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- [00:03]
A
Welcome to season three of Derms on Drugs, a video podcast brought to you by Scholars in Medicine, the best educational platform in dermatology and provided no cost to medical providers. Germs on Drugs is where cutting edge derm meets sediment comedy. I'm Dr. Matt Ziras, doc Dermatology, and each week I'm joining my residency buddies, Dr. Laura Faris from the University of North Carolina and Dr. Tim Patton from the University of Pittsburgh. And we use our 60 years of combined derm experience to discuss, debate, and dissect the the hottest topics in dermatology. It is everything you need to know to be on the cutting edge of derm, and you'll actually have some fun listening. New episodes drop every Friday on Scholars in Medicine, Apple Podcasts, Spotify, and other major podcast platforms. And I highly recommend that you download the Scholars in Medicine app to access the full podcast video archive and explore the best derm educational content on the planet. We're talking real pharma, independent coverage of all of dermatology, a robust core curriculum, the, you know, analyses of the latest stuff going on in the field, and it is supported by an amazing AI clinical consultant called Ask Simon. All right, so this week we've got one of our deep Dive episodes, and we are so excited to have Dr. Chris Syed from the University of North Carolina, who is a deep, deep HS expert. Chris, great to have you on the show.
- [01:21]
B
Thanks so much for having me. Glad to be here.
- [01:23]
A
So first question that I think any. Any reasonable listener would wonder, why the heck did you choose to go into hs? Like, that's you just, you like, like dealing with the most miserable people. You're not miserable because they're bad. Like, miserable because it's an awful disease. It is an awful disease. So how'd you get into hs?
- [01:44]
B
Yeah, I mean, that's part of what kind of drove me to it. When I was in residency, I think I saw a lot of patients come in, and it's not that people weren't trying to get them better, right? But there was so little to offer them. They were so miserable leaving. And when I was finishing up, I was like, okay, I'm going to be out in a few months, and I've got to take care of people on my own. How do I do you know better than this? Right? How do I fix this really challenging bunch of patients when I'm on my own and don't have somebody to back me up all the time? And so partly was just a challenge to learn more, how to try to do better for Them at that point, you know, that was 2013. So it was two years before adalimumab was approved. Nothing was approved. So everything was a fight if you wanted to get it approved at that point. And at that point, patients came in on doxycycline. They left on minocycline. Like, nobody in the room, me or the patient thought they were probably getting better at that point. Right. So it just felt like we were throwing out random stuff and there wasn't really anything satisfying about it. So, you know, that's why I just took an opportunity to sort of research a whole bunch and try to learn it. Well, we had to give a senior talk, and so I picked HS as a way to force myself to read more about it. And, you know, there it was picking up a few things like antibiotic combinations that we weren't really using all that much around, you know, kind of where I was training at least, and then things like surgery coming up a lot and something I had never had any exposure to or never done before. But the idea that, you know, it had an important role and how to best use that, including in the dermatology setting, which, again, I never saw a case done in training or really talked about. We did intralesional steroids occasionally an ind, but it was clear there was more to do and a bigger way to make an impact. And it would be a challenge. You know, it'd be difficult many times. And like you said, like, miserable patients can make for miserable doctors very easily. Right. So that, that, you know, misery loves company. And it's easy to sort of feel worn out by the end of the day, but it just felt like a good opportunity to do more. And I absolutely had people tell me when I was like, maybe I'll see HS patients. And like, you know, like, it's sort of a pause and then like, why are you doing that again? Like, what is it you think you're going to accomplish? Are you trying to drive yourself into the ground? But, you know, there was just this huge need and so few other people doing it. Right. It just felt like, you know, partly just something where it was a gap that needed filling, partly an opportunity to do things better and do like, you know, sort of pioneer and try to do some different things procedure wise. You know, that was sort of the point of academic medicine, was to offer something that others weren't, right? That patients didn't hit the end of the line and be told, sorry, nothing else I can do for you, that somebody had to think creatively. And so it felt like, again, a good opportunity.
- [03:59]
A
And where did you. Where did you do residency?
- [04:02]
B
Yeah, so I grew up in North Carolina and then went up to UNC for undergrad. Never left. So I did like, undergrad, med school, internship, residency there, and then joined the faculty. So I found a good place and didn't leave. So it's been fun to see it kind of evolve over the years. I got to, you know, work with people who are my attendings. We still have some of them on faculty now. And so it's been. Been a good place. Couldn't. Didn't find a better place that. That put. Pulled me away yet.
- [04:23]
C
Hopefully you never will. That's the goal.
- [04:25]
B
Hopefully not. Yeah.
- [04:27]
A
All right, so let's go ahead and get started. We've got three different articles we're going to cover this week. We're going to start with Dr. Patton kind of talking about how do we figure out who's got disease that's bad enough to really warn aggressive therapy. Dr. Patton, why don't you get us started?
- [04:44]
B
Yeah.
- [04:44]
D
So my deep dive paper, March 2026 edition American Journal Clinical Dermatology titled Defining Moderate Disease and Progression in Hydroidinitis Supper tiv An Expert Framework to Unlock the Window of Opportunity for Prompt Treatment by Martorell et al. Dr. Syed was also one of the authors on this paper. So if you're not familiar with the whole window of opportunity concept, figure one has a nice little visual representation. You have an HS patient. They have disease onset, an inflammatory nodule in the armpit. It becomes an abscess. That's mild disease. HS becomes moderate with multiple nodules and abscesses, and then a tunnel forms and then the disease progresses from there to severe. So the window of opportunity is between mild dise.
- [05:25]
B
Severe disease.
- [05:26]
D
The thought being, hey, let's introduce biologic therapy in that window. I mean, I definitely got a, like, how can we get more patients on biologics? Vibe from the paper. Novartis was involved in funding and hiring medical writers, and two of the listed authors are Novartis employees. So it's kind of like a letter that says, dear Doctors, put more of your HS patients on cosentics. Sincerely, Cosentics. Right, But I think the problem being addressed is a real one. Like, when do we start? Biologics in HS patient? Who's a candidate? The paper. So it's like a sort of a consensus. They. They call it a framework. But, you know, 10 HS experts. What defines moderate disease? Table one, list criteria and you know, which patients have moderate disease. Every single HS patient. You've ever seen. Table 1. So moderate HS, they define it as patients with inadequate control of HS symptoms or one active tunnel draining or non draining, or at least four inflammatory lesions inclusive of inflammatory nodules and abscesses involving at least two anatomic areas. Table 2 provides definitions of progressive disease in HS. Pretty straightforward. You know, what defines progression. So my thoughts on the window of opportunity. While it's never explicitly stated, it implicitly argues for initiation of biologics in all HS patients. And so that like the definition of moderate HS is such that there's no such patient with mild disease. That's kind of like the way I felt about it. So this is the only concern I have. So you have an HS patient with a few inflammatory nodules post inflammatory changes, no tunneling, no prior treatment. It's a reasonable candidate for like your topical therapy. Clindamycin, hibiclens, bleach baths, maybe put them on doxycycline. 3 month plan Spironolactone if they're female, maybe you do a three month follow up on their window of opportunity framework. If that patient develops a tunnel at follow up. Technically I've missed the window and could be criticized for mismanaging an HS patient. Even though like stepwise care, like that initial sort of management plan seems appropriate, you throw in the fact that window of opportunity concept strongly promoted by industry, like, is it putting providers in a tricky situation where we feel compelled to prescribe biologics to all HS patients from the very first visit, which again, like, I lean towards aggressive therapy. Like I put patients on isotretinoin that think other, other providers are like, why are you being so aggressive? Like, I'm an advocate for aggressive therapy, but you know, having this window of opportunity and did we miss it? Did we miss it? Aren't we kind of saying like, if we're not using biologics and one tunnel forms, we're kind of in a bad situation because that window of opportunity is gone. Like, who are we not considering biologic therapy on with this notion of like moderate disease being like not, you know, like two abscesses and you have moderate disease right now?
