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Derms on Drugs
From Blood Vessels to Mighty Mites: What’s Hot (and maybe not) in Dermatology Right Now
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- [00:02]
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 ID 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, where 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 derm and you'll have some fun. Listen. New episodes drop every Friday on Scholars in Medicine, Apple Podcasts, Spotify and other major podcast platforms. The video component As a reminder, everybody has some of the key figures and tables from the articles that we talk about. So this week we've got one of our patented six pack episodes where we are going to talk about the stuff that we have found most interesting in the literature over the last few weeks. Dr. Farris, what do you got?
- [00:55]
B
Okay, so I decided to pick this paper on small vessel vasculitis. Why? Because I feel like I'm bad at vasculitis. And two, because they are classified by the Chapel Hill criteria. And I feel like now that I'm in Chapel Hill I can't be bad at vasculitis, but so maybe I'll be a little less bad.
- [01:17]
C
Okay.
- [01:18]
B
Okay, so this is point of care, risk factors for systemic disease in patients with small vessel vasculitis of the skin. Margin et al. And this was data from the Brigham and Pennsylvania. So what did they do? They looked at 430 cases of patients with small vessel vasculitis of the skin and they classified them as either being skin plus systemic involvement, which is 87 versus 434 who had cutaneous only vasculitis. And so how did they. They basically had to have a minimum of six months of follow up and to have received a diagnosis of. Of systemic vasculitis. So, and also if they al. If they had small vessel vasculitis associated with underlying connective tissue disease that was considered systemic. And or if they had end organ dysfunction that was considered systemic.
- [02:14]
A
Wait, tell me, tell me those one more time.
- [02:16]
B
Okay. To be considered a patient who had systemic involvement, it was. You had in your chart a diagnosis of systemic vasculitis, underlying connective tissue disease associated with that vasculitis or organ dysfunction.
- [02:33]
A
Okay, so you could have, like, a creatinine of 1.4 and they would have called it systemic.
- [02:39]
B
Yes, because it would have. Yes, because it was. Or. Well, they didn't go into, like, what was the exact cutoff. But if you had organ dysfunction, that counted. All right, so like renal dysfunction did.
- [02:53]
A
So, like, if you're. If you had HSP and had some GI pain and a little bit of blood in your poop, that they probably called you as systemic. Okay.
- [03:02]
B
Well, you had to have actually have, like, underlying organ dysfunction. So, you know, I'll go into some of the criteria that would make you go, okay, maybe. All right. Okay. So what they did was they looked at odds ratio of having systemic involvement, and they did multi univariate and multivariable analysis. Okay. Most common vasculitis that they saw was IgA vasculitis, followed by connective tissue disease associated vasculitis, then cryoglobulinemic vasculitis.
- [03:32]
A
These were the most. The most common systemic vasculitis is not.
- [03:36]
B
No. Of all the vasculitis that was in the cohort. Okay, no, no, sorry. That was the most common of all of the systemic.
- [03:43]
A
Yeah, because.
- [03:45]
B
Yeah, yeah, yeah, yeah, yeah.
- [03:46]
A
Okay.
- [03:47]
B
Okay. And so multivariable analysis showed the factors that were significantly associated with systemic disease were nausea, vomiting, odds ratio of 3.92. So that tells you, Matt, that's not just like, oh, I feel sick. Oh, it's systemic. Right. Like, that was. It put you over. You know, you had to actually have systemic involvement. Ulcerating or necrotic skin lesions, odds ratio 3.26, abdominal pain, cramping, odds ratio 2.7. And then fatigue, malaise, or lethargy. And that was odds ratio of 2.6. So if they complain of those, they're more likely to have systemic involvement. And the cohort who had urinalysis, and I'm like, doesn't everybody get urinalysis? But dipstick hematuria of three are. And so most of them did, 388 did UAS, but some did not. Whatever that is. The difference under 100, dipstick hematuria of 3 or more was had a 2.4 odds ratio of 2.4. So those were all, like, the things that were predictive of having systemic involvement. The thing that was inversely associated was recent antibiotic use. So it was, like, protective for. Right. So if they recently had antibiotics and they have vasculitis, it was probably going to be cutaneous only.
- [05:08]
A
So that was probably just a drug reaction to the antibiotic or possibly part of the immune response to the infection.
- [05:14]
B
Yes, that is what I'm taking. And then other things associated with systemic disease in only univariate but not multivariable were joint pain and younger age. So what was not associated? No association. Skin pain, blood in the stool, melania, and then trace hematuria or proteinuria on the dipstick. So it really had to be 3 plus on the dipstick. And also recent URI did not have an association either way. So, you know, I thought this was helpful. You know, who do I need to worry about more? Who do I need to be working up more? I personally get a UA in everybody who comes in with cutaneous vasculitis, but now I don't have to worry about trace hematuria as much.
- [05:59]
A
Okay, do you get. So, you know, the number of people I've ever seen who cutaneous small vessel vasculitis was the initial presenting sign of something meaningful was kind of vanishingly small. Right. You know, it's almost always, you already know they, if it's. If they have connective tissue disease. You already know they have connective tissue disease or whatever. Like a normal healthy person who gets some small vessel vasculitis just seems, you know, maybe if it's HSP and they had an preceding infection, but you know, that tends to not turn into anything big. What, I mean, what do, what do you, what's you guys take on kind of the quote, run of the mill, small vessel vasculitis patient?
