cardiologist & naturopath) independently of each other felt I had ME/CFS. I began my research and saw that I met criteria for ICC and CCC definitions. When I finally went to OMI (still hoping maybe I didn't really have it) it was confirmed by my doctor who said I was a classic case of CFS and no doubt in his mind that this was my diagnosis. He had no doubt that I had a chronic viral-reactivation of EBV, which my body was not able to control, and anti-virals were my best bet (and in my case we chose Famvir.)

He also explained there was a significant co-morbidity between CFS and Hashimoto's (and what come first the chicken or the egg- I do not know) but they are two separate entities and I need to treat both. I am not saying any of this to be defensive (I know in my heart and soul that I have received the correct diagnosis at OMI and finally on the right treatment) but more so because you are a doctor who is voluntarily devoting time to understanding ME/CFS and helping us here on PR and I want to make sure that we are all really on the same page.

 

[Jonathan Edwards]

Dear Gingergrrl,
Don't worry. I am not wanting to make a diagnosis for you. I am simply trying to piece ME together, as I think you realise. My idea of ME4 is not just Hashimoto's. Most people with Hashimoto's do not have CFS symptoms, even if they have some unexplained symptoms in that sort of direction. Most people who I think might have ME4 have thyroid antibodies but normal TSH, I suspect. So ME4 would be a sort of cousin of Hashimoto's, with some mechanism in common related to autoantibodies but other things not in common. But it would not be so surprising if they turned up together. And as I indicated, this does not in any way rule out EBV triggering the CFS. I think I said I could see it as ME7 (EBV type) with a bit of 4 linked in or the other way around.

I tend not to see these processes as completely separate. I am used to thinking in terms of mechanisms with 50 interlinked steps. But I realise that for you it makes more sense to think of them separately. From the practical point of view your analysis has to be the right one because it leads to decisions. Mine is just speculation - maybe useful for decisions in the future, maybe not.

Maybe to put it another way I am not sure I am sure enough to put anything on a page yet. I am still moving my ideas around.

 

[Gingergrrl]

Dear Gingergrrl, I tend not to see these processes as completely separate. I am used to thinking in terms of mechanisms with 50 interlinked steps. But I realise that for you it makes more sense to think of them separately. From the practical point of view your analysis has to be the right one because it leads to decisions. Mine is just speculation - maybe useful for decisions in the future, maybe not. Maybe to put it another way I am not sure I am sure enough to put anything on a page yet. I am still moving my ideas around.

@Jonathan Edwards Thank you for explaining and I am happy when doctors take an interest in solving ME/CFS and I am the last person to claim to have the answers! I agree there may be 50 different mechanisms intertwined but that it was easier for me to separate them b/c (at least in the U.S.) each specialist sees and treats a different part of the body. My endo properly diagnosed and treated my Hashimoto's but didn't know anything about CFS. My cardiologist has also been wonderful but didn't know anything about CFS. My naturopath has helped me tremendously but has strong feelings re: natural anti-virals and supplements vs. meds (and seems to feel threatened by other perspectives.) Whereas my other doctors do not know anything about supplements. The first doctor to tie everything together for me and know about BOTH meds and supplements and communicate with my other doctors is Dr. Kaufman at OMI. He put all the pieces together which is very rare (at least in the U.S. where care is very fragmented.)

 

[SOC]

As you say, at the bottom the Labtestonline site mentions reactivation occurring in immunocompromised individuals. The problem for me in the claim that ME patients are immune compromised is that the major research groups working on ME seem to be agreed that we simply do not know that. (And quite a lot of people on PR seem to get no problems with infection - something that researchers comment on as well.)

To what major research groups are you referring? Clearly Dr Klimas and the people at the Institute of Neuroimmune Medicine (Klimas, Fletcher, Broderick) and the research team of Griffith University (Brenu, Marshall-Gradisnik, Staines) don't agree with you. Nor do the top ME/CFS clinicians who are using different immune modulators and antivirals.

What definition of ME are you using? I'm considering the ICC which says:

Myalgic encephalomyelitis is an acquired neurological disease with complex global dysfunctions. Pathological dysregulation of the nervous, immune and endocrine systems, with impaired cellular energy metabolism and ion transport are prominent features.

