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Derms on Drugs
BCC Treatment Goes Viral: Find out what happens when you unleash a genetically modified herpes virus on difficult BCCs
01:02:12
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- [00:18]
A
Hi, I'm Dr. Matthew Ziras, and welcome to Derms on Drugs, a video podcast brought to you by Scholars in Medicine. Derms on Drugs is where cutting edge derm meets mediocre comedy. I'm Matt Sires, and each week I'm joined by my residency buddies, Dr. Laura Faris and Dr. Tim Patton. And we're going to use our 60 years of combined derm experience to discuss, debate, and dissect the hottest topics in dermatology. It's everything you need to know to be on the cutting edge of derm, and it'll be the most fun you've ever had while learning something useful about the skin. So tune in every Friday when we drop a new episode only at Scholars in Medicine and Spotify at this point. So we are going to go ahead and jump right into it. I know Dr. Farris had a big night last night at the Duke UNC game. Now that she is chairwoman of dermatology. I think she took some poor student seat, told them they're not allowed in anymore. So. But, you know, let's go ahead and see what she's got to tell us about today. Dr. Ferris, why don't you go ahead?
- [01:30]
B
All right. Hopefully I'll fare better than the Tar Heels did last night. But. So the first paper that I'm going to talk about, it was just published in Nature. Cancer Efficacy and Tolerability of Neoadjuvant Therapy with. We're just going to call it TVEC because I can't pronounce the formal name. Cutaneous basal cell carcinoma. It's a phase two. It's the NEO BCC trial. And so this is a small study. It was 18 patients with what we would call difficult, or what they call difficult to resect basal cell carcinoma. So that. How do you determine which patients are difficult to resect? Or what do you call is like locally advanced. Is always sort of this ongoing trial with basal cell. But 18 patients, open label study. They got six cycles, and then they had this sort of interesting primary endpoint, which is, was the tumor then resectable without the need for plastic surgery to do the reconstruction? So basically, did it need a flap? Did it need a graph? And so this actually was terminated early because it met that endpoint. And so what they found was that 50% of patients did not need a flap or a graft. They also were able to. There's a lot of basic science in here. I'm gonna kind of focus on the clinical aspect of this. But, you know, big thing in Treatment of locally advanced tumors, or neoadjuvant therapy particularly, is what percentage of patients reach a pathologic complete response? It was a third of patients here.
- [03:10]
A
Wait, hold on a second. So do you inject this stuff into the tumor or do you. Okay, so it is.
- [03:19]
B
So there are intratumoral delivery.
- [03:21]
A
All right, so that's why TVEC just.
- [03:23]
B
To remind people, HSV engineered to express GM csf.
- [03:29]
A
Okay, so it's a herpes virus. And you inject. So that's why they're studying it for basal cell. Because as I was looking at this, I was like, why the hell aren't they using this for, you know, pancreatic cancers and liver cancer and brain cancer? Because it's easy to inject it into.
- [03:43]
B
You have to have accessible tumors. So this is FDA approved for melanoma specifically. All right, so, you know, so this is looking at it for basal cell. Why basal cell? Basal cell tends to be sort of a cold tumor microenvironment. They can be hard to treat. And so, you know, key just to go not too deep into the science, but if you look at the patients who had good pathologic responses, they had increased levels of CD8 positive T cells, CD20 positive B cells, C, CD68 myeloid cells, and a decrease in CD4 positive T cells, and particularly Tregs. The tumors that did not do well were infiltrative basal cells. And then the other thing that they said was they looked and said, what percentage of people had subsequent basal cells. It was two, which was lower than they would have expected. So their argument was potentially this is going to prevent future basal. Everybody kind of did better. All the tumors got smaller. Small study, hard to know what to do with it, but, you know, interesting. And potentially this is a way to sort of change the microenvironment in basal cell carcinomas. Maybe make them more likely to regress, maybe even make them more likely to respond to other therapies too.
- [05:04]
A
Do they get. This is going to sound stupid. I say a lot of things like that, like, do they get her. Like, do they get cold sores on the lesion?
- [05:14]
B
So interestingly, one patient had to had early termination because he had basically like pyrexia. So he was the one. And he did not have pre existing IgG and IgM to HSV. So it was like getting a primary HSV. If this gets out of control, you can actually treat them with like acyclovir as well.
- [05:34]
A
Huh. So do people who have a history of herpes do better or worse or did they not really talk about that?
- [05:42]
B
They did not really talk about it. There may be data from the melanoma world, but I don't know. But you know, interesting. Intralesional oncolyt viral therapy. Probably sort of where we're going to, I think, start moving with particularly non melanoma skin cancers.
- [05:56]
A
Be super cool if we ended up doing it for warts like one virus and another virus and see if it worked. All right, Patton, what do you got?
- [06:04]
B
Very expensive warts there.
- [06:06]
A
Expensive wart therapy. Agree. Okay.
- [06:08]
C
I mean there are these risks, you know, difficult to resect basils and so it's going to be interesting to see what wins out in the neoadjuvant care. Right. There's. They're studying intratumoral immune checkpoint inhibitor therapy. You know, the systemic therapy to shrink these guys before surgery is. It's just kind of toxic. It's hard, hard to tolerate. So I think intratumoral treatment makes a lot more sense, less toxicity. Right now it's going to be. Is it going to be the TVEC or is it going to be the.
- [06:41]
B
Map or will it be both? Maybe it'll be one, then the other.
- [06:43]
A
It would make sense to use them together. All right, Patton, what do you got?
- [06:47]
C
All right, I did the. Buried a ritless switch in alopecia areata. So.
- [06:51]
A
Oh, wait, wait. So before you start, I want to say last week Patton said, doesn't make sense to switch from one jack inhibitor to another. I. You. I remember that.
- [07:04]
C
I think.
