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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 dermatology and provided at no cost to medical providers. Derms on Drugs is where cutting edge derm meets hit or miss comedy. Dr. Matt Ziers from Docs Dermatology. And each week I'm joined by my residency buddies, Dr. Laura Ferris from the University of North Carolina and Dr. Tim Patton from the University of Pittsburgh. And we use our 70 years of combined derma experience to discuss, debate and dissect the hottest topics in dermatology. It is everything you need to know to be derb and you're having fun listening. New episodes drop every Friday and Scholars of Medicine, Apple Podcast, 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. Explore the best derma educational content out there, and I mean real pharma independent coverage of all of dermatology. Just get on there and Google Scholars in Medicine and you will find it. And it is supported by an amazing AI clinical consultant called Ask Simon that uses all of the curated knowledge and expertise of the faculty to answer your questions. This week we've got another one of our patented six pack episodes. And let's just get to it. Dr. Farris, what do you got?
- [01:16]
B
All right, so I have a paper from the recent jad. The cost of superficial radiation therapy are greater than Mohs micrographic surgery for the treatment of non melanoma skin cancer. Analysis from the CMS provider and service data set. So we talked a little bit about superficial radiation therapy for skin cancer here in the past. So we know this is like having its moment in dermatology. A lot of people are doing it, lots of controversy. And then there's the fancier cousin, image guided SRT or ig srt, which is basically SRT with some ultrasound. So, so what this group did was, and they were, you know, I'd say primarily Mohs surgeons. So I'm going to put that out there. But they pulled Medicare claims data from 2018 to 2022 and they looked at, you know, how are dermatologists billing more? Superficial radiation therapy? Yes. Are they billing more with image guidance? Absolutely. And over that time period that actually the image guided SRT went up by 250%. Simple radiation simulations, which, you know, used to be like, oh, do the ultrasound. That used to happen about half the time, about 50% of sessions. Now it's up to about 90% of, of sessions. And so here is the thing that's interesting. So you know, people will say well, you know, radiation, it's, you know, it's, it's not expensive, it's not expensive or you know, most surgery is a very expensive modality and, and image guided, you know, radiation is just simple, it's easier for the, you know, patient. We haven't had a lot of data on cost. So here is what is, I think the top line. That was really interesting. If you look at a typical course, which is 20 fractions, IGRT is 428% more expensive than standard Mohs with complex closure. So that's a, a pretty significant difference. Even at the low end. If you said, you know, what about if you just do 12 fract, you're still looking at 200% more than Mohs. And so, and then, you know, true srt, you know, they also looked, you know, people will say well, every case doesn't, you know, course doesn't have to be 12 or 20 cases. If they looked at the percentage of cases that were, you know, the majority of the cases were, you know, 15 to 20, they weren't mostly like the 5 fraction cases. So if you look at the difference in costs, you know, a 5 fraction case was about 1450, 12 fraction case, 3480 bucks, 20 fractions $5803 and 25 fractions over $7200 versus the most cases were either with complex repair, about 1600 bucks or with an additional, that's, you know, one most with one additional stage in a complex repair, that's the 1500 bucks. If you add one additional stage in a flap, it was like almost 1900 bucks. So you know, other than the 5 fraction cases, sort of 12 and up fractions, IGSRT costs more. And you know, the, the numbers are the medical, the Medicaid or Medicare costs are going up and up. So you know, interestingly, it is going to be interesting to see what happens. So this is actively being litigated sort of in the coding world right now in 2026, a new Medicare, there's these LCDs or local coverage determinations said that you cannot just repeat the simulations, which is the ultrasound, you know, to look at where there is tumor and to guide your therapy. And they're being denied as being not medically necessary. The American College of Mos Surgery, the American Society for Radiation Oncology have jointly come out in support of restricting, you know, the, the daily ultrasound and simulation codes. So you know, there's, there probably is a role for radiation, but it seems like you Know, it's maybe not like a very cost effective option for the average run of the mill patient, particularly one who could have Mohs with maybe just a complex closure or even based on this data, even with a flap. So thought this was interesting, putting a little bit of data behind something we've discussed and debated for a while.
- [05:59]
A
I think it's going to be cool to see what happens now that. So I, when I was looking it up as you were talking about this, right. They changed the codes. And the first thing I came up was with, oh, the code is 300% higher than it used to be. And I was like, what they meant they like. But no, it was that they got rid of, as you said, I think they got rid of the image guidance on every billing and just the code. So they said it probably went down to like 3 grand from 7400 down to like 2700. So still more than Mohs, but not as bad. It's, it's still an interesting thing. Like, I think if, I still think if I had a tiny little basal cell on the tip of my nose, I still think I would want IGSRT and then I would get it mosed if it came.
