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- [00:05]
A
Welcome to season two of Derms on Drugs, a video podcast brought to you by Scholars in Medicine. The best educational platform in dermatology and provided at no cost to medical providers. Derms on Drugs is where cutting edge derm meets hit or miss comedy. I'm Matt Zyrus from Docs Dermatology and each week I'm joined by my residency buddies, Dr. Laura Faris from the University of North Carolina and Dr. Tim Patton from the University of Pittsburgh. We use our 60 years of combined derm experience to discuss, debate and dissect the hottest topics in dermatology. It is everything you need to know to be on the cutting edge of dermatology, and you'll actually have fun listening. New episodes drop every Friday on Scholars in Medicine, Apple Podcasts, Spotify and other major podcast platforms. And a reminder that there is a video component that has some of the key figures and tables from the articles we talk about. This week we've got another one of our patented six pack episodes where we are going to talk about the stuff that has caught our eye in the literature as the most interesting and useful over the last few weeks. Let's go ahead and get into it. Dr. Farris.
- [01:08]
B
All right, so I am going to start with a paper that was published in JAMA Dermatology, and this is by Breglio et al. And this is looking at everybody's favorite vitamin, niacinamide, or, sorry, nicotinamide, not niacinamide, nicotinamide, B, vitamin B3. So this was, you know, we've had a few papers that have been small randomized control trials looking at nicotinamide and the prevention of skin cancer. And, you know, the first one, like made it into the New England Journal of Medicine. Then there has been some, you know, thought that, well, other studies have maybe refuted it, but this was one that was looked sort of done on a really big scale. So they looked at 33,000 patients from the VA system. So what does that mean? They're all going to be like, male and older and they're mostly going to be white, but that's okay. So they pulled 12, about 12,000 patients. So first of all, they picked people who had had at least one skin cancer. And then they pulled, they found 12,000 who had been on at least 30 days of nicotinamide, 500 milligrams twice a day, and then did like propensity score matching. So matched controls about 21,000 people. So then what they could do is then look at, you know, incidence of skin cancer over time. So who are These people mean age was 77, they were 98% male, 95% white. They were pretty similar in terms of those demographics. The nicotinamide group was more likely to have had cll, to have had a solid organ transplant, although this was definitely the minority of patients and to have been had acidretin treatment in the past. The median number of skin cancers before starting nicotinamide was 3. But 15% of them actually had 10 or more skin cancers before starting or before going into this cohort. So what, what's the top line result? Nicotine.
- [03:18]
A
Just to make sure here. So again, they only looked at people who had had at least one skin cancer.
- [03:24]
B
Yep.
- [03:25]
A
Okay. All right.
- [03:26]
B
Yeah, so you couldn't, it wasn't like anybody went on nicotinamide for anything. So I think the idea was like they were hoping that actually like they were on it for skin cancer prevention. So top line result, 14% reduction in skin cancer risk and in the nicotinamide group versus the group that did not receive it. So, you know, that's not insignificant given the size of the va, the number of non melanoma skin cancers. What really drove it was cutaneous squamous cell carcinomas, 22% reduction overall. There really wasn't protection from basal cell carcinoma that was sort of overall. However, if you looked in the group that started it early, like they'd only had one, there was actually a little reduction there. Biggest bang for your buck was, you know, if you started it right after you had your first skin cancer in that group, the risk reduction was 50%. So I thought that that was interesting. In the solid organ transplant recipient group, again, it was like a couple percent of the population, they did not see a significant benefit. But if they looked at people who started it, who had had a solid organ transplant, if they started it once they'd had just one or two skin cancers, then they actually had nearly a reduction in subsequent squamous cell carcinomas. So you know, I thought this was helpful. So, you know, this was, this was good. They matched to like the number of past skin cancers, the timing of their primary skin cancers. They broke down the results by like, you know, did they started after 1, 2, 3, 4, you know, 10 skin cancers, etc. So you know, I think like the take home point is if you're going to do it, start early, you get more bang for your buck if you start after that first skin cancer. And so, you know, I thought that was good. It's the va. So like one of the things, so you know, what are the limitations. Right. So you don't need a prescription to start nicotinamide. Anybody who's worked in the VA knows that the vets want a prescription for absolutely every over the counter medicine, like Tylenol, that they might possibly take. So you actually probably have some decent records where is, if you tried to do this in one of our health systems, people might not put down the nicotinamide. So probably better, you know, accounting for it. But, you know, their point was, even if people were taking it outside, that should bias you toward the null. So if they didn't get it through the va, you know, you could have people in the control group who were taking it, but that should bias toward the null, not sort of bias you toward nicotinamide being protective.