- [08:32]
B
It's a good question. You bring up lots of points. Or you want, did you want to go first? Or I can, I can give some initial comments.
- [08:38]
D
Oh yeah, take it.
- [08:39]
B
Yeah. So you know, the paper had a definition for moderate disease which included patients who I think were recalcitrant to other therapies. And so like, it's not that all people who have like just a few nodules would necessarily qualify as moderate disease. It doesn't always say like moderate disease has to equal, you need to do biologic therapy. It's just the idea that if they have disease that hasn't responded to other conventional therapies, they should qualify. Right. Like you've been through spironolactone, antibiotics off and on. They're not tolerating those things. You know, at that point, you shouldn't have to wait for them to develop a tunnel if it's conducive with what they want to do. I mean, it's always a patient provider discussion. And like, if you look at, you know, psoriasis, appropriate use criteria, like any genital or scalp involvement is supposed to qualify you for systemic therapy based on guidelines. Right. There are a lot of patients who can do fine with topicals in that scenario. So it's not we have to do every time. It's just that if that patient is not responding, you think they qualify at that point. They should be able to be on one if they've been recalcitrant enough and had enough quality of life impact that you think is necessary for that patient. So it's more about like it could be appropriate, but it's not saying you have to use it in that scenario because. Cause the other definition was at least four, like, you know, four or more inflammatory nodules or any draining tunnels at all. Which is the idea that if they make tunnels once, they're going to do it again. They've got surgical burden, irreversible damage at that point. Like that's a pretty straightforward, like if they feel like they would want to be on a biologic with where their disease is. I think if they have a tunnel, they should absolutely be allowed at that point. You know, four nodules is, you know, you're not going to catch them on a day when they're that active. But that's the idea that, look, are we really going to waste time, force them to do an antibiotic for three months when you can just kind of tell already they're advancing quickly, They've got pretty active disease, a pretty big impact on quality of life. So I don't think there's ever a situation where we'd say like it is inappropriate, like you, you know, you must treat this or you're doing something inappropriate. In that moderate disease category, you should absolutely be able to do antibiotics, spironolactone, laser hair removal, lots of other things in that context. And even a patient with one draining tunnel, it's context dependent, right? Like if I Have a young female. Like, there's a subset of patients, 3 or 4%, they get like one. One area that flares over and over again. They're really not developing widespread disease. It has been three or four years every month in abscess on the labia. And if you take care of that one spot surgically, they might do great and really not need any medicine at all. So it's more about, you know, if they hit these criteria. You should be thinking about biologic therapy. This is the chance to act if there's momentum moving the wrong way. But it's not that you have to do it. It's tough when there's bias. Like, you said that that study, you know, Novartis helped organize it. You know, the experts get together and they sort of get to say their message and have veto power. Like, it's not to where, you know, but it has an uneasy feeling to it for sure. And there is like a whole nother effort, very similar to finding moderate disease, you know, which is maybe going to come out different and make it even more confusing. But that's the problem is you have, you know, groups that aren't talking to each other, developing different guidelines. And we really probably just need is appropriate use criteria of, like, when should you consider it? As opposed to saying, this is moderate disease and therefore, you know, maybe we should consider it for those patients.
- [11:35]
D
But if you had a patient come in and say, like, you know, let's say they got one nodule in each axilla, one in each groin, so four nodules.
- [11:45]
A
Wait, the person.
- [11:46]
D
And they said to you, like, hey,
- [11:47]
A
you're saying the patient has two groins?
- [11:51]
D
Yeah, a right one and a left one. So they, and, and they said, hey, I have hs. I've seen the commercials. I mean, like, if they wanted to start Adalimumab or any of the biologics, like, I think it's totally appropriate. Right? I mean, I, I do you. Do you start people on biologics where other people are like, what are you doing? Like, this isn't that bad a disease.
- [12:18]
B
I mean, I don't think we get that much pushback. I think most people feel like, again, that's a personal. I'd say, like, sure, it would be reasonable for you to do it. If you're motivated, you feel comfortable with escalating, it's having a big impact on you. And especially if you're young and it's advancing and the momentum is in the wrong direct. Again, if it's somebody where things are, like, relatively stable, they've Never tried anything else. I would absolutely lay out options at least and let them pick. Right. Whether that again, be things I mentioned earlier, you know, laser hair removal, things like that. Like sometimes you do just fine with those things. You don't have to escalate over time. But yeah, that person was highly motivated. Again, just like somebody with congenital psoriasis or sort of other things where we consider treating them or getting like acne. Like you mentioned, like you got a low threshold to treat nodular acne because, you know, it can form scarring. Right. Once it starts, you should get ahead of it. So, you know, maybe some people would say that it's overly aggressive. I, I also think, you know, I'm skewed towards patients with really bad disease. Like, I have a lot of patients who come in there. It's a referral center. They often have bad disease. I don't have 100 of people on biologics. Right. So I have plenty that we're doing other things for. But I think it gets to the point where it is very reasonable to offer it. Like if it's conducive to the patient's sort of risk, benefit profile. And these are pretty low risk drugs for the most part, I think it's, it's a reasonable thing to try to get ahead of it if you can.
- [13:33]
D
Do you find that? I mean, this. We probably know the answer to this. It seems to me like papers like this are trying to encourage earlier use of biologics. Do you think that's a huge problem? Like patients come to you and they've never even been offered a biologic. Is that, is that sort of picture changing because of the, you know, the fact that it was approved, Adalimumab was approved as long as it was, or
- [14:00]
B
it's, I mean, it's better than it used to be. But there are still, you know, a lot of dermatologists who've been practicing a long time in the community that are just minimally comfortable with biologics in general. Like minimally comfortable with hs. Don't really know where that threshold is. They're waiting to pull out the big gun to the last minute. Right. They have this idea that I'm really only going to save it for if you get bad enough, because then I'm not wasting it too early, which I think is the wrong way to think about it. Like the earlier you treat somebody, the better their response tends to be. So I do think sending that message is important for a lot of folks out there who don't maybe see as hs as often or aren't thinking about it as often. And part of it's also, you know, you're partly speaking to payers with this kind of thing and the idea that you can't put barrier after barrier in front of access for some patients who do need it because they're not checking whatever box you think is required that you just kind of made up when you don't really know the disease very well. So I think the more precedent there is in literature when we think it is appropriate, the easier it should be to access it over time.
- [14:53]
C
Do we have good data that, you know, certain therapies will actually prevent like progression, like let's say from early stage one to two or two to three. And so I like the window of opportunity. Like I think a psoriasis, like, you know, I do a lot of psoriasis. I don't think of psoriasis as having a window of opportunity. Right. Like I can start somebody when they're pretty bad. And that's, I mean arthritis, that's another story. But just playing like skin.
- [15:21]
A
It's just a big window. Really big.