- [06:47]
B
But okay, 20 fractions, 5,800 bucks. That's a lot.
- [06:52]
A
It is a lot. But what my insurance will pay for it.
- [06:55]
B
And that is, that's srt. Sorry, that is SRT without the image guidance. If you've got Image Guidance with 20 fractions, it's 8,400.
- [07:07]
C
Like if you had a little teeny ditzel on the tip of your nose, you'd go to a Mohs. They would take like a good Mohs surgeon, minimal tissue. I mean, it may be secondary intent healing. You'll be healed in two, three weeks.
- [07:20]
B
Yeah. And I will say, like operating on something that's had 20 sessions of radiation is not like a super straightforward easy thing either. Right? So you, you change the, the healing, you change that sort of field. It, it, you're not going to get the same result from Mohs if you just do the SRT first.
- [07:40]
C
So I honestly think like a very, very good radiation oncologist would be like, this is a bad choice. Like really, really think about getting the most and then, you know, and that's their job. You know what I mean?
- [07:54]
A
I mean that is literally when we had the radiation oncologists on. That is literally what they said.
- [07:58]
B
That is literally what they said.
- [08:00]
A
Yes.
- [08:01]
B
Yeah. And if you look in like 20, $22, the amount of total Medicare expenditure, if I You know, roughly add this up, it's like $70 million.
- [08:14]
A
Could, could I maybe get it done? But then get one of those skin substitutes that cost like $22,000.
- [08:20]
B
Yeah.
- [08:20]
A
Put on there instead.
- [08:22]
B
I think those are also, there's a big lawsuit against those. Going on right now is like Medicare fraud. So I, I would say don't open up your superficial radiation skin substitute clinic. We're going to radiate your IGS RT skin substitute.
- [08:37]
A
Right. We're going to radiate it till it gets an ulcer. Then we're going to put a skin substitute on. There it is.
- [08:44]
B
Get you a good connection in jail to be able to have you continue to record with us. But so interesting actually to have data out there.
- [08:53]
A
Yes, it is. Thank you, Ferris. All right, Patton, what do you got?
- [08:56]
C
All right, my first six pack is a pre proof article available online from the JID in June of 2026. JID is for like smart dermatologists. I almost never read it. The title is Charting a New Melanoma Risk Factor Satellite Nevis Prevalence in High Risk and Population Based Cohorts by Nima Gahari et al. The authors spell Nevis with an A. That's how smart they are. Like they're just like, they do everything different and better.
- [09:22]
A
N, A, E, V, U, S. Correct.
- [09:25]
C
It was done in Australia. They use the Vectra platform. So that's the 3D total body photography machine. Satellite Nevis was defined as a Nevis that was in within 5 millimeters of a neighboring nevus. And with vector you can do like all these sort of crazy analyses.
- [09:43]
A
So you're not talking like satellite, like, because when you, when you hear satellite nevi. I was thinking like a congenital ne.
- [09:49]
C
Congenital? No, no, no. They defined it as you. You're doing your skin check and There's a mole that's 5 millimeters away from another mole or less.
- [09:58]
A
Okay, okay.
- [09:59]
C
They actually did it like 3mm, 10mm, but they, they settled on the five and that's what I'm going to stick with. So figure one is really cool. It's like the photo of the upper back shoulder of a patient. They use these avatars and all of the Nevi in the photo are circled and each Nevis has a number next to it and the number is the distance from its closest, neatest neighbor. So like vectric can like, they can like probably do that in a second. This study compared high risk melanoma patients to a population based cohort and asked the question if the high risk cohort had more satellite NEVI. And they did. Satellite NEVI were present in 62% of the high risk cohort compared with 26 of the population based cohort. And the mean number of satellite NEVI was higher as well. It was 3.83 in the high risk versus 0.57. Figure 2 is a forest plot showing that like unadjusted, the high risk cohort said seven times more satellite NEVI than the population based cohort. When adjustments were made for total knee discount, other risk factors like age, sex, sun exposure, high risk cohort still had significantly more, like roughly twice as many. Oh, oh, just. Yeah.
- [11:09]
B
This means they've got like two nevi that are really close together. Yeah, you're like. So you're more likely to have like kissing nevi almost.
- [11:17]
A
Yeah.