A. Postexertional neuroimmune exhaustion (PENE pen’-e): Compulsory

This cardinal feature is a pathological inability to produce sufficient energy on demand with prominent symptoms primarily in the neuroimmune regions.
.
.
.
1. Flu-like symptoms may be recurrent or chronic and typically activate or worsen with exertion.e.g. sore throat, sinusitis, cervical and/or axillary lymph nodes may enlarge or be tender on palpitation
2. Susceptibility to viral infections with prolonged recovery periods

While I think we can all agree that the precise nature of the immune dysfunction is not yet fully established, research done on well-characterized patient cohorts is showing abnormalities in the areas of NK cell number and/or function and CD8+ cell numbers.

As we all know, to our great dissatisfaction, research claiming to include patients with ME/CFS include people who probably do not have the neuroimmune illness we talk about here at PR. That has distorted the body of research literature on a number of physical abnormalites in "CFS". I prefer to look at the more recent literature using patients that meet the CCC or the ICC.

Certainly we are much too early in the research history of ME/CFS to claim that there's any well-established knowledge/treatment for ME/CFS. The research into the physical abnormalities of the illness is far too new to have made its way into medical textbooks and the knowledge base of most physicians. That does not mean that patients should have to wait until any ME/CFS treatment is accepted by the medical mainstream, which will take 10-20 years, before they get appropriate treatment.

When I chaired the IiME Research Colloquium I made a slide to put up at the end that started 'What do we already know'. It got a laugh from anaudience that included Dr Hornig, Dr Kogelnik, Dr Scheibenbogen, Dr Blomberg, Dr Newton, Dr Bansal, Dr Marshall-Gradisnik and several others and they all chimed out in unison 'nothing'.

I think you may be misrepresenting Drs Kogelnik and Marshall-Gradisnik, if not others, if you are suggesting that because an audience in which they were included chimed out "nothing" in response to "What do we already know?", they think we know literally nothing about ME, particularly about immune dysfunction in ME.

Nobody has a blood test that can be reliably predicted to even separate a population of ME patients from controls even on statistical grounds. I know that because I am desperately trying to find one to help design a trial. I would not need Canadian Criteria if I could just do a blood test that said 'immune compromised'.

Yes, we are early in research and we're not even sure we can separate ME/CFS patients from other groups with idiopathic fatigue. That doesn't mean our researchers literally think we know nothing about the illness, or that patients who have lab results showing immune dysfunction should not be treated for chronic infections and immune dysfunction when possible.

We patients can't wait 10-20 years until there's a fully certified blood test for ME/CFS before we get treatment that will improve our conditions. Many of us will be dead before then, and huge numbers of us will have lost any form of normal life -- which is something of a living death in itself.

We can agree to disagree about immune dysfunction in ME/CFS. I've kept a copy of this discussion so 10 years from now you and I can discuss the wisdom of our different approaches during those 10 years once the research has actually played out. If thousands of patients have died or become seriously impaired by the use of immune modulators and antivirals during that time when it turns out those treatments were completely unnecessary, I will humbly concede that my position was totally wrong and harmful to the patient population. If, on the other hand, it turns out that ME/CFS patients are immune impaired, but thousands of them lived in misery because they were denied necessary immune modulators and antivirals,... well, I leave that up to you.

I sincerely hope that your investigations into the autoimmune aspects of ME/CFS reveal the truth about the illness, and provide a treatment path for the many suffering patients. I am confident that I am only one of tens of thousands of patients who are grateful for your efforts on our behalf.

 

[Gingergrrl]

Wow, @SOC, I was going to quote your post but don't even know where to begin because you made so many outstanding points! All I can add is that my doctor at OMI referred to CFS as "Viral re-activation disease caused by immune system impairment." These are his words not mine and when he offered me the anti-viral treatment, it was the first moment that I felt even a glimmer of hope that I could get my life back.

What kills me is that I have the opportunity to get tested and to try an anti-viral while people outside of the U.S. (except for KDM patients and a few other exceptions) do not. That is a tragedy to me that I do not know how to fix (but that would also take this thread off topic so I will leave it at that.)

 

[barbc56]

We patients can't wait 10-20 years until there's a fully certified blood test for ME/CFS before we get treatment that will improve our conditions. Many of us will be dead before then, and huge numbers of us will have lost any form of normal life -- which is something of a living death in itself.

