Plaque Psoriasis: Current Expansion of the Therapeutic Landscape

Brad Glick, DO, AOCD: Hello and welcome to this HCPLive® Peer Exchange titled “Expert Perspectives on the Utility of Real-World Data in the Management of Plaque Psoriasis.” I am Dr Brad Glick, a dermatologist and dermatologic surgeon at the Glick Skin Institute in Margate and Wellington, Florida. Joining me today in this discussion are my colleagues, Dr George Han, an associate professor of dermatology and the director of clinical trials and teledermatology at the Zucker School of Medicine at Hofstra/Northwell in New Hyde Park, New York; and Dr Neal Bhatia, the director of clinical dermatology at Therapeutics Clinical Research and a dermatologist at Therapeutics Dermatology in San Diego, California.

Our discussion today is about the standard of care in the management of plaque psoriasis, along with the newer interleukin [IL]-23 inhibitors class of biologic drugs. We will also focus on the long-term safety and efficacy of these interleukin 23 inhibitors. Welcome everyone, and let’s get started. Dr Han, I’m going to start with you. Can you talk about the implications of the current expansion of the therapeutic landscape and the approval of various biologics and therapeutics for the management of plaque psoriasis?

George Han, MD, PhD: Thank you for having me. This is a fascinating subject to talk about because it’s almost in some ways an embarrassment of riches. What I think it means practically is that our psoriasis consultations are taking longer and longer because we just have more to talk about. I think it’s a nice thing to be able to offer our patients not only new biologics. There are 11 biologics on the market and more that are probably coming. We’ve got new oral options and new topical options, so it is a great time to be able to treat our psoriasis patients with medications that are targeted toward the pathogenesis of their disease state, rather than throwing broad immunosuppressive medications at them, as has been done in the past.

When you think about where these medications fall in our arsenal, they really do have a role, and it is helpful for us to have all of them because you will find those patients who just keep having issues with keeping a response to some of the medications. I remember there was one patient who I was treating who had tried 8 or 9 [medications] already by the time I saw them. There’s a real need out there for novel mechanisms and novel treatments. The way that I lay it out for my patients is that the evolution of psoriasis therapies has been such that we’ve gone from medicines that are broadly immunosuppressive and block a lot of the immune system to target the psoriasis to medications that very narrowly block just the pathways that are overinflamed. In essence, in psoriasis, we have overactivation of certain immune mechanisms, and now our medicines pretty narrowly target that and leave the rest of the immune system to do what it needs to do. I think it makes for a very compelling conversation with our patients, being able to offer them these medications, and really giving them a chance at a much better quality of life.

Brad Glick, DO, AOCD: Neal, what about you? What do you think about the current landscape for our therapeutics for plaque psoriasis, in particular with the focus on the biologics?

Neal Bhatia, MD: Well, I’m glad you said landscape and not landslide, because that would’ve been years ago like George said, with blowing up the immune system and not having a way to focus. George is actually very articulate in the discussion of targets of pathways and process. I think that’s really where the psoriasis patient deserves our attention. We’ve been so used to trying to shut down cellular responses and think about what’s going to put out the fire, and the bandage we can see. Now we have the focus on what is going to turn off the faucet and what’s going to try to keep things under control for the long run, not just for what we see in front of these patients. I’m sure we’ll get into this a little bit later, but the concept of what else is going on under the hood in terms of metabolic syndrome, screening for arthritis, or making sure that any other comorbidities are taken care of with the right approach to treating the disease as a whole. I like the way George also phrased it about blowing things up because you stop dendritic cell surveillance, you stop lymphocytic surveillance, you basically put those patients at higher risk for consequence vs when you stop the cytokines that are building blocks that make the disease, you allow other things to continue. I think that’s now the generation we live in. I’m sure we’ll also get into costs and thinking about the long term. We have to think in terms of the cost of not treating these patients; that’s always been my major concern.

TRANSCRIPT EDITED FOR CLARITY