- [06:43]
B
So I, I think, and again, prefacing, not that great at vasculitis, but I think that for the most part those are cutaneous, limited. I mean, I definitely go look for things, but I have not. I mean, I can't remember the last time. I think I've had like one person with some who had renal involvement, but I don't feel like I've seen a lot of it. How about you, Patton?
- [07:06]
C
It's not common, but I mean, I, I can recall the, the patients with cryoglobulinemia and Wegner's and, and HSP most.
- [07:16]
B
Commonly was like cryoglobulinemia. The one like, was that how they presented though, was just with skin findings and then it ended up being. Yeah, yeah, I guess actually that's true. I have had a couple of those. Yeah.
- [07:32]
C
I mean, it's, it's rare. Right. What were the numbers in the study? Right. It was, it was 70 some that had systemic disease and 400 where it was limited to the skin.
- [07:42]
A
Yeah.
- [07:43]
B
Yes, it was 87 with systemic and 343 with just cutaneous only. So that. I mean, to me, I would. Okay, that sounds about right to you. I would feel like I see even more. That's just cutaneous, but. Yeah, but then if.
- [07:58]
A
If you take. If you didn't look that hard and you took out the IgA vasculitis ones. Right. So the people who had basically had HSP and had some GI involvement or had HSP and some renal involvement. If you didn't look that hard, their HSP would go away. They'd be fine. And then you'd probably be at like, 30 or 40. You know, it'd probably be at. Less than 10% of people had something systemic.
- [08:23]
C
Yes.
- [08:24]
B
So what were tim of those? Like, what was your. What were, like, your worst vasculitis, like, systemic vasculitis cases? Like. Oh, God, I'm so glad I worked this up, because. Blank.
- [08:34]
C
Well, I mean, a guy with Wegner's who was admitted to the hospital with renal failure who refused dialysis and died.
- [08:41]
B
That's kind of sad.
- [08:43]
C
Yeah.
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A
And.
- [08:43]
C
And. But he had leukocytoclastic vasculitis in the skin. And then pan's not good. Now, some people would say that's not small vessel vasculitis. That's medium vessel vasculitis. That's little. That's not palpable purpura. That's more of kind of that reticular pattern with painful nodules. You got to go a little bit deeper for that biopsy. But pan's bad. I mean, but it's a. Yeah.
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A
The big thing is those don't really present with, like, a whole bunch of little, you know, 6 millimeter palpable purpose spots on your ankles. Right. I mean, that's. That's not. Whenever I've seen pan or Wagner's, it's been like, you see it and you're like, oh, this is not normal vasculitis.
- [09:23]
C
Yeah. Right. I mean, the Wegner's patients that I recall are. Were sick. I had a cherg. Strauss. I know we're not supposed to use these names. Eosinophilic granulomatous, ptosis and polyangiitis. A chirk Strauss guy that was pretty sick. That was a little bit odd because he kind of had hyper eosinophilia for a while, and his skin disease was actually more kind of these urticarial lesions. And then he evolved into egpa, which. That's been described where it starts off as hyper eosinophilic syndrome, but. Yeah, I Think going into the room if they feel otherwise. Well, really no complaints. They're, they're pro. It's probably LCD and. Yeah.
- [10:06]
B
Okay, you got it Like a ua.
- [10:08]
C
Work it up. Right?
- [10:09]
B
I mean, cbc. Yeah, yeah.
- [10:12]
C
I do rheumatoid factor. Kind of the poor man's cryos before I actually order cryos because cryos just technically is, is difficult and I, I, I don't think I would if I thought it was cryoglobulinmia. And cryo test was negative. I don't know if I would trust that. So rheumatoid factor is kind of my cryo screen before I actually order cryos. But yeah, hep B, hep C. I do these C anchors when if they're not sick, the likelihood of the cause being positive or is low. But I'll check it. It's an easy test. I think it's cheap. Okay. And ua, Right.
- [10:47]
B
Okay. New chest X ray or anything like that in these patients or not.
- [10:52]
C
I mean, I always ask about lung symptoms. If they don't have lung symptoms, I don't get a chest X ray.
- [10:57]
B
Okay. I do not typically do it either. Just wanted to make sure. And then I didn't want Matt to be the only one who overachieves and does extra. So I, I just found this one interesting case report. I'd never really heard of it. It's called recurrent cutaneous eosinophilic vasculitis. In the Journal of Allergy and Clinical Immunology in Practice. So it was a woman with five year history of intermittent recurrent rashes. It was palms and soles and then they become painful and then they become like pruritic purpura. And they would recur every two to three months. She had an eosinophilia of 16%, which is high. And then biopsy, neutrophil infiltration, nuclear dust, and then prominent eosinophil infiltration.
- [11:44]
A
Why do we care?
- [11:46]
B
Because I thought like this is not something that I thought like if you, I'll throw, I'll give you the slides. It like I look at this and it almost looks like urticarial wheels. And then like they, they do look like these like deep purpuric things. It was mostly palms and souls. But I, it just like, I wouldn't have thought like, ah, this is just a manifestation of vasculitis. Okay. And it goes away with prednisone. So I thought, you know, vasculitis with a bunch of EOs. Think about this. And you can treat it with prednisone so. Because it's not in the Chapel Hill consensus criteria. That's why I care.
- [12:22]
A
All right.
- [12:22]
C
Okay.
- [12:23]
A
All right. All right, all right. All right. Patton, what do you got? What's your. What are you. What are you going to talk about? Yeah.