- [11:17]
C
Which honestly, that does look weird. I mean for all the skin checks we do when two moles like are close together, that always mentally stood out to me. Like, that's weird looking. Never really thought, do those patients have like higher rates of melanoma? And actually the, the paper really didn't. They, they kind of went backwards. So what does this mean for everyday practice? I have no idea. But now that I know the association, whenever I see a nevus within 5 millimeter of another nevus, especially in women and young patients where that, that was more prominent, I'm going to panic and say they should come in for like weekly tbs. I think that's the takeaway. No, seriously though, I think as we, we, we try and define high risk patients versus lower risk, you know, is, you know, who should be undergoing regular screening, who shouldn't, are satellite NEVI going to be factored into that? This was, you know, it was like sort of retrospectively, you know, and they defined high risk going into it. Like if you had a melanoma and one melanoma and you were under 40, if it was two melam, two melanomas under age 65, a strong family history of melanoma, multiple atypical nevi. They put you in the high risk cohort and then they kind of work backward and said, well, how many, you know, how many satellite nevi? So they, the author said, you know, prospective studies and things like that would kind of be the next thing to, to set to look at, but just kind of, I don't know. Interesting. I never thought of satellite NEVI could be like potentially associated with higher risk of melanoma, but maybe they are.
- [12:48]
A
Now did it show both in general, these, this is an additional risk factor or it is a specific risk factor for the Two satellite nevi. Like, if I'm looking at an EVIS and I'm like, that looks a little funny, but I think it's okay. But, oh, there's another one that's within 5 millimeters. Should that make me be like, whoa, that's because.
- [13:12]
C
Because one looks odd.
- [13:14]
A
Yes.
- [13:14]
B
But it's not that a Nevis with a close neighbor is more likely to be melanoma. It's that people who have these Nevis double pairs are more likely to have melanoma anywhere somewhere else.
- [13:27]
C
Yeah. And it was just like normal Nevi, like they didn't have to be like any typical Nevis and then a satellite one next to it.
- [13:33]
A
Crazy to me that that survived the adjusting for Nevis number.
- [13:38]
C
Yeah, yeah, it did. I mean, it dropped, but, you know, but seven times. It was really high. You adjusted for neva's number and it came down to like one point. Whatever. When they factored in neva's number with all those other factors still twice as high. Yeah. And even that one point, whatever, it was still statistically significant. Like the, the error bars didn't touch one. So I don't know.
- [14:01]
B
Yeah, I think what's going to be interesting is when we can have all these whole body images and then we can have people have been followed and then develop melanoma. So it's, it's an oddball, interesting association. Right. Now what you want to know is like, can AI say here, you know, this is the pattern of, of a person at risk of melanoma, especially without
- [14:21]
C
any other risk factors. Right. If it just, if satellite NE became a new risk factor, kind of interesting. They did. You know, they, they need to do a lot of work before we can definitively say that. But I just thought it was kind of neat.
- [14:33]
B
Yeah.
- [14:33]
C
And I just think it's neat, like potentially like just what vector can do. Right. I mean, they reran the analysis. They said, all right, well, let's do it with 3 millimeters. Let's do with 10 millimeters.
- [14:44]
A
Yeah.
- [14:44]
C
And vector, like they can just like process that. It's impressive.
- [14:49]
A
And is it the one that does the dermoscopy on all of the moles too? Yeah.
- [14:56]
B
It's not the machine, though. There is this machine that's coming out. I forget what it's called, but that goes up and down and it does such high resolution illuminated images that it actually shows, it looks, it's the quality of a dermatoscopic image. I think I presented that paper. That is not the vector. The vector you have to actually use Contact.
- [15:16]
C
Yeah. And they, they did for this, they had like a dermatoscopic images, but.
- [15:20]
A
Right.
- [15:20]
C
I think you have to do that on your own.
- [15:22]
B
Yeah.
- [15:22]
A
Okay. It doesn't do them automatically. Is the one that does them coming out soon. Do you know fairs?
- [15:28]
B
I don't know the timing on when that will be like commercially available. I think it's being developed and somewhere in Europe.
- [15:33]
A
Okay. All right, that's, that's good stuff, Patton. That is good stuff. Good, good work this week.
- [15:39]
C
Thank you.
- [15:40]
A
Attaboy. So my.
- [15:43]
C
Try my best to please you, man.
