Improving Quality of Life in Atopic Dermatitis With Targeted Therapies - Episode 3
Matthew Zirwas, MD, highlights therapies that are available for the treatment of atopic dermatitis, including corticosteroids, calcineurin inhibitors and JAK inhibitors.
Linda Stein Gold, MD: That brings us to the next topic: our treatment approach. When we’re dealing with a patient with atopic [dermatitis], we want to have a short-term game plan to get that flare under control, but we can’t forget that long-term strategy because they’re going to have this disease for decades or potentially a lifetime. We’ve seen many new developments. It’s an exciting time in atopic dermatitis, with many new developments. Matt, give us an overview of where are we in terms of treatment options.
Matthew Zirwas, MD: The classic treatments for atopic dermatitis were topicals. We still have the same topicals we’ve always had. We have topical steroids. The main benefit of topical steroids is that they work fast and are easy to get. Patients love to hear, “I’m going to send this to your regular pharmacy, you’re going to go pick it up today, and you’re going to start using it.”
The downside with topical steroids is steroid phobia on behalf of the patient. No matter how hard we try to educate them around that, topical steroids have a very good safety profile when they’re used appropriately. There’s still steroid phobia, and that’s a challenge to get past.
Obviously, we’ve got our nonsteroidal topicals, which were our traditional agents. We’ve got the TCIs—topical calcineurin inhibitors—pimecrolimus and tacrolimus. Those 2 drugs have fabulous safety profiles. The biggest challenge is they’re relatively slow and not terribly efficacious. They’re good drugs, and they work. But compared with some of the newer topicals, they don’t have great efficacy.
We’ve got our PDE4 inhibitor, crisaborole. It’s a really nice drug but relatively slow and not as impressively effective as something like a high-potency topical steroid. But it has a wonderful safety profile and is approved for a very young age, so it has some benefit there.
Then we’ve got our newest topical therapy, topical ruxolitinib, which is the first topical. We’re going to get more into this, but it took the best of both worlds. It works fast and is highly efficacious, like a steroid, but has a very good safety profile as a nonsteroidal. We don’t have the steroid phobia, but it works fast and it well. It’s the first topical that took the best of both worlds and brought them together. That’s exciting. We’ve got good systemic agents.
With these nonsteroidal topicals and new systemics, I emphasize to patients that this isn’t like the steroids they’ve used in the past. This isn’t going to be like a systemic steroid, where we say, “You’re going to get better, but we can’t keep you on it, and you’re going to get worse again.” With topical steroids, you’re going to use it for 2 weeks and notice a big improvement, but then you’ve got to stop it, and then you start to get worse. These are medications that you’re going to stay on long term. You’re going to get better, and you’re going to stay better.
We’ve got wonderful options for any type of patient. In general, we’ve got our biologics with wonderful safety profiles that work very fast. The challenge with them, the downside, is that they’re injectables, and a lot of patients have some difficulty. There’s some challenge in getting them past the idea of giving themselves a shot. With appropriate education, that’s very doable, but it can be a little challenging. For our biologics, we’ve got dupilumab, which was the first 1 approved, and then tralokinumab as our other option. Dupilumab is approved down to 6 months of age. Patients, especially adults, love that this is safe to give to infants.
We’ve got tralokinumab, which is approved under 18 years of age. The big benefit with tralokinumab is that once a patient gets better, they have the option to space their injections out to every 4 weeks instead of every 2 weeks. That resonates with a lot of patients. That’s the main differentiator with tralokinumab. We’ve also got systemic JAK inhibitors…. I think about some of the details with them, but these are the fastest agents that we’ve got. For clinicians who aren’t experienced with JAK inhibitors, I describe it as prednisone without the steroid adverse effects—in terms of how fast it’s going to work and how well it’s going to work. If you haven’t used JAKs, it’s shocking how regularly I hear from patients, “The first day I took the pill, that night my itching was better.” I’m waiting for somebody to be like, “I unscrewed the cap, and I must have smelled it because I immediately got better.” When you look at the diary data, it’s more like a couple of days, but 1 month out, they’re remembering what happened. Their memory is a little different from what really happened. The JAK inhibitors and speed of onset are amazing.
For our needle-phobic patients, they’re really good. The safety profile is very good, but it’s relatively difficult to talk about because of some of the boxed warnings that the FDA put on these medications. Whether they deserve those boxed warnings is a good argument. Regardless, they’re there, so we have to talk about them.
To summarize that for our viewers, we’ve got our traditional topical steroids, which are still the most common topicals that I prescribe because they’re easy and quick to get. If cost and ease of getting them were not an issue, I’d probably never prescribe a topical steroid again. If topical JAK inhibitor was cheap and easy to get—if I was confident that I was going to write it, and you were going to go to your pharmacy and pick it up—it’s hard for me to think of why I’d ever write a topical steroid prescription again. That’s fascinating.
We’ve got topical steroids, which we still use because of ease of access. We’ve got a number of nonsteroidal topicals. We’ve got topical ruxolitinib, our latest and greatest, which is the best of both worlds of steroids and nonsteroidals. Then we’ve got systemic agents, our injectable biologics. They work within a week or 2. We start seeing real benefit. Then we’ve got our systemic JAK inhibitors, which start typically working within a day or 2. But they have a more challenging safety profile to discuss with our patients.
Transcript edited for clarity