- [12:29]
C
First six pack. October 2025 edition of Skin appendage disorders called Dermatologic Implications of glucagon, like peptide 1 receptor agonist medications by Burke at all. We recorded an episode talking about GLP1 receptor agonists a couple of weeks ago, but didn't really get into side effects. I mean, this is a review article. It's not like technically challenging, but more and more people will be using these meds, so figured we could review some of the dermatologic side effects that we might be seeing more of.
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A
I didn't even know.
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C
Isn't that a great idea? What's that?
- [13:01]
A
I didn't even know there were any hair loss. That's it. You lose too much weight and your hair falls out?
- [13:06]
C
Well, then pay attention. 6% of side effects reported to the FDA were dermatologic in nature. First side effect paper talks about ozempic face. How could you not include Ozempic? Halloween of the cheek, Sunken eyes, sagging jowl. Seems to me that most cosmetic derms could manage these pretty easily with their various procedures and torture devices. The paper talks about injection site reactions, hives, hypersensitivity. Recommendations include typical recommendations for injection site reactions. They do also mention that switching GLP1RAs can be considered because cross reactivity is not always present. So. Okay, I thought that was good to know. Dysesthesia, this was interesting one, I had not heard about this have been reported. And these seem to be more common in the oral version of semaglutide. So Rebelsis, which is FDA approved for diabetes. 3 milligrams daily for 30 days, 7 milligrams daily after that can go up to 14. Although apparently Novo Nordisk is pursuing weight loss indications at higher doses. And this actually just got FDA approved to treat like cardiac prevention of cardiac side effects in diabetes patients with certain risk factors. So it just got FDA approved for that. So the oral version. Just something to know that the dysesthesia, that was kind of interesting. A list of very rare reactions. Bp, what sounds like age up psoriasis form reactions, vasculitis. These are so rare that you don't.
- [14:44]
A
Know if they're actually related. Right. You got millions of people on these drugs. Occasionally somebody's going to get something pretty much right.
- [14:51]
C
Paper Talks about hair loss. Right, so that was what you mentioned. Recent trinetic study published in the JAD found an increase in TE with tirzepatide compared to other weight loss drugs. But there was another real world study that didn't find that disproportionality signal for hair loss. And there was even a case report of AGA improving significantly after 6 months of tirzepatide use. So hair loss is confusing. TE occurring in weight loss makes sense. Right. Especially if it happened really quickly and they weren't really good at. You know I, I think some people like literally don't eat. Like you have to actually counsel them on. You have to have some sort of caloric plan.
- [15:33]
A
So that it was. I've told you guys that I was. When I went on tirzepatide after my. Which I'm now off of course. But my first shot, I didn't eat for three days. Like literally did not eat for three days. It was right at the start of the ad. So I hadn't eaten for two days. Show up at the aad, go out, you know, having some libations. I couldn't get. I could. I was so hungover because I hadn't eaten in two days. I couldn't leave my room for a day. It was, it was embarrassing.
- [16:03]
C
Your bed was covered in TE hairs. The paper ends with potential uses for GLP1RAs in dermatologic conditions. But we kind of talked about that on our previous episode so I wasn't going to go into that there. So pretty simple, easy paper that I thought.
- [16:25]
A
Yeah.
- [16:25]
C
You said the dysesthesia was interesting to me. That one I had not heard of.
- [16:30]
B
I think like 10% of the United States is on a GLP1. I mean it feels like it's even more when I look at patients medless but like, like this is a huge proportion of the people in the US and I.
- [16:44]
A
And I think they're going to get cheap pretty quick. I think they're already starting to. I think it's going to make a huge population health difference. It is really interesting.
- [16:54]
C
One of my residents brought up. This was not in the paper. One of my residents brought up Ozempic butt. Have you guys heard of that one?
- [17:02]
A
No.
- [17:03]
B
Is this just like you lost fat so whatever you had becomes more saggy? Like couldn't you have a arms?
- [17:10]
C
Yeah, I don't. The I. The butt thing. She said. Oh no. It's very like they, she goes. I think she said they look like pancakes.
- [17:19]
B
Okay, okay. I don't know, it wasn't.
- [17:24]
C
It wasn't in the paper. That's just a little side side note.
- [17:27]
A
Okay, I'm going with that from now on. Anytime from now, whenever I take my shirt off, I'm going to be like, I've got ozempic muscles.
- [17:35]
C
This is an ozempic body.
- [17:37]
B
Yeah.
- [17:40]
C
I look like a giant pancake.
- [17:44]
A
All right, let's. Let's go on to my two papers that I did for this. Number one. So there was a study several years ago that. So the title of the study. An Interventional Comparative Prospective Study to Determine the Optimum Concentration of Intralesional Triumphant Alone Acetonide Treatment of alopecia areata. So there was a study a few years ago where they looked at like 10 milligrams, 5 milligrams, 2.5, like, milligrams for ML for alopecia areata and found that the lowest concentration that they studied, which was 2.5 mgs per milliliter, worked just as well as the higher concentrations, but caused less problems in terms of, like, atrophy and that kind of stuff. So these people did a study where they looked at 2.5mg per ML versus 1.25mgs per ML, and they showed pretty conclusively that if you go down to 1.25 mgs per ML, it doesn't work as well. So that was because I've often wondered, like, how low could you go? Could you go down to, like, 1 mig per kilogram, like. But no. 2.5 milligrams per milliliter is the lowest dose you want to go to for intralesional tackle for alopecia areata. The. You know, nowadays, I always kind of hated doing this because it was just. Do you guys still do a lot of. I mean, what. I guess. What the heck else are you going to do for somebody who's only got a little bit of alopecia areata?
