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Author Topic: Change regimens because of barely detectable viral load?  (Read 1593 times)

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Change regimens because of barely detectable viral load?
« on: February 13, 2012, 08:25:20 AM »
Any advice or thoughts would be greatly appreciated.
Tomorrow I have an appointment with my doctor.  Iíll get my latest labs and will need to decide whether or not to change my drug regimen. My last three labs over the past nine months have each shown barely detectable viral loads (between 10 and 40 copies) with no real change in my CD4. Over the years, Iíve had occasional tiny blips in viral load but never a sustained period like this. Should I jettison this otherwise satisfactory treatment because of these low viral levels if my latest labs continue the pattern?
Some background info: Iíve been on treatment for about 12 years. Iíve been on various regimens, but never failed one. Iíve changed regimens for various reasons, principally due to side effects. Five years ago genotypic testing showed my virus to be susceptible to all drugs. Currently taking Norvir, Reyataz and Truvada.

Offline newt

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Re: Change regimens because of barely detectable viral load?
« Reply #1 on: February 13, 2012, 10:05:17 AM »
In answer to your question about changing combo, personally, I think no. I wouldn't.

The target is a viral load consistently under 50/40, not beating the test.

- matt
"The object is to be a well patient, not a good patient"

Offline eric48

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Re: Change regimens because of barely detectable viral load?
« Reply #2 on: February 13, 2012, 06:35:43 PM »

Clinically speaking, I, personally, not being a doc, tend to agree with the above.

The VL is coming from somewhere. Everyone, even with VL below 1, had some tiny VL.

2 suspected and possible sources:
- cellular (most probably latent CD4, this is the research lead by Dr Siliciano at J hopkins and others) (school A)
- compartmental (organic): an other group is claiming that the virus also hides in some isolated part of the body (can't remember the research group but work is quite convincing) (school B)

Both seem to agree that it is clinically irrelevant for the patient, yet, their opinion differ and matters in looking for a cure.

School A hopes that, for those patients who do not have the problem identified by school B, it is worth pursuing eradication attempts. On the millions of people under treatment, there is, statistically, a number of people, not yet identified, who could benefit from School A R&D and achieve some kind of a 'cure' (there are several proposed scenarios)

Once this is demonstrated, then, most likely the effort by group B to clear anatomical reservoirs will become relevant.

Whenever I have a meeting with my Doc, he is quite insistingly developping the current argument within the scientific community whether it is worthwhile to have commercial instrumentation than can measure below 20, since, as stated above, there is no demonstrated clinical relevance. I realized he was kind of trying to get my opinion since I work in that industry. In other words, he is repeatedly asking MY opinion.

I decline, since, I would have to charge him my hourly rate ;-)

I pay him for his opinion and not the other way around.

My opinion is irrelevant, nor is the opinion of ANY doctor in the field. Cobas Taqman is manufactured by Roche. Version 2.0 reaches a detection limit of 20. with a very good accuracy and analytical confidence. There are already some preparation techniques out there that can improve this, at fairly low additional cost, but not with 100% confidence. There is currently no instrument in real competition with Roche on that spec. Once there is, then the manufacturers will compete again to grab or keep their market share. Until then, Roche is keeping competitive margin under the hood. There are also some manual, labor intensive, methods for research labs to go down to 1, but that is for R&D only.

As soon as one manufacturer comes on the market with an instrument capable to challenge the leadership of Cobas Taqman, (and not until then), there is no reason to believe that Roche will not be able to integrate the laboratory twicks in their instrument, and offer a guaranteed detection limit of 10 or 5 to commercial labs. Once one commercial lab gets this improved instrument, then competition and willingness to keep market share will push other labs (in competitive environments) to get this newer instrumentation. Non competing labs (such as the VA) are fine with a detection limit of 75. Most hospitals are fine with 40 or 50.

The only reason why there is no instrumentation going down to 10 or 5 or 1 is simply that there is no economical or strategic reason for corporations do unveil such instrumentation. There is no public funding either.

There are arguments in favor of improving the detection limit. One of which is to identify those patients who have smaller reservoirs and have a larger pool of candidates for eradication trials.

There are arguments against improving the detection limit. One of which is that it creates useless patient anxiety.

That being said, anatomical reservoir is not a minor issue in a very limited number of cases. there is one (and one only) case report of a patient whose brain what not getting enough of raltegravir and hence developed resistance to RAL in the brain. The case reports are very very few. At that point, the resistance gets detected and a change of combo solves it.

Better penetrating drugs may seem attractive, but, as they penetrate more into the compartments (e.g. the brains) you do not know what collateral damage they may create on the long run...

If you are satisfied with the immunologic and virologic response of the drug, then there is no reason to change regimen. there is no reason why not change either.

It is a personal choice. I, for example, am a listed applicant and volunteer for eradication trials (my application not yet approved). then, it makes sense for me to include in my combo selection criterias the penetration capabilities of the meds.

In the situation you describe (where you do not report any neurologic or brain related issues), I do not see any rationale in changing combo

Hope thishelps put things in perspective

NVP/ABC/3TC/... UD ; CD4 > 900; CD4/CD8 ~ 1.5   stock : 6 months (2013: FOTO= 5d. ON 2d. OFF ; 2014: Clin. Trial NCT02157311 = 4days ON, 3days OFF ; 2015: https://clinicaltrials.gov/ct2/show/NCT02157311 ; 2016: use of granted patent US9101633, 3 days ON, 4days OFF; 2017: added TDF, so NVP/TDF/ABC/3TC, once weekly


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