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A
So have you, Are you guys already using this? Have you been. Do you, do you routinely recommend nicotinamide to everybody? With what, like, what is your thing?
- [06:19]
B
I was. And then I kind of was like, well, then the transplant study didn't show it worked and those are the patients I worried about. Then I was reading other studies. I was like, maybe I meh, maybe I shouldn't do this. And then, you know, I think the problem is then when I do it, I'm like, oh, God, you've got like 85 squams. I mean, try nicotinamide. But that's actually the wrong approach to take. You should be like, you've had a skin cancer. This is a vitamin. It's pretty safe. You know, why don't you, why don't you do this?
- [06:50]
C
Yeah, I am not as good as I should have been. And I think I'm actually going to be even better now. I mean, I had a guy yesterday who had like history of aks, lentigines, never had a skin cancer. And he's, he was just one of those guys. Like, I like to keep a close eye on things. I want to keep coming on a regular basis. And I actually brought up nicotinamide to him. I mean, right. If you started after one and it's better, maybe if you started before you even get one, it'd be even better.
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B
High enough risk. Yeah.
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A
Yeah.
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C
But then I kind of want to say we're going to be like, just recommending this to everybody because it's in a ton of the skin health supplements along with collagen and vitamin C. Like nicotinamide is in a lot of those overall. This is for your healthy skin. Are we just going to be recommending this to everyone?
- [07:42]
B
I mean, I thought, I thought this paper was helpful. The other thing My pearl that I do. I'm better at this. With skin cancer patients, look at their med list and make sure they're not on hydrochlorothiazide. That is associated that too. I'm. Yeah, I've gotten better at that. So, you know, clear association with, you know, cumulative use of hydrochlorothiazide. New squamous cell carcinoma risk. So I do a better job of looking for that. But now I'm gonna, like, I have a. I have a resolution. I'm gonna do both.
- [08:12]
A
The. One of the things that's always interesting to me is why are all the studies 500 bid? Why can't it be 1000 once a day? People are much more likely to take 1,000 once a day. They are to take 500 bid.
- [08:26]
B
That's true. I wondered that too.
- [08:28]
C
Question I. The other thing you said nite at the beginning, then said, oh, no, nicotinamide. Those are the same. Exact.
- [08:35]
A
They're the same thing. But I, I have a case.
- [08:37]
B
People give niacin, which then, yes, causes flush. Nicotinamide makes it much more clear. If you just say nicotinamide, then they're not like niacin, niacinamide. But yes, they are. They're be.
- [08:49]
A
I had a patient who we worked up out the wazoo for flushing, and she be, you know, I'm on niacinamide and blah, blah, blah. And I finally had her bring her meds in and it was niacin. And she was like, oh, no. The pharmacist told me that was niacinamide. And I was like, oh. So, yeah, that's a. It's worth being very. If you get somebody who's, who's flushing, definitely. If they say they're a niacinamide, definitely make sure of that. All right, let's. Let's move on. Patton, what do you got?
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B
All right.
