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Government Study Finds Protease Based Triple Combination Keeps Patients Alive Longer Than Double Nuke

Changing the standard of care

Results of AIDS Clinical Trials Group (ACTG) 320, one of the most important studies of triple-drug antiviral therapy in people with AIDS, were recently released by the National Institute of Allergy & Infectious Diseases (NIAID). The principal investigator was Scott Hammer, M.D. of Harvard Medical School. ACTG 320 is the first study to prove that the protease inhibitor indinavir (Crixivan), when added together with a second new drug (in this case 3TC), to an underlying AZT or d4T treatment regimen, prolongs AIDS-free time and extends survival in people with fewer than 200 CD4 T cells and over three months of AZT experience — compared to simply adding one new nucleoside analogue (in this case, 3TC).

The study is also the first to prove clinically that combination anti-HIV treatment strategies — adding at least two new drugs when making a decision to switch therapy — are more effective than adding single new drugs to antiretroviral treatment regimens. The study was also innovative and flexible in allowing participants to change underlying regimens based on toxicity — those experiencing AZT toxicity were allowed to use d4T instead. Finally, the study may be the last of its kind, demonstrating as it does that AZT+3TC alone, which only last year proved its superiority to AZT monotherapy, is inadequate as a treatment for advanced HIV disease. Double nucleoside combinations are no longer appropriate control arms in people with AIDS or fewer than 200 CD4 T cells.

ACTG 320, combined with data from the Abbott advanced study M94-247 and Roche saquinavir+ ddC study NV14256 (which demonstrated a survival benefit to the protease inhibitors ritonavir and saquinavir, respectively) when added to nucleoside analogues, further strengthens support for changing the standard of care for people with AIDS and under 200 CD4 T cells to triple-drug therapy including a potent protease inhibitor plus two nucleoside analogues, at least one of which is initiated when the protease inhibitor is begun.

Starting in January 1996, ACTG 320 enrolled 1,156 HIV-infected persons who had fewer than 200 CD4 T cells, more than three months of AZT experience, less than seven days of 3TC experience and no protease inhibitor experience. They were randomly assigned to receive AZT+3TC or AZT+3TC+ indinavir and followed for a mean of 38 weeks (maximum one year). Persons intolerant to AZT at baseline were allowed to take d4T, and persons experiencing moderate, non-AIDS defining disease progression were allowed to switch underlying nucleoside analogue therapy to any combination of the nucleosides AZT, d4T, ddI, or 3TC. They were followed for an AIDS-defining illness or death.

Participants were stratified at baseline by CD4 above or below 50 (38% below, 62% above). 83% of participants were male and 17% female; 27% were black, 19% Hispanic, 3% had hemophilia and 16% had a history of injecting drug use. The mean CD4 count at baseline was 86, and mean age was 39. Virologic analyses are not yet available. The dataset was closed on January 27, 1997. An independent Data & Safety Monitoring Board (DSMB) analyzed the data on February 18, 1997 and recommended that ACTG 320 be stopped early. Study participants were unblinded (told which arm they were on) and offered a number of follow-up treatment options.

ACTG 320 is the third, and perhaps the most well-designed, study to demonstrate a survival benefit by adding a protease inhibitor to nucleoside analogues. Previously, in January 1996, Abbott showed that the protease inhibitor ritonavir, when added to underlying nucleoside analogues (AZT, ddI, ddC, or d4T), prolonged survival during six months of study in people with under 100 CD4 T cells. Later in 1996, Roche showed that its protease inhibitor, saquinavir, when added to the nucleoside analogue ddC, prolonged survival compared with saquinavir or ddC alone.

Like the Roche study and unlike the Abbott study, all ACTG 320 participants received at least one new drug, and those on triple therapy received two new drugs. Unlike the Roche study, however, whose control arms were ddC or saquinavir monotherapy, all ACTG 320 participants were on two nucleosides or two nucleosides plus indinavir. Therefore, ACTG 320 more clearly defines a new standard of care than either of the two previous studies, but all three demonstrate that protease inhibitor regimens confer a survival benefit (a 50% reduction in death) in advanced, AZT-experienced people followed over six to twelve months.

