Expert Perspectives on the Utility of Real-World Data in the Management of Plaque Psoriasis - Episode 3
Brad Glick, DO, AOCD, George Han, MD, PhD, and Neal Bhatia, MD, discuss the current role of topical therapy and the use of non-biologic oral systemic and standard therapies for plaque psoriasis treatment.
Brad Glick, DO, AOCD: While I have you here, and we’re talking about therapeutic protocols and that we have to look at the whole patient, their medications, their comorbidities, their social circumstances… comment on the bigger picture. We’ll take a step back and discuss the current role of all of our therapies and the standard of care. Maybe mention topical therapies, your approach there, and how we approach our patients. Then, where the oral systemics come in and, ultimately, where we get to when we utilize biologics and where our focus and our discussion is today about biologics, particularly [interleukin]-23s. I’ll start with you, George, since you were just talking, and then we’ll hand it over to Dr Bhatia.
George Han, MD, PhD: It’s interesting when you look back at the data. We have these studies that were undertaken at a global level about looking at treatment patterns in psoriasis. What’s always striking is the number of patients who are getting only topical therapies. Even patients with psoriatic arthritis, half of them were only on either topicals or no treatment. Patients with severe psoriasis just on the skin, even more of them were on topical or no treatment. Whatever we’re getting in terms of advances in our science doesn’t seem to necessarily be translating. Now, that large global study was done before a lot of the newer biologics came out. I think newer data is probably going to paint a slightly different picture, but I still think that undertreatment is rampant in our country, especially. I hear plenty of stories about people out there who are going to one dermatologist after another. That’s not to say that there’s anything wrong with what people are practicing out there, but these are patients who come in [with an affected] BSA [body surface area] of at least 50%.
Any day of the week, I would at least talk to patients about systemic therapy, about biologics, about orals. They come in, and they’ve never had that conversation with the dermatologist. Some of them will say, “I saw the commercials on TV and I asked about it, but I was told that that’s not for me.” I’ll ask, “Why is it not for you?” and they don’t have a good answer. I think we owe it to ourselves to really advocate for our patients in order to get them appropriate treatment because the psoriasis is more than just skin-deep. We know that it’s associated with numerous comorbidities, both medical and psychiatric. We’ve been talking more and more about the link between psoriasis and cardiometabolic syndrome. We know that the same cytokines that are elevated in the skin and psoriasis are elevated in the bloodstream. Some of those cytokines have also been implicated in the pathogenesis of atherosclerosis. So we have all the ingredients here together to think about this question more deeply. I think a lot of people are doing great research…on this front. I fully believe that at some point we’ll have a better understanding of it. But for now I think we should start to think about these questions. [And consider psoriatic] arthritis as well, which probably remains underdiagnosed.
I think taken together, we generally collect a more severe population, but we do have patients who we manage just on topicals because they have very limited skin disease. We always make sure that we ask them periodically about joint pain via the PEST [Psoriasis Epidemiology Screening Tool], which is actually very quick and easy to deploy. I’m a big advocate of that because you can have it for your psoriasis patients in the waiting room. Just instruct your front desk staff to keep a copy of it on hand and to give it to anybody who’s coming in for psoriasis, and you don’t really have to do anything much additional during your encounter. I think easy things like that we should still employ with our patients with limited body psoriasis who are managing just with topicals.
Of course, now that the topical game has changed, we’re dealing with new mechanisms of action with nonsteroidal topicals, which is really exciting; we have phosphodiesterase inhibition, we have aryl hydrocarbon agonism. These are completely new pathways that we’re discovering. We’re starting to learn how to put that into our armamentarium. Figure out where does this lie in terms of how we use it for inverse psoriasis, how we use it to try to maintain clearance in certain areas. It’s become very exciting on that front, but for patients who have a little more skin disease, to be honest, I often skip over the conversation about oral agents just because of the really high efficacy and safety profile of biologics.
There’s more to the oral landscape, also. I think in this day and age, I’m glad to not have to use much cyclosporine or methotrexate, at least for psoriasis for the most part. Apremilast is a little limited in terms of its top-end efficacy, but I think it definitely does have some role in scalp and maybe palmoplantar psoriasis. That is where I sometimes will use it. The new medicine, which is deucravacitinib, has also come in and shaken up that oral landscape with a new pathway in TYK2 inhibition, which really flows along the same path as IL-12/23 inhibition.
Then, of course, we have the biologics. For me, it’s a little rare to be reaching for the TNF [tumor necrosis factor] alpha inhibitors first line. I think there are just more negatives to it. It’s a bit more immunosuppressive. There’s that slight signal for nonmelanoma skin cancer. There are multiple reports out there about other potential side effects, even weight gain, on TNF alpha inhibitors that you really don’t have with IL-17 or IL-23 inhibitors, which are quickly becoming the most used part of our armamentarium because they’re just so efficacious. Safety signals through 5 years and longer for a lot of these medicines look good. We’re not being surprised about anything post-marketing because, as Dr Bhatia said, we’re not trying to target T-cell activation. We’re not looking at removing a basic building block of your immune system. We’re looking at a very hyperfocused area. By the way, it’s an area where we know that if patients are born without this pathway functioning, they live normal lives and maybe have a little more fungal infection. I think this is all very reassuring. We’ve come a long way from those early days where people used to get up in meetings and say, “I don’t want to give anybody lymphoma. I’m never giving one of those drugs.” Thankfully, no study’s ever shown that kind of signal for psoriasis patients. We really have come a long way since then.
TRANSCRIPT EDITED FOR CLARITY