Transcript
Dr. Naiem Issa: And in our last couple of minutes here, just to be cognizant of time, we're going to bring up seborrheic dermatitis. Because I think it really deserves its owncouple of minutes here, even though that's something that we treat day in and day out and is maybe simple at first to the clinicians, but I think from a pathophys standpoint is actually quite complex. And tell me if you agree with me about this, is that seborrheic dermatitis, according to gene transcription studies, is showing us it's not a malassezia or tinea story. It's not a fungal story. This is a marriage between atopic dermatitis and psoriasis components with some chronicity in between. So you have Th1, Th2, andTh17. Oh my goodness, so where do we begin? And I think PDE4 is also an excellentand elegant story to tell on how to regulate all that, no matter what component of that type inflammation is going to be upregulated more or downregulated more compared to others for different patients. So that being the case, it's also nice to havethe roflumilast foam at the 0.3% where it can be used for any part of the body, most classically the scalp, the face. Don't forget the chest and the back, especially for men. And here's a little secret area, sometimes you can get it in the genital area as well.
Dr. Maureen Offiah: That's right.
Dr. Naiem Issa: I see a lot of men have that, and some females. So I think whatis really interesting with seborrheic dermatitis is that we typically try to hammer in a topical antifungal, which we know is probably ketoconazole shampoo or thelike, and some topical steroids. But in your experience, has that been successful in the long-term or even the short-term for seb derm patients?
Dr. Maureen Offiah: Not really. I would say if there's been any cases of success thatI've had with the topical antifungals, it will be with, I'm talking about the mildest of the mildest forms of seborrheic dermatitis. One of the things that you mentioned that'sreally important is the fact that we have this disease condition, that even though ittends to be simplified and minimized, in fact by a lot of our colleagues it has a reallywide spectrum of severity. So you have patients that can have really, really mild disease. Like you said, the anti-inflammation property of the topical antifungal may be appropriate for them. But then you have the moderate to severe disease state patients where you really would need to come back and address the pathophysiology of this disease. And the reason why over the years historically we've just done what we did, throw antifungal at it and scream, "malassezia, malassezia," because that was what we all learned in residency, that it was simply an overgrowth of malassezia. And of course, because of the way that this disease condition was always minimized and shoved to the back side like, "Oh, you're not as important as AD and psoriasis," there was not very many literature and lots of studies as far as trying to investigatefurther into the pathophysiology. But thank God for new studies that have now shown us that the primary issues going on are the immune dysregulation, which we said right now are trying to be, "Oh, we're part of AD or part of psoriasis family," thelittle confusion there. But also that barrier dysfunction, which we always assumed was just something we saw mostly in AD, sometimes in psoriasis. But now we know that seborrheic dermatitis has its own distinct barrier dysfunction that's separatefrom AD and psoriasis. And that to me, it was like a eureka moment. Everything finally made sense, because then you’d be like, "Wow, this patient's getting better," especially moderate to severe. Even when you give them really strong class one topical steroids, there is nowhere that clobetasol is used more than on the scalpof patients with seborrheic dermatitis. You and I know that. With the antifungals, why do we still have these patients that are trapped in the loop of where they're just not having adequate relief from this chronic condition? It's like one moment they have a little bit of improvement, the moment they try to taper down the steroid, oh, they're back flaring again, was because we were not addressing the primary issuethat these patients have. And I think the barrier dysfunction in seb derm is actuallymuch more of an issue, in my opinion, than even in AD and psoriasis, because itwould make sense as to why these patients respond dramatically the moment you actually switch your thinking and your treatment plan to addressing more barrier dysfunction and inflammation rather than addressing fungal overgrowth. The moment you shift away from antifungal, antifungal and try to focus your treatment with using a nonsteroidal topical medication with an elegant vehicle that would help the skinbe the best version of itself, start to repair ... Go back again, the brick and mortar phenomenon, try to build back the protein and the lipids that have all broken apart. The moment you fix that, you see that the patients have less frequent flares. The flares are all spaced out, farther in between, few and far in between. And even that, they'reable to get on maintenance therapy and they're happy. I see a lot of skin of color patients in my practice, obviously, and I can tell you that the antifungal shampooshave never worked in this population. This population, especially the female ones, this is not a population of patients that can wash their hair twice a week. So theantifungal medications work optimally when used twice a week. That's not going to happen with your African American females. We have hairstyles and sometimes elaborate, sometimes in a wig, sewing and braids, and we're just not able to apply this medicine after that medication, the inconvenience of having four or five different prescriptions for just a disease that affects such small BSA, if you will. Mostly the face, the scalp, the ears. We talked about maybe on the chest in some patients and maybe in the groin, but still generally small BSA. It was just unbelievable that for such a small BSA-involving area we'll load these patients up with five different medicines because you have to have a different steroid for different locations, the antifungal, the nonsteroidal, and the list goes on and on. But thankfully, now thatwe now have a better idea of what's really going on as far as pathophysiology, we can then shift our thoughts from focusing on antifungal medications and fungal overgrowth control to focusing on barrier repair and anti-inflammation.
Dr. Naiem Issa: That's a beautiful answer. And you brought up a couple of conceptsthat I want to bring home for seborrheic dermatitis, especially now that we have thefirst nonsteroidal FDA approved medication, which is roflumilast PDE4 inhibitor, a 0.3% foam. So a few things. One, you talked about barrier disruption. Of course, we have cycling of the topical corticosteroids on the scalp. You're going to thin the barrier even more over time, so that's paradoxical.
Dr. Maureen Offiah: Right.
Dr. Naiem Issa: So we want to move away from that. And here we have an elegant formulation for any type of hair. If you're thinking about hair-bearing areas, kinky hair, straight hair, textured hair, no hair, what have you, to have a formulation of this foam that really likes to attach first because of electrostatics and then kind of goes down like a fireman pole down to the scalp. So no matter how bad you are at applying the medication, it's still going to get there whether you like it or not. And so you don't have to try very hard. And then there's some nice elegance to that and it doesn't mess with the texture as well, especially for skin of color patients that you talkedabout. And then for the long-term chronicity, we actually have long-term 52-week data for roflumilast foam that showed that with as-needed usage, not continuous, but as needed, patients were able to maintain over time. And one more kicker because you brought up skin of color, which I think has been very important, is thatpigmentary alteration has been so important, hypopigmentation, hyper, especially along the hairline. Well, guess what? Roflumilast foam has even shown through their long-term data as well that the investigator clinicians have shown improvement in both hyperpigmentation and hypopigmentation in the majority of cases as well. So quite an elegant MOA, quite an elegant vehicle, quite an elegant active ingredientas well to tie it all together. So in the last 10 seconds here, Dr. Offiah, thank you very much for your time. It was very nice to talk about topical steroid stewardship, talk about the acute and chronicity of our inflammatory dermatoses, the fact thatwe have PDE4 being an important mechanism of action to think about as a holistic way of looking at inflammation and barrier repair and itch across all the disease states, atopic dermatitis, psoriasis, as well as seborrheic dermatitis, and that we have precision in the way that we treat the different patient types and different formulations to meet those patient types. Thank you to our audience for listening to us today. We hope you found that informational, and we will see you next time. Bye-bye.
Dr. Maureen Offiah: Thank you.
I preserved the transcript wording rather than fact-checking or editorially correctingthe medical claims, while standardizing the speaker names and formatting.