- [09:19]
C
My first six pack was from the July, August 202025 edition of Dermatitis titled New and Emerging Pharmacotherapies for Pruritus A Systematic Review and network meta analysis. Speaking of network metalysis by Lee et al. Authors wanted to compare the efficacy of medications studied to treat pruritus using just one measure, and it was the four point reduction in the peak Pruritus numeric rating scale, also sometimes referred to as PPNRS. The numbers are confusing. Figure one says that 48 studies were included, but then table two says only 31. And it seems like they finally settled on 29. And it wasn't 100% clear how they whittled that down. Fifteen studies in atopic derm tendon psoriasis, four in prurigo nodularis. So, you know, four studies and a meta analysis. Is that helpful? Figure three has kind of three separate force plots, one for each disease. For. For atopic dermapadacitinib was the most effective itch reducer. I want to say that they combined the 15 and 30 milligram dose data. That's what I gleaned from going through the supplementary material, which is what a dedicated and conscientious podcaster does. We. We go through the supplements. Abro, berry, doopy. They were around the same. Lebry and Treo rounding out the rear, so to speak. For psoriasis, 10 studies were evaluated. Ixakizumab, Ustekinumab were the winners. They didn't go up against, like, the big boys. Like, the Twilight 23s weren't really in there. Did they not focus on itch in their studies? You guys did clinical trials for the 23s. Was itch not a huge component of that?
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B
I feel like that's a question in all of them, but I don't know.
- [11:00]
C
Yeah, I don't remember. But maybe it just wasn't nrs. Like, they didn't do NRS for, like, that was what they the. So I don't know. For Purago Najula. Pure Purragollaris. You know, the trouble with that word, pruritus was I saw the P and then the U and the R. And so for me, that was pure. And then you tried to throw an R ahead of a P, a U and an R, and you can't say that. You can't say pru or error. And so I just. I ignored the first R and went with puritis. That was how I said it, because I just couldn't get past the fact that really just ignore the second R and think of the word prune, and that's pruritus. But, man, that. That. I really had to rework my brain network, it looks like.
- [11:52]
A
For anybody who's wondering, we have been making fun of Patton since residency for the way that he's always said pruritus.
- [12:01]
C
Well, I just wanted to explain why. I think maybe garner a little bit more sympathy.
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A
You didn't need to explain why. It's just that you're an idiot.
- [12:09]
C
Oh, that's the short story. Fine. All right. I'm just going to call it pn can we just go with that?
- [12:14]
A
Okay.
- [12:15]
C
Nemo was the most effective at itch reduction, doopie Next most effective serlopatint. I'm not sure if I'm saying that one right. And vixarilumab. So CIN was a neurokine in one receptor blocker. Substance B binds to NK1. We itch. They halted that trial. Vixerellumab, it's an oncostatin M receptor blocker. I think they halted their PN studies as well. So I, I, this didn't really add much. Right. UPA is good for ad Ixekizumab being like I, I guess if you have your itchy, itchy psoriasis patient, maybe icsi. I, I think I, that was kind.
- [12:55]
B
Of their thing for a while when it came out. Remember the itch of psoriasis. I feel like ixacizumab really like pushed that when they came out. So I think they asked better and more questions about it.
- [13:05]
C
So yeah, my sense is that risen kidumab is probably just as good for itch and maybe they just didn't look at it, I don't know.
- [13:14]
A
So I am a, I'm going to use this as my moment to wax poetic about itch a little bit and itch measurement because it drives me nuts. Right. So when you look at the studies about NRS scores for psoriasis and atopic dermot, they say that psoriasis is just as itchy as atopic derm. Right. And that is just crazy talk. Right. It's crazy talk that patients with psoriasis don't complain about itching like patients with atopic derm. And here's the reason why. So if I said to somebody it's easier to think about it with a pain scale. If I said to somebody who's never had a major injury in their life nothing terribly painful has ever happened and I squeezed their finger in a little vice and, and said okay, rate that on a 1 to 10 of how painful it is and I grease it really hard. Oh, oh, oh. And let's say then though that that was a 28 year old woman and then after that she got pregnant nine months later, natural childbirth, no pain meds at all. And then after she gave birth we gave, we came back and gave her the same test and squeezed it again. You think she's still going to call it an 8? No, she is not. Right. So any kind of a scale like that is very susceptible to anchoring and Right. The itchiest you can imagine being is based largely on how itchy you've ever been. Any of these 10 point scales. I'm very suspicious of because as you know, I don't know if most people know this. The, the pain 10 point scale is the, the main bad guy in the world of like, what caused the opioid epidemic. Forget Purdue Pharma. If they, if somebody could sue the 10 point pain scale because at, at one time it was. If somebody said their pain was a seven, like quality indicator was. You gave them an opioid. Right. And. And what about the faces?