- [19:12]
C
Oh, my gosh. Yes.
- [19:13]
B
Yes. That's like, first line.
- [19:15]
C
Oh, my gosh.
- [19:16]
B
Come on.
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C
And I still do the tac 5, because the ma, then I can just tell the ma. I'm like, draw two saline and two of tac 10.
- [19:25]
A
Okay.
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C
If I had to do the 2.5, they would ask me and I'd be like, I. It. It would take me too long.
- [19:32]
A
So I still stick with the 5.3mls of saline, 1ml of tack. Yeah, there you go, Patton girl math.
- [19:40]
C
Well, I know, but that's. If I wanted four cc's, they'd be like, well, you only want one cc, and then. How do I do that?
- [19:47]
B
It's fine. I've seen residents not able to calculate it.
- [19:53]
A
Ferris, that should be part of your.
- [19:54]
B
You really not do that.
- [19:55]
A
That should be part of your residency interview process. Like, have. Have them.
- [20:00]
C
I need three and a half cc's of TAC 2.5 now. Go.
- [20:04]
A
Right, I need. I need two CCs of lidocaine, 1.8% plus epinephrine, one to 487,000. What's the concentration of meat right now?
- [20:17]
B
I would have to retire. I don't. I couldn't calculate that.
- [20:21]
A
But you would know. Make the resident do it.
- [20:24]
B
I would already know. Yeah.
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A
The applicant do it. Right.
- [20:26]
C
That's the idea.
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B
All right, all right, I'll consider that.
- [20:28]
A
That was article number one. So 2.5 MIGS promo number two. This was interesting. So, hydrocolloid dressing versus petroleum ointment for scar appearance after derm surgery. So basically, after you do a normal excision, the, you know, one group, they did, you put the petroleum and a dressing over it. You change it every day. You know the whole thing. You clean it, you put new petroleum on normal wound care versus you put a hydrocolloid dressing over it. Because hydrocolloid dressings now are really cheap and really easy to get. They're really sticky. So can you just slap a hydrocolloid on there, leave it on for a week and make it, like, super easy for people? Well, the takeaway here was that first, in terms of the scar appearance, the ones who got the hydrocolloid dressing looked better at a week, but long term, it made no difference. So the hydrocolloid. So it healed a little faster with the hydrocolloid than with the petrolatum, but it made no difference in terms of the actual scar appearance. However, it was very interesting whenever they looked at convenience. So did patients think it was convenient and comfortable? So the hydrocolloid dressings were pretty dramatically higher degree of convenience and comfort compared to changing it every day with petrolatum and were significantly more comfortable than changing it every day with petrolatum. So more convenient, more comfortable. But in these. None of these things were really statistically significant, but it was only like 60 people in each group. Surgical site pain was higher with the hydrocolloid, so a little over 20, 21.2% versus 12% with the petrolatum. Wound dehiscence was higher. So four patients, 6.2%, had dehiscence with the hydrocolloid and zero with the petrolatum. And postoperative bleeding was higher. So 20% with the hydrocolloid versus 20.6% versus 8.8% with the petrolatum. Again, none of those were statistically significant. But if those numbers are real, it just means if you, if you did enough. Right. So there was like twice as much post operative bleeding. There was nearly twice as much surgical site pain.
- [22:52]
B
So infection, did they look at infection?
- [22:56]
A
Yes. Required antibiotics. Zero in both groups.
- [22:59]
B
Okay.
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A
So.
- [23:01]
B
So, you know, it's interesting. I like, like the hydrocolloid dressings, like the duoderm ultra thin. Yep. And so, but I don't, I guess I don't really do them with sutures. And I wonder, like, were they using gut suture? Were they using like, were they using absorbable or, you know, like proline or whatever? Non absorbable. So I could imagine the hydrocolloid would kind of disintegrate gut suture or absorbable suture.
- [23:26]
C
And it depended on the location. So on the face they use four monocryl and topped it with fast gut. On the trunk they used four. No, three monocryl and then maybe four as a running subcuticular. Those were the sutures they used. I, I don't use a lot. I barely ever use monocryl.
- [23:48]
B
So yeah, I would use it for like ED&C sites. Right. So like if you just slap that on and leave it on for like six days, especially in the summer, people can go in the water. They're waterproof, you know, or even like other old people who are getting shave or anybody who's getting a shave biopsy on their back. Those band aid hydro seals are basically cheap hydrocolloid. And you know, people are like, I can't change the band aid. I'm like, I'm going to put this on and just leave it and then at some point it'll fall off. And you're done with wound care.
- [24:19]
C
Yep.
- [24:19]
A
And those are.
- [24:20]
B
They can swim with it. What's that?
- [24:22]
A
And those are. And they're really cheap. Like really cheap. Now do you guys think that mighty patches and all of the mighty patch type things. Do you ever tell kids to. Not the kids asking us, but they're all just using them anyways. Do you think from watching my kids use them, I think they do make a difference. I think they make acne lesions get better faster.
- [24:40]
B
Yeah, my kids all believe in them. My girls.
- [24:44]
C
Yeah, exactly that.
- [24:45]
A
I'll tell people the other place that I think those are useful. Well, we'll get to it in my, with my next. Oh, no, I talked about it last week. The, the fissures with Hand with. Hand with the fingertip fissures. Hydrocolloid dressings, which they make mighty patches kind of for this, are actually really good for that.
- [25:01]
C
There's.
- [25:01]
A
They're stickier and more waterproof than band Aids, so I think they're actually pretty good for fingertip stuff and help it to heal underneath there.