- [15:23]
C
It's a big. Yeah, it's a bigger window. It's like a, it's like a picture window. But no, it is not. Yeah. So, you know, I guess that's. But my gut feeling is that with HS it is a little different. Right. So once somebody has early stage three disease, I can never make them iga. I can never make them feel as though they are clear or, you know, I. Whereas with psoriasis I can take you from 80% BSA to 0% BSA.
- [15:51]
A
It's a lot.
- [15:52]
C
But I guess. What's that?
- [15:55]
A
It's a lot like psoriatic arthritis. Right. I mean if you get an arthritis mutilans, you've missed your window of opportunity.
- [16:02]
C
Yes.
- [16:02]
A
Right.
- [16:03]
C
No, absolutely.
- [16:05]
A
Yeah.
- [16:05]
C
And like, do we know, do you actually like, you know, there are markers of fibrosis and things like that, like do the biologics change that?
- [16:14]
B
So there isn't. It's going to be really hard to do that study because you'd have to look at patients with early disease. You'd have to put them on a, you know, biologic or placebo for six months and see or like at least six months, maybe a year to really get a sense of who's going to progress and who's not. And do you truly slow it down? I mean, there is some evidence that like, you know, patients who have shorter disease duration before you start treating tend to have better outcomes. You know, Those that have sort of less severe numbers of like, you know, fewer numbers of draining tunnels, that kind of thing, they probably do respond a little bit better overall. So the idea is that like the ceiling of how much improvement you can get declines the further you wait and the worse you let things get. Right? So the percent of patients who get, you know, 100, you know, 90 and 100%, you know, high scores, you know, like high score 900, like, you know, that really sort of dramatic reduction disease, those responses are better for patients who aren't as bad at their baseline. So the worse you let them get, the lower your ceiling becomes. And the other big thing is that they have higher surgical burden at that point. Like to get them that much better, that means they have to have a lot more surgery done, which is also a burden on its own. You know, it's not a magical thing. You get to wave the one and it happens. That's recovery and downtime and more time to get the same level of improvement overall. See, I agree with you. It's different than psoriasis or eczema. Like, we can put a patient on a drug who has terrible, terrible disease for a long time. Six months later, their skin can look normal, right? Like they have. No, they might have some dispigmentation. It's possible that you can get scarring with those things. But, you know, and what's different with joints even is like, say even you can recover, like the skin itself, you know that like there's not inflammation around, you know, there are marks left behind forever. Right. And it is for a, you know, a teenager or somebody in their 20s who was trying to get romantically involved to have to explain away, you know, what it is that has permanently changed them. Like, you cannot take that back once it's happened. Even if you get the. Even if you get high score 100, 0 nodules, 0 abscesses, no drainage anymore. Right. Like, it is still something they have that burden of living with forever if you don't jump in early and do something about it. So the moment there's tunneling, the moment they're scarring, just like an acne patient, like, yeah, we have, I think, necessarily a lower threshold to treat. Like, there are more psoriasis patients out there in the world, but I think we have a greater number of HS patients ultimately that might need biologics. Because even if it's a quarter of many people with HS compared to psoriasis, like, what the disease does is just that much worse and that much more long lasting.
- [18:30]
C
No, that's I. I would agree. And then my other question is laser hair removal. So, you know, I know that's something that you do. We do a lot here at unc. And so my question is, do you think that you can prevent people from going from her, like, early stage one to two and how about two to three? And where do you think laser hair removal is helpful? When is it. Is that an early intervention thing? Is that more of a. You've got a bigger window?
- [19:00]
B
Yeah, I mean, earlier is probably better. You know, once somebody has an armpit full of scars and tunnels, like, you can't fix that by removing the hair follicles on the surface. And half the time, the hair follicles are mostly gone from all the scar. So earlier is probably better. And I do think it can have, you know, a relatively lasting impact for some patients. You know, the idea is that fewer follicles around, fewer inflammatory nodules that pop up, and each nodule, you know, maybe has a chance of spiraling, leaving some scar and some tunneling behind. And so, yeah, like, earlier is probably better. Like Hurley 1 and 2 patients. There are some Hurley 3 patients that, you know, you clear certain areas with surgery and you treat the rest of the surrounding area with laser, and it probably helps to stabilize that disease a little bit better. But it's hard to predict. You know, just like with any medicine, you know, some people can do the laser and still just plow right through and get worse regardless. But I do think. I think we do a better job stabilizing patients when we add that to the mix, especially in kind of that earlier moderate disease. You're gonna have some patients who, again, inflammatory disasters, and it's just. It's not enough for early stage.
- [19:58]
A
An early stage patient, like we were just talking about with Patton, if. If they came in and you had no barriers, you could either put them on whatever biologic you wanted or do laser hair removal with. Like, which one would. If. If it was your. Your child, you know, who's 23 and started to get HS, would you want the hair removal, the biologic? I know both are. Don't really. You can't do both. But which one would, like, can. Can it be curative, you know, for these patients, if you get it early with the laser hair removal?
- [20:35]
B
Yeah, I mean, I think it can be stabilizing to the point that you get them through their most active years of disease with much less activity, and you maybe spare them, in many cases, the need for escalating to a biologic. Like, I think it's really foolish of these companies sometimes to not be like really gung ho about covering things like laser hair removal and paying docs a few hundred bucks without question. Because even if you just delay the start of a biologic by a month or two like that, that pays for your year of laser. Right.
- [21:01]
A
If you skip, if you get rid of one dose of a biologic, it's the same thing with psoriasis. It should be that the day you get your first psoriasis, you know, systemic, before you, every single patient gets a home narrow band box, just spirit, end of story. Right. If it, if it prevents one dose, it has now paid for itself.
- [21:24]
B
Yeah, I totally agree. I mean, I think it is. Yeah. If I had a kid who was a teenager, you know, early 20s, you know, if all they were getting were, you know, a few lesions, you know, every month or two, like along the bikini area. Yeah, probably I would encourage something like laser before committing them to, you know, a couple years or a decade of being on a biologic. So I would start there and then escalate over time rather than going straight to a biologic. But again, the moment it's, you know, they've had a few sessions, they're not improving, they're not stabilizing and have a low threshold to do something sooner rather than later. Okay.
- [21:55]
A
All right, but Ferris, let's go ahead, let's talk about your paper.