- [07:05]
A
Yeah.
- [07:06]
C
I don't know. Did I. Is that what I said?
- [07:08]
A
I thought he said that. Ferris.
- [07:09]
C
I said. I said just stay on the Jack we were talking about.
- [07:14]
A
Okay.
- [07:15]
C
Basically. Stop.
- [07:18]
A
Okay. All right, all right. Patton, where'd you go?
- [07:21]
C
I don't. I disappeared. There I am.
- [07:25]
A
There you are.
- [07:26]
C
Well, I mean I'm the. I'm the beauty of the show. You lose me.
- [07:31]
A
Yeah.
- [07:32]
C
All right, so 20 December 2024, clinical and experimental dermatology efficacy and safety is switching from baricitinib to ritless. It have been severe alopecia areata by Chen et al, who is a retrospective case series. Fifteen patients. So these patients, three things they had severe alopecia areata had been, you know, so salt score of 50 or higher had been on Barry for at least six months. Didn't want to continue or increase the dose and had stopped Barry for at least three months. So these weren't really switchers. These were. I stopped the medication and. Hey, do you want to try this other one three months after you Stopped it. Switching kind of implies like right away. Yeah, not that that may make a difference, but I think the point being berries washed out of your system. So this isn't a berry effect, this is ritla, which may or may not be true, but anyways, they were placed on RITLA 50 milligrams daily, followed for 24 weeks. 60% of those 15 patients responded, 40% did not. So you know something, you can tell your patients even if you haven't had a great response. In this one study, more people than not responded.
- [08:40]
A
I mean that's actually a little better than their phase three results of just treatment naive people.
- [08:48]
C
Yeah, I think they were prime. I think the, the baricitinib did prime these people a little bit.
- [08:53]
A
Oh yeah, yeah, I couldn't.
- [08:54]
C
So anyways, two graphs. Median SALT score, median dlqi, both improved with patients that started RITLA univariate analysis. If you had no response to bear, you were much less likely to respond to ritla. And no other factor like age, sex, comorbidities, duration of current aa, AA type was found to correspond to achieving a response. They have a table that really allows you to go through each patient's. Five patients had no response to Barry. Like 0% improvement in salt score while taking the berry. Four out of five of those patients had a zero improvement in salt while taking Ritley. So if a patient has absolutely no response to Barry, it's not like there's a chance it really isn't going to work, but it's not looking good. The responder really responded. Went from assault of 100 to assault of 11. A couple things about her, she was 12 years old, which was a lot younger than the other non responders and she was also on 2mg whereas the other non responders were all on 4. So I do think Barry primed them a little bit. I know they stopped at three months, but you know, there was a discontinuation trial with Barry and at three months only 20% of patients lost their benefit. So I still think Barry was still having a biological effect. So I think Barry people may say, well it's not really fair. If these people stayed on Barry, we probably would have seen the same responses and the same non responses. But you can switch. I, I did it with one patient, he was at six months. It was kind of like the study, he was at six months and he wasn't really getting a great response. And that, you know, Ritless, it may be knew it was available and so we did switch him. I Haven't seen him back yet. It's kind of a cute story. He has alopecia universalis and he doesn't care. He's married and has a kid, but his kid has AA and so he was like testing himself out to see, you know, it was this a medication that he would like put his kid on. It was, it's kind of, it's like a little, a little Hallmark movie now.
- [10:51]
A
I'm going to announce it officially right now. People have now learned everything they need to know about Jack inhibitors for alopecia areata from derms on drugs. You don't need to listen to Brett King or any of those other supposed experts anymore. Ferris told us last week you give them six months on Jack. And that was Riddle was the study. And if they haven't gotten better, they're not going to get better. And so now we know after the six months if they've had no regrowth. Yeah, it's not even, probably not even worth try. So that's. If you get six months on Illumina at 4 milligrams and nothing happens, it's probably not even worth trying Riddle. I mean you still can, but you give them six months, they haven't gotten better, you switch and there's a 60% chance they'll get better whenever you switch them. That's it.
- [11:35]
B
If they had some response, all you need to. So yeah, having a little like, like there's. With a little bit of a response.
- [11:43]
A
Right. If they get a little bit of a response, it's still reasonable to switch. But if they get absolutely no response at six months, probably not even worth trying the other one. Would you.
- [11:52]
C
What would you do in that? I think we talked about it last week. I hitting them with pred at that point maybe makes sense and keep them on the Jack.
- [12:00]
A
Totally makes sense. Hit them with pred. I would do like probably 20 for a month, 10 for a month, 5 for a month. You could do 40, 20, 10. That was the study. Right. The eight patient case series was doing that and then all of those patients regrew and then maintain their regrowth. But I think you really are immunosuppressed. I mean hell, I wouldn't want to be on a JAK plus prednisone.
- [12:25]
C
Yeah.
- [12:25]
A
You know. Yeah. Okay. All right. Ferris, you got anything else? Nope. All right, got it. Let's go on to my study. So this was the treat. No, it wasn't treat, it was something else. I can't remember the name of the study. Chat check the check Study Chronic Hand eczema in adults cross Sectional Survey 60,000 people in Canada, France, Germany, Italy, Spain and the UK. This basically confirmed, so this was a big study that basically confirmed everything we already knew. So now we can be pretty damn certain that the prevalence of hand eczema and physician diagnosed hand eczema was a little lower than expected. So it was about 5%. Now if you use non physician diagnosed, just hey, might get hand eczema. My hands get an itchy rash, the number goes up. But basically things that I thought were interesting, 20% of people had dermatitis at some point in their lives. 9% had hand eczema at some point in their lives. 6% reported hand eczema in the last 12 months. 4.7% physician diagnosed hand eczema in the last twelve months. Biggest things were, as we already know, male versus female females have more than males. It was interesting. There was a big difference in countries. So like in Germany it was very low at 3.5%. In the UK it was high at 6.4%. People with jobs had more hand eczema. Interestingly people in urban areas had more than rural areas. But the survey was like 80% urban, 20% rural. So hard to know what to make of that. And then the highest prevalence was in people 30 to 39. We can really see that in the forest plot. Right, so it's really 18 to 29. Then it goes up for 30 to 39 and then drops by decade up to the age of 60 to 69. Don't know, that might be that like old people don't wash their hands. Or it might be that old people's skin gets tougher but kind of hard to understand because you would think of less barrier function in old people.