- [25:10]
B
Okay, so. Yeah, yeah, yeah. No, I still think the EDC site and especially like on the leg where I'm like, I know all the water is going to run down and get them infected. I really like having. Having it for those. So. And then. Yeah.
- [25:24]
A
All right. So reasonable to offer to surgery patients as a. Would you rather something more convenient or something that's, you know, less likely to be painful or do any oozing or that kind of stuff? So worthwhile, you know, new. New information. All right, let's go, Ferris. What do you got?
- [25:43]
B
Okay, so my next paper is actually gene expression profiling to predict melanoma sentinel node cell status. This is the Merlin 001 study. So this just came out like a couple days ago at the time of recording. And so this is a prospective study conducted at nine academic medical centers with experienced melanoma surgeons. And basically, to be enrolled, you had to be a patient with a biopsy. Proven invasive melanoma T1, like high risk to T3 tumor and clinically negative nodes. All of them got the Merlin test just to remind people what that is. It's cpgep. So there's eight genes. I will not read them all off. We can put them in the show. Notes. Different. This is very different than, like the decision DX Castle test. And then they also do cp, which is clinical pathologic core factors, which are age and breslow thickness. So you put all that into the model and it comes out as low risk or high risk.
- [26:43]
A
Okay, yeah. Hold on. Why did they use Merlin instead of Castle? Is. Is one better than the other?
- [26:52]
B
Because this was done by the Merlin people to show that they're. How their tests work. So this is truly prospective. Like, we've got a lot of different, you know, tests out there. This was, you know, what makes it different than what's out there? It's not like we took a series of, you know, 500 people who had sentinel node biopsy, we went back and tested their tumor, and now we can classify. And this is like, prospectively. They did it. Everybody got sentinel node. Everybody got the test. They were blind. Everybody was blinded to the test result. And then they unblinded it. Okay, so in the end, in the study so 1761 patients, good size, 37% of them had a low risk result. And the other set, whatever that other number is, 63% had a high risk result. Among. So now the like the big question is what percentage of those low risk cases were sentinel node positive? So what you would say as your pre specified endpoint is it should be 5% or less. Right. That if you know in NCCN guidelines, if the probability of a positive sentinel node is less than 5%, you don't do it. If it's 5 to 10%, you discuss and consider. And if it's greater than 10%, you discuss and recommend. So what they, what they found in this low risk group was, was that the positivity rate was 7.1%. So that still falls into the discuss and consider negative predictive value of like 93%. Among the high risk cases that two thirds that were high risk, they had a sentinel node positivity rate of 23.8%. So you know, it's good that it's this large scale study. If you look at it, the majority of these tumors were kind of thicker tumors, so 40% of them were T2A. Um, there was, you know, among like, you know, if you look at other studies, like Casel studies, there's a lot more T1 as in there. There was only 26 or 1.5% were T1 as in this study. So you know, if you do look kind of like just among the T1Bs, and you said among those patients who are among. Yeah, the T1s. So T1a and T1b, that number was 4.9% of low risk had a positive node. But you know, that is like just over the edge. If you look at the T1BS, which is where I think these tests can be the most helpful. It was 5.2% of those patients with a low risk result still had a positive node. You know, so was a, it was a rigorous, well done. It was a rigorous study with a rigorous endpoint. It did not however, show that it could really pull out a nice low risk group that could safely forego sentinel node biopsy if you really want that risk to be below 5%.
- [29:46]
A
Interesting. So like, because it's my initial take, whenever I looked at this was like, well, shit, it definitely is telling us something like the high risk ones had way more center lifto positivity than the low risk.
- [29:58]
B
Yeah, it's definitely telling us something. It is definitely saying this route, this group is truly lower risk and the high risk group is truly Higher risk. It's just if you want to get down to like, what do the NCCN guidelines say? And you want to be able to say you are safe, you really want to be below 5% in that cohort. And the only group that. That was truly below 5% were T1As, and there's only a couple of them. I don't think most of us would recommend this in a T1A, but T1B was 5.2%, so.
- [30:29]
A
So, Patton, anything you want to say before I talk about something vaguely related?
- [30:35]
C
No. I mean, there was the accompanying editorial and they basically said this, you know, we're still looking for GEP data. Does this test help us figure out who we can not send for sentinel note? And it said, no, it didn't. Didn't answer that question.
- [30:52]
A
Okay.
- [30:52]
B
That was the thing. Now, you know, again, this was in JAMA surgery. This is done by surgical oncologists, editorials by surgical oncologists. They still very much believe that sentinel node biopsy prevents progression in that lymph node basin. And there's data, you know, if you look at postdoc analyses do support that. But I don't think that they're looking for a reason to use GEP in general. But yes, the study did not give it.
- [31:18]
A
So the vaguely related things I wanted to talk about. So first, there was somebody in my office this week who they now have a commercially available circulating tumor DNA test, which you guys maybe already knew this. So, like, if you want it, you send the path report to them. They get the tumor specimen from the path lab, come up with, like, here are its genetic things, and then you send them some blood and they're able to, I guess, do a very sensitive analysis for circulating tumor DNA to give people more prognostic information about residual disease. Now, apparently you gotta wait at least a month after the surgery because doing the surgery on the tumor releases all kinds of, you know, circulating DNA. So you don't wanna, like, get picked that up. So you gotta wait at least a month. But I have no idea what it costs or if it's available or I didn't go into anything to date at all. But it was just interesting to me that it is now commercially available.
