Tenofovir (Viread) / Raltegravir (Isentress) Cures ME/CFS Patient Sick for 20 Yrs + Tenofovir Poll

[Hip]

some of Dr Weir's patients moved from 20 on the Bell scale to 80-90 using tenofovir

If we equate 20 on the Bell CFS Ability Scale to say half way between moderate and severe ME/CFS, and 89-90 on the Bell scale to somewhere between mild ME/CFS and remission, then that jump is a two-level improvement on the scale of Severe ➤ Moderate ➤ Mild ➤ Remission/Cured.

 

[fingers2022]

I think I'd call my improvement a "long-lasting" one rather than "permanent". I am realistic about the fact that this could just be a window of partial remission. I have had boths ups and downs during the time since I stopped Viread/Tenofovir. My ability now is substantially higher than it was in 2015 - when I could hardly function at all. However I have had dips that halved the gain for a period of time.... thankfully I'm currently not in a dip.... BUT I am very aware that my well-being is still ... what's the word? .... tentative?

Or Tenofovirtative?
Some good discussion. I must check out that severity scale - is it function-based? Absolute or relative to pre-ME?
Hang on, I'll be back.

 

[fingers2022]

If we equate 20 on the Bell CFS Ability Scale to say half way between moderate and severe ME/CFS, and 89-90 on the Bell scale to somewhere between mild ME/CFS and remission, then that jump is a two-level improvement on the scale of Severe ➤ Moderate ➤ Mild ➤ Remission/Cured.

I find the wording of the Bell scale very difficult to interpret, making it difficult to apply.
What does 'expected' mean? It could mean average function of person of same age and gender. Or it could mean what the person could achieve pre-ME (possibly adjusted for age if they became ill many years ago).
Also 'no symptoms at rest' is useless. We all get symptoms at rest - it's called PEM ffs! I think it should read 'no symptoms if no physical exertion undertaken'.
Next, the percentages don't align very well to the qualitative descriptions.
Another...'mild/moderate/severe' symptoms - it needs a definition of what these designations are. They are separate to function. So, for example, someone may feel like complete crap but still get out of bed and go to work - does the fact that they got out of bed say that their symptoms were mild? I think not.
Without wishing to blow one's own trumpet, one reason I've maintained physical fitness in 26 years of ME is that I frequently exercise when I feel bloody awful. I have lived with a lot of PEM. I know I'm lucky to be able to do this and eventually recover. It's personal choice, with some luck thrown in - I do count my blessings compared to others who can't get near this. However, I see otherwise healthy people who do physically far less than I do. That's their choice, but it says to me that we all have different levels to which we are prepared (or motivated) to push ourselves, and different standards of what level of discomfort we are prepared to tolerate.

Sorry, that sort of turned into a rant - I hope not, just trying to further the discussion.
Very good day today BTW
Ask me again tomorrow lol

 

[Keela Too]

Or Tenofovirtative?

Not sure what you mean? I was on Tenofovir, which is also called Viread. - or are you referring to my tentative remission?

Some good discussion. I must check out that severity scale - is it function-based? Absolute or relative to pre-ME?
Hang on, I'll be back.

When I was most ill, I always said I was moderate - but looking back, I think I was severe, or at very least, at the severest end of moderate. Denial plays a part in how you describe yourself. Anyway, I was horizontal most of every day (but I chose to recline on a recliner in the kitchen, rather than in bed) and I left that -almost totally horizontal state- for only very short periods each day. Longest probably about 2 hours in one go, but that came with payback. Mostly it was 15 to 20 minute upright-ish at a time. I didn't do standing, and walking was only to the bathroom and back.

At that stage every time I allowed a payback /PEM incident my long-term ability levels were pushed lower and lower - it was a sort of ratcheting downwards thing. It was frankly scary. ANY small thing I did (and in no way was I ever "pushing" myself - certainly much less than I'd have pushed myself when well) had dramatic effects on my ongoing health. I was in a bad place when I started the drug.

I think there are some folk who can get away with taking a day or two of PEM, and a week later they get back to where they were previously. I didn't seem to have that luxury. Even a small activity that I felt I'd coped with on the day, could end up leaving me permanently less well. I know all this from having measured things like my step-count etc.

If it's possible to say that ME has different versions like MS has, (eg a relapsing/remitting version and a progressive version) then I'd say I had the progressive version of ME.