- [14:29]
B
Or they're not going to work, so they're not getting work exposure.
- [14:33]
A
Yeah, that makes way more sense than anything I said Ferris, that's why we're here, man. Good. That's why I got so good work. So, so really nothing terribly new here. This is what we already thought, but it's a 60,000 person study, so really confirms it and gives us good, you know, stuff on it. Biggest pearl I have for hand eczema was during COVID we actually got a number of good studies of like what mattered, what kind of soap you use doesn't matter much how much you moisturize, doesn't matter much. So moisturizers don't help a whole lot. What does help is washing your hands in cold water. And it goes back to, we tell our patients, don't shout, you know, if you don't take long super hot showers because it melts your intercellular lipid, lets it get rinsed away. Same thing in hand eczema probably that the hotter the water the more you can remove the intercellular lipid. That's the one pearl that I've got for people right now. You guys have anything else you want to chime in about this one? Before we bring our guest on do.
- [15:39]
B
We think weather like Canada UK had higher rates? Do you think weather matters in chronic hand eczema?
- [15:46]
A
That's actually a great question. So I think that changes in weather matter a lot. So going from hot to cold and cold to hot. Right. Our skin isn't terribly well designed for that and I do actually think cold weather matters but again because of the changes. Right. So you're our evolutionarily our skin is never in the, in the, until the last 50 years, our skin never experienced going from 10 degrees to well it kind of did but from 10 degrees to 80 degrees, you know, 10 times a day as you went inside and outside. So when it's hot, when it's 90 and you come inside and it's 70, that's not nearly as big a switch as going from 10 degrees to 90 degrees or from, you know, from 10 to 70. So I do think temperature matters. But I'll be, I'll be interested to hear what our, our guest thinks about this. Patton, what do you got anything?
- [16:42]
C
No, I, I wasn't quite sure what the, the point of this was. Like you said, it was kind of stuff that. Okay, yeah, maybe never been studied on this big a patient, but is anything shocking here? I mean Le Leo was one of the authors. So I think they're doing like a little pre marketing type of they got.
- [16:59]
A
A new drug and they sponsored it and they're right. They got the JAK inhibitor coming for hand eczema. And so let's, let's go ahead and bring our guest on. So we've got Dr. Jakob Thyssen who is a professor of dermatology at the University of Copenhagen in Denmark. He was the lead author on the European hand eczema guidelines that came out several years ago. Now conflict of interest. Dr. Thissen does work now doing R&D at Leo, but he is looking for new molecules, not really doing work on their existing molecules. So we're not really going to talk about Trilokinumab I E Adbri or Delgo Sitinib, which is the new hand eczema drug that is coming because those really aren't the areas that he's working on. But. So, Dr. Thissen, great to have you on.
- [17:51]
D
Pleasure to be here. What a wonderful way to spend a Sunday afternoon in Denmark. So thanks for the invitation.
- [17:58]
A
You got it. So first let's go right into kind of what Dr. Ferris asked, because I think it's a great question. So, and I will again tell everyone, I think of Dr. Thissen as the world expert on hand eczema. Right. The European guidelines are comprehensive. The Danes have done the most work on hand eczema. Sort of their classification system is what the whole world uses. And so Dr. Thistle, why don't you, you know, what do you think is the role of weather in the seasonality of hand eczema? Let's start there.
- [18:30]
D
It's such a good question. I'll tell you what, if you come to Denmark in the winter, you wear your sneakers out and you know, it goes from, from plus, like plus Celsius to minus Celsius, your skin will crack like your toes will crack, your fingers will crack even though you have good mittens on. So the point is that cold is very, very important for skin barrier function. And you have a bunch of animal studies showing the same. But what's interesting is we have very big nationwide registry. So every Dane is basically recorded in the reg. If you pick up a topical corticosteroid or what have you in the, in the pharmacy, you will be recorded. And we had a PhD student from the US, Dayton, by the way, you.
- [19:12]
A
Just made all Americans nervous about Denmark. You will be recorded.
- [19:17]
D
But it's great for research, I will tell you. But we had, we had Carson Hammond, so he's a dermatologist out of Phoenix, Arizona. He was here doing a PhD for a few years and he came up with the idea to study this like, what's for 80 patients? Is there a higher consumption of topical medication and oral medication, systemic medication in the winter? And there was, and I'm fully with you, that transition also is very important. What you just raised, and I know Peter Lies have done some very impressive studies showing when you take mice in and out of humidity, it actually weakens the barrier and then you have more eczema prone skin. So I'm right with you.
- [19:58]
A
Okay. All right. So I usually monopolize our guests. So I'm going to give Pat and Ferris a chance to ask some questions here. Before I could, I could sit here and pepper this in with questions for the next four hours. So I'll let the two of you jump in first.
- [20:16]
B
Yeah, I guess my Question would be how much of hand eczema do you think is. Is really sort of either irritant or allergic contact related. Right. Like, so how much of this is, you know, if we could actually change exposure or change what we're doing, how much of it do you think would get better? And how much of it do you think is sort of more immunologic or genetic?