- [32:18]
B
Some centers are doing this and using it. It's not totally clear, like, exactly. We don't have great studies. There was a adjuvant MRNA vaccine study where they looked at CTDNA in patients and they did find that higher levels of CTDNA was, were predictive of lower survival. And, you know, there is Evidence that like, you know, it's like it, it sort of varies with tumor burden. Right. So if all of a sudden your CTDNA is going up, that's probably a reason to do imaging and think about it, but we don't have. It's not like firmly in the guidelines, but I think it's very interesting.
- [32:54]
C
Yeah.
- [32:54]
A
The other thing, I got an email today. So I get, you know, I don't get colonoscopies. I get cologuard, where you poop in a bucket and mail it in and they tell you if you're high risk for colon cancer. Well, cologuard now has a thing called cancer guard, which is a blood test that detects 50 plus cancer types and subtypes with one blood draw. Obviously it's not covered by insurance, but it's like $689 to get it done. And I was just like, man, I don't want that done. I don't want to, I don't like if it seems like it's gonna, it just, again, it was just weird. Like, well, wow, okay, now we've got blood tests. Okay, you're cancer free. Like the amount of testing that this seems like it's going to drive. It seems like it's going to.
- [33:45]
B
Yeah, you know, we, I, I was doing that study in Pittsburgh for the Grail gallery test. So just because we had a clinical trials unit and lots of patients through. And so it's multi cancer early detection. You're basically looking for, you know, circulating tumor fragments that are, that they can then put back to a certain, you know, class. And so it is for detection. And then, you know, the study was to follow, like, how often was their cancer and then also follow the negatives to see how often those people did develop tumors. It was also looking at things like adverse events from, you know, additional testing and what additional workup was done. It was really interesting. I did have one patient who came in to me and said, like, oh, I've, you know, he, I put him in. He was like a, I don't know, psoriasis patient or something. I put him in and then I got back a positive, like anal cancer signal. And so I, I was looking through his chart and I saw I'd been seeing one of the gips for treatment of hemorrhoids and they kept bleeding and he kept going back for his bleeding hemorrhoids. And so I called him and I said, you know, I actually would like you to go like, I'm going to call your gastroenterologist. And they Went in and they biopsied it. And what was being treated as a hemorrhoid was actually like a friable tumor. So he actually did have the tumor, which was, you know, unfortunate. So, you know, things like that happen, but there's also, you know, false positives.
- [35:08]
C
How, how is the cologuard cancer test? It would, they would just mail you it directly. It wouldn't go through like a doctor or anything like that. They mail you the test, the cancer.
- [35:17]
A
Test I'm talking about. Yeah, I think you can have your doctor order it or you can get a telehealth and they'll order it and then you go somewhere and get a draw and mail it into them.
- [35:29]
C
Yeah, drive on. College is kind of crazy, right? Are going to have these. Find my cancer.
- [35:36]
A
Well, Ohio State University now they advertise it on tv, has like a, a whole unit developed dedicated to like, I think I have cancer. And you, they're like, we'll get you hooked up with oncologists and we'll scan your whole body and we'll do okay. Like it's, they advertise it like in Ohio State Buckeye games and I'm like, okay, I think I got cancer. I'm coming in. Like, yeah, I don't, I don't know if there's like a heavy duty screen, like if you've got to get a referral from your primary care doc that's like, oh, there's a shadow on your, you know, lung, your tent.
- [36:10]
B
Those are truly for asymptomatic patients, but they are supposed to be ordered by a physician and they're only supposed to be done it like, you don't want to give that to a 20 year old. You know, it's certain ages and things like that. You're old enough.
- [36:21]
A
All right, next, Next. What do you got, Ferris?
- [36:24]
B
No, that was me. I'm done.
- [36:25]
A
Oh, that's right. Circularly. That's right.
- [36:27]
B
Now you do like 50 bazillion papers. So. Yeah.
- [36:31]
C
My second six packs article from October Jad titled Efficacy and safety of the oral Janase kinase Janus kinase inhibitor Povorcitinib in patients with extensive vitiligo in a phase 2 randomized double blind dose ranging placebo controlled study by Amit Panja et al. So it was exactly that non segmental vitiligo. Study design was in the supplementary materials. It's, it's not labeled correctly, but basically randomized placebo and then three different doses of Porv citinib for 24 weeks. There were about 40 patients in each group and then everybody got porcitinib up to week 52. The 45 milligram group stayed on 45. The placebo 15 and 75 all went to 75. And that's where it's mislabeled because it says that they went to 45. So that's not right. Yeah. Primary endpoint change from baseline in the total vasi at week 24 and all of the POVOR patients had improvements in TVASI. Percentage improvement was almost like 20% improvement in all the doses. And this improvement continued through week 52. Similar improvements were seen in the face VASI scores, all doses showing statistically significant improvements compared to placebo at week 24 with continued improvement at week 52. Were these clinically meaningful differences? It's hard to say. The key secondary endpoint was the total Vasi 50. So this would be like 50. I mean, the way I'm reading this, 50% improvement in repigmentation. I mean, like, that would be the very least of it a LIGO patient would want to have, I would think. And at week 24, no statistically significant differences in the percentage of patients reaching this endpoint. Whether you were on porvo versus placebo, it was numerically higher for the Porvo people, but yeah, it didn't reach statistical significance. There's this whole table in there that looks at the T Vasi 57590 and the F Vazi 50, 70, 90. It's, it's a ton of numbers and I don't think we can meaningfully go into all the data. If you looked at, let's say like the face Vazi 90, so you got 90% repigmentation in the face. And I think that's what a patient with vitiligo would, would very much like to have. I mean, obviously they want to have 100%, but if you could tell them your face is going to be 90% better, I think they'd be like, okay, yeah, I think I'm going to do this. So in the highest dose group at week 52. So basically patients that were on 75 milligrams a day for 52 weeks, only about 30% of patients reached F VASI 90. And it just doesn't like seem that good. But you know, vitiligo patients on the face, they may be happy with that sort of improvement. There are some patient court, sorry, patient reported outcomes that the supplementary materials had. I mean, again, it's just a ton of ton of charts. The facial patients, global impression of change. I'M going to put that one in the slideshow. For the highest dose patients on 75 milligrams daily. From the beginning of the study, 69% of patients reported very much improved or much improved after a year. That kind of seems good. It's just really slow. Percentage of patients at six months with the same scores was something like 22%. So at six months in, you're not going to have a lot of people that are like, hey, this is much improved or very much improved. And then what had to be the most disappointing results were the quality of life measures. Vitiligo, specific quality of life, dlqi, some other ones. And there were no meaningful improvements in any of those. You know, take away Vitiligo is hard to treat and nothing really jumped out like on the safety data. Typical stuff you see with Jax. What did you guys think?