Now I still get some small measure of PEM (a feeling of a virus returning, not just tiredness) but it is much milder, and I don't think it has the same potential to alter my long term abilities. It helps also, if I do things slowly... if I try to hurry and use any aerobic capacity, I quickly am unable to do so, and the after-effects are more unpleasant. So I'm learning to accept that although I can now achieve more, I cannot return to my old ways (pre-ME) of dashing about doing stuff at speed.

Although I might appear "well" to others, and certainly I am "well" in comparison to where I was in 2015, I am not "well" in how I react to aerobic exertion. Basically that has not been restored.

 

[Keela Too]

Without wishing to blow one's own trumpet, one reason I've maintained physical fitness in 26 years of ME is that I frequently exercise when I feel bloody awful.

This is totally opposite to how I was. I think you were lucky to be able to do this.

Edit to add - Or perhaps as illness duration increases the sensitivity to exertion - and the long term damage it might do - decreases? I only became ill in early 2012, so was still in comparatively early days (years)! ??

 

[heapsreal]

If there is only 2 people who did try this or three this is not the patients mistake ! It's the medical system issue !


Why we don't get ARV trials like ALs or MS ?

Because they think its a psych issue.

 

[Keela Too]

That's their choice, but it says to me that we all have different levels to which we are prepared (or motivated) to push ourselves, and different standards of what level of discomfort we are prepared to tolerate.

No.. I disagree - it is not a personal choice. See my above post #145. Sometimes it is the illness that dictates how very little we must do. xx

 

[heapsreal]

I will post this again just to confuse people. It shows tenofovir reduces inflammation but also increases immune function. The big but is if its treating a RV than it will also increase the immune function if the RV is immune suppressive similar to hiv. Treating a RV will also reduce inflammation. Bottom line is we dont know really how it works but the obvious reason is a RV and researchers should be looking for it before falling back on it only working on inflammation etc. Agree with the above with a treatment trial of cfs patients starting with specific immune abnormalities like low nk function and a general leaning towards the immune system looking like its fighting some type of infection.

https://www.poz.com/article/hiv-tenofovir-inflammation-20217-1101

 

[lansbergen]

Or perhaps as illness duration increases the sensitivity to exertion - and the long term damage it might do - decreases?

Don't think so

 

[fingers2022]

No.. I disagree - it is not a personal choice. See my above post #145. Sometimes it is the illness that dictates how very little we must do. xx

I do agree, for me too, sometimes there is really no choice, have to rest unless I want to go backwards - I call them my viral cycles, they are pretty frequent. Although Tenofovir seems to me shortening them and making them less severe.

 

[fingers2022]

I will post this again just to confuse people. It shows tenofovir reduces inflammation but also increases immune function. The big but is if its treating a RV than it will also increase the immune function if the RV is immune suppressive similar to hiv. Treating a RV will also reduce inflammation. Bottom line is we dont know really how it works but the obvious reason is a RV and researchers should be looking for it before falling back on it only working on inflammation etc. Agree with the above with a treatment trial of cfs patients starting with specific immune abnormalities like low nk function and a general leaning towards the immune system looking like its fighting some type of infection.

https://www.poz.com/article/hiv-tenofovir-inflammation-20217-1101

Although the article posted by Nandixon (if I understand it correctly) talks about different pathways of action. Does this mean that researchers can actually tell how a drug like Tenofovir is working, i.e. as RV or as cytokine regulator?

Here's that link again (credits Nandixon):

Tenofovir selectively regulates production of inflammatory cytokines and shifts the IL-12/IL-10 balance in human primary cells

 

[Hip]

I find the wording of the Bell scale very difficult to interpret

I am not so keen on the Bell scale either. When the Bell scale says something like "activity levels 30% compared to the healthy state", it's actually quite hard to get a sense of what "30%" means.

That's why I like the mild, moderate and severe scale, because when you read the descriptions of these three levels, most ME/CFS patients can instantly place themselves in the correct level (there is also a "very severe" level, on this scale, which is quite distinct from severe).

There are other ME/CFS scales, such as Dr Lerner's Energy Index Point Score (which is perhaps a bit easier to relate to than Dr David Bell's CFS Ability Scale). And there is Dr Charles Shepard's ME Disability Scale (which is reasonably easy to understand).

And there is the ME Ability and Severity Scale devised by ME/CFS patient Jodi Bassett (which is interesting in that it uses one scale for physical abilities, and another for cognitive abilities; there are some ME/CFS patients who have far more physical disability that cognitive disability, and vice verse, so it makes sense to measure these two facets separately).

Does this mean that researchers can actually tell how a drug like Tenofovir is working, i.e. as RV or as cytokine regulator?

