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Improving Care: Rationale for Switching HIV Therapies

MAY 16, 2017 | PANELISTS: PETER L. SALGO, MD; IAN FRANK, MD; PAUL E. SAX, MD; JOSEPH ERON; ERIC S. DAAR, MD


Transcript (slightly modified for clarity)

Peter L. Salgo, MD: People sometimes do have to be switched from one ART regimen to another. So, what are your triggers for doing that?

Paul E. Sax, MD: A perfect example would be someone for whom I was recently contacted about his refills, and he’s taking old tenofovir (so, the more nephrotoxic one) plus twice-daily raltegravir. I could very easily ask him, “You want to take 2 pills a day instead of 3 pills a day and you want to take a safer medication?” And to him it all sounds great, and so we made the switch. He’s virologically suppressed. He’s never had trouble with this regimen. I offer him the opportunity to take something safer and easier and he’s happy to do it. That said, there will be some people who say, “I don’t want to switch if it’s working.” It’s our responsibility, as clinicians, to identify those patients and switch them if they’re taking something that we think is harmful to them.

Eric S. Daar, MD: So that’s the convenience and subclinical tolerability?

Paul E. Sax, MD: Right, exactly.

Eric S. Daar, MD: Then, there’s the clinical tolerability issues, where people are having side effects. That’s another reason. And then virologic failure and drug–drug interactions.

Peter L. Salgo, MD: Clearly, some of your patients are going to get resistant to some of this stuff, right?

Paul E. Sax, MD: I have a patient on rilpivirine-based treatment right now. That’s a medicine we haven’t mentioned, and she’s having terrible esophageal reflux. She needs to go on to a proton pump inhibitor. Her rilpivirine treatment has to be changed. That drug requires stomach acidity for absorption.

Joseph Eron, MD: I will say, and Eric just mentioned it, we need to consider the number of people that actually fail with resistance. We have patients that we’ve treated since the 1990s, that have a lot of resistant virus below the surface. But people who are started on therapy now really suppress or they don’t take it very well.

Eric S. Daar, MD: Not taking it very well really means not at all or very little.

Joseph Eron, MD: Right. You just don’t see much resistance. If you look at the British Columbia data, and we have some data that will be at CROI (the annual Conference on Retroviruses and Opportunistic Infections), it’s just not very common.

Ian Frank, MD: I want to say a couple of things about switching therapy. First, I think it’s important for providers to know that “It ain’t broke, don’t fix it” is not a good way to manage patients. Sometimes patients do have intolerances that could be improved upon, and I think to ignore those, just because the viral load is undetectable, is a mistake. Patients need to understand that if they switch off of what they’re currently on, they can always go back—assuming that they don’t have resistance issues that develop after the switch.

Joseph Eron, MD: Right, if they’re suppressed.

Ian Frank, MD: That’s one of the reasons why a lot of patients don’t want to switch—because they feel like this combination has saved their life and they are so enamored with that combination that they just don’t think that they can switch off.

Peter L. Salgo, MD: But you’ve got to convince them that it’s saving their life, that we’ve got something better, and that this older drug may be doing something that’s shortening their life.

Ian Frank, MD: The question is, what kind of car do you want to drive? There are some old cars that will get you where you’re going, but now these days, they’ve got cars that have a fax machine in them and you can put a USB port in there and can play your own music. Wouldn’t you rather drive an updated vehicle if you can?

Paul E. Sax, MD: We all have anecdotes of patients referred to us for a consultation for antiretroviral therapy. Can you simplify their regimen? And to use one example: I saw someone recently who was on 4 nucleosides, efavirenz, and boosted darunavir. That was the regimen that saved his life, so that’s the one he’s still on; he’s been on it for years. That’s just too toxic.

Peter L. Salgo, MD: What do you do with a patient who’s got constant low-level viremia—500; 200,000 copies? What do you do with that guy or that woman?

Eric S. Daar, MD: It’s probably one of the areas, I think, where you can say there’s most controversy, especially between that undetectable and maybe 200. We do have quite a few people (although I think less since we’re using more integrase inhibitors) that are just cooking along in that range. And in the majority of them, it doesn’t seem like when we switch therapy or add drugs, anything happens. So we don’t help them. And the majority of them don’t seem like they’re failing. I tend to just watch them closely. I make sure that they’re taking the medications consistently, that there are no drug–drug or drug–food interactions, and just sort of keep an eye on them. And most of them end up doing just fine.

Paul E. Sax, MD: Weirdly, in some of them, you can have resistance if you do the GenoSure Archive. Occasionally, you’ll get one of those and they may have 1a4v.

Eric S. Daar, MD: Although we have undetectable people, we do the GenoSure Archive and they have resistance to what they’re on. I don’t know what it means.

Paul E. Sax, MD: Yes, I don’t know what it means either. Resistance in some of the regimen they’re taking.

Joseph Eron, MD: Yes. I know.
 
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