- [15:45]
A
My, my paper I'm going to stick in the skin cancer theme. So I really like this one. So it was a study where basically they. Well, here, let me look up the name of the study, which I don't usually pay that much attention to, but it was interesting. And so I want to say what the actual name of it was. All right, so the takeaway of this study, so it was the burning question, does exposure to low dose and low irradiance ultraviolet radiation lead to cutaneous DNA damage in people with skin types 1 to 3? And so basically they took a bunch of people, these were in Australia who were skin types 1 to 3 and they did biopsy and then radiated them with one either 0.7 or 1.6 standard erythema doses. And a standard erythema dose is just like a standard dose. It's not an md, it's not adjusted by your skin type, and it's a very low amount. So one SCD equivalents to like five minutes in the midday sun in Raleigh, Durham, for example, in the winter, it's like an hour of, of midday sun. But so it's a small amount. It's, it's generally non burning even in skin types 1 and 2. And then they said, does this cause DNA damage? But more interestingly to me, they looked at, does it, how well does your body repair that DNA damage? And so they looked at things like, so they basically radiated biopsy, then radiate, then 15 minutes later do another biopsy and then do, you know, another biopsy 24 hours after that, and then do radiate again on day two, radiate again on day three, radiate again on day four, and then do a biopsy 15 minutes after the day four radiation. And so it lets you see how many mutations does it cause, like right after the, the radiation, how well does your body clean them up over 24 hours. And then if you do it day after day after day after day, four days in a row, is there an accumulation. And it's an interesting. Whenever you look at their numbers, and this might have been largely because it was underpowered, but when you look at their numbers, as you would expect, there's significant DNA damage. In particular cyclopyridine pyridine dimers accumulate and then. But they pretty much all get taken care of within 24 hours. And whenever you do, repeatedly over. So if you look at 15 minutes after the first day versus 15 minutes after the last day, there was no accumulation. So there wasn't like more damage after the fourth day whenever you look at the cyclopyridine dimers. So the, the P values were like 0.9. So not 0.09. Like 0.9 now exactly the same. Yes. So it was, you know, if they did a huge, you know, could be that it just didn't do nearly enough people because what they were doing was doing it and then staining the cells to see how many of the cells show CPDs, how many of the cells show the eight OX G levels and how many showed P53 exposure. And as you would expect, CP53 went up because as you get DNA damage, CP53 gets upregulated. But my take on this study was that a low dose exposure to UV was very well repaired. Now obviously if you do. Because the question is, it's obvious that if you get enough uv, it doesn't get repaired day to day because if it did, then nobody would get skin cancer. So, you know, does this, I take this as being like, okay, we, a tiny little bit is actually okay.
- [20:00]
B
You only need like one mutation. Right? So the whole thing is like, you know, the reason patients with XP get horrible skin cancers is that like they can't repair any of them. Right? We repair 99.9 of our mutations. It's the very few that we retain. And then you got a second hit years and years and years later. So yeah, the average person without xp, we're like, you know, or making and repairing mutations all day long.
- [20:31]
A
So the question, as you guys know, I'm a believer in the benefit, the cardiovascular benefits of sun from nitric oxide release, blah, blah, blah. The question I always get from people is like, well, how long can I spend in the sun? And so the takeaway from this to me was it gave me like a reasonable, okay, 1.6 SEDs didn't show accumulation. And the numbers that it spit out whenever I had AI calculated all out were like, okay, in the middle of the summer, five minutes outside in the like fall and spring, like 20 minutes outside in the midday versus. Or it just, it gave, it gave me some answers to. Like, okay, here's something that you make an argument that it, not that it's totally safe, but that it looks like you can repair. You're not overwhelming your repair system is the way. That is the way that I would put it.
- [21:25]
B
I believe that is a lot of extrapolation from one study of sun over five days.
- [21:34]
A
You're accusing me of extrapolating?
- [21:37]
B
Yeah.
- [21:37]
A
Come on, Paris.
- [21:38]
B
You and your paid AI system. I, you know, look like, yeah, a little bit of sunlight is fine. I had to walk a block to pick up lunch and walk a block back. I did not like put on sunscreen to do that. It's index, UV index of 11 here. Like I, I get like, you know, a little bit is okay. But this to me is not enough data to say fair. This is you now because again, you can't, like, you don't, you don't need a detectable amount of DNA damage. You need a. You just need the wrong gene at the wrong, you know, to be damaged and not be repaired and then wait for that second hit. So I'm still not convinced, right?
- [22:21]
C
It's not, it's not realistic. But in the situation where somebody said, look, I live in a cave and I run out to my mailbox and because I live in a cave, my mailbox is very far away and I am exposed to five minutes of sun, should I wear sunscreen? I would be like, no, you don't have to wear sunscreen. Five minutes probably actually a good idea if you're living in a cave.
- [22:48]
A
It would actually be because the five minutes is if it's perpendicular. So it would be since you're upright, you're.
- [22:55]
B
Okay, we need to move on. This is like the dumbest argument for not wearing sunscreen.
- [23:02]
A
All right, let's move on. Ferris, what do you got?