- [20:43]
D
Yeah, so it's a great question. I'd say that, you know, irritant contact dermatitis, that that's really the most important exposure that causes eczema, whether you have atopic background or not. And then I think that at least in my country, if you go 30, 50, 70 years back, allergic contact dermatitis on the hands was something of great importance. But today, when I saw my last patients about a year ago, I would rate it's about 1 out of 10 chronic hand eczema patients where allergic contact dermatitis could play a role. But that could also be in concert with irritant contact dermatitis. Just remembering that many of these chemicals both have irritant and allergic potential. So what it brings me forward to is as a clinician, I mean, you have to take that interview and hear about irritant exposures and allergic exposures. You have to look at the hands, let's say you have a very localized lesion just where the metal piece from a dog leash or something is exposed every day. And then you do the math. But, but I think that always keep in mind it could be allergic contact dermatitis. Do advise your patient if you're suspect this to remove. That could be fragrance, allergens or metal exposures, whatever. And if it doesn't solve or if you have easy access to patch testing, then absolutely, why not make the patch test? So, so that's the way I see it. But I mean it's just my gut feeling. 10 to 15% of patient with have relevance or of relevant allergic contact dermatitis, but not more, to be honest.
- [22:18]
A
Jakob, do you. So the, the thing that I have learned kind of helps my colleagues get this and helps patients get it because I think that irritant contact dermatitis is a factor in essentially every single case of hand eczema. And the terminology, what I learned to say to people is imagine you got five showers a day because the average, well, the average American washes their hands six times a day. So imagine you got six showers a day, got in there, hot water, soaped up. Would you not expect that every single person would be walking around with dry Itchy, flaky skin. And so some people are washing their hands 10, 15 times a day. But even if. Unless you're so I actually think a big part of the reason men have less hand eczema than women. And I say this frequently on the show, I think men are disgusting and we just don't. And we wash our hands like twice a day, whereas women wash their hands like, you know, ten times a day. And so that's why the average is six, because it's disgusting men and clean women. But. All right, Patton, what do you got?
- [23:26]
C
I was wondering because you've also done some work about topical steroids and systemic effects of topical steroids with bad hand eczema. I, I just, I never thought that that would be an issue. The, the skin on the hands is very thick, systemic absorption. Even if you're putting on steroids twice a day for, you know, two weeks straight and can only take a few days off, I kind of tell those patients, don't worry about it. You know, the back of your hands might get a little bit thin and you're going to see, you know, telangiectasias and things like that and atrophy. Am I, am I like under, under counting just how dangerous topical steroids can be or am I ignoring the side effects in those patients with hand eczema?
- [24:09]
D
I think your guess is just as good as mine. There's no, there's no research I'm aware of that will show that, okay, you'll get systemic exposure after putting clobetazole on your hands for, for a certain number of times. But, but I will say is if you have other skin areas, let's say genital, where we know the absorption is just enormous there, you know, two, three weeks of clobetazole for lignosclerosis there, you can have Cushing syndrome. So I mean, we know these are very potent drugs. And in ad I really do think that it matters for systemic absorption and exposure. And I think we have pretty good evidence for this that is very, very good register based studies indicating this. But we also, about a year ago ran a study where it was an RCT taking tacrolimus versus mometasone furate and show that, you know, with system or with full body exposure for two weeks, you do see corticosteroids go into circulation and it will suppress insulin sensitivity. It will affect bone homeostasis. So for me, I think, yes, that we know. I'll just try to go down to my point. But my point for, for hand eczema is just that. And this may be controversial, what I'm saying now, but I try always more or less completely. Unless it's hyperkeratotic eczema to avoid clobetazole. I think in hand eczema, it works, but it's just too much because it will relieve some symptoms here and there. But there is a price to pay, and it comes down the line because you will destroy the barrier. And that's my point. So I think steroids on the hands, you know what, they work great. But if you take two potent steroids, there is a price to pay for patients. That's my experience.
- [25:57]
A
Pat. Before, I got, like, nine follow ups to the things Jacob just said. But before, again, before I jump in, Patton, you got any follow ups? You want to ask them? No, no.
- [26:05]
C
Take it away. Go.
- [26:06]
A
Oh, God damn it. So, all right, listen. Sorry, sorry, by the way, I apologize for just taking the Lord's name in vain. So listen, because I think Patton's Catholic. He has five kids, so he's gotta be. So this is so. All right, number one, you just said something that nobody in the world of derm gets, right? So I'm sure you've seen Elias's papers from, like, back in the 90s, that three days of clobatazole and you stop making and releasing lamellar bodies. So you stop making intercellular lipid. Right? So for people who, like, think in terms of bricks and mortar, you start making the mortar, and you can't do barrier repair after three days of clobatazole. Which is why topical steroids have never worked as well for atopic derm as we would think. Because while we're helping with the symptoms, we are reducing barrier functions, and we're making the fundamental problem of the disease worse. But my response to that has not been to not use clobazole. It has been. I have people use clobatas all for two days at a time. So since Elijah showed three days, I tell people, use. You can use it for two days a week, and then the rest of the time, I got them on something else. Historically, that's been a tci, which I don't think does a whole lot, but. But that's been my. So do you use any steroids in hand eczema? Do you. Is there. Like, you use betamethasone, you use mometasone, or you just stay away from them completely?
- [27:31]
D
No, no, no. I would say tzi. I don't use for hand eczema on this. It's, you know, atopic hand eczema and not really anything palmar. So dorsal TCI is fine. The rest that has been for me, topical steroids, really the workhorse in and out, week in, week out. But I'm just saying that except for the hyperkeratotic one, my experience is that clobetasol is just too much. So I swear to betamethasone, I swear to mometasone. So I take it down a notch. And then one of my favorite studies is a Nils Vien from 1994, I think in the British Journal of Dermatology, showing, you know, you use mometasone for chronic hand eczema and then you can taper to twice weekly or three times a week. I know it works fine both of them, but you do see more side effects if you do it three times a week compared to two twice a week. So for me, you know, my clinical, clinical experience mixed with evidence from the literature is that a European group, three steroids. So, you know, moderately or potent topical corticosteroids, that's the one I prefer. But I'm not against clobetasol. But when I teach, when I taught my, my residents back in the day, I would always say, be careful. It's a very powerful tool.