- [40:20]
A
So quality of so looks not great. And so the quality of life stuff said nothing. Wow.
- [40:28]
B
Right. I, you know, I think this is going to be a like using combination with narrow band or other things. Right.
- [40:36]
C
Like, I think so too. Yeah.
- [40:37]
A
I mean there's been some data looking at it with narrowband and it wasn't that much better. Not Pavro in particular. I think this was tofa.
- [40:47]
C
I thought the Berry data, the Berry study we did Barry and then maybe it was Barry band alone, narrow band plus berry. I thought those patients did better.
- [40:56]
A
They did, yeah.
- [40:56]
B
I think that they do. And then, yeah, I don't know, anecdotally, like I've kind of done that or excimer laser, which is, you know, basically. And then polypodium leukotomus. There's some data for adding helio care when you do like, for. To narrowband for treating vitiligo. I will say anecdotally about a couple times I felt successful and it was polypodium and narrowband and then some sort of like topical. Jack.
- [41:26]
C
Yeah, I mean, I, you know, the, the ruxolitinum data, I think when. What do I. I think it was the, the rucks data. Their primary, primary endpoint was the F Vazi 75. And for this trial at week 24, topical rocks actually did better. Higher percentage of patients that reached that F75. But at 1:52 weeks it was about like 50% in. In both the topical rucks group and as well as this oral porvo group, about 50% reach that F Vazi 75. And I think topical rocks is like pretty good for vitiligo. I mean, they, they have to stay on it. They have to keep using it and it's going to be slow, but. Right. I've had patients where you give them that because you know that like topical steroids for atopic derm. I think I can counsel patients use it on and off and that's fine. And here's when you do use it, here's when you don't like vitiligo. There's no break. If you're using a topical medication, it is every day forever until you start to get that repigmentation. And you just can't do that with steroids. That's why I like the topical calcineurin inhibitors because they could use those forever. And that's why I like the topical jacks because just like use it forever, it's fine. And combining it with narrowband and maybe some other things that are out there, I think it'll be nice. It's just, you know, systemic jacks. I think dermatologists are a little bit wary of prescribing them and I just don't know how willing they're going to be to prescribe something where it's going to be slow. A fair number of patients are going to be like this isn't any better. It's tough. Like that's going to be a tough indication.
- [43:19]
A
Yeah, yeah, it's going to be. I don't like. And right. You can add on. Right. There's data for Plaquenil, there's data for PDE4 inhibitors. There's actually some data for Vitama. There might be. Like if you combine Vitamma with Opsalura, maybe it's even better. But you obviously never get that covered. The other thing that can be interesting, there's some data for using latanoprost. So like the, you know, the eye drops there and those are. That's cheap. Use that once a day and you're opsoler twice a day and it seems to make it work a lot better by stimulating the melanocytes.
- [43:55]
B
Yeah, I've seen people talk about and I'm not like a micro needler but microneedling the matter prost onto areas of Italy. I actually saw paper once for like microneedling 5fu, which seemed crazy to me. But like I, I think there's probably different things. We could be hard disease only I were that interested in it.
- [44:13]
A
Yeah, hard disease. Right. All right, let's move on to my last couple. So we've got number one. I mentioned this in last week's episode. Topical timolol for treatment of spider angiomas in children A case series. Basically they treated six spider angiomas twice daily for six to 13 months. Two of them went away completely, two of them got a little better. And whenever you look at the picture, like they got a little better and then one of them had no response. So, you know, this can be something. If some parents come in with a kid with a spider angioma, maybe it would work in adults too. This is something cheap and easy to do. Topical timolol is dirt cheap. You know, dab a little bit on there a couple of times a day and maybe it'll help, you know. You know, I think a lot of times people are okay with leaving them alone, but if they want to do something, this gives you something to do that is easy, right?
- [45:14]
B
A solution, looking for a problem.
- [45:16]
A
Yes, but it's a cheap solution though.
- [45:19]
B
Yes, cheap. Looking for a minor problem. So it's good. They're a perfect match.
- [45:26]
A
It's good.
- [45:27]
C
Faris, that's good.