While I understand the sentiment of this statement, I don't understand the thinking.

If we jump to therapies that are not up to scientific scrutiny, this only detracts from the causes of me/cfs. Maybe if only science based treatments had started many years ago, we might have better options today. I'm talking about science based medicine which is a bit different that evidence based medicine. Click this link for a description of the difference between evidence based and science based medicine.

http://saveyourself.ca/articles/ebm-vs-sbm.php


I know it's frustrating but we may not have any choice at this point in time. Yeah, that's really depressing but we want to find out what is going on with patients and sometimes this takes time.

I know this is not a popular notion. It's not for me but I think it's an important issue. We may not have something in our lifetime but if it helps the next generation, so be it.

I guess to sum it up is do we go with the devil we know or the devil we don't know. I know what my choice is but others may disagree.

Barb

I find it greatly disappointed that some of the me/cfs "experts" are treating patients with treatments which may be problematic and possibly harmful..

 

[Gingergrrl]

I guess to sum it up is do we go with the devil we know or the devil we don't know. I know what my choice is but others may disagree.

I find it greatly disappointed that some of the me/cfs "experts" are treating patients with treatments which may be problematic and possibly harmful..

@barbc56 What is the devil that we know versus don't know in regard to CFS? I am honestly not sure what you mean since there is no standardized approved treatment that I am aware of?

I was also curious which treatments you meant were harmful? I can only speak for myself but I am taking Famvir which is FDA approved for herpes and shingles with many research studies showing that it has helped EBV (which is also a herpes virus.) I don't feel it is that risky and I am taking it at a much lower dose than others I have compared with. I am a pretty cautious person but do not see this as a risk. The thought of not trying and living my life in it's current state is more of a risk to me.

 

[heapsreal]

We arent talking cures but there is enough people on here who have improved greatly by treating infectious agents with antivirals, antibiotics and immune mods etc. These treatments arent just given to patients without any thought but are used after what testing is available and a smart thinking doctor who is joining the dots.

To say these treatments are dangerous just doesnt make sense because if they were as dangerous as some are making out then they wouldnt even be on the market. These patients are being monitored by their doctors, so if issues arise then they can be treated accordingly. Theres also a risk to benefit ratio and many believe that not treating cfs/me is a much bigger risk.

Lets look at antidepressants being prescribed, doctors dont test for a great deal before prescribing these, when was the last time anyone heard a doctor testing a patients serotonin levels before prescribing an ssri. This sort of non science medicine i think is alot more dangerous then antiviral treatments which are tailored to patients and monitored closely with blood work.

Its just insane to tell people to wait for science to develop some type of treatment or cure for cfs/me. Maybe say this to someone who has had cfs/me since the tahoe outbreak in the mid 1980's, yep just need to wait another 10 or 20 years for a treatment, dont worry about your quality of live.

Its this off label treatment by experts like dr lerner and dr montoya and co who have kept research going in cfs/me, not to mention the amount of patients who are greatful for reducing their pain and suffering.

I have thought many times on where i would be if i hadnt had treatment for viral infections. I probably would have lost my job, my house, maybe my family. Then i would have been pushing shit up hill to get an ME diagnosis to obtain a disability pension. Then i probably would have ended up with many other comorbid conditions with all the things that come along with severe chronic illnesses.

So for someone to tell me that taking antivirals is dangerous and i should wait 10-20years for some type of treatment is just rediculous and stupid. This would have cost me so much in many ways.

I am currently able to keep working 30hrs a week and support my family and able to keep my house and able to keep making my house payments which keeps a roof over our heads of my family and myself. My symptoms are greatly reduced, so my pain and suffering isnt anywhere near as bad as i once was. Am i cured, no, but i would be in alot worse a place if i hadnt gone after treatments.

Doctors like montoya, lerner, klimas, peterson, cheney, koglenek, chia etc etc are all trail blazers and have done so much for cfs/me. Any new doctors entering this new field would benefit greatly about this illness if they would only look into the research these gurus have created, they not only have theoretical knowledge and experience but even more important is alot of hands on clinical experience treating cfs/me patients, some have treated thousands. Just cant beat that type of experience.