It's known that tenofovir works both as an antiretroviral and a cytokine regulator, and that both of these mechanisms could potentially explain this drug's benefits in ME/CFS. But as to which one of these two mechanisms is responsible for the benefits, that's not known at this stage. It could be that both mechanisms are responsible.

 

[fingers2022]

It's known that tenofovir works both as an antiretroviral and a cytokine regulator, and that both of these mechanisms could potentially explain this drug's benefits in ME/CFS. But as to which one of these two mechanisms is responsible for the benefits, that's not known at this stage. It could be that both mechanisms are responsible.

From the study abstract: "The observed drug-induced changes in cytokine production were independent from transcriptional regulation through the mitogen-activated protein kinase and nuclear factor kappa B pathways."
This suggests that it would be possible to conduct a trial which looks for correlation of perceived (or objectively measured) benefit in ME/CFS with regulation of cytokine production which is independent from transcriptional regulation. If that showed a statistically significant correlation, I think we'd all say 'sod the RV theory' let's just get on it anyway.
I'm still quite liking that there are at least two possible ways this $h1t may be working.
I'm well into my 4th month now - I think that's around about the time that CD counts go up with ART. Feeling pretty good. No discernible side-effects whatsoever.

 

[Keela Too]

I'm well into my 4th month now - I think that's around about the time that CD counts go up with ART. Feeling pretty good. No discernible side-effects whatsoever.

Sorry probably being dumb here but "CD counts"?
I'm assuming when you say ART you mean Anti Retroviral Therapy (and not Agressive Rest Therapy, which is what I have also seen ART refer to. )

I had a significant up tick at 16 weeks. Hoping you also will experience that.

 

[fingers2022]

Sorry probably being dumb here but "CD counts"?
I'm assuming when you say ART you mean Anti Retroviral Therapy (and not Agressive Rest Therapy, which is what I have also seen ART refer to. )

I had a significant up tick at 16 weeks. Hoping you also will experience that.

White blood cell counts - don't know if this is the best source...
http://www.aidsmap.com/CD4-cell-counts/page/1044596/

Haha, yes Aggressive Rest has proven particularly effective for me, but I get too restless.
Thanks for the good wishes on the week 16 uptick

 

[Binkie4]

@ Keela Too
I hope you don't mind if I ask if you tried antivirals first since quite a few people in UK are using them. I have only just got to hear of tenofovir. Do you know what is the determinant of whether your doctor sends you down the antiviral route or tenofovir.

I am in 6th month of treatment with Dr Bansal on acyclovir. May be beginning to see some improvement but I have been diagnosed as needing a mitral valve repair which is contributing to symptoms so it's difficult to estimate.

Aggressive rest is all that's possible for me at the moment.

I am glad you have achieved some improvement Sally. I wondered what your treatment was when I read your blog. I have a lot of reading to do to get to grips with this thread. Hope you continue to see improvement.

 

[Keela Too]

I didn't try antivirals first. Perhaps I should have, but this was suggested to me, and so it's what I took. I'm not sure that knowledge is far enough on yet with any of these treatments to work out what works for whom... I feel a lot of it is largely down to luck. I feel like I was very lucky, and I sure hope that luck holds

@Binkie4 Wishing you every success with the treatments you are on. We are all just flailing in the dark at the moment I fear. One day the science will catch up and help us properly.

 

[NelliePledge]

I have received word (albeit secondhand) that some of Dr Weir's patients moved from 20 on the Bell scale to 80-90 using tenofovir monotherapy for 6 months. He has said that getting them through the IRIS is the toughest part because he doesn't use steroids in the fear it will make them worse again

Sorry if this is a basic question what is IRIS an acronym for?

 

[Jesse2233]

@NelliePledge IRIS = Immune Reconstitution Inflammatory Syndrome

It's a phenomenon seen in AIDS. This is a pretty interesting read (may deserve it's own thread due it's similarities to a "Herx").

Note that this quote is in the context of AIDS and not ME/CFS

Some people who start antiretroviral therapy (ART) get health problems even though their HIV comes under control. An infection that they previously had might return. In other cases, they develop a new disease. This is linked to improvements in the patients’ immune systems. The problems usually occur in the first two months after starting HIV therapy. This condition is sometimes called Immune Reconstitution Inflammatory Syndrome or IRIS. It may occur in about 20% of people starting ART.

-----

Several patients developed cytomegalovirus (CMV) disease after they started HIV treatment. See Fact Sheet 504 for more information on CMV. In some cases, these patients had not been diagnosed with CMV before they started HIV treatments.