- [15:14]
B
One like, where you make like, you have to pick which face looks the most. 1. I think those guys are. They should go to jail.
- [15:24]
A
For both itch and pain. They should be functional questions. Right. So for itch, what I. Basically what you want to say is, okay, like, is, are you so itchy that, like, you notice it, but it doesn't really bother you? You can go about your day. Are you itchy enough that, like, you're thinking about it a lot, but, like, you can still do stuff, or are you like, so itchy that, like, you're just thinking about it all the time? Like, it's, it's hard to like, because it should be functional. Right. So either no impact on function, some impact on function, or a lot of impact on function.
- [16:02]
B
That's why I like the studies that look at sleep disturbance. Right. Is it like making the scratchy things, the things that, you know, measure if you're scratching, you should give everybody poison ivy and scabies the month before they go into the study. And then you'll be like, how itchy are you?
- [16:19]
A
That's. I, you might have some trouble getting that through the irb.
- [16:22]
B
You think so?
- [16:23]
C
I do not think maybe up in Canada, maybe Drucker can do it.
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B
Yeah.
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A
The biggest thing that I would say also about this, that was kind of of interest to me, you know, that Nemo is so much better for Prigo nodularis, but it, it. I don't think it was even in the network meta analysis for atopic dermatitis. Is that, Is that correct?
- [16:51]
C
That's correct. It wasn't included in the atopic derm part, at least in the little forest plots they did. And I, I don't know. You know, they talked about, oh, there was a really quick onset of itch improvement with topical ruxolitinib, but for whatever reason or another, just didn't make the final cut. And I don't know if they explained that well or didn't.
- [17:14]
A
Yeah, it's. It's a, it's hard any. It's always hard to compare anything that's topical and systemic, but it, You Know, I'd say this was, you know, the, the psoriasis ones. I don't care. I think that was kind of silly to put in. But I, I would say in general this, this was in line with, with my experience of which drugs work the best. Nothing really, you know. Okay, great. Nemalizumab is probably the best drug we've, best biologic we got for itch. JAK inhibitors are probably better than Doopy Doopy and the other biologics for itch. But you know, okay, great. That's what we got.
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C
Yeah, yeah. Wasn't, wasn't anything earth shattering. No, sorry, sorry.
- [17:56]
A
I'll forgive it, I'll forgive it. Let's jump onto mine. So I am now doing a couple of articles, two this week instead of my normal three.
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C
Excellent.
- [18:08]
A
Number one was interesting. So a randomized double blind trial of oral minoxidil 2.5mg vs 5mg for male androgenic alopecia. So title of the study, oral minoxidil 2.5 mg versus 5 mg for male androgenic alopecia. Double blind randomized clinical trial. This was in, published in JAD online. So far what was interesting is that whenever you look at the dermatologist assessments, there was no statistical difference between 2.5mg and 5mg. However, whenever you look at self assessed clinical improvement and the patients were blinded as well, there was a significant difference and it was interesting. So when you look at, you know, how many patients said they had great improvement, the people who got 2.5 milligrams it was 46%. So about half people who got 5 milligrams it was 72%. So about 3/4 meaningful difference. When you look at great improvement from the dermatologist perspective, the rater's perspective, they said that in the 2.5 milligrams it was 25% and in the 5 milligrams it was 32%. So just a big discordance between the dermatologist assessed improvement versus the patient assessed improvement. That was one of the biggest things that I took away from it. And also that this was a relatively small study, so 50 people in each group. I would bet that if you redid this study with 200 people in each group, there would be statistical, statistically significant differences. That was my other takeaway from it. But you know, so it, it suggests to me that the 5 probably does work better, but that the 2.5 works pretty well also. What do when you guys use oral minoxidil, what do you usually do for dosing?
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B
I start with males, 2.5. With females, I start with 1.25.
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C
Okay.
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A
Patton, same how often?
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C
Up to 2.5 in females. And I had one female patient, I think we talked about this before. She wanted to go to five because she was tolerating it and she wanted to see if it would be better. So I took a female patient up to five. I routinely take guys up to five.
