Despite a recent influx of new treatments, it is crucial to remind patients there is no cure for atopic dermatitis and follow-up care is important, explained Jerry Bagel, MD, director of the Eczema Treatment Center of New Jersey.
A better understanding of the pathogenesis of eczema has brought new biologic agents and oral medications to market, which have proved effective in treating atopic dermatitis (AD), explained Jerry Bagel, MD, director of the Eczema Treatment Center of New Jersey.
However, despite the recent influx of new treatments, Bagel asserts the importance of reminding patients that AD is a chronic inflammatory disease. Remission is possible, but follow-up care is crucial.
In part 1 of his interview with The American Journal of Managed Care® (AJMC®), Bagel also argues that mitigating risk factors for AD is not as important as treating the disease appropriately.
AJMC®:What are some risk factors for atopic dermatitis, and could you please discuss both modifiable and non-modifiable risk factors?
Bagel: I think the first risk factor is your genetics, and people have a genetic predisposition to atopic dermatitis. Many have family members that either have atopic dermatitis, asthma, hay fever, sinus conditions, or contact allergies. They're all within the same kind of syndrome of atopic dermatitis, T helper 2 types of anomalies.
Other than genetics, I think the other key factor is emotion. I see many people coming in for eczema, and they have eczema on 20% of their body, and we're waiting for them to get their drug approved, and 2 weeks later they come back and it's on 35% of their body or sometimes 10% of the body. It's very capricious. It waxes and wanes. There is a lot of itch involved, and when people are more stressed out—and that happened over the pandemic, and it happens during hurricanes—it can really exacerbate people's eczema.
In addition, changing in seasons—when it gets really hot and people go outside, or when it gets really cold and people go outside, their skin doesn't tolerate it as well because their epidermis is not functioning as well as normal epidermis.
As far as modifiable and non-modifiable risk factors, it's not about the risk factors that you can modify as much as the disease itself. And if you treat the disease appropriately, you can get their skin to be less itchy, less inflamed, and slightly less affected by the environmental factors that they're facing.
AJMC®: How has the treatment landscape for atopic dermatitis evolved over the past few years?
Bagel: There has been a tremendous uptick in research resulting in newer treatments for atopic dermatitis. It has only been 5 years since we have the FDA approval for Dupixent (dupilumab), the first subcutaneous treatment for atopic dermatitis, which has helped so many people diminish the amount of eczema, inflammation, and itching that they have. Subsequent to Dupixent, there has also been Adbry (tralokinumab), which is another biologic agent interfering in IL-13 metabolism and thereby decreasing inflammation that way.
Understanding the pathogenesis of eczema and knowing that IL-4 and IL-13 are produced too much by T helper 2 cells, and these interleukins result in B cells, which produce immunoglobulin (Ig) G to convert them to IgE, and IgE induces histamine; now that we know by blocking all this, we can really help the patient. Recently, there have been 2 oral medications, Janus kinase (JAK) inhibitors, that have been quite effective and acting even quicker to treat eczema than even some of the biologic agents have. There is going to be a third biologic agent, lebrikizumab, that's soon to come out to market that also has high efficacy.
AJMC®: What is the role of biologics in the treatment of atopic dermatitis?
Bagel: Of the 2 biologic agents currently available—Dupixent and Adbry—both affect IL-13. Dupixent is a receptor blocker that blocks IL-13 and IL-4, whereas Adbry simply blocks IL-13. As I mentioned, IL-13 is germane to the pathogenesis of eczema, because it increases spongiosis in the epidermis, where the epidermal cells are spread apart. When they're spread apart more allergens can come in from the outside and induce even more of an inflammatory result. That gives you more itching, more scaling, and more redness. If you can stop the skin from becoming spongiotic and stop a lot of the itching, which is what IL-13 does, then you can get people to get back to normal skin.
AJMC®: What is your approach to treatment sequencing for atopic dermatitis?
Bagel: It depends on the severity. If someone's severity is mild, I used to use a lot of topical steroids, but we know that topical steroids, when used for prolonged periods of time, can result in atrophy of the skin and can result in telangiectasia of the skin. There are now newer medications that are non-steroidal and work well, like Opzelura (ruxolitinib). Used twice a day, it’s very effective at ameliorating itch and also improving eczematous skin, so in localized areas, like let's say 6% or less, it would be really worthwhile to use Opzelura topical therapy.
Sometimes we still use increasing increments of narrowband ultraviolet B, but that requires 3-times-a-week of treatment. Ten weeks is a big nut to crack for people to get in here 3 times a week these days, but some do, and it is effective for the treatment of eczema and it's safe. When those are not working, then I probably will go to a biologic first and give it about 16 weeks to see how its efficacy goes. We start by measuring Physician Global Assessment, which rates the severity of the rash—is it mild, moderate, or severe?—on a scale of 0 to 4. We also look at body surface area percentage and the severity of the itch, which is rated on scale of 0 to 10. When you take those 3 factors into consideration, you then can see 16 weeks later, are they 15% percent better? Are they 20% better? Are they 100% better? Then, you can continue on with the treatment, which some people really have a problem with, because after a while, they want to go off it. Since it's such a capricious disease, sometimes they talk me into getting them off it, although I don't like that approach.
Now, if the biologic agents don't work, then I go to Rinvoq, a JAK1 inhibitor, which is more effective, but it has some risk factors. I've got to check more blood work, make sure the complete blood count is ok, make sure that the patient’s not hepatotoxic, and that their triglycerides don't go up too much. However, in many cases it is effective. Sometimes I use Rinvoq before a biologic agent. If they're really flaring badly, and they need to get better quicker, then I think Rinvoq will work better than the biologic agents.
AJMC®: How do you promote compliance and adherence with atopic dermatitis therapies with your patients?
Bagel: I try to see them every 3 months. For many of them, in order for them to continue to get their treatment approved, they need to get approvals from the physician's office. So, they have to come in for that. But I tell them that this is a chronic immunologic disease. Somebody comes in and they're 27 years old: “How long have you had it for?” “Oh, I've had it since I was 8 years.” I say, “Well you've already had it for 20 years.”
Then I tell them that this pill or this shot, is not a cure. It suppresses it. It might give you some remission, but it's not going to cure it. Therefore, if you start and stop a biologic, it might not work the second time, because you may develop antibodies to it. I tell them this is not a 3-week disease. This is not poison ivy. This is a chronic inflammatory disease of your skin. For instance, if I told you that you had diabetes, you wouldn't ask how long you need the insulin. You know you're going to need it. You know you're going to have to monitor it.
That's really my spiel to patients, to kind of instruct them that this is a long-term ordeal.