- [28:46]
A
Yeah.
- [28:46]
D
And it is. Yeah.
- [28:48]
A
And for those of us in America, a high potency topical steroid is a Class 2 or 3, which I agree with the Europeans, by the way, that it should be low, medium, high and ultra high. But then the other thing Patton brought up, which I think is a great question. Right. So. So yeah, you've done the work showing that there is a direct correlation between the probability of getting diabetes and the total amount of topical steroid used and the probability of getting osteoporosis and the total amount of topical steroid used. Do you have anything in your head that is like a, I guess the bigger question, do you ever bring it up? Do you ever say to a patient like, hey, or does it, does that risk ever influence your.
- [29:35]
D
Never, never practice, never whatsoever. But I will say caring for 80 patients where you have significant body surface area there, it comes into mind. So I can have patients that are well treated with not kilo after kilo of topical steroids, but I mean, when you have significant usage and they are very disciplined and they do listen to your advice about put it on as soon as you can and then taper and go to twice weekly application. So very adherent, disciplined patient with large body surface area. I'm like, even though it works fine for you, it's time to move you to a systemic or a biologic because it's not good in the long run. But I never had the conversation around diabetes and osteoporosis. It's something in my own internal algorithm. It's too much, I think, for patients to digest.
- [30:25]
A
Okay, last big question first. So I'm going to be the first author on the phase two study that Insight did on. And we're allowed to use brand names on this show. So Opzelura for hand eczema. And I gotta tell you, it was freaking insane how good it was. So like, and these people were supposed to be non atopic, just hand eczema, whatever. And I was like, I, I like it was an order of magnitude better than clobetazole would be my guess. And I was like, oh my God. Like, I think this is because you don't have the barrier impairment. But I think JAK inhibitors and conflict of interest. Right. Jakob works for Leo, who's got a JAK inhibitor, who's gonna be coming to market for hand eczema. But right, based on what I saw with Abzelura, I was like, oh my God, this is like. Do you think JAK inhibitors are going to completely change the world of hand eczema?
- [31:26]
D
Let me try to give a political answer with my bias here. I think what we see is the topical steroids. They have worked well for decades. Germs know how to use them. There is a certain element of patient fear and it works well for most patients. But there is also a need because of tcs reducing inflammation, but come at the cost of the barrier. I think there is a need for these innovative topicals, JAKS being one of them. And among the new innovative topicals, I would say that the JAK seems to be the most potent. You know, fast onset of action, very strong itch reduction. And therefore I also see that these can be very useful for crowning hand eczema, where it looks like they will have the indication, or at least we see in Europe, that there is one topical JAG inhibitor that has the indication for chronic hand eczema. So I see this, this is a very good combination for patients because it reduces inflammation, but not at the cost of barrier impairment.
- [32:24]
A
And do you guys have tapiniroff in Europe?
- [32:27]
D
Like, no, not yet. And I don't know whether the Organon has any plans to, to take it to Europe. But that's also a good, a good product when you look at the data.
- [32:39]
A
Yeah. And what's fascinating about it is that it's the ERA hydrocarbon pathway is the only pathway I've ever seen that actually stimulates barrier formation beyond just you remove inflammation and barrier gets better. So I'm picturing in my head that the most effective topical regimen I could ever imagine would be to pin her off once a day and a jack once a day to pin her off, to stimulate barrier recovery, Jack inhibitor to take away the inflammation. I got one last question for you before you go. So you have been, you were sort of a mentee early in your career of Torkoal Manet, correct?
- [33:23]
D
Yes.
- [33:24]
A
So he is the one who's done the best work on dietary nickel. Yeah, I think dietary nickel is the most underdiagnosed thing in the world of dermatology. I think that it is. 1 to 2% of the population I think is walking around with inflammatory something from dietary nickel. What do you. Having worked with Torkel and because I've never actually talked to him about this, do you think about dietary nickel on a regular basis with hand eczema and other patients, or is it something where you're kind of like it exists, but man, I'm not too worried about it.
- [33:59]
D
The answer is I don't. But let me just, you know, flip back 40, 50 years because it's interesting. There were two professors at the time. You had Torto mening and then you had this Nils vine, actually the same guy I just spoke about before on Ometazone, furiate and tapering to twice weekly, three times weekly. So they had two ambitious career ahead of them. And Tor Delmene, he chose to go into regulating nickel exposure from jewelry, from buttons, from zippers, what have you. And that led to the European regulation on nickel exposure, limiting exposure, limiting nickel allergy prevalences to a bare minimum. Now, Nils Fine, he did the opposite. He believed very much in what you're talking about that oral Nigel exposure leads to a lot of eczema's problems. And he wanted to understand and study that. And it was very important at the time. So he showed in very convincing studies how much it matters and how sick patients were and how changed when they had an nickel free diet. But what just happened in Europe over the years with the success of Torgumene's work on regulatory efforts, is that it became less and less relevant with the dietary exposure because patients, and we've documented this, they went from having, you know, very often three plus nickel test, patch test reactions to two plus to one plus to now doubtful. So you know this. The severity of Nigel allergy in Denmark just decreased decade by decade by decade. And the more decreased, you know, the cutaneous response, the less nickel, the less diet, less diet mattered. So I mean it's just that, you.