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A
Do you see much hypertrichosis at five? You know, fuzzy, fuzzy faces.
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C
No, that's just not a frequent reason for discontinuation. It's not like I never stopped it because a patient calls and they're like, no. Or they don't want to try it. And I'm seeing them for the first time and they don't want to try it because they got it with it. But it's not a lot. It's not high. It's got to be less than 5%.
- [20:52]
B
In men or in women.
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C
Are you talking about like, well, nobody. No guy's going to complain about that, I don't think. But females, yeah, it's less than 5%. I just don't get that complaint a lot.
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B
I see it in women if I.
- [21:05]
C
Maybe I have horrible follow up and they're quitting it and I don't.
- [21:10]
B
No. It may just be the patient population. I gave one woman when I first started using it, I was like, didn't know where to stop. And I think I went up to like 7.5 or something and this poor woman like came in with horrible hypertrichosis. I was like, sorry about that. Go back down to half a pill. But, yeah, no, I, I do see it. And like, you know, sometimes it's just like, it's just like a little bit kind of along the lateral cheek. It's like I have to ask about it or look for it. But now that I've been diligent about that, I do see it. Yeah. And I mean, men don't care, right. If you're going to shave anyway, you don't care. Some like it.
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A
Well, unless they're getting it like on their forehead or something. I mean, it's, you know.
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B
But I. In men, it's always in the beard area. I've never seen it on, like the forehead.
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A
Patton, how long have you been taking it?
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C
I don't need such things.
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A
It's obvious.
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C
You think so I had a hair transplant in Turkey.
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A
All right, let's go to my second article. This was just a Case report but it was a premolast in the treatment of pityriasis like anoides et varioliformis acuta. A case report pretty like pretty bad leva and initially treated with 80 milligrams a day of prednisone plus azithromycin, 500 milligrams a day. Then they stopped the steroid after a week due to steroid side effects. Put them on acetretin. That didn't work. Then they put them on a premolast and it worked really well. And the main takeaway here is I'm always looking for new reports of PDE. Systemic PDE4 inhibition working. So now reflum Elast should be a go to drug for Pleva and probably for PLC as well if it requires treatment. That was my takeaway there.
- [22:59]
C
I don't know. Podcast should be changed to derms on Rofluma last.
- [23:03]
B
Exactly.
- [23:05]
A
It's not a bad idea.
- [23:06]
C
We really do.
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B
I wonder if they sponsor us.
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A
I doubt it since it's $6 a month.
- [23:14]
C
All right, I'll take anything. I'll take 5 cents. I don't care. Give me it.
- [23:18]
A
All right, let's move on. So Ferris, what do you what's your next article? What do you got?
- [23:22]
B
All right, my next article was just came out in the Lancet and was.
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A
Such a special journal.
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B
It's very special. It's a very European kind of experience. It was also extreme. It was also presented at EADV once daily oral icotra kinra versus placebo and once daily oral ducravacitinib in patients with moderate to severe plaque psoriasis. This is iconic advanced 1 and 2 to phase 3 studies. Linda Steingold is the lead author on this. Okay, so, so what was this? So this was basically a head to head science, you know active comparator study of look in of two of them. So hang on trying to get my numbers in front of me. Okay, iconic one and two over about 1200 adults. Moderate to severe plaque psoriasis. What does that mean? 10% BSA IgA 3 or more PASI score 12 or more 20% about 20% of the patients were severe at baseline. Most of these patients not support surprisingly in this day and age had tried systemic therapy 2/3 they're about 25% were biologic experienced and so co primary endpoints were PASI 90 and IGA 0 and 1 week 16. So I coach or Kenra 70% of patients achieved IGA 01 versus 10% on placebo and and if you look at and then Pazi 90 which was the other endpoint versus placebo like 55 to 57% versus like 1 to 4% on placebo. So we already kind of knew that from previous studies. Now how does it do, how does ICOTRA Kinra do compared to Ducravacitinib? So Pazi 100 was 30% in the Icotra Kinra group versus like 12% in the, in the Ducravacitinib arm responses with you know, with Icotra Kenra and Ducrabicitin to some extent keep improving through week 24 safety. So you actually had active comparator to safety. So they were numerically lower in the ICOTRA Kinra group compared to the Ducravacitinib group. So about 50 adverse event rates of like 57 versus 65%. So you know, I think like if you want to do the non official network meta analysis, we know that Ducrabacitinib was superior to Otesla and head to head studies. So I think that this would say then you know, we can say ICOTRA Kinra once a day is going to be superior to both Otesla and Ducravacitinib.
