Speculation about drug reaction

I ended up stopping tenofovir after five days. The symptoms that I experienced when I added the tenofovir were more consistent with a flare of my disease than anything to do with the known toxicity profile of the drug. In addition I had repeated my TGF beta-1 (the only potential marker I’ve ever found of my disease) and C4a which was high normal at baseline. TGF beta-1 was still astronomically high and C4a shot way up, on AZT/raltegravir, even though I didn’t feel worse when the labs were drawn. Shortly after that draw, I started to feel and function much better, then plateaued until I started the tenofovir. Repeat TGF beta-1 and C4a from just prior to starting tenofovir are pending. By the way, I am having safety labs every two weeks (blood count and metabolic panel).

I am following eight X+ patients from a distance (and one long term CFS patient who has chosen to start treatment with a negative culture). It is a mixed bag so far, but the two people I know of that started raltegravir alone didn’t do well in very short order (days). AZT alone seems to bring about a very modest improvement with little problems over a month or so, which is when the three patients I was following who were on it alone added raltegravir. Very small numbers and completely uncontrolled, but it’s all there is for now.

I took tenofovir for five days, by which time I was quite a bit worse than before I started it. At that point, I decided to stop raltegravir as well. It turns out that tenofovir can raise the level of raltegravir though it doesn’t seem to be clinically significant in AIDS patients (Raltegravir drug interactions). It is possible that raltegravir is such a potent inhibitor of XMRV integrase that there is a build-up of unintegrated DNA in the cell cytoplasm. DNA in the cytoplasm could activate production of interferons and thus, a resultant inflammatory response.  That is how it felt to me. Treatment with interferon alpha (example is treatment of Hepatitis C) can be associated with a plethora of side effects, many of which are CFS-like symptoms. 

Below are links to a few papers on measurement and modeling of the decay characteristics of HIV with treatment. It is worth noting that there is a first-phase rapid decay and a much slower second-phase decay. Though the exact mechanism for the later is still unknown, it is likely related to the infection of long-lived cells. Second-phase decay in AIDS patients treated with HAART takes years.

Personally, I feel best about AZT right now of the three drugs available. It prevents replication at the most basic point in the virus’ life cycle. It is the broadest spectrum if you will. It has been around the longest. There is vast experience with it over many years of treatment. It may be that raltegravir requires reduction of viral load before adding. Or it may be that we are like the genetically susceptible infected mice for whom it isn’t the right drug (Raltegravir autoimmunity). We desperately need viral load measures and organized clinical trials. But until then, I’ll keep reporting… 

I have heard from people considering AZT alone, sometimes at below HIV doses. I would still prefer more than one drug. We can’t know anything about how readily this virus will become resistant to drugs. We don’t know anything about XMRV’s RT error rate. We don’t know anything about viral load in target tissues.

I stayed off both drugs, on AZT alone, for 5 days. I continued to get sicker until I was well below baseline. Last night it seemed clear to me that I had been better off on the AZT/raltegravir protocol, so I decided to go back on raltegravir. Amazingly, I feel much better today. The horribleness seems to be fading into the background again. I am reporting now because I don’t know how it is going to turn out. But it is an almost A-B-A experiment. However the experiment turns out, what has happened already greatly surprises me.

It would have been a fairy tale if the drugs had just worked. So much for logic! I actually didn’t expect it to be that easy. The good news is that if the drugs can move the illness, it is supportive of the hypothesis that XMRV is causative in the pathogenesis of the disease. It seems to me, that if altering the viral load, or altering the build-up of viral particles in the cytoplasm can shift the clinical picture in either direction in days or weeks, viral replication must not be so slow. It is a pretty stunning observation if you think about it. Must be a really good (successful) pathogen to be replicating so freely in relative equilibrium with the host over so many years. Doesn’t kill for a very long time. Clinical observation is that trying to alter things often doesn’t work out so well with CFS patients. Hence the observation that the patients are “sensitive”. Actually I think we are very tough.

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6 thoughts on “Speculation about drug reaction

  1. >Jamie, thank you for sharing your experience with us Me/CFS patients. It is very valuable! I would like to know if you are worried about mitochondrial dysfunction that AZT can cause? (Of course there is always benefits and drawbacks to any decision one takes)

    Thank you and good luck !

  2. >dr. deckoff-jones,

    thanks again for keeping us informed on all this. it is invaluable information!!! and it is amazing indeed that within one night/day, you noticed a difference in how you feel when you re-started the raltegravir with the AZT.

    if the 8-9 other xmrv+ (and one xmrv negative) folks you know who are taking these same meds are willing to let you post more about their experiences (anonymously), that would also be helpful to us.

    i know that turns you into a conduit for their info, but it could be so helpful.


  3. >just wanted to say thank you. i've suffered from this for a long time too and with fibro which makes my life a living hell… it's hard to have hope but you have given me some today. ~laura tattoo xoxoox

  4. >Thank you so much for the early reporting. It is on all of our minds.

  5. >Dr. Deckoff-Jones,

    Can you comment more on the TGF Beta as a marker? What is considered astronomically high?

    I am particularly interested in your CFS case because my highest aberrations are also C4a and TGF beta. Also, like you my fatigue/PEM tends to be much more on the cognitive side than the physical side.


  6. >I've also taken that medication before and it worked for me. There are some medicines that I've taken in the past that makes me sicker and have allergic reactions at the same time. Allergic reactions can happen if medicines are not measured well so the companies are now upgrading their near infrared technology to ensure clients excellent medicines.

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