- [22:00]
C
All right, so we're going to move on to a biologic. So we're going to talk about bimakizumab. So, so this is the two year data for patients with moderate to severe HS. Pooled results from two phase 3 randomized control trials and their open label extension. Dr. Syed is the senior author here. So this is pulling data from B herd 1 and BEHRD 2. So these are two phase 3 studies. So bimakizumab is a monoclonal antibody, inhibits IL17a and F, which are both important drivers. And so these are two identical 48 week randomized placebo controlled phase three trials. And then once they finish the 48 weeks, they could roll into the open label extension, which is planning to go for 188 weeks. Right. So that's some strange number. That's a little over three years. So in total they had 868 patients on bimkizumab, 146 on placebo in the parent trial, and then they had 657 that went into the extension. So pretty good size trials. So, you know, what they looked for was safety data. And then efficacy data. So the dosing is kind of interesting. When you rolled over, you were stratified on whether or not you had achieved a high score 90. So that's a 90% reduction in abscesses and inflammatory nodule count with no increase in abscesses in kind of appropriate or, you know, reflecting back on what we were just talking about. No increase in draining tunnels. Okay. And so the people who were. Who did not have a high score 90 went on 320 milligrams every two weeks. And the high score 90 responders got to pull back a little bit to every four weeks. And then, you know, they could go back up to every two weeks if they. They were, you know, not responding well, basically with, you know, with criteria that I won't go into. Okay. Safety. They did not see treatment emergent adverse events go up from year one to two, and they did not see, you know, that they saw, like, stable or decrease numerically the number of serious adverse events too. Most common ones were Covid, probably due to when they were doing the studies, oral candidiasis, which I think is something that's really. I'm always amazed by how common that is with bimakizumab in particular. So 12.5 per 100 patient years. So that is, you know, pretty frequent, mostly mild to moderate, rare, you know, rare serious infections. And there were, like, low events of ibd, Mace, malignancy, suicide, et cetera, et cetera. And there were no new safety signals. Okay, Moving on to the efficacy. By year two, 85% of patients achieved high score 50, 77% achieved high score 75, and 57% hit high score 90, and then 44% achieved complete clearance or high score 100. Mean abscess and inflammatory nodule counts drop from about 6, 17 at baseline down to 4 and then down to about year one and down to 2.3 by year two. For the patients who had draining tunnels at baseline, which was about three quarters of that cohort, the mean count dropped from 4.9 to 1.8 at year one and then 1.4 at year two. So, you know, that was pretty, I thought, pretty interesting. So it actually looked like the draining. So I would imagine they still scarring there, but their tunnels are no longer draining. And then for the people who had none, they basically, very few of them developed. They went from, on average, from 0 to 0.2 tunnels by year two. So about one in five, I guess, would develop one draining tunnel. If you wanted to look at it that way. Quality of life measures were Kind of as expected, they went along with, they tracked with lesion response and roughly a third of patients had a DLQI of 0 or 1. So that means essentially no impact of their disease on their quality of life by year two. And so, you know, I think that's pretty significant because of the, you know, profound impact on quality of life that HS has. So what are the strengths? This is a pretty large cohort size. It's two years. It's going to go on, you know, even longer. So, you know, what, what could we say that's like critic critical? Patton really started us off on the snarky criticism side. So how can I add to this? You know, there's actually not a ton. I mean, I guess what you would say is, you know, with an open label extension, there's no control arm after week 48. I also think it's hard to enroll and probably not ethical to put people in placebo controlled studies for two to three years. Also I think that, you know, the other important thing anytime you got an open label study is to realize that people do, there is attrition, people do drop out. So there is some attrition bias that the sickest or least responsive patients tend to be more likely to drop out. Which means that if you're looking at the results and the people who are left, they're going to generally be the people who are responding better. So you know, there you can look and compare this to other data, but we don't have head to head data. Again, this was like a single drug study. It's not, you know, compared to like Secukinumab or compared to Adalimumab. So you know, I think that this was good evidence that you know, patients one, this is a long term disease and it can be a progressive disease. If you look at the curves, patients did tend to do better over time. I think that the tunnel reduction is probably more important than the, the like inflammatory nodule reduction because that's very much a snapshot in time and what they have at that study visit. I think that tunnels are harder to resolve. So, so that, that was my take on that paper. Chris, anything else, any other data from there that you think are important that I didn't talk about?
- [28:22]
A
I'm jumping in. Hold on here.
- [28:23]
C
Okay, Matt, sorry, I know how much you like to interrupt me. Go ahead.
- [28:27]
A
Well, I let you finish. So technically I interrupted. Technically I interrupted. Chris. So Chris. So Laura touched on this, but it is a soapboxy thing for me, attrition. So that like, because in, in some of the ad literature, there's like, oh, 98 of people will do great at three years. And it's like, no, you started with 600 people, you finished with 82. You don't know what the hell happened with. And so I, I may, when I did a really deep dive on was the idea that you can assume that it is not data missing at random. It is, it is non random. And exactly as Laura said, the people who are not doing as well tend to be the ones who drop out. And in that setting there is absolutely no way to correct for it. Like people like to be. Oh, we did Monte Carlo mixed model bootstrap analysis and so we accounted for the. No, you didn't, you didn't. It's impossible. It is literally impossible. So I'm a believer that they should all be locf that that LOCF is the best. Because if you're not doing great and you drop out, then we'll see that. Because your last observation will like. And I, but everybody pushes back on me in farm and, and just like I've had.
- [29:51]
C
Just to give you numbers, I, I know what you're saying. Just to give you numbers. At week 48, the number of subjects that were in Washington, 556. And then at week 96 it was 446. So you're losing about 110. So you're, it's about 20% attrition from week 48 to week 96.
- [30:15]
B
Yeah.
- [30:16]
C
So if you said it's 20% attrition and if you look at it, the numbers go up a little bit. Like for your, you know, your high score 100 goes up by about 14%. So it's not just the people, the non responders. But you know, that's just to put it into context, it's not that 90% of people drop out, it's about 20% at least in the study.
- [30:40]
A
Yes.
- [30:40]
B
Yeah.
- [30:40]
A
Yeah. And that's, Yeah. I mean it's like when you, to me, whenever you look at like the high score 75, for example, there were fewer people. Although it went from 64% to 77%, there were fewer people. Right. So meaning there were 356 people who got high score 75 at 48 weeks and there were only 344 people who got it at 96 weeks. So for all of these. So like high score 90 did actually go up a little bit and high score 100 did actually go up a little bit in terms of the absolute number of people. But that, that's what I always look at to try and like give me a sense.
- [31:22]
C
Yeah, that's a good point. So the lower, the lower response rates, the fifth high score, 50, 75, you would imagine those patients are more likely to be on that cusp of wanting to drop out. And that number does go down. The high response rates, it's a lower percentage. But the act, the absolute number, the numerator goes up and the denominator goes down.
- [31:47]
A
All right, so Dr. Clyde, what do you think about all this?
- [31:50]
B
Yeah, so I'll give you both sides of it. Yeah, like, you know, I have some beef with how this is reported even though again I'm one of the folks on there. Like, you know, OC data is the rosiest way of looking at it. And so every pharma company that publishes a paper is going to want OC data to make it. The numbers look as inflated as they could. I agree. The lost last observation carried forward is like usually my preference. And I think there's a supplemental figure that I had pushed for for either last observation carried forward or at least even like a non responder mutation. Like if you really want to be stringent, you do non responder mutations that anybody leaving is considered a non responder, which isn't always fair. In a long term study people lie
- [32:24]
A
about this all the time. They'll call it a modified NRI and then whenever they modify it, then it's not an nri. Like a pure nri.