- [26:24]
A
The interesting thing is going to be we've also got two second generation.
- [26:31]
B
Tick.
- [26:32]
A
2 inhibitors coming out, the Zasocytinib and I forget the name of the other one and to see how those, we're not going to have any head to head trials of those but we should have had to head trials of those versus Ducravacit nib. So it should allow for a assessment of you know, how do they compare to Ecotra Kinra.
- [26:54]
B
Right. So just a little reminder, what is Icotra Kinra? It is a peptide that is taken orally that binds to the IL23 receptor. So it's a pathway blocker but it is, it works a little differently than the, than you know, Skyrizi tremphy. So you know, I think it's interesting, I'm very interested to see like, you know, what it's like when this drug comes to market. You know, it's an interesting technology. We're going to see this. So you know, I was looking a little bit at the history of it. So you know it started out as a peptide that had like enhancers in it that you, it started out being looked at just for like ibd. Right. So you can imagine it's going to sit in the gut and actually they do have IBD studies ongoing for this drug. So but it turns out that like they, when they optimize the drug, they don't even have to put anything in it that makes it, you know, preferentially go into systemic, into circulation. It's actually just that the drug is absorbed and goes right into circulation. I like the idea that, you know, just like when we talk about like nanobodies for hs, we think about small molecules might be good for penetrating tissue that's inflamed. And so, you know, I'm really curious, I'd love to see like if you labeled this peptide, does it penetrate into the skin differently? You know, I, I think it's going to be, I think it's really interesting. So. And I think it should be something we can use across diseases and then to that effect, like what's it going to do in the joints? Right. So maybe getting into synovium is going to be easier if you're a little peptide versus a big antibody. And is this going to be like an IL23? Again, this is all complete speculation. I have no idea.
- [28:39]
A
But I always interesting, like inflamed tissue has higher vascular permeability to begin with. So I always feel like that whole, like whole smaller molecule might get into the tissue better, doesn't it? Always seems like baloney to me. Maybe in the joints.
- [28:55]
B
How about non inflamed tissue?
- [28:57]
A
Yeah, and maybe synovium might be different as well since that's an avascular space.
- [29:02]
B
Right, Right.
- [29:03]
A
Maybe, maybe. I don't know.
- [29:05]
B
So I think the big question is going to come down to do patients want a pill or do patients want a shot? And I think that's like a big topic that companies are really interested in and looking at. I think to some degree want to, you know, have that narrative like do patients want pills or shots? I, you know, I think that it, there's patients who want pills and there's patients who want the least frequent dosing that they can get.
- [29:29]
C
Yeah, it's not just like a shot. Right. It's like once every three months. You have to remember to take it right every day. So it's going to be tough.
- [29:37]
A
Ferris, just I wanted to give you a heads up that after the end here I'm going to be asking you what was the biggest scuttlebutt at the eadv? Was there anything that people were like, ooh, really talking about?
- [29:49]
B
All right, I was barely there. I flew in, gave my, like my flight got delayed. I was on the ground for like 24 hours. So I'm not the scuttle, but okay, I barely made it out alive.
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A
All right, All Right, Patton, what do you got?
- [30:05]
C
All right, second six pack was September 2025 edition of Allergy, Asthma and Clinical Immunology was titled Avapritinib reduces symptoms and Mast cell burden and systemic mastocytosis.
- [30:19]
A
I have got to stop letting you pick your own papers.
- [30:22]
C
This is so interesting. Listen up, people. Maculopapular cutaneous mastocytosis has always been kind of interesting, right? Impressive clinical findings. You make the diagnosis with a biopsy, you work them up for systemic serum tryptase, CBC, LFTs, maybe send off a C kit and it's all negative. And then literally, there's nothing you could do for the skin. Nothing ever worked for cutaneous mastocytosis. Well, now there is, so low dose ivapritinib, 25 milligrams a day. This is a report out of Germany.