- [23:05]
B
This is something much more practical. This was, this is a paper in clinical and translational science. Real world efficacy and safety of Tophositnib for patients with alopecia areata. A retrospective multicenter cohort study done in China. Okay, so you know, like Topacit and the OG JAK inhibitor, but you know, we don't really use it that much in dermatology because we got much more selective ones. But as we all know, it's now generic and it's now like a dirt cheap JAK inhibitor. So, you know, I think tovacitinib is actually where we first got the idea of, oh, My gosh. JAK inhibitors could be great for alopecia, but it's not FDA approved or other. We've got three other ones that are FDA approved. So this might be like tofacitinib's moment to shine. Okay, so how did it do? This was a retrospective study of like I think 61 ish patients. Yeah, 61 patients and who had refractory or severe AA who had at least, you know, 12 weeks to up to two years of toacitinib treatment for alopecia areata. So baseline mean salt scores, so that's the percent of, you know, scalp involved or percent hair loss was 70.9. So that's pretty good. Like the average clinical trial, you need to have a salt score of 50 or greater by at the end of Note, at a 12 week endpoint that dropped to 41. So a 41.6% improvement in salt score. By week 24 that went down to 28% and got it kind of, you know, plateaued from there. Over the full study they saw that 67.8% of patients had a 50% or greater improvement. And just over 20% of patients got down to a salt of 10, which you would say is pretty much like regrown hair. They also looked at eyebrows and eyelashes. And the patients who had alopecia universalis, they also regrew a little faster than the scalp eyelashes were sort, but they sort of plateau, plateaued out. By about week 12 they sort of had like a one point improvement in the eyelash eyebrow scale. So how does this compare to the FDA approved drugs? Baricitinib, JAK1, JAK2 inhibitor. It had two phase three studies and at the 4 milligram dose, about 35 to 39% patients hit assault of 20 or less by week 36 and that was like only 6% on placebo. So you know, this retrospective study, we don't have a placebo control obviously. And then eyebrow and eyelash regrowth. With about third of patients, Ritinib or Litfulo, approved for age 12 and up, which is sort of a selling point for that drug, JAK3Tech family kinase inhibitor and that one in the Allegro program, about 23% of patients hit assault of less than 20 and that was about a third by week 48. Also eyebrow eyelash Duroxolitinib, which is Laxelvi, our newest drug, and that one has JAK1.2 selectivity. And so on those phase three studies, about 40% of patients had a SALT of less than 20 by week 24. So, you know, where does, you know, that actually means that like tofacitinib's data and this is a retrospective study, but, you know, pretty surprisingly strong. But there's a couple other things. You know, all of the patients in this study, they did not have to have at least a scalp. They did not have to have at least a salt 50. So you have patients who did have less hair loss. And so it's a little bit easier obviously to get them to like assault 10 or 20. And you know, the, the severe group was like 46 out of the 60. So the other 15 were sort of more, less severe. And then the other thing is that, you know, these patients were not treated with like, they weren't like washed out, embarrassing or. I'm sorry, topacitinib monotherapy. You know, they could have like intralesional steroid, they could have minoxidil, they could have topical steroid, they could have oral immunomodulars. They had like microneedling with red light. So we really can't like compare. It's not apples to apples. So, you know, what does this do? And the safety data looked really good. Like there wasn't anything that looked terrible. But again, it's not like regular labs and the same amount of monitoring as you'd have in a, in a clinical trial. But I thought it was interesting, like, you know, for the patients who, like, there are insurance companies like the one that I used to work for, the institution of Pittsburgh where I used to work their payer, like their, their insurance company was like, alopecia is cosmetic. We will not pay for any treatments for alopecia. Done. End of story. So no appeals, nothing. So, you know, for those patients, toac at about 25 bucks a month out of pocket could I think be a good option for them.
- [28:34]
C
They. Was the dosing standardized or.
- [28:39]
B
I do not know that they actually reported. Reported that, that they looked at a standard dosing for that. So there was more variability with this being open label or, you know, whatever. Retrospective.
- [28:54]
A
Yes, that's. I mean, the, the data was pretty good. I'm trying. Yeah, I'm looking at it.
- [29:00]
C
I, I'm seeing initial dose adults 5 milligrams, bid juveniles 5 milligrams. But when they say initial, that makes me think they could bump it up.
- [29:08]
B
But they could have bumped it up. Yeah.
- [29:10]
C
I don't know if they got into that.
- [29:13]
B
Yeah, they did talk about dosing. I'll try to get that answer for you. But yeah, I'm sorry, what you guys think?
- [29:19]
C
Yeah, I, I Put a patient on topacit and it was amazing. He was so happy.