- [35:37]
A
Know, that part of it I never thought about that. Right. We've got pretty good data that the longer you go not being exposed to an allergen, sort of the less, the more it takes to wake up your memory effector T cells. So your allergy gets less, you know, intense. And so it hadn't occurred to, I was thinking of the nickel regulations as just bringing down the prevalence of nickel allergy. It never occurred to me that it also, but it's obvious whenever you say it that it would also bring down the severity of nickel allergies.
- [36:09]
D
Went down. So I think the message for listeners here or viewers is that if you have a very niggle allergic patient with a 3 + or 2 + reaction, it may matter. But if you have one of those, it's a doubtful or three pluses in a row, you're like, don't worry about it.
- [36:24]
A
All right, okay.
- [36:25]
B
How about Matt, can you drop in for listeners? Where do you send them for nickel free diet information?
- [36:31]
A
So there's a website called www.thelownickeldiet.com. there's also a textbook or not a textbook, a cookbook of the same name called the Low Nickel Diet that's on Amazon. It's like 30 bucks. I wrote a chapter in there called about nickel, dietary nickel for doctors. That is literally because most dermatologists and allergists don't know about this. And so it's to literally cop for the patient to copy it, take it into their doctor. And it's got all the references, everything else. So it really is the only diet that we have. So yeah, compared in the US we don't have any nickel regulations. So nickel was still 20% of people horribly allergic to it. It's the only diet of all this anti inflammatory diet, bologna and the Paleo, this and the whole 30 and the that and the whatever. There's no real evidence behind any of that. Low nickel diet is rock solid proof. We know which cytokines we know like and it has systemic effects. The Italians talk about this systemic nickel allergy syndrome. This is the only truly anti inflammatory diet. If you and you can get a test, right, you get a true test. If you're allergic to nickel, the diet might help you. If you're not allergic to nickel, it's not going to help you. But www.thelownicklediet.com and the textbook called the Low Nickel Diet on Amazon. And I have no conflict of interest, although I wrote a chapter in the book I don't get, I don't, I don't make a penny.
- [38:03]
D
A penny?
- [38:04]
A
Yeah, penny. Not one. All right. So unlike Patton, who's very conflicted, don't listen really to much of. If he recommends anything, forget it.
- [38:13]
C
Yeah, horribly, horribly, horribly in bed with pharma.
- [38:18]
B
Just go on to openpayments.gov you'll compare.
- [38:22]
A
19 cents over six years for Pat.
- [38:25]
C
I think I owe them money.
- [38:27]
D
I'm probably gonna get kicked out of the show. So just one anecdote before I leave. That's a case report from Japan with an old woman or a middle aged woman who went out to her well every day to carry in water. And it was so much nickel in this water and she would wash her, her head in it. She actually got allergic nickel dermatitis on her face and it was diagnosed. And when she stopped using the well water, he was fine.
- [38:53]
A
You're kicked because I get asked all the time by patients, do I need to worry about whenever I shower? And I'm like, no, it is impossible for there to be enough nickel in.
- [39:02]
D
Your water to get this one anecdote. Yeah, one case.
- [39:06]
A
Listen. All right, so Jakob, thank you for coming on today. This was so much fun. And I want you to stick around if you don't mind, for a few more minutes. So Patton typically does some trivia for us and it's, it's kind of the three of us against each other. You're gonna, we gotta wait for Patton to finish answering the question. Reading the question, then once you finish reading the question, you just shout out the answer. So far for this season, it's Ferris 2, actually Ferris 3, Cyrus 1. So she's won twice and we tied once. I, I have yet to win a round of trivia. But let's, let's see, let's see where we go here.
- [39:44]
C
All right, I struggled this week. These are the worst questions. So I'm just setting this up because I did like hand dermatitis and then I started to get into allergens and Cyrus would have cleaned up there. Can't have it. We got two that kind of focus on Denmark, so definitely favoring Yakov. I don't mind favoring our guests.
- [40:05]
D
And then I was a chip in if I know the answer.
- [40:09]
A
Oh, yeah, that's the idea. You're competing, you, Ferris and me.
- [40:14]
D
Yeah.
- [40:14]
A
Okay, let's go.
- [40:15]
C
And then one does have to do with patch testing, but it's pretty obscure and it may actually Be wrong. Okay.
- [40:20]
A
And I have already lost to Jakob several times in ping pong. And I think of myself.
- [40:24]
D
That's true.
- [40:25]
A
I think of myself as a very good ping pong player. And he just wiped the floor with me.
- [40:29]
C
Wow. Okay. All right, first question. These are a bit wordy. I couldn't shrink them down. My research team took off this week. All right, number one. According to World Population Review, 68% of the population of Denmark is blonde, which put them at number six when ranking countries according to the percentage of blonde people. Of the five countries ranked above Denmark, which is the only one that is generally not considered to be a Nordic country.
- [41:05]
A
Germany.
- [41:07]
C
Germany's not Nordic. And it wasn't Germany.
- [41:10]
A
You said which one's not Nordic?
- [41:12]
C
Yeah, not Nordic.
- [41:14]
A
5.
- [41:15]
D
So there's.
- [41:15]
C
There's Finland, Iceland.
- [41:18]
D
Iceland.
- [41:19]
C
They all have a bunch. They. Most people consider Iceland Nordic.
- [41:24]
A
You guys own. Oh, no. No, you don't. That's Greenland you guys own. Well, for now.
- [41:29]
D
Let's see about that one. So we have five countries. Iceland, Norway, Denmark, Sweden. Finland. That's five. And then you want the sixth one with blonde.
- [41:36]
C
Yeah, there's one in there. There one in the top five. That is not.
- [41:41]
D
Okay. Could that be Holland? No.
- [41:44]
C
No.
- [41:44]
A
Kazakhstan?
- [41:46]
C
No. Really?
- [41:48]
B
Switzerland was not it.
