Advances in the Management of Plaque Psoriasis - Episode 7
Mark Lebwohl, MD: Let’s go to the next agents. One’s been mentioned already, IL-12/23 [interleukin-22 and 23], which is the next agent to be approved, ustekinumab. Do you have patients on ustekinumab?
George Han, MD, PhD: I still have plenty of patients on ustekinumab. It’s been a great drug through the time it’s been out, about 10 years now. We have great safety data for the drug. And for a lot of patients it has a pretty good durability. Safety profile is excellent, as I mentioned. But there are some newer agents too, which I think we’ll be discussing, the IL-23 agents, as well. But this was a really great example of a newer class of medication that upped the bar for efficacy for psoriasis. Maybe for psoriatic arthritis, as you mentioned earlier, it’s not as effective as our TNF-α [tumor necrosis factor-alpha] inhibitors. But really a lot of patients I have are still very happy on it.
Brad Glick, DO, MPH: That’s been my experience, too, with psoriatic arthritis, with ustekinumab as well. But I have a lot of patients still on ustekinumab, and for me, whether they inject at home or not, most of my patients are injecting with me in the office every 3 months. Now, one of the things about infusing Remicade, one of the things about using ustekinumab and the newer generations of IL-23 blockers in the office, is that it really keeps that doctor-patient relationship. It really keeps that patient-office staff-physician relationship and a lot of the patients like it, just like your patients like coming in for their Remicade infusions, even if they have some residual plaques.
Scott Gottlieb, MD: And not to mention compliance, and so I think sometimes long-term efficacy is certainly enhanced by these drugs that we give in the office because I think their compliance is much better.
Brad Glick, DO, MPH: You want 100% adherence to therapy, have them come in to the office and inject. They’re going to get their medicine.
George Han, MD, PhD: At least that way you know if they’re not doing quite as well, is that the treatment failing or is that because they’re using it or not using it? You remove that out of the equation, which I think is really good. Because one of the things that we see is that the most expensive thing to do is to switch from one biologic to another. And that adds cost to our health-care system. So really removing that I think is kind of important. But I totally agree that those 3-month follow-ups for psoriasis where you just do an injection are some of the most pleasant visits of the whole day. Because that next person has hair loss, they’ve been to 4 other dermatologists, and now they’re here to see you, and I’m just dreading that one. But the psoriasis one is where they’re pretty clear, you catch up about family, how everything is going, and that’s a very pleasant visit. If all of my visits could be like that, I’d be very happy.
Brad Glick, DO, MPH: I think the other thing about ustekinumab is that the PSOLAR registry really imparts some fantastic information for our colleagues when it comes to malignancies and infections. It’s really a fantastic agent where adverse effect profile is concerned, in my opinion. And that data are very, very helpful for me as a clinician.
Scott Gottlieb, MD: I totally agree with that. When patients are averse to starting a systemic agent and they say, “Hey, doctor, what is the agent that’s the safest that we know as much about as any other agent,” I do go to Stelara with that because of the PSOLAR data. And I explain to them about that 8-year registry, and I think that’s very helpful. Most dermatologists who use a lot of biologics, after we got comfortable with Stelara, started to get a little more comfortable with the other classes of drugs, and maybe we were using them a little bit more quickly than we were say when Stelara first came out because we were a little bit more comfortable with the safety profile of the more targeted agents.
Mark Lebwohl, MD: I must say I use the safety story about Stelara if I want to give the patient another IL-23 blocker. What I say to them is this drug blocks even less than Stelara, which blocks IL-12 and IL-23, but it blocks IL-23 better so it works better. It’s certainly going to be as safe as Stelara. We don’t have 10 years of data to prove that, and I say that, but by its mechanism you would expect that.
Scott Gottlieb, MD: Right. We’re all saying we’re big fans of Stelara, but some of the newer agents might work better, might be safer, or what have you. First of all, when you block IL-12 and IL-23 versus just blocking IL-23, I think there was some question in my mind of whether those 2 similar mechanisms of action, whether the newer agents, would work similarly to Stelara or whether they would be better than the first agent because of their similarity of mechanism of action. Some of the newer trials of some of the drugs have actually used Stelara in the head-to-head comparator in their primary clinical trials, and the newer agents have worked better, some of the IL-23s.
In addition, there have been a couple of studies in which Stelara failures were then put on to IL-23 drugs, like NAVIGATE, where patients who were failures to Stelara were then switched over to Tremfya. So you’re switching a similar mechanism of action to a similar mechanism of action, and patients did better on Tremfya than they did on Stelara. I think that those sorts of data are also important in terms of making treatment decisions, both as a first-line drug as well as a second-line agent.
Transcript edited for clarity.