- [32:33]
B
Not, not always. Like, because some, some non responder modifieds are actually worse. Like, and the sort of initial study for this one was if you got an antibiotic, like a rescue antibiotic, you were also considered a non responder. So it actually worse than a standard non responder invitation. But you're right, people fiddle with it to try to like you know, juice their numbers a little bit. But this, I'll tell you why. Like I think it's overall a very positive story. Like, and again this is the context of the only people included in this analysis were those who entered the open label extension. They had to stay for a year, which automatically gives you a more favorable look. Right. People who dropped out in the first year would have been less likely to respond to in three years later. So you're already filtering, you know, through that lens and then you get to the end and you say okay about, if you really want to look at the number I care the most about, it's high score 90 and 100. Like those are the folks who are super happy, high score 50s. They're better, they're probably not super satisfied. But if you want to look at who is really responding really, really well consistently, who's the patient who comes to you and is super happy with the drug, it's your high score, 90 to 1/ hundreds. This study started with about 800 people that were getting drug from day one and then over the course of time, like you said, they got to about 400 by year two. So even if you assume that everybody who left was a non responder and you cut your numbers like in half almost, you know, you say a 20% high score, 100 response rate, 20, 25% with that, you know, if you just looked at everybody who entered on drug on day one and went to year two, that is still like pretty darn good. Like 25% of people with no active disease after two years, you know, I think is better than what Adalimumab did. I think it's a little bit better than what cosynthex does. And that'd be sort of the harshest way looking in reality. I think a lot of people who leave the studies, they do it because it's a, it's you know, a big time burden. It's a big travel commitment. I had people driving three hours during my involvement in the study for every single visit. And over time some of them were actually really good and said, you know what? Like I just can't keep doing this, you know, I'm glad I did it. I'm way better than what I was. I just can't keep it up. Or they moved across the country because they had got a new job over the course of two years or had to be close to family. So I have people who are very sad to leave the study because they were doing much better when they did leave. So it's a bit of a mixed bag, especially if you filter for, for people who have been there for a year, like they were probably pretty happy at a year, like they didn't all leave because they suddenly become unhappy at week 52 as opposed to week 48. So I don't think a lot of the attrition in this type of follow up is purely because people aren't doing well most of the time. It's just you lose like to only lose a hundred folks out of 550 over the course of the of from week 48 to 96 isn't that bad actually. And those, those numbers do dre up or to some extent that's the reality is that I think people, if they do well with IL17s. You know, TNFs tend to wane over time. That's the one of the biggest problems with adalimumab. You know, responses between Benzelix, Cosentyx and Humira like all look pretty similar at week 12 and 16. But when you get out further is when you see things improve. Whereas I think adalimumab levels off early and then starts to wane. Cosynthex holds up pretty well. Bemzelix, I think is the, is the best of them in terms of its ability to maintain response and probably have continued improvement, improve response as more time passes. So I do think this is, it's an overall positive story. But yeah, there are ways where like things could be reported more fairly. Like this is not a story of if you start a person on the drug, 45% have high score 100 two years later, like that's too rosy of a picture. And I think you could get that impression looking that slide to start with. But, but yeah, it's somewhere in the middle of those two things.
- [35:52]
A
So Chris, I'm kind of ready. I'm going to go on to the, to the next paper. But it really, that paper was really just a first. I want our readers to know or our listeners to know about it because it is such a useful article. So Dr. Seib was a author on this one as well. It's in the American Journal of Clinical Dermatology 2025.
- [36:12]
B
Can I give you two more points on that study? Is it okay if I give you like two more quick things? Like one was about thrush, because you mentioned thrush, but that is a nuisance side effect for sure. And I tell people one in eight folks are going to develop thrush through the study if you notice it. I give people fluconazole, 300mg, take once weekly as needed, give them 10 tablets, they have control over it. If they notice symptoms coming back, they can use it and stay on top of it. Most people are willing to put up with that. The other side effect that comes up in about 12 or 15% of patients after that first year or sort of, if you look out at the one year data and two year data, it's about 15% get dermatitis, which is a broad spectrum. And so that's one of the more important things to look out for because it's probably more of a barrier that gets in the way of treatment. Some people you treat through and it's fine, it clears after three to six months and their HS does great and they're really happy. There are some word is like rip roaring, like awful. You may be in like 2% and it can be. It's most often an inverse pattern. So they might come in and say my, you know, armpits are hurting. Like it's really raw and sore and their HS looks pretty good. It's just the dermatitis. And so if you can get them through it sometimes they still do great in the long run, but that's maybe the more important thing to watch out for.
- [37:16]
A
So I gotta say, that is such a.
- [37:18]
C
How do you treat that topical? Like try and cinnamone and talk them through it or what do you do when that happens?
- [37:24]
B
Yeah, it depends on how severe. You know, you're dealing with intertriginous sites a lot of times. So it is difficult to have them do topical steroids, you know, for a long period of time. But that's how I would start. You know, I don't think there's that much yeast growth that complicates things. I'll sometimes do like a, you know, it's heresy. Some people think it's terrible to give somebody like a topical steroid and an antifungal, but I'll give them ultrasound because it's easy. And like they're worried about yeast growth because we talked about it at some point. I know. So yeah, but, but you know, it's moist areas, it's macerated, like, you know, I'm covering all the bases. I don't want to have to keep changing it over time. And so, so, you know, it's. You can start with something like that. You can try to do a non steroid, but it's often sort of macerated and sore. So protopic and things like that don't do great a lot of the times there's just too, too much sting to it. And then you can try to just call it atopic dermatitis or inverse psoriasis and get whatever other topical you like. And sometimes that's where I'll transition to things like a JAK inhibitor, add a jack in inhibitor, saying we're managing that. So, yeah, sometimes you can manage through, other times you got to switch something else.
- [38:20]
A
Yeah, it's a fascinating topic, this whole cytokine shift phenomenon, because we see it in Brighton doopie get. About 5 to 7% of people will get either nuanced Seb derm, new onset psoriasis, new onset psoriatic arthritis. And it's fascinating to me that with the IL17s, it, it goes along with efficacy. So it happens the least Least with cosentics, then tuls, you get a little bit more dermatitis, and then bimselix, you get the most. And that. That cytokine shift is just. It's pretty cool. And it's pretty fascinating to me that. That it goes both ways.
- [38:58]
B
Yeah.
- [38:59]
A
Dr. First, do you know, do you get as much of that in psoriasis as you do in hs? Like, I feel like the number that. That I see in psoriasis is more like in the 5% range. I think is the kind of what I've seen in the literature. But that's kind of a random question.
- [39:18]
C
I mean, we don't see that very much. I think in part, it's also because most of our psoriasis patients, we do have on topical steroids as well. I think that they just sort of end up treating through it. That's my impression.
- [39:34]
A
Okay, all right, so. All right, let's go on to that. That last article. So. American Journal of Clinical Dermatology 2025. Comprehensive and updated algorithm of Hidradenitis Suppurativa Management from the experts. Again, Dr. Sled was an author on this, and it has a phenomenally good flowchart that really is a pretty comprehensive overview of all of the different therapies. I mean, you. You guys killed it with this. The. You've got lines of lid in there, which is by far my favorite therapy
- [40:15]
B
for
- [40:17]
A
helping in the acute setting. You've got, I think, oral refluma last in here. Like, you guys really brought everything good in. I just think it's such a phenomenally good resource. Just bravo. Bravo. Was my. Was kind of my takeaway from it.
- [40:36]
B
Thank you. Yeah. You know, Dr. Shao was, I think, senior author. I'll give her, like, the bulk of the credit, and I came in and sort of helped in a few ways. But, yeah, it's nice because it covers a lot. It's kind of all there. It's also maybe overwhelming of like, where do you actually start? Or which, you know, what do you actually follow? Because it is just there's so much different stuff you can do when it's unpredictable. So it's easy to get lost too. Yeah.
- [40:59]
A
So it. And it's.
- [41:00]
C
So that likes anything that talks about oral refluma last off label. So you really, like you had them at reflumalast, but do you actually use oral refluast at all as a. obviously not as, like, monothery, but as an adjunct NHS. Have you done it?