- [29:25]
A
Yeah, I think it's. If I had to bet, I am going to bet that it's as effective or more effective than the ones we've got and has a similar safety profile. That's what I'm gonna bet. But the problem becomes like, okay, we've got FDA approved options. You know, you're using the off label, the one that if there is a risk, it's with this one. Like okay, so now if they get a heart attack or a stroke or a blood clot, like it seems difficult to use it for a disease where we have other FDA approved options. Yeah, unlike say lichen planus or lichen plano pilaris where like we don't have any FDA approved options. So it would make sense. But it's hard to.
- [30:16]
B
Yeah, yeah. They did not go into more than the initial dosing of the toquestinib. I didn't think I saw it anywhere else. But yeah, so you know, we don't know what they did. So you know, interesting. I mean this at least gives some data to say, you know, if you cannot get an FDA approved drug, might be worth considering.
- [30:37]
A
Yep, 100% on board I think. And I think for a lot of other things when people are not happy, you know, if they're, if you've given them appropriate informed consent, like here's. We don't think it's a problem, but here's what the data is very reasonable. Long as you document it.
- [30:56]
B
Yeah.
- [30:57]
A
All right, Pat, what do you got?
- [30:59]
C
All right, my second six pack paper. I came across this horrible case report. A 58 year old male, Hillary, stage 3 HS and he developed an sec within his groin, HS lesions. So like they have this little timeline. Originally he got adalimumab in 2022, that didn't work. They bumped him up to Cosentics in 2024. He got the Squam in 2024 and it was non operable. It was considered like invasive. I don't know if they really got into all the details there but basically they gave him semi and I mean he just, he did horribly. He developed.
- [31:36]
B
By semi you mean semiplumab.
- [31:38]
C
Semiplumab. And he developed all these complications and he developed septic multi organ failure. So you know we HS is common. We see these patients all the time. Immune checkpoint inhibitor therapy is super common. It's like approved to treat every single cancer that exists. And I don't think I've ever seen an HS patient on ici. Therapy. And you know, if I did, after reading this case report, I'm like, oh my. Like, is this something we really need to worry about in our HS patients? So my second six pack paper is from the June 2026 edition of Skin Appendage Disorders and it's titled the Effects of Immune Checkpoint Inhibitors on Hydride N Supper. A Scoping review by Carmela Marquez et al or Camilla Marquez. The authors review PubMed Medline. And honestly, there's just not that much out there. Like, you know, I'm surprised it was this small. Five articles that described 13 patients seem like there should be more, but it is what it is. Pembro was the most commonly prescribed ICI. The number of cycles of ICI therapy, the average number was 18. Eight of the 13 patients had history of HS prior to immune checkpoint inhibitor therapy. Five patients, it was nuanced at hs. In the eight patients with a history prior to the therapy, six patients had quiescent disease and two had active disease. At the time of the immune checkpoint inhibitor initiation, only three patients, only three of the patients with a prior history of HS had a flare of their hs, whereas five had stable disease. So that was eight patients going in that had a history. Only three of them flared. And the five patients that developed new hs, mean time to onset was three months. Paper outlines therapies, nothing crazy there. Standard HS therapies that none of the patients were started on biologics, which I think I'd be a little bit nervous if patient was getting a immune checkpoint inhibitor. They probably don't want to put them on a biologic. It seems that immune checkpoint inhibitor therapy was stopped in only one patient because of the severity of the flare. So overall the takeaway is most patients with HS don't seem to flare. I mean, all the caveats, this is a very, very small study, retrospective and all that. So the horrible case report seemed to be an outlier. Most patients with HS didn't flare. No onset disease did not appear to have severe enough disease to warrant ICI discontinuation. So kind of nice to know, I think, when, if this comes up, kind of counsel the patients and their oncologist that it seems like in most cases it's not going to wind up being that severe. Case report that was reported, but so
- [34:15]
B
were they kind of scary on an ICI for a squam that developed in their HS or for another cancer?
- [34:23]
C
For the case report. Oh, and the, in the, the retrospective scoping review. Scoping review, it was not related to the hs.
- [34:32]
B
Okay, but case report it was related to the hs.
- [34:35]
C
It was, it was an HS that developed within the, the groin where his HS exists.
- [34:40]
B
So I guess my concern is I feel like there is SQUAM that is driven by like cumulative mutations like, you know, lung squamous cells, cutaneous squamous cell and sun exposed skin. There's also squams that develop in areas of chronic inflammation like hs, like margalins ulcer. I feel like I would be more nervous about using a checkpoint inhibitor in a, you know, an inflammatory setting squam than I would in a cumulative mutation squam.
- [35:13]
C
Yeah, sure. But I guess the question would be would you say don't use an immune checkpoint inhibitor or I would say are
- [35:25]
B
there options other than an immune checkpoint in those settings? But I don't know that that's the right answer. Like that's what I see. Thinking acetrant.