- [30:54]
A
Is that a. Is that a drug that's on the market?
- [30:57]
C
Yeah, it's FDA approved to treat indolent systemic mastocytosis. Metastatic gastrointestinal stromal tumor that has the pdgr. PDGFRA mutation. It's approved? Yeah, it has a brand name. I don't remember it.
- [31:19]
A
Okay, but so we could send these people to like a HEMOC doctor to get this.
- [31:24]
C
Yeah, so, yeah, so they, they talked about two patients and, you know, they had like sort of indolent disease. They had pretty impressive cutaneous disease. There's photos in the. In before and after.
- [31:37]
A
Yeah.
- [31:37]
C
But they also had elevated tryptase and they had systemic symptoms. And so it wasn't just like, hey, you have maculopapular cutaneous mastocytosis. But the skin did get better and I was just amazed at that. And so that's why I picked it, because clinically it's very impressive for a disease that literally we had nothing for these patients and now we have something. I mean, their skin is, is kind of clear. I. I have a feeling, you know, the next person I see, I'm really gonna be like, but isn't your stomach hurting too? And don't you have brain fog? Then I think this might be insolent systemic. And then I'm gonna get them avipritinib.
- [32:15]
A
Okay.
- [32:16]
B
I mean, I've seen this marketed to derms. Like, I feel like everything I open, they're like, let's talk about indolence. Systemic mastocytosis.
- [32:25]
C
That was a thing. I am getting emails once. It's. I do compare this. I know you guys are going to yell at me. It's like the emails that I get every week for gpp I have seen one GPP patient ever. I know that specializumab works really well, and I know that you actually want to give it subq low dose, long term, because that spends more money. No, I think that's a more effective way to manage GPP as opposed to waiting for them to flare. I'm just kidding. Spazolumab. Don't. Don't send me hate mail. But, man, like, the proportion of how many GPP emails I get compared to how many patients I have, it's. It's a million to one. Stop sending me GPP emails.
- [33:09]
A
Wow. Million to one. That's a lot of emails.
- [33:12]
C
Okay, yeah, I'll forward them to you.
- [33:15]
A
Okay. No, please don't. Okay. All right, so we had a new drug for even indolent cutaneous mastocytosis. All right, good. Good to know. Good to know.
- [33:26]
C
Are you really gonna. Are you gonna really pick my papers from now on? No, I'm not on probation.
- [33:32]
A
Nope. That would take too much effort. And now that I know that it's. It is a drug on the market, then I'll. I. It's allowed. It's allowed. All right, so my next one was psoriasis and atopic dermatitis overlap, pathogenesis and therapeut. For the clinician, this was in dermatitis. The senior author on it was Peter Leo, who the derms on drugs know and love. And basically the takeaway here is it's. They go through kind of the pathophysiology of, you know, is this a real thing? Right. So is. Is it that there's some eczema that has some psoriatic components or esoform eczema, and there's some psoriasis that has some dermatitic components where it's psoriasiform dermatitis, or is it. Or, you know, eczematized psoriasis? Or is. Are there people who really do kind of have both, and they're making the argument that there are people who do really kind of have both. And their. Their takeaway is that in somebody who's got real clinical manifestations of both diseases, our first line therapy should be a JAK inhibitor that the drugs that make the most sense. If that didn't work, if you think it's more psoriasis, you should go il17. If you think it's more atopic dermatitis, you should go IL13. And then if that didn't work, you think about doing a combination therapy with an IL17 and an IL13. You know, essentially all common sense would Be my main takeaway that if your main issue is, I just want to get them better, you put them on a jack. If you don't want to put them on a jack, then you think about, okay, which one do I think is more likely? And you try a drug, and if it doesn't work, you try the other class. And then if none of that works, you can either put them on both drugs or you can try a jack at that point, if you haven't already tried one. But just in useful article, because this comes up a lot, right?