- [41:18]
B
Yeah, every now and then. I mean, the PD4 inhibitor is probably just not that great in HS. I mean, they're only so. So and psoriasis when it comes down to it, you know. And like, you know, a third of patients get too much stomach upset with a formula just like with like a premolast. And so it's got its limits, but you know, it's super cheap to get it from like, you know, like we'll get it from like Mark Cuban pharmacy for you know, 20 bucks or something like that a month. And it can fill a gap for somebody who's not quite ready to be on a biologic or doesn't want to be on for some reason. You know, maybe we're adding it on top of their biologic. I've tried it sometimes for things like if people get the sort of sore acid form eruptions with whichever biologic they are on to see if we can calm that down and maybe has modest effects sometimes. I will say that I don't think I have a single patient on refluimolast right now. And so it's not something that I'm doing all the time. But you know, it's in the back of my mind as an option that's cost effective if you know, somebody's having trouble accessing other things.
- [42:08]
C
And then one other question because one of the things I think that's a, that has been amazing when I've seen it done. I have not done it, but is ertapenem iv. Ertapenem. How often do you use that? How would you say for like the average dermatologist who's listening, who maybe isn't like, oh, I've got an order set for getting a PICC line put in and blah blah, blah, like how, how do you use it? When do you. What's your off ramp from it and how hard is it to actually get for patients?
- [42:41]
B
Yeah, so I mean, first of all, you know, it's not the long term fix. You know, antibiotic. You know, resistance is a real issue. We're mostly doing this in the outpatient setting. So it's less of a problem than when you're sort of incubating superbugs in the hospital and putting everybody on strong IV antibiotics like that. But you still have to be careful. And it's a, you know, it's a bit of a burden. People have to get their PICC line place they got to keep it wrapped up and protected. If it's, you know, somebody who's young and active physically, they have to be careful with exercise and stuff like that. I mean, I probably use it, you know, once or at most twice in a month. And so. And I see a lot of patients with terrible disease who wouldn't be unreasonable. But again, you know, I'd say maybe a third of the time I offer it, somebody actually does it and I offer again a few times a month, something like that. I mean, even though it's a hassle, it is like you said, it's like miraculous sometimes. I mean, people who are like your worst patients, bedbound three weeks later, like up and at it doing things and you know, they get, the problem is they get worse once they go off. You know, they got a little bit of a tail, maybe you know, a few weeks on the short end or sometimes three to six months where they can be pretty good after they come off if we do it for 12 weeks. But it is a bridge, right? Or it's a rescue. Somebody who's just falling apart. You have to kind of get them, you know, out of the house. You're trying to not make them get hospitalized and have bad things happen to them. It is a way to rescue or to. And at the same time I'm starting and I'm usually making some other big change in the background of what is the long term, like you said, exit strategy. So it's either somebody who's terrible that we're starting up for the first time, getting the ball rolling on other things, or I've had them on something for a while, it's just not working. They're falling apart. Okay, let's transition you to that next thing or get you teed up for surgery for some of those worst areas. Just get it calmed down, less inflamed to begin with. But it, it's not as complicated as it seems like the first time you do it, everything is really complicated. I mean, I never did like infliximab during my residency. I never set up an IV drug. And so I do that all the time now still with this, you know, I basically send like a pre filled out order template that I just wrote out, you know, IV or dependent, one gram daily, you know, cbc, cnp, esr, CRP every two weeks. And I said fact, you know, I have a contact at one of the home infusion companies, option care or I'll use, there's a couple other ones I'll use sometimes I just send that to them and they set up home health. They set up, you know, all the, you know, all the drugs get ordered through the pharmacy, like through the pharmacy and stuff. It's actually like very easy kind of like, if you set up IV infusions at another clinic where once you set, set the order rolling, like all that, like, they handle the authorizations, they get everything kind of set up maybe 10% of the time there's somebody who's got a high coat, like, you know, high out of pocket cost, and they can't do it for that reason. But it almost always gets approved. It's just a matter of whether something at the last minute they get a high quote of what it's going to be every week to have somebody come out. And the nurse goes out once a week, does the draw, like, kind of make sure the PICC line looks good. But for the most part, the patients are taught to do it and it's pretty easy after that first day. And then you just set them up for the pick line or sorry, bad.
- [45:29]
A
How long do you keep them on it?
- [45:32]
B
12 weeks. Usually, you know, like, the early literature was aiming for more like six weeks, but usually 12 weeks, you know, by the time they hit six weeks, they've been good, pretty good for a few weeks. At 12 weeks, you know, things settle down a bit more. You give more of a break and you've got more time to work with it because it just, you know, by that time they're on the third line biologic, and you're having to wait for the insurance approval. If you do six weeks, half the time you get there and they've like barely started that next thing.
- [45:54]
D
So a question about ertapenum, because I have used it on a couple patients. We're fortunate enough there's a. A person in the infectious disease department who does it. Like, we just email her and she said, yeah, I got it and takes care of everything. Pick line placement, all that, like, the responses blew me away. So much so that I was like, what are we. Like, what are we doing with hs?
- [46:19]
A
It's.
- [46:19]
D
If we're calling it, it's inflammatory and TNF and it's an antibiotic, absolutely kills the disease. So is this all bugs? Is it all bacteria?
- [46:33]
A
I'm giving my theory question. I want to give my theory first. I think it is a inflammatory.
- [46:39]
D
I did not ask. I did not ask Doctors. I know Dr. Cyrus this question.
- [46:46]
A
I want to see what Dr. Said thinks about my. My theory is that it is skin commensals that people are having inflammatory reactions to because skin commensals are resistant to all normal antibiotics, all of them. I think it's like an inflammatory reaction to staph EPI or to some other distance or you can't clear it. But yes, that's, that is my theory that it is an excessive inflammatory reaction to a skin commensal. All right, Dr. Seib, what's the real answer?
- [47:16]
B
Yeah, yeah, I mean I, I, my thinking is very much along the lines of that is that there is something abnormal in the immune response. And I think people argue whether, you know, there is a defect in the immune response so that you don't sort of contain and sort of limit the certain types of bacteria on the skin that trigger that response. So there could be a defect of some kind that allows altered proliferation and then an overactive response to that, or there's just an overactive response happening. There is something about probably the innate immune cell responses like you know, NK cells and mate cells and things like that that react to, you know, preserved bacterial antigens across lots of different species of bacteria that trigger that initial insult, you know, alert the rest of the immune system to respond like there is an infection present. So it mimics the response to infection and so that, that may kick it off and it's possible there's like some effect on the gut microbiome as well and that also sort of fuels that inflammatory response. That could certainly be playing a role too because yeah, it doesn't make sense. I mean it's not an anti inflammatory antibiotic. I think you really are shifting, reducing the microbiome and then you kind of take the fuel out of the fire in doing so. And ertapenem, like in some ways it gives me hope that we're going to do better. Like, you know, if you look at adalimumab, cosynthix, benzelics, like there is a little bit of a step up between those therapies but they don't touch erdipendum. Right. Like, you know, it is like 95% of the time a home run. And so yeah, there is somewhere in there, you know, a signal or cascade that if we can block it more specifically, like we should be able to get better drug responses over time. Like it is possible. I don't think it's an impossibility that we find something that hopefully does that well over time. I just don't know that we're always looking in like the right corners of the immune response. So far we don't have, you know, easy targets, you know, where drug companies are sitting on things that are T cell and B cell specific or whatever else. And they just, you know, don't have that in their stable to try yet at this point point. So to me it at least is a glimmer of hope that we're going to do better as time goes on.
