This Month in HIV: Breaking HIV/AIDS Research From CROI 2007
A few years ago there was a lot of talk and some studies about a higher rate of heart disease in people with HIV -- perhaps because of HIV, perhaps because of the protease inhibitors. Any news on this?
"I think the good news is, we've got new [HIV treatment] options that don't appear to affect cholesterol and heart disease risk like the old ones did."
[There wasn't] too much news at this conference, but I think subsequent follow up data from some of those original studies showed that it didn't appear to be true across the board. So in other words, if you looked at people who were on non-nukes, like Sustiva, they didn't really appear to be at much increased risk. If you looked at people who were on PIs [protease inhibitors], [you saw that] that group accounted for most of the increased risk. But if you then treat their cholesterol or treat their blood sugar problems, you reduce the risk. So I think the good news is we've got new [HIV treatment] options that don't appear to affect cholesterol and heart disease risk like the old ones did. The other [good thing] is that we're getting better about realizing we need to be treating these problems when they occur. So I think that's going to decrease the risk [of heart disease] quite a bit.
Didn't several studies presented at CROI show that up to 40 percent of people with HIV smoke cigarettes, which increases the risk of heart disease?
If you're smoking, it's kind of crazy to be worried about your cholesterol and your protease inhibitors because the amount of benefit you would get by stopping smoking just dwarfs the risks [from those factors]. Smoking is such an enormous risk for heart disease that cholesterol and protease inhibitors are tiny in comparison. So if you quit smoking you have accomplished most of the battle.
I think people are also concerned about data showing that the incidence of cancer in people with HIV is growing. Anything you can tell me about that?
There was one interesting study, looking at cancers that are not typically thought of as being HIV cancers. [Click here to read coverage of studies on cancer and HIV presented at CROI.] So the HIV cancers are lymphomas and Kaposi's sarcoma, and things like that. But they were looking at the other cancers, and interestingly, found that the risk of those cancers was increased in people with HIV, and it was increased more in people with low CD4 counts. Obviously, although they are not strictly HIV-related cancers, there's clearly a link between immunosuppression and your risk of getting these cancers. This has actually been used as another argument for why we should be starting therapy earlier, to help prevent that risk.
"I do think that immunosuppression is a bad thing, and it can increase your risk for all sorts of things, other than just the traditional list of HIV-type complications."
Now, it's a little complicated in some studies, because people with HIV tend to smoke more and tend to do things that could increase their risk of cancer that's apart from their HIV status. But still, I do think that immunosuppression is a bad thing, and it can increase your risk for all sorts of things, other than just the traditional list of HIV-type complications.
What was the big news for people who have multidrug resistant HIV?
This conference is always about drugs and this was no exception. In fact, new drugs really took the limelight, I think -- at least [among the] clinical presentations. Probably the drug that got the most attention was raltegravir, which is the new name for the Merck integrase inhibitor, MK-0518. We heard data from two large, simultaneous multicenter clinical trials called the BENCHMRK trials, in patients who were highly treatment-experienced, had a lot of drug resistance. [Click here to read coverage of the BENCHMRK studies.]
The bottom line is, people did very well with raltegravir combined with other agents. They did much better if they were on raltegravir than if they were not on it. They especially did well if they were on raltegravir, along with at least one, if not two, other active drugs.
For example, if they were on raltegravir with Prezista and Fuzeon, they did extremely well. Or if they were on it with one of those drugs [they did well]. This drug is out there in expanded access right now. We hope it will be approved this year. The key thing is that, when it comes out, as with any new drug, it's going to be critical that you're taking it with something else that really works.
The other news was about maraviroc, which is the Pfizer CCR5 entry inhibitor. There was kind of a similar study -- or two studies -- called the MOTIVATE trials. [Click here to read coverage of the MOTIVATE studies.] [They were] very similar in design [to the BENCHMRK studies], people who were treatment-experienced and had drug resistance got an optimized background regimen, and then they either got maraviroc or placebo. People did better if they were on maraviroc.
The clincher with maraviroc, though, is that it is a CCR5 inhibitor, and so you really should only take it if your virus is R5-tropic -- which means that you have the kind of virus that uses the CCR5 coreceptor to get into the cell. So you have to do a test, called a Trofile assay, before you take this drug. If you're not R5-tropic, if you have other types of virus, specifically virus that gets in through the CXCR4 coreceptor, then you probably shouldn't be taking this drug. Of the people they screened for the trial, 44 percent were not able to join the trial because they had that kind of virus. This is not going to be a drug for everybody. But for those who had R5-tropic virus, it worked very well.
So is it reasonable, if you are resistant to many HIV meds, to be able to switch to medications that will get your viral load undetectable now? It used to be unreasonable. Now, is that an expectation anyone can have?
Yeah, absolutely. In fact, both the DHHS guidelines and the IAS [International AIDS Society] USA guidelines have changed their wording. [Click here to view a PDF of the International AIDS Society treatment guidelines.] They now say that the goal of therapy for everybody, regardless of the amount of treatment experience, is an undetectable viral load of less than 50. That's a major, major change.
Because they used to say that that was not a realistic goal for a lot of people. I think that by the end of this year, if we really get multiple drugs approved this year; I think it will be a realistic goal. But it will require that both people with HIV and their clinicians understand that no great drug is great without other backup. If you use a new drug without considering resistance, and without combining it with something else, then it's not going to be a great drug for very long. That rule has not changed in the many years of antiretroviral therapy. I hope that everybody knows that rule by now.
For my final question, I wanted to get your idea about mortality issues. Everyone newly diagnosed wants to know what his or her chances of living a normal lifespan is. Are there any new data about that?
Well, not so much data. You've heard different presentations, trying to estimate lifespan. There was a lot of fuss about the one that gave an estimate of 24 years. I tell my patients: Ignore those studies. Not that they are not good studies; they are very useful. But they are talking about large populations. In those populations are included people who don't take their medications, people who are actively injecting drugs, people who have hepatitis C, people who have renal failure .... If you're not one of those people, if you're just a healthy person who plans on taking every dose of your medications, then those kinds of estimates are meaningless to you.
"I tell my patients that they should expect to live a normal lifespan, and to die of something other than AIDS, when they're old."
I tell my patients that, granted, these new therapies ... the whole idea of suppressive therapy has been only around for 11 years, so it's still relatively young. But [in] people who have undetectable viral loads we're not seeing their virus evolve and become more resistant or harder to treat. So I tell [patients] that they should expect to live a normal lifespan, and to die of something other than AIDS, when they're old.
Can I promise this 100 percent? No. I do think that it's a pretty realistic prediction. But I know that every time somebody publishes some study about what the average lifespan is I'm going to get 40 e-mails and 20 calls from people, saying, "But you told me that I was going to live a long time." So, be careful how you extrapolate data to your own personal situation.
Basically, on the whole, would you say the news from CROI was positive for patients living with HIV?
Oh, yes. I think definitely the news from CROI and from other recent conferences, like [the International Conference on AIDS in] Toronto and some of the other meetings, [has been promising]. The fact is, we've got incredibly good initial therapy now that could last you for decades if you do it right. Then, if things don't work out with the initial therapy, or if you get toxicity or side effects, we've got a lot of options to go to that will work when the first line therapy fails.
We used to say you have got one or two good shots at antiretroviral therapy, and I would say we can go much further than that now. At the same time, people on initial therapy are much less likely to fail than people were in the early part of the HAART era. I think the news, from a treatment standpoint, is great.
Thank you very much.
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This article was provided by TheBody.com. It is a part of the publication This Month in HIV.
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