- [35:34]
C
Interesting.
- [35:35]
B
Yeah.
- [35:36]
A
This is a situation that I hope I never face clinically because that would be like. Really? Because. Yeah, there's no. It's one of those deals where there's no good option. Kind of like you're darned if you do, darned if you don't. You just don't know what's. I mean, you don't know what's going to happen. Right. It might go great, it might be a disaster, but it's hard.
- [36:02]
B
Yeah. And I think like, you know, one ICI work in tumors that have high tumor mutational burdens. I don't know if we know the answer, but my gut feeling is that TMB is not high in those like squam associated, those HS or marginal and ulcer associated screams. It'd be interesting to find or study that. Yeah.
- [36:24]
C
You know, this actually came up in a, in a tumor board that we had recently because I said the same thing. I'm like, it was a, it was a stasis ulcer that developed a squam. And I asked that same thing. Like typically Those have lower TMBs tumor mutational burdens. So is there less of a response? And one of the oncologists said that they had done a recent study where that didn't seem to make a huge difference. Like they, those patients with low TMB squames actually had a decent response to the immune checkpoint inhibitor therapies anyway, so.
- [36:58]
B
But. Right.
- [36:58]
C
I thought the same thing.
- [37:00]
B
All right. Yeah. Well, we're gonna hope we don't have those patients.
- [37:04]
C
Yeah.
- [37:04]
A
Yes. We're gonna hope that we can send them to Chris Syed if we have patients.
- [37:10]
C
Honestly, like looking back on this and I Thought I remember that like in the chart. I don't think they gave the indicator, like of all the things that they gathered in this information, I don't think they gave the indication for the immune checkpoint inhibitor therapy.
- [37:21]
B
Interesting.
- [37:22]
C
Yeah.
- [37:22]
A
Okay. All right, all right. My last, my last two are just kind of an interesting technology thing. So just that these came out at the same time. So one was randomized trial of manage standard care for atopic dermatitis versus teledermatology care. And so people had to have a preexisting diagnosis of atopic dermatitis. And then they were randomized one to one to either come in for standardized care or just store and forward teledermatology. Like type in your stuff, take pictures, upload them. We'll tell you what we think you ought to do. 300 people in the trial. So decent size and the, the AD was reasonably mild. That was one of the like things about it that made it a little harder to like really figure out. So the easy scores at baseline, like the mean was around 5. So it was like pretty mild ad to start with. But for all of the things that they talked about, all of the endpoints. So easy scores, iga, poem, patient oriented eczema measure, all of it. Like the teledermatology care was just as good, so they to take it. And so the people who got randomized to Teledermatology only had 0.07 visits per year. So most of them never saw the dermatologist at all and were totally fine. And so it was just interesting and unexpected result. Is what I would describe it as kind of suggesting that you can manage AD pretty well via store and forward telermatology. The second one was a psoriasis study that was looking at target lesion assessment. Basically an app that you put on your phone, you pick one of your psoriasis lesions and you just take a picture of it every day. And they compared that to kind of one of these total lesion severity score things compared to in person assessment and it was basically just as good. So again, just another kind of take on we can probably. That one there wasn't even like a dermatologist monitoring it. It was AI. Total lesion severity. They're just kind of an interesting.
- [39:55]
B
Not total lesion. Target lesion.
- [39:57]
A
Target lesion.
- [39:57]
B
Yes. Yeah, yeah, yeah.
- [39:59]
A
Target lesion severity. Yes. Not. Yeah, total lesion severity score is tlss, not tls. So target lesion severity. So and it was monitored pretty purely by AI and can at least get
- [40:12]
B
an objective measure from AI of degree of improvement.
- [40:16]
A
Yes.
- [40:16]
B
Yeah. No, I think that's interesting. I really think telemedicine is probably the future for the care of a lot of inflammatory skin diseases. Like dragging people into the office and going over things and you know, doesn't necessarily make a lot of sense. It's not necessarily the best utilization of resources.
- [40:37]
A
Oh, great.
- [40:38]
C
For that they did the store and forward. Because I've done both that and video visits where you have the live, like Storm Forward. I like, I just can't stand. I mean, it's like you, you say, okay, well here's your therapy. And then they, they send a message back. You know what? I forgot to mention it. I already was on that one. And it burned. And then you're like, oh, okay, well, are you moisturizing? And they're like, well, which one should I like? It's this, it's this back and forth that in a live visit you can knock out like that and the Storm forward. I mean, unless you have like really good nerd. Like, did they, did they go into number of messages back and forth. That was always the thing with Storm
- [41:21]
A
Forward for me is they did go into that actually. And let me see if I can. So first, my take on store and forward is the same as yours. Like, I, I hated it. I didn't mind it if I was messaging with their primary care doctor instead of them. But direct, direct doing it with the patient was really painful. And. But I could see doing like a store and forward and video. Because the problem with video visits is you're often like, well, this connection sucks. I can't. Because. Right. You just don't get to say so. I feel like the combination of. Upload some pictures ahead of time.