- [41:49]
C
Switzerland was not it.
- [41:50]
A
Island.
- [41:51]
C
It's in the neighborhood.
- [41:52]
A
It's close to Kazakh. I don't know what's close to K. No.
- [41:56]
B
All right.
- [41:58]
C
Estonia.
- [42:00]
A
Estonia.
- [42:01]
B
Okay.
- [42:02]
C
All right. Estonia. 70% of the patient, apparently blonde population.
- [42:07]
A
About patients, just so they get sick more.
- [42:10]
C
No. No population. Well, blonde hair. Yeah, sure.
- [42:13]
A
Okay.
- [42:14]
C
All right. So that was. I mean, that's a little bit. Okay, let's move on. All right, ready?
- [42:17]
A
That's a good question.
- [42:20]
C
Bruno Block is considered to be a pivotal figure in the development of patch testing. Yadison is, like, the father of patch testing. Bruno Block worked under him, and he was the one who, like, standardized it. He's like, here's our standard panel. Here's how you do it. Here's how long you apply it. Before then, it was like, no. People would just stick people on. Stick things on your skin and see if it was a reaction. Okay. So he developed the standard series of nine allergens. Of these original nine allergens, which one is still included in the European and American standard patch test series? What. What would you say, Jakob?
- [43:01]
D
Nickel?
- [43:02]
C
No.
- [43:03]
A
Thimerosal?
- [43:04]
C
No.
- [43:05]
D
Chromium?
- [43:06]
C
No.
- [43:07]
B
Formalin.
- [43:08]
A
Oh, what?
- [43:10]
C
Stretch.
- [43:10]
B
Formaldehyde.
- [43:11]
C
I mean, formaldehyde.
- [43:12]
B
Yeah.
- [43:13]
A
Is that it? Yeah.
- [43:15]
C
Formaldehyde.
- [43:16]
A
Son of a. You've got two okay, one world renowned patch tester here and thisin I'll never.
- [43:27]
D
Be back on this show.
- [43:30]
A
Say whatever we want.
- [43:31]
C
We can say what. Yeah, so the other ones were mercury, turpentine, naphthalene, arnica, a leaf iota form in quinine and formaldehyde. That was his original nine.
- [43:42]
A
You know I was close with thimerosal, but thimerosal is actually not on the American standard panel anymore. So that does. You're right, that doesn't count.
- [43:50]
C
All right, third and final question so.
- [43:55]
A
Far it's Ferris 1 this and Zyra 0. Okay.
- [44:00]
C
Okay. So last week we talked about Niels Ryberg Finson and his Nobel award winning discovery of treating cutaneous TB with UV therapy. Remember won the Nobel Prize in 1903. I think Dr. Finson was born a subject of the Danish kingdom, but he wasn't born in Denmark. Where?
- [44:19]
A
Greenland. Oh wait, I gotta wait for the.
- [44:21]
C
Where was he? Faroe Islands. I knew Ferris and Cyrus had no chance of getting Faroe.
- [44:29]
A
I don't even know what the Faroe Islands are.
- [44:31]
B
They make good salmon. You get good salmon from there.
- [44:33]
A
Oh no, that's. Is that the fur? Is that the Faroe Islands?
- [44:36]
C
Yeah.
- [44:37]
A
Huh. Okay, so this in one fairest one, Zyra zero. I remain far behind.
- [44:44]
B
You remain defeated. That's right. You're very consistent.
- [44:51]
A
All right, that was, that was good stuff. Yakov, thank you for coming on today.
- [44:56]
D
This was my pleasure.
- [44:57]
A
This was a great, great time. And Yakov, just so you know, last week our guest was Dr. Weller from the UK because Jakob and I have talked pretty frequently about the sun and effects on mortality stuff. So the, that new study that just came out, he, that was a. Yeah, it's, it's, it's. You Europeans know what you're talking about.
- [45:20]
D
No, it's great. I love that topic. Great, thanks for having me. It's a pleasure.
- [45:24]
B
Thank you.
- [45:25]
A
Thanks for being on, Yakov.
- [45:26]
D
Thank you.
- [45:27]
A
We are now going to break into our final segment of the week. So I hope you enjoyed our first two earlier this week. And so this is the six pack where we're going to go over six more articles that we thought were interesting and clinically relevant. And so let's get right into it. So Dr. Faris, why don't you tell us about article number one.
- [45:46]
B
So this was an article in JAMA Dermatology, Babette et al. And this is imiquimod cream preceded by superficial curettage versus excision for nodular basal cell carcinoma. So this was basically a randomized study of 145 patients, half of them got superficial curettage, which is basically like curetting to the level of the adjacent skin, followed by imiquimod. 5% a week after curettage, five days per week. So five days on, two days off for six weeks versus, you know, standard surgical excision. So this was the five year study. This is a five year follow up. At the one year follow up, they actually did kind of see the same thing, which is that surgery is better recurrence rate, it's higher at a year, but this was looking at five years. And so if you look at, you know, what percentage of patients were recurrence free, it was 77.8 in the curettage and 98% in the excision arm. You know, takeaway for this is that excision does seem to work better. They did say that, you know, investigators thought that the scar looked better for patients who had imiquimod, but there was really no difference in patient rating. So kind of a long process to go through this for patients and maybe in the end excision is just sort of better and one and done.
- [47:14]
A
Yeah, it's hard, it's hard to see using this instead of curettage, EDC or curettage and cryo. Hard to see any reason to do this instead of those. Patton, any thoughts?
- [47:27]
C
No. Right. I, I don't see a lot of patients going for however many weeks of putting a cream on, you know.
- [47:33]
A
Yeah, I'm with you. All right, so curettage and imiquimod out derms on drugs not recommended. All right, Patton, what's next?