Doctors concluded that these patients were infected with CMV before their HIV treatment. However, their immune systems had been too weak to react to the CMV. When they started HIV treatment, their immune systems got stronger and then they responded to the CMV. That’s when the patients developed what looked like a new case of CMV disease.

There were similar cases in other patients and with different infections. It was called “immune recovery syndrome.” Some patients developed fever and swollen lymph nodes. Others had inflammation in various parts of their bodies. Nearly all started ART with very low CD4 (<100) cell counts. These problems showed up after the patients had a large increase in their CD4

-----

No one wants to develop inflammation or an infection. However, most cases of immune restoration syndrome go away with continued HIV treatment.

What’s probably more important is in the name of the syndrome: immune restoration. It is a sign that the immune system is getting stronger. It also shows that the immune system is responding to specific germs. Before HIV treatment, there might have been no response to these germs because the immune system was too weak.

Even in patients who develop immune reconstitution syndrome, antiretroviral therapy should be continued.

---------------------

WHAT PROBLEMS CAN OCCUR WITH IRIS?

IRIS has been linked with the several types of infections or inflammation including:

Cytomegalovirus: CMV IRIS can affect different organs, including the brain, eye and colon.

Cognitive (memory and thinking) problems:

Cryptococcal Meningitis: See fact sheet 503 for more information. The first symptoms are headaches and fever.

Hepatitis B and C: Some of these were cases of hepatitis C that had not previously been diagnosed. Fact Sheets 506 and 507 have more information about hepatitis.

Herpes Zoster (Shingles) and Herpes Simplex outbreaks. Fact Sheet 509 has more information on shingles. Fact Sheet 508 discusses herpes simplex (cold sores and genital herpes.)

Molluscum Contagiosum (a viral skin infection. See fact sheet 513).

Mycobacterium Avium Complex (MAC): This opportunistic infection is caused by a bacteria related to tuberculosis. It can flare up during immune recovery. MAC IRIS during immune recovery may show unusual symptoms, including fever, fatigue and night sweats. Fact Sheet 514 has more information on MAC.

Progressive multifocal leucoencephalopathy (PML): See Fact Sheet 516 for a description of this viral brain infection. Immune recovery can cause a serious worsening of PML.

Swollen lymph nodes, also called “lymphadenopathy.” This can indicate general immune activation.

http://www.aidsinfonet.org/fact_sheets/view/483

 

[Jesse2233]

I went back and looked at my notes from a conversation I had with a doctor who corresponded with Dr Weir on ME/CFS treatment and notes from talking to one of his patients.

• It appears Dr Weir has only treated a handful of ME patients with tenofovir to date
  
  
• He uses tenofovir monotherapy in a single daily dose of 245 mg because that's what he can get in the UK
  
  
• His first two patients went to 85-90% on the Bell scale from around 10%
  
  
• He stopped treatment at one year because of concern for long term side effects
  
  
• He believes a year of tenofovir treatment helped these patients' immune responses clear a retrovirus
  
  
• He has had patients show no response after 6 months
  
  
• Two further patients recovered to 90% on the Bell scale. It's not clear where they started
  
  
• IRIS side effect can happen in month 3 or 4, sometimes it's severe, and in one patient treatment was stopped because they could not tolerate it
  
  
• Steroids are not advised to help with the IRIS since it would defeat clearing the retrovirus
  
  
• Dr Weir would like to know how to identify responders, whether 1 year is enough time, and if just tenofovir is all that's required or if a cocktail would be better (similar to ones seen in HIV)
  
  
• He has heard from an old patient in France who recovered by combining tenofovir and raltegravir (as @Hustler/@Elkyare did).
  
  
• He believes that ME/CFS is more likely to show full remission and allow for discontinuation of ARVs than HIV due to the occasional spontaneous recovery seen in his ME patients
  
  
• He posits that responsiveness to ARVs is due to a patient's unique immunological profile. Dr Weir bases this on his background in tropical disease and the different drug cocktails needed to treat leprosy
  
  This is doubly interesting because Dr Richard Horowitz is now using Dapsone (a leprosy drug) to treat Lyme.
  
  
• Dr Weir believes that the ME/CFS retrovirus damages the mitochondrial genome in some way, and that is the core problem causing symptoms
  
  
• He wishes that a double blind, large study could be done examining mito function and mito genome of ME patients before, during, and after ARV treatment. He unfortunately does not have the funding for this and is nearing retirement.

Man wouldn't it be great if Dr Weir, Dr Chia, Dr Nath, Ron Davis, and Ian Lipkin could all get in a room together and discuss this.