- [45:29]
A
And then the other one, this was interesting. So title of this article was demodicosis mimics acneiform eruptions in patients with inflammatory bowel disease receiving upadacitinib. A case series. So Basically they had 509 inflammatory bowel disease patients. 30 of them got acneiform eruptions. And of those 30 who got acneiform eruptions, 20 were demodex erupt. Were, were ended up were caused by Demodex. Now here's where it gets super interesting. Of the 509 patients, 181 got biologics. Not, let's see here, one patient got a Demodex in that group. Right out of 181, 308 people with conventional therapies, two of them were diagnosed with Demodex. There were 18 patients treated with Rinvoq. 16 of the 18 treated with Rinvoq got Demodex, like 90%.
- [46:34]
B
Maybe that's what Jackne is. It's just Demodex.
- [46:38]
A
That was exactly my whole thing like seeing.
- [46:41]
B
All right, from now on we all, for the next month they're gonna scrape every jack knee, see if there's Demodex.
- [46:48]
A
See if there's Demodex in there. And even if we don't see the Demodex, maybe you just give them a few doses of Ivermectin, you know?
- [46:56]
B
Yeah.
- [46:56]
A
See what that's, that's because this is. I, I will tell you, I am a believer that all papulo pustular rosacea or at least, I don't know, I'm making that up, that a lot of Papulopustular rosacea is Demodex driven, even with a negative Demodex prep. So my go to. For, like, somewhat resistant rosacea is combined oral ivermectin and metronidazole. So you do ivermectin 1 milligram per 10 pounds, repeat it in a week. The same day that you start the Ivermectin, you start oral metronidazole 500 milligrams twice a day for, you know, 14 days. And that is stunningly effective for rosacea. Like, papulo pustular doesn't do anything for, like, you know, just erythrillen, blah, blah, blah. But for the papulo pustular, super effective. I think. I think of Demodex as one of the most underdiagnosed things out there. So I'll do the ivermectin metronidazole orally and then follow it up with the compounded ivermectin metronidazole azelaic acid from one of the compounding pharmacies as maintenance therapy. And that's. Yeah, but that.
- [48:13]
C
This.
- [48:13]
A
That's what this article made me think about. Was that Jackney, maybe is. Is Demodex.
- [48:19]
C
Yeah, I think that Demodex is going to be diagnosed more frequently because now they're advertising the eye drop. Have you seen these commercials?
- [48:28]
A
No.
- [48:28]
C
They're on in football all the time. So there's a little woman, like, dressed up like, how'd you like to be that actress? Like, I got your perfect job, but I am.
- [48:38]
B
I.
- [48:38]
C
You're a mite.
- [48:39]
A
You're a demet.
- [48:40]
C
She's in her little mite costume, and then they splash the things on and all her friends, like, disappear, get washed away. So I think people are going to be like, hey, I saw this commercial with these mites that can be living on me. What do you have for me?
- [48:57]
B
We should just de worm humans like we do.
- [49:00]
A
It's not bad.
- [49:01]
B
Dogs and, you know, like, horses. It would probably be good.
- [49:05]
A
Patton, what's. What's the active ingredient? That eye drop?
- [49:09]
C
I'm pretty sure it's ivermectin. I. I don't know.
- [49:13]
A
Okay, hold on.
- [49:14]
C
Let me. Let me find out. Yeah, no, you guys talk amongst yourselves. I also like this paper. They said that we obtained the samples using the thumbnail. Thumbnail squeezing technique. Like, that's a thing we all.
- [49:30]
B
That's. No, you know what? You, I think, taught me this. The best way to get a Demodex prep is to use a comedone extractor. And you just push on the pustuler. Even just on a red, juicy papule. Get a little oil and put that on there. That is by far the best way to extract.
- [49:48]
A
That's useful. I always do it. I use two glass slides and, like, use the two of them to squeeze a pustule and, like, let it pop. But it hurts like hell.
- [49:58]
B
Oh, yeah. No, do the. Do the calming extractor. You just kind of.
- [50:02]
C
Yeah, like, rub it over. Squeezes them out. Yeah.
- [50:05]
B
Yeah, it does. It really does work.
- [50:06]
C
Well, XDEMVI is the name of the drug. Xdemvi ophthalmic solution. The active ingredient is Lotilaner. Lot of laner. I don't know. It's a gabigated chloride channel inhibitor that paralyzes and kills mites without affecting humans, which would. That would be a bad thing if. Yeah. Also paralyzed.
- [50:30]
A
Can we inject it and it'll make wrinkles go away?
- [50:33]
C
I don't know.
- [50:35]
B
Because it doesn't work on us.
- [50:36]
A
It's paralyzing things. That's always the first thing that comes to mind. Could it.
- [50:40]
B
I was thinking head lice, and we could use it for that.
- [50:44]
A
By the. I'll put that out there, too. That's another thing. If for head lice, you can give people massive doses of ivermectin, there's a fair amount of resistance now, but that's another possibility.
- [50:55]
B
New England Journal of Medicine. Good trial of that years ago, I think it was. Yeah.
- [51:00]
C
Okay.
- [51:01]
B
No, that is. That is a favor of somebody who has treated head lice in children before. Yeah, I sure would prefer a pill because I can't smoke. When I put malathione on them, that makes it worse.
- [51:14]
A
All right, that's enough. So I want to thank everybody for joining us this week. I hope you learned a few things. Hope you laughed once or twice. And mostly, I hope you're planning to join us next week. Until then, I'm Matt Zyrus.
- [51:27]
C
I'm Tim Patton.
- [51:28]
B
And I'm Laura Ferris. And we are Derms on drug.