- [35:39]
B
Because then people I think, also, like, these are the patients I like methotrexate for, sometimes cheap. And it can work for both. I, I, you know, I have seen patients where it's like, I remember one patient, it was like, you'd put them on dupixent and they'd break out, horrible psoriasis. You're like, all right, it's clearly psoriasis. And you put them on like, I don't know, Humira or Cosentyx. And then they were like, examinish. You're like, all right, it's clearly atopic. Like, I think the cytokine inhibitors are so targeted and polarizing that you can. You just sort of make them flip back and forth, whereas a little bit more, this is the time when non targeted can be helpful. So, yes, a JAK inhibitor is good sometimes methotrexate is still a useful drug, even though there are JAK inhibitors out there. I think that, that I'm sure you could try Reflumel, Asmat.
- [36:32]
A
There you go. I was waiting for you to get on the right path, Paris. All right, Patton, any comments?
- [36:39]
C
My experience has been that it's more often I'm looking at him and it's spongyotic, like, more heavily spongotic. And I put him on doopy and it gets worse. Like, is that what happens more frequently with you guys?
- [36:53]
A
It's hard to, it's hard for me to say if I think it.
- [36:57]
C
I don't know. Yeah, I don't know. I was just curious. Like, do you say, like, the psoriasis that becomes exematous with a 17 or 23 or 1223 TNF? I. I don't know if I've really ever seen that.
- [37:13]
A
And it, well, it is. It. It certainly, according to the literature, happens more commonly with io17s than with 23s or TNFs to get an examinous reaction.
- [37:23]
C
Interesting. Maybe I don't use enough of those. Okay, okay.
- [37:27]
A
All right. My, my other article was just since Opzelura just I think last week down to age 2. And the article just came out. Efficacy and safety of ruxolitinib cream in children aged 2 to 11 years with atopic dermatitis. Results from True AD3, a Phase 3 randomized double blind study. Main takeaway actually worked even a little bit. This was mild to moderate atopic dermatitis randomized double blind placebo controlled trial numbers were actually even a little bit better for IgA treatment success with kids than it was for adults. So 56%. That number is more like 51% in adults, but really effective in kids. Obviously the challenge is talking to parents about the boxed warning. And there is a little bit of systemic absorption. So we can't say like hey, you don't need to worry about this at all. Like, well it's baloney. The blah, blah, blah, blah, blah. Like there is a little bit of systemic absorption and you know, is it enough that it should have any immunologic effects or any, anything? No, it shouldn't be. But there is some systemic absorption. And is it imaginable that if you use it over a big enough body surface area there'll be some kids who get a high enough level that it could do imaginable is unlikely, but it's imaginable. So it's, you know, that's going to be. The challenge is talking about the box warning, you know, with parents, you know, what do you guys think? You think you'll be using much obsolera in the 2 to 2 to 12 age range?
- [39:09]
B
I don't try very hard not to see kids of that age.
- [39:13]
C
You know, that's a great question for. Because if you're putting it over that much body surface area, given that doopie's approved down to six months, why in the world would you not have that little kid on doopie? Other than they may scream their head off when you attack them with a needle every two weeks. But still aside, my kids would scream and cry at me and I didn't give them doopy. Yeah. So you're. That's just part of childhood.
- [39:39]
A
It. But it can be a big, like there are kids who. It's like a, a huge, you know, four year old who. You can't really explain anything to them. And it's just like I there we.
- [39:54]
C
Have, I share an office with a pediatric dermatologist and so those kids do come in. It's. It's heartbreaking.
- [40:03]
A
It is, it is. Yeah, it is.
- [40:07]
C
I mean I laugh a lot but my first response was oh, that's really heartbreaking.
- [40:15]
A
Yeah, it sucks. It sucks. Yeah, it sucks. All right. Well, that's it for our six pack for this week. I'm gonna sign us off here. So for all of our listeners, thank you for joining us. I hope you learned a thing or two. I hope you laughed once or twice. And mostly we're hoping you're planning to join us next week. Until then, I'm Matt Zyrus.
- [40:36]
C
I'm Tim Patton.
- [40:37]
B
I'm Laura Ferris. And we are Derms on Drugs.
- [40:41]
C
It.