ACTG 320 also proves the benefit of changing more than one antiretroviral therapy at a time. ACTG 320 was the first controlled study to prove survival benefit not just for the protease inhibitors as a new class of drugs, but to prove the survival benefit of a new and revolutionary anti-HIV treatment strategy. In ACTG 320, all participants had received over three months of AZT, and all participants were given at least one new drug — 3TC — and half of the participants were given two new drugs — 3TC and indinavir. This study proves what, after Vancouver, we only guessed and hoped: that, when people with HIV make a decision to switch therapy, the best way is to add at least two new drugs, in order to reduce the chance that the virus can develop resistance to any one new drug. This means that the era of sequential monotherapy, as practiced since 1987, is over, and that the new treatment strategy, at least for people with AIDS, should attempt to administer potent antiviral combination therapy designed to reduce viral levels beneath the limit of detection.

Particular praise goes to the study investigators who are planning a state-of-the-art salvage trial for ACTG 320 participants now on AZT+3TC, rather than simply offering them open-label indinavir, as was done in the past. ACTG 320, like its predecessor protease studies, offers new hope for antiretroviral-experienced people with HIV.

ACTG 320 also suggests that people taking therapy likely to cause maximal viral suppression have superior clinical outcomes. The results of ACTG 320 confirm earlier suggestions from surrogate marker trials (trials measuring viral load and CD4, but not clinical endpoints) Merck 035 and Merck 039, which showed that AZT-experienced persons adding 3TC and indinavir experience a high likelihood (65-85%) of having their plasma HIV levels go below the limit of detection (400 copies of HIV per milliliter of plasma). ACTG 320 suggests that this benefit — of having virus go “undetectable” — is associated with significant clinical benefit — a 50% reduction in AIDS-defining events and death. However, virological analyses of ACTG 320 are incomplete.

AZT+3TC+indinavir is just one of many combination therapy regimens which can drive viral load below detectable limits, and thus slow down progression to AIDS or death. There is nothing unique about the particular combination of AZT+3TC+indinavir. What is new is the clinical confirmation of the ability of maximally-suppressive antiviral combinations to extend health and prolong life. What remains to be determined is whether there is some sort of qualitative difference between going “undetectable” with a potent protease inhibitor combination and going “undetectable” with an all RTI (either nucleoside or non-nucleoside) combination. People who are already taking AZT+3TC should be encouraged NOT to rush out and merely add indinavir to their regimen. This is not what ACTG 320 tested: all 320 study participants were essentially 3TC and protease inhibitor naïve. That is, they had never taken them. When protease therapy is begun, at least one underlying drug– and possibly both — should be switched at the same time.

ACTG 320 may (and probably should) be the last trial of its kind in people with AIDS. Although AZT+3TC only last year proved clinical benefit in PWAs (in the CAESAR study), and AZT+ddI only did so in 1995 (with ACTG 175), double nucleoside combinations with approved agents should no longer be the standard of care for PWAs. Triple therapy with two nucleosides [at least one of them new] and a potent protease inhibitor should be recommended as the standard-of-care for people with AIDS or fewer than 200 CD4 T cells. The Abbott and Roche studies plus ACTG 320 demonstrate significant benefit for the class of drugs plus nucleosides versus nucleosides alone.

ACTG 320, like the Abbott and Roche studies, does not prove clinical benefit for people with over 200 CD4 cells. We still don’t know when is the best time to start antiretroviral therapy. We don’t know enough about resistance and cross-resistance among the protease inhibitors; in particular, whether choosing indinavir as “first-line” protease therapy will make it less likely to later benefit from second or third choice protease inhibitors. Healthy asymptomatics not currently on antiretroviral therapy who wait to begin therapy may have additional treatment options in six months or a year from now. In any case, people initiating triple-drug regimens need to strongly consider how their first regimen will affect future treatment options.

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