- [49:05]
D
We should probably move on to surgery, right?
- [49:09]
A
Yes. But there's one more drug we got to talk about.
- [49:12]
B
So the.
- [49:12]
A
I think it is the. Because most germs are really not going to use ertapenet, just not. Line is phenomenally effective. I use it all the time as rescue therapy. Now for people who haven't used Linezolid, it's 600mg bid. As long as you do it for 10 days or less, it's got an incredibly benign safety profile. Do it for more than 10 days, you start to get into risk of neuropathy. But I have a fair number of patients who are like on a biologic and then are also getting 10 days a month of Linezolid and they get like, they'll be good those 10 days. They'll be great. Usually about 10 days after they'll be good and then the last 10 days they're like back to normal. But it's better than like it's it. And it's cheap, right? It's dirt cheap. It's not dirt cheap. It's like 50 bucks. For 10 days. For 10 days. If you have to pay cash. Do you. If I. It is possible. I've just been super lucky. Tell me how you use linazolid. I'm assuming you, you use it which, what's in place therapy.
- [50:20]
B
Yeah, like you said, it's not something where there's long term safety. I mean lots of antibiotics have a long track record of safety. Whether it's like, you know, we freak out about Bactrim but you know, people use Bactrim for prophylaxis for, you know, decades and it's not a problem. So there's plenty of things you can use long term. But lines aid is short term. Like 10 to 14 days is kind of a rescue. You know, people talk about using triple therapy with metronidazole, moxifloxacin and rifampin and that you can do for couple of months or a few months. The eleonzolid is like a short term flare. Rescue can be very reasonable. I haven't put somebody on like every month due 10 days as a way to kind of, you know, have them on an ongoing adjunct. But it's an interesting idea and something that, yeah, like it, it probably can work pretty well. It's not as good as erapenem, but it's, it's probably better than the average antibiotic. Is okay.
- [51:05]
A
Yeah, it's a, it's a, it's a easy drug to use. And for a patient who says, oh, I've been on so many antibiotics, never the linezolid will work like it is, it's reliably effective. All right, now let's. One last question before we move on to some surgery of the ancillary drugs, the metformin, the spironolactone reflumelast we mentioned already. Are any of them really very useful? Do you have many people on those in addition to their biologic?
- [51:41]
B
I mean, probably my favorite thing in that, I mean like spironolactone, metformin, like I said, like dapsone. I'm not very impressed with like they're all sort of okay. I mean, oral contraceptive pills, if you do content, like for patients who flare before their menstrual cycle, if you do continuously active pill and suppress cycles consistently, you do get quite a bit out of that sometimes. And so that's a pretty easy thing where you just, it's four packs for a three month supply, you know, throughout the sort of last row of pills, go straight to the next pack. And most patients you'll suppress cycles for, some will have spotting and it's irregular and you can't keep it up. But it does get around those premenstrual flares for a lot of patients. And infliximab is probably that. I mean, I use as much infliximab as like any other biologic, even though it's off label. And you have to fight for it because it is, it is probably still like the fastest and most consistent of them, like probably, you know, as good as been the Kismab or better. It's just, you know, it's more of a hassle to do infusions. The approvals are kind of hit or miss. And like J and J used to do a free drug program for Remicade. They've stopped it for Solara and Remicade in the last, like starting this year for any new enrollment, enrollments for people who can't get it through insurance or who don't have insurance. And so that's been kind of a blow actually because usually we could fight the insurance and if we couldn't get it, we had an out. But now we're kind of stuck. And none of the other biosimilars, you know, offer free drug programs for off label use in particular for hs. So it is, you know, an issue that there's sort of some advocacy for. I told Them. I wouldn't stick anybody on them yet. But yeah, if you, if you ask your JJ reps about, you know, what happened to the free drug program and, you know, if they're supporting all the patients they care so much about, like, why. Why have they taken away this drug? That's very important to some of them. Fair. Fair.
- [53:13]
A
So that my takeaway answer there was none of those ancillary drugs are that great.
- [53:18]
C
So I think that's a good point, that this is a chance for us to try to advocate for patients. This is. Infliximab is not expensive for the company or the biosimilars. Should not be expensive for payers. It would be great if we actually had this as an option for HSI patients. So hopefully the more that we all speak up, the more we can get this.
- [53:38]
B
Yeah, but it.
- [53:39]
D
So, Chris, isn't it? So I had a patient who actually wanted to go on Infliximab. They had failed Humira. They were placed on Cosentyx. The groin disease got worse. And so they asked about Infliximab. And at first the insurance company said it's not FDA approved. And I said, well, Benzalex is, and it's a lot more expensive. So don't you want to do the infliximab? I mean, and they did. They paid for the infliximab.
- [54:04]
B
Do.
- [54:05]
D
Do you see that with insurance companies where, like, infliximab is the cheapest option,
- [54:09]
B
so they still fight you on it sometimes. So, you know, it's off label, so it's easy for them to reject it if it's not in their algorithm. A lot of insurances do have it in their formulary for treatment of hs and so for some, they'll go along with it pretty easily. It is very expensive, even with biosimilars, like the dose we use because it's 10 mgs per kg. Yeah. Sometimes the patients can be heavier. Like, you know, we're not talking about two or three vials for like a, you know, RA patient who weighs 60 pounds, like, you know, 100 pounds or something like that. Like this is. It adds up quick sometimes. And so it can be like very, very costly when you do it, especially every four weeks. I mean, that being said, it does just work the best. And so you get something out of all that. For a lot of patients where they're especially those that have like terrible pyoderma and HS overlap, like those inflammatory, like sort of inflammatory syndromic patients, you know, they high dose infliximab is like the one thing that works for them mostly the time. So, yeah, so it's. It's a challenge with some insurances it's in guys, you know, the old treatment guidelines of 2019, you know, talk about infliximab like other international ones talk about. So there is plenty of precedent for it. A decent number of studies, usually with an appeal, you can get a cover, but there's, you know, 10% where they won't budge. They. They'll tell you you can only do five mix per kick every eight weeks, which never works well enough, or patients, you know, lose insurance. And they've been on it for five years, and all of a sudden they have no way to get access to it anymore. So, yeah, it presents some challenges, right?
- [55:30]
C
So I know we're running low on time, but one, if people wanted to learn more about surgical intervention, which I just think is so key and underutilized, A, what's the procedure you would tell people to learn to do? And B, what's the best way to learn how to do it?
- [55:46]
B
Yeah, I mean, there are, like a fair number of videos online now that kind of walk through the roofing. You know, I always tell people, if you ever want to come hang out with me, like, I have plenty of people come through the clinic and spend a day or two. And it's not like rocket science. I mean, the residents that we train, you know, I'll get some exposure. And almost all of them go out and they're like, how do I order those probes afterwards? They're all out there doing it in the community now. So if you know somebody else doing them and you can watch a few, and you've done plenty of other skin surgery for things like skin cancers. Like, you have all the basic tools already. It's just kind of like, okay, where do I look? Where do I numb that kind of stuff. You know, there's the SHSA meeting, which is. I mean, we don't always do, like, sort of like the nitty gritty of how it works, but there's lots of meetings where somebody's getting a surgery. We'll talk on hs. They're going to show you some videos and walk you through it. You know, you can reach out to me, like, I'll send you some videos or talk to you about it. The HS community in general is like, super willing to help and teach others. So I don't think you'd have much trouble if, you know, somebody's doing them to join them for a day or something or Again like just have a phone conversation, look at some pictures and videos and talk it through. It's. It's scary at first.