- [41:59]
C
Yes.
- [41:59]
A
And then we'll have a video visit. Because the other thing that I loved about doing Telederm was lower expectations. So meaning the patients were much more. You know when somebody takes a half day off work and drives in to see you and waits and the whole thing like, they want a. Like, here is the plan. Here's what we're going to do. I've got an answer for you. The blah, blah, blah, blah, blah. And whenever it was like, okay, jump on your phone at 2:15 and like, we'll do a FaceTime call. Like, I didn't do them on FaceTime, but it was the equivalent, like they were much more okay with like, well, I don't really have any. Great. Like, try this. We could try that. Like,
- [42:39]
B
I just think it narrows the scope of what you're covering. Right. So like, yes, my problem Is like, I'll go in and it's like I have a rash and I want a skin cancer screening. And I'd like to talk about why my nails feel brittle at 87.
- [42:53]
C
Yeah, it's. It's. They flip it, like, flips.
- [42:56]
A
The.
- [42:57]
C
The timing of the. The visit. My. My manager said this. She's like, when they come in, they're. They're on your time and they don't, they don't care about how long it takes because you're. But when it's a video visit, that's like their time that they're on.
- [43:12]
B
Yeah.
- [43:12]
C
And so they're like, let's, let's get this over with as quick as possible. I want a quick answer. I'll put together a treatment plan. That's fine. We don't need to go into a lot of detail. It's. It's like remarkable, the difference between those two visits.
- [43:26]
A
Yeah, Yeah, I agree. Like, I. If I could do most visits via that, I would have.
- [43:34]
C
Yeah.
- [43:34]
A
Like, it's. Especially now with, like, if you could screen, like have AI transcribe the whole thing and do the note.
- [43:42]
C
We have.
- [43:43]
B
I use like a bridge. I run it. You know, it's sitting there. It writes basically my whole note for me, listening to the conversation with the patient.
- [43:52]
C
Yeah. The trouble with the bridge, though, is you still have to sit there through the conversation. Not that, like, it seems like I'm badmouthing patients, but you have to. You're actually there to interact with a human being.
- [44:02]
B
You can't get away from that. Yeah.
- [44:04]
C
But because you had to sit there for that history. What would be nice is like in a bridge prior to the visit where the patient sits down with the bridge and says, I'm going to give you my whole history and it's going to be maybe like a five minute history. And I think good AI narrows that down to one or two paragraphs where you're like, okay, I got it.
- [44:24]
B
So I think we make an avatar of you as the AI asking them questions, and then that gets summarized and then that goes in and then you.
- [44:33]
C
My personality. I don't really think AI could.
- [44:37]
B
It would be. It'd be like, you are AI. Yeah. People would refuse Matt to do it. We can make Matt as an avatar doing that.
- [44:46]
A
So, I mean, but you guys have played. I know you guys have played a little bit with Doctronic. That is basically what Doctronic does. Yeah.
- [44:53]
C
Yeah.
- [44:54]
A
Right now it's via typing. It's not an avatar yet, but it takes a really good history. Gives you a summarized soap note and a preliminary assessment plan.
- [45:03]
C
I mean, it's kind of. It's kind of insane that, like, clinics just don't start. Like, just don't do that. Right? Like, put in your whole thing to Doctronic and I'll see you in a week. And then when they come in, you have everything there, and you just walk in and be like, okay, yeah, I'm looking at it. I agree. Or this is. Yeah, I mean, it's kind of crazy. We're not doing that.
- [45:26]
A
Well, it's what I do now. Whenever any of my family asks me a medical question, I'm like. I'm immediately like, okay, go to Doctronic, fill out the thing. Send me the assessment and plan and the soap note, and then I'll tell you what I think that is awesome. Excellent, right?
- [45:43]
B
That's what I do when my kids are like, can I spend quality time with you? I'm like,
- [45:49]
C
can I play catch?
- [45:51]
B
Yeah.
- [45:52]
C
Call up Doctronic.
- [45:57]
A
Okay. On that note, thanks to our listeners for joining us. I hope you laughed once or twice. Hope you learned a few things, and mostly, I hope you're planning to join us next week. And until then, I'm Matt Zyrus.
- [46:07]
C
I'm Tim Patton.
- [46:08]
B
And I'm Laura Ferris. And we are derms on drug.