Addressing Itch Symptoms in Plaque Psoriasis
Margaret Bobonich, DNP, FNP-C, DCNP, FAANP: We’ve talked about the skin. We’ve talked about the joints. The one thing I want to throw in there is the itch.
Melodie Young, MSN, RN, ANP-C: Signs and symptoms.
Margaret Bobonich, DNP, FNP-C, DCNP, FAANP: I know. We have formal questionnaires and we can use those, or you can use the partner questionnaire. You ask the person sitting next to them in your office—their partner, their spouse, their girlfriend—and you can ask the patient, “Does this bother you? Does it itch?” “No.” And then the partner says, “You keep me up all night scratching and itching.” Or, “I vacuum the bed sheets because you scratch all night.” So I just want to throw in that itch is an incredibly powerful thing that can be distracting. You may not be able to focus at work because you’re not sleeping, or your spouse isn’t. So itch is one of the things that I think drops off the radar.
Melodie Young, MSN, RN, ANP-C: We used to say that psoriasis didn’t itch. I was actually trained by one of the most brilliant people in the psoriasis community, and I well remember, in the late 1980s and in the 1990s, telling patients psoriasis doesn’t itch. Rather, eczema itches. And that’s one of the differentiators—not just the location but the pink, scaly patches that itch. They would complain about the bleeding. They would complain about the flaking. They would complain about soreness. But when we started asking patients what their biggest complaints were regarding the signs and symptoms of disease, itch and pain came up as No. 1 and No. 2.
We’re terrible in dermatology with pain. We’ll just admit that. Everyone’s afraid to manage pain now. But usually with pain, if pain hurts then pain hurts. That’s kind of an oxymoron. If you have pain and you’re hurting in some way, there are some things that you can do. Unfortunately, sometimes people will abuse substances trying to get relief from their pain, including prescription pain medicines or other things. But we’re just now starting to talk about itch in dermatology and what a miserable, miserable experience it is to be itchy and scratchy all the time.
Margaret Bobonich, DNP, FNP-C, DCNP, FAANP: Let me give you an example. I had a patient who had severe plaque psoriasis. He actually became erythrodermic, with about 80% of his body covered. He went to see his provider, and nobody, nobody… They kept giving him topicals or prednisone here and there. He came to us in such severe distress that I’ll never forget. He looked up. He was sitting on the bed. He looked up at me and he said, “If you cannot fix this itch, I will kill myself.” I think that’s very impactful to tell us about the quality of life for patients, and how does this translate into what we choose to treat them with?
Melodie Young, MSN, RN, ANP-C: His goal was not to be clear. His goal was to not be miserable. And clearing, unfortunately, or fortunately, is the way you manage signs and symptoms of this disease. You have to get their skin clear, and you have to get those inflammatory cytokines that are feeding the itch component within the skin and the synovial fluid. Those cytokines that are found in both places are what cause itch, and an overgrowth of skin cells, and increased blood flow into the area. People will tell me they won’t go out to lunch with their friends. They’ll find out who’s driving because they don’t want to be in a car with someone who’s got dark interior. They know when they get up you’ll see the flakes everywhere. It’s those things that you learn about people. You’re thinking, “Oh my gosh, I can’t believe you’re so miserable and are living your life in a way for which we can make such a big impact.”
Douglas DiRuggiero, PA-C: Well, the good news about this is that the treatments we have available to us do address itch very nicely—both the biologics and oral apremilast do that. All of the trials for these things didn’t really set any primary endpoints at addressing itch. Primary end points are looking at clearance.
Melodie Young, MSN, RN, ANP-C: They are now.
Douglas DiRuggiero, PA-C: But as they’ve gone back and done a lot of post hoc analyses and have initiated investigator-initiated trials, we’re seeing that we not only see that these newer treatments are phenomenal at helping itch in practice, but we’re starting to see data telling us that as well. That kind of brings us to the next point about if they’re itching and they’re severe and severe in different areas and quality of life, what are we doing? What’s our experience with these biologics? I’ll give you my experience quickly from the beginning, and then people can kind of open up.
When etanercept was approved for the treatment of rheumatoid arthritis, it was November 2, 1998. I remember the day because I put a patient on it. I was in internal medicine at the time, in 1998, and I had a patient who wanted to be on it. The patient came in and told me about it. “I want to be on this medication.” They educated me.
Melodie Young, MSN, RN, ANP-C: And you were brave enough to move forward.
Douglas DiRuggiero, PA-C: And I said, “Let’s do it.” So we put him on it. When you fast-forward to 2004, when it finally got approved for psoriasis, by that time I had moved into dermatology. The guy came in to tell us about it and I said, “I’ve had 15 to 20 people on this medication already.” So I have a long track record of putting people on these biological medications, like etanercept, and then all of the ones that have come after that. Now, etanercept was not the first TNF [tumor necrosis factor], because Remicade [infliximab] actually was approved about 3 to 4 months prior to that, in 1998. They were both getting their approval, not for psoriasis at that time but in terms of hitting the market.
So when we look at our tissue necrosis factor inhibitors, we’re looking at etanercept, adalimumab, which is Humira, infliximab, and then a newer option to us in dermatology, certolizumab. These products have been great. We know that they’re great for our joints, and they have multiple indications. They do have some black box warnings that we have to look out for, such as infections and some cancers. But they’re here to stay, and they’ve been very helpful to us. As we move into IL-12/23, when Stelara [ustekinumab] kind of hit the market, and then we moved to the IL-17s that followed on the footsteps of those. Then we kind of said, “Look, we don’t need the IL-12s. Let’s focus on the IL-23s.” And those have been the new kids on the block.
What’s exciting is over the last 7 to 8 years we’ve had a biologic launched, FDA approved, at least 1 per year for the last 7 to 8 years. I know it’s a lot, because now the pool, as you guys now, we now have 11. We have 11 that we can choose from that are biologics, with almost all of them being monoclonal antibodies. That’s what the -mab means in secukinumab. The only one that doesn’t have
-mab at the end of it is etanercept, Enbrel, and that’s -cept. That’s a human fusion protein. It’s the only one that differs. The rest are monoclonal antibodies that have been launched, and we do have a few more on the horizon.
I use all of them. I see advantages to all of them. We can talk about the peculiarities of which patients should go on which, but I have a great comfort level with these because I see them changing people’s lives in every aspect—psychosocial, joint, itch—and we’re going to see some data potentially discuss that it may be helping with the other comorbidities, improving those as well. We can talk about that a little bit, too.
Transcript edited for clarity.