- [56:47]
A
Do you have a video repository for this?
- [56:51]
B
I have some videos that we've taken and a few that are like published, you know, in sort of review articles about surgery and stuff like that where you have to go and you have to dig for them a little bit. We did one on like there's one on our website now that I just did that goes through like it's more patient directed of like this is what to expect your procedure. Like it's got a video of what that procedure itself looks like and what the wound care looks like, how to take care of it afterwards. So we just posted that in the last couple of weeks and then. And it's on YouTube right now. If you look up probably like slide debriefing or something like that, I would guess it would pop up. I don't know exactly how do you have to search it but, but yeah, there's lots of videos that talk through, you know how to go about doing it.
- [57:29]
A
At this point I'm going to make a suggestion here that I think would. Would take that lousy Durham department in UNC that's kind of really struggling and put it on the map. Would be. And for cheap and easy, right you get a medical student. An iPhone camera would probably be good enough. But a medical student and a decent camera to come and spend a couple of weeks with you or do a one month research rotation and really. And then you know the AI video editing tools now are so good to edit them together into. Here are 20D roofings. Here are, you know, wide local exit. Like a medical student could easily put that together and if there was somewhere that had that a bunch of high quality videos I think that could be a real needle mover in the world of hs.
- [58:24]
B
Yeah we have some like paid for right.
- [58:28]
C
There are codes that get it paid for which also becomes a barrier sometimes to people doing it. So.
- [58:34]
B
Yeah, but it's. Yeah, if you do small things. Yeah the codes pay well for small things. If you're doing big stuff all the time then yeah it's. You can spend a lot more time than what you're getting back compared to treating skin cancers. But it's kind of a wash like you know, I'll have some patients where I treat three things that are small in different locations and that reimburses really well and then somebody else, you know, it doesn't work as well for. But it, it's all Fine. In the end, Dr. Ferris hadn't fired me for not meeting RVU expectations yet, so I. It's working out.
- [58:59]
C
Oh, yeah. Not yet.
- [59:00]
B
Yeah.
- [59:03]
A
All right. Anything that we haven't touched on that you want, you know, that's where the biggest podcast in dermatologists that dermatologists listen to and derm providers. Is there anything that you want to get out there about HS that we haven't. That we haven't talked about already?
- [59:23]
B
Yeah, I mean, you know, it's. It's getting better all the time. You know, it's still challenging to manage, but like, when you get these patients better, you know, the patient who comes in is a total disaster and it's like, where do I even start here? I mean, there is a path to getting those patients better. I didn't understand that when I started it. You know, I questioned myself the most that first year or two when those patients that walked on the door, I said, I'm going to be the HS expert. And then, you know, the bomb drops and it's like, how do I even, like, start with this person who's got Hurley 3 disease everywhere? I don't have any drugs that are approved, but like, over the course, you know, it's a project. It can take a year or two or a few years of, you know, stabilize it with medications and we've got more options for that now. Again, figuring out how to do some procedures yourself and sort of finding some servants who are willing to help you. But, you know, you can put light at the end of the tunnel. Like, I didn't even. I couldn't see it at first because I hadn't seen that path sort of to its end in the beginning, but. And patients have never seen it for themselves and so they don't have much hope sometimes. But you can make a huge difference over time, even in those worst cases. And the better our drugs. I mean, there's 20 drugs and trials right now. Like, we are going to have some step ups over the next five years that are going to do even better. Um, so there is absolutely a way and like, you know, there is nobody else to do it. Right. Like, you know, we. I mean, on the dermatology end, like, we know these drugs well, we know the procedures well. Like, there's no place else for them to go. And so they. We really do have like a unique skill set where we can serve these patients in my mind better than anybody else can. You know, it's a team effort sometimes, but like, if you're not the quarterback for them like they're going to walk out the door and be stuck right where they are and there is again like no needle being moved if we don't step up and do it it for them. So yeah, just realize that you have the skills and a very unique power and like place in society to help these people who suffer terribly. It's just a matter of like jumping in and figuring how to do that.
- [61:03]
A
Okay, last, last question of problem JACK inhibitors when they come into hs. So I'm doing the, the POVO trial and I think it works better than any of the biologics is, is my take or you know, we're not going to have head to head data but that's what it seems like. But I'm nerv. Like you know, they're the, the AE reports come through and you know, these are immunosuppressive drugs in people who have abscesses. Like I'm, I'm kind of nervous about JACK inhibitors and hs. Like what are you, where do you see them fitting in once they get approved?
- [61:40]
B
Yeah, I mean, you know, I think Jack's made everybody very nervous, you know, and it's all based on like, again there's not enough time to talk about oral surveillance and sort of true risk around JACK inhibitors and stuff. I, I'm, yeah, I am somebody who like, I feel like JACK inhibitors are safer than a ton of the drugs we've used historically. Like they're very great options and I think they get sort of an unfairly bad name. The safety profiles in the HS patients I think are gonna look very similar to other drugs ultimately. Yeah, my take, you know, I've been part of like the POVER sitting in trials. Like, you know, I use a fair bit of UPADA sitting up off label and so, you know, they're not perfect. I think they're going to come out like relatively similar to where like Cosindex and Demi are probably. There's going to be some patients who happen to respond better to a JAK inhibitor than to whatever biologic we've had them on so far. So it's going to be a great additional option. There will be some patients who would rather take a pill than an injection. So for them it's going to be first line. For others it's going to be, you know, second or third depending on what their preferences are. But I don't know that they're going to be a step up as much as an alternative. I think both UPA and POVO are going to be, you know, good options to have. It's going to put, you know, another quiver, another arrow in our quiver. But it's not going to be, you know, the thing that supplants everything else as number one efficacy, like an atopic derm. Like Jacks work better than all the biologics. I don't know that we're going to see something similar from an efficacy standpoint in hs, though. They'll be good. I'm going to be happy to have them.
- [63:00]
A
And we are big Jack supporters on Derbs on drugs. We've talked numerous times about why oral surveillance. It did not actually show that Tofa increases the risk. What it truly showed was that Humira reduces the risk. Like it's. And that's what the label says. The label table says compared to a tnf, the rate was higher. But. Right. It. It was that the TNF lowered it. Right. That's. That's the key thing.
- [63:26]
B
But yeah, if you, yeah, if you look at similar controls and like, with severe, moderate, severe rheumatoid arthritis and all those risk factors, like, they had lower rates of those side effects in the trial than they had, like, what we expected in real life. So. Yeah, it's just. Yeah. It's not a fair comparison. Yep.
- [63:40]
A
Well, Chris, I want to thank you for coming on. It's been a fantastic episode. I'm. Anybody who is an HS person is the saint in my. Like, you guys are the saints of dermatology. No, no question about it. Just really appreciate you coming on the show and to our listeners, hope you learned a few things. Hope you laughed once or twice. Mostly. We're hoping you're planning to join us again next week. Till then, I'm Matt Cyrus.
- [64:09]
D
I'm Tim Patton.
- [64:10]
C
And I'm Laura Faris. And we are derms on drugs. 1.