Questionable medical advice?

[tamsinasia]

I started treatment in August 2008 with a CD4 count of 155 and viral load of +/- 650,000.  I responded well to Atripla, and by January 2009 my CD4 had risen to 511 and my viral load had dropped to 57.  Then I moved to Thailand and switched to Stocrin + Viread + Lamivir (3TC).  This is is lieu of Atripla not being available in Thailand, and I am aware that Viread and Stocrin (Sustiva) are also components of Atripla.

My problem is that my recent lab results are poor.  My CD4 fell from 511 to 389 and my viral load increased from 57 to 2,050.  Short of accusing me repeatedly of not sticking to my regimen (I have never missed a day), my doctor had little to say, and spent most of the visit fumbling with the numbers.  I finally suggested that perhaps the hot weather had compromised the strength of my meds - a suggestion which she grabbed and ran with. 

She prescribed me 3 more months of Stocrin + Viread + Lamivir and said "see you in three months." 

QUESTION:  With a downturn such as this, wouldn't it be prudent to have perhaps received a prescription for one - two at most - months of meds, and have a blood test in 30-45 days, followed by a visit to the doctor?  I really don't think it's wise to wait 3 months!  Thanks.

[Assurbanipal]

Tamsin

While it may feel better to have an explanation, not sure that ithere is any biological advantage to the strength of the meds having been compromised by heat rather than by lack of adherence .  With your viral load rebounding more than 3 times to above 1000 copies, you might want to ask the doctor whether it would be worthwhile to check again (for lab error) and then to check to see whether the virus might have developed resistance to this set of drugs .

Do you have the option of a second opinion? 

If you can get a second test taken and the viral load is still above 500-1000 copies, you might want to consider getting a genotype done to check for resistance.

Note you may find the following excerpt from the US guidelines helpful -- hope so

"Assessment of Virologic Failure. There is no consensus on the optimal time to change therapy for virologic failure. The most aggressive approach would be to change for any repeated, detectable viremia (e.g., two consecutive HIV RNA >50 copies/mL after suppression to <50 copies/mL in a patient taking the regimen). Other approaches allow detectable viremia up to an arbitrary level (e.g., 1,000–5,000 copies/mL). However, ongoing viral replication in the presence of antiretroviral drugs promotes the selection of drug resistance mutations [11] and may limit future treatment options. Isolated episodes of viremia ("blips," e.g., single levels of 51–1,000 copies/mL) may simply represent laboratory variation [12] and usually are not associated with subsequent virologic failure, but rebound to higher viral load levels or more frequent episodes of viremia increase the risk of failure [13, 14]. When assessing virologic failure, one should assess the degree of drug resistance and should take into account prior treatment history and prior resistance test results (AII). Drug resistance tends to be cumulative for a given individual; thus, all prior treatment history and resistance test results should be taken into account.

Management of Virologic Failure.
General Approach. Ideally, one should design a regimen with at least two, and preferably three, fully active drugs on the basis of drug history, resistance testing, or new mechanistic class (BII) [15-20]. Some antiretroviral drugs (e.g., NRTIs) may contribute partial antiretroviral activity to an antiretroviral regimen, despite drug resistance. Because of the potential for drug-class cross resistance that reduces drug activity, using a "new" drug that a patient has not yet taken may not mean that the drug is fully active. Drug potency and viral susceptibility are more important than the number of drugs prescribed. Several clinical trials illustrate effective therapeutic strategies for treatment-experienced patients [17-21]. In these studies, patients received an antiretroviral regimen optimized based on drug treatment history and resistance testing and then were randomized to receive a new active antiretroviral agent or placebo. Patients who received more active drugs (e.g., a ritonavir-boosted PI and a drug with activity against resistance viral strains with or without a new mechanism of action) had a better and more prolonged virologic response than those with fewer active drugs in the regimen. These studies illustrate and support the strategy of conducting resistance testing while a treatment-experienced patient is taking a failing regimen, designing a new regimen based on the treatment history and resistance testing results, and selecting active antiretroviral drugs for the new treatment regimen. Early studies of treatment-experienced patients identified factors associated with better virologic responses to subsequent regimens [22, 23].They included lower HIV RNA at the time of therapy change, using a new (i.e., not yet taken) class of drugs, and using ritonavir-boosted PIs in PI-experienced patients. More recent studies show that higher CD4 T-cell counts and higher genotypic and/or phenotypic susceptibility scores (indicating a greater number of active agents) are associated with better virologic responses [19, 20]. In general, adding a single, fully active antiretroviral drug in a new regimen is not recommended because of the risk of development of rapid resistance (BII). However, in patients with a high likelihood of clinical progression (e.g., CD4 T-cell count <100/mm3) and limited drug options, adding a single drug may reduce the risk of immediate clinical progression, because even transient decreases in HIV RNA and or transient increases in CD4 T-cell counts have been associated with clinical benefits (CI) [24]. Weighing the risks (e.g., selection of drug resistance) and benefits (e.g., antiretroviral activity) of using a single active drug in the heavily treatment experienced patient is complicated, and consultation with an expert is advised. Discontinuing or briefly interrupting therapy (even with ongoing viremia) may lead to a rapid increase in HIV RNA and a decrease in the CD4 T-cell count, and it increases the risk for clinical progression [25, 26]. Therefore, it is not recommended (BIII)."

pp53-54 of the pdf http://aidsinfo.nih.gov/ContentFiles/AdultandAdolescentGL.pdf

Assurbanipal

[Inchlingblue]

I remember reading somewhere, although I can't cite the article right now, that when a genotype test is done with a very high viral load, there's a chance that the results will not reflect the genotype of the entire viral load. When most of the viral load is then suppressed after starting meds there's a small amount of virus with resistance that remains (which was not caught in the initial genotype test) and then has a chance to take over? (Hope I'm making sense, I'm kinda sleepy).

I'm not saying that's what happened here but it sounds like it might be a possibility.

As far as not feeling comfortable waiting three months, are you able to voice your concerns about this to your doctor?  Maybe you can ask her why she suggested 3 months to get retested and doesn't she think that one month or at most two makes more sense?

 

[mecch]

I'd start following the US guidelines and start bugging who ever you need to bug to get more and faster attention to this. Maybe it was a screwed up test. Maybe the drugs were bad.
I wouldn't wait three months, you don't need that anxiety and, (it seems to this non expert), your test shows a treatment failure, so find a Thai doctor who gives a crap to figure out if it is, and why, and now.

[Inchlingblue]

  This is is lieu of Atripla not being available in Thailand, and I am aware that Viread and Stocrin (Sustiva) are also components of Atripla.

I was under the impression that Viraday, which is "generic" Atripla, is available in Thailand, are you sure it's not?