- [47:43]
C
Trelo Kinumab for BP. January 2025. British Journal of Dermatology by Maglia et al. Off label use of triloquinumab in the treatment of bullis pemphigoida K series. It was a retrospective series of five patients at tertiary referral centers. They were, they had bp, they were deemed to be bad candidates for immunosuppression or had failed immunosuppression or had an adverse event from a prior BP therapy. They did atopic derm 8, atopic dermatitis dosing, and four of the five patients were also started on 0.5 mgs per kg per day of prednisolone that was tapered. But they didn't really go into the details of that tapering, which I think is the, the most important thing in how you manage BP patients with other therapy, you know, with whatever steroid therapy, steroid sparing therapy. You're going to put them on. So what was it? The figure 1 showed the clinical photos before and after and the patients that had a complete remission. Two other patients achieved partial remission on doses of prednisone of 5 and 7 and a half. The text actually said 5 migs per kig, but that had to be a type you would, you would kill old people on that dose. And they did it at 12 weeks of treatment and then they followed them out longer. So yeah, longer term, follow up. One patient died, he had esophageal cancer going into the treatment. Three of the other four had either complete or partial remission. Still required prednisone, albeit at low doses, two and a half or five milligrams. So of the, like the. The one guy. Take the guy who died out. You had three of the four patients that still needed prednisolone therapy. That's comparable to the Adept Liberty. No, Liberty BP Adept study where 80% of patients treated with DUPY still required. I mean that's a totally unfair comparison because that was a very well controlled trial.
- [49:38]
A
So the take. So the takeaway is probably similar. Probably similar to Doopie. Yeah.
- [49:44]
C
Interesting to see if these other IL13 will go after that indication.
- [49:51]
A
Yeah, interesting.
- [49:53]
C
But you would expect that they would work similarly in the treatment of BP just like they do in atopic term.
- [50:00]
A
Well, but it tells us at least that IL4 blockade doesn't appear to be necessary for pemphigoid, which was an interesting question.
- [50:11]
B
In two years we could talk about should you switch from one to another for bp.
- [50:15]
C
That's right, switching these days.
- [50:17]
A
Right. All about switching.
- [50:19]
C
That's all right.
- [50:19]
A
All right, so we'll go on to the next one which was mine. This was interaction between blood pressure medication use and skin. Well, not skin cancer, actinic keratosis. And essentially they did a tri. So this was association between the use of anti hypertensives and the treatment of actinic keratosis. A trinetics population based study by Mendoza et al in the jad. And this was interesting. So we've kind of known for a while that it looks like hydrochlorothiazide in particular increases the risk of skin cancer, probably because it's somewhat photosensitizing. So they looked at a bunch of different blood pressure medications and the need for treatment for actinic keratosis. And basically what they found was that hydrochlorothiazide did increase your likelihood of getting treated for actinic keratosis. Probably increased it by about 20%. So interesting, right? Pretty. Pretty. We now should be thinking, if you've got somebody who's got tons of AKs and BCCs and squames and they're on hydrochlorothiazide, they should probably go on to something else. Interestingly, look like there might have been a little bit of risk with some of the other ones, but not nearly as big. So beta blockers. So metoprolol had a little bit of a risk. Losartan had a little bit of a risk associated with it. Looks like the blood pressure meds that have the least risk appear to be diltiazem and clonidine. But really my takeaway is that other than just kind of stay away from hydrochlorothiazide, if you've got somebody who's got a ton of UV induced premalignancy malignancy, you guys have any other real takeaways from this one or other thoughts on it? Because we now have like four or five articles that have. Have that have confirmed hydrochlorothiazide increases this risk.
- [52:10]
B
Yeah, I think this just sort of brought a case into it, as most of the data was on squamous cell carcinoma. Specifically. I counsel patients to try to get on something else if they're on hydrochlorothiazide and they've had a couple of particularly squamous cells.
- [52:24]
C
Yeah, I'm. I'm terrible at this. I really do need to get into the habit. I don't think. I, you know, immunosuppression. Sure. But I really don't. That's not on my radar and it needs to be. I pledge here. Forth.
- [52:40]
A
Yeah. It doesn't cross my mind.
- [52:43]
B
I tell PCPs, like, when you give those, like, derm lectures, like derm pearls for PCPs, throw this in there. It's an important one for them to know.
- [52:50]
C
Cool.
- [52:51]
A
Okay. All right, let's go on to our next article. Dr. Faris, what do you got?
- [52:56]
B
So this was basically, AI is better at talking to patients than we are. So this was over 1,000 clinical questions, 59 messages. Basically, either the doctor responded or they tested two AI models and they used the Stanford AI GPT model. And if you looked at patient satisfaction, it was higher with the AI responses than the physician ones. Interestingly, the physician ones were liked better by patients when they were longer, but the AI ones, that didn't really make a difference if they were longer. So, you know, maybe we ought to think about having AI rewrite our patient portal messages.
- [53:42]
A
But there was a huge difference in how long? Right. The AI ones were like a thousand 1500 words. The physician ones were like 200 words.
- [53:51]
B
Right.
- [53:52]
C
I mean, 200 words. Do you. I'm like, yes, it was characters.
- [53:58]
A
Yeah.
- [53:58]
C
Okay.
- [53:59]
A
Okay.
- [53:59]
B
And don't forget like 250 versus 14. 1500.
- [54:04]
A
And these were real. These were real doctors, not dermatologists. The. Now, did they look as well at the quality of the messages? Because if it was like, the course of. Patients are going to like it better if they're like, hey, do I need to avoid McDonald's in the air.
- [54:21]
B
That they were like appropriate clinical information. So that was. It wasn't that, you know, that they were giving the wrong information and just telling people what they hear. It's not like, oh, here, you can have an antibiotic for your cold. It wasn't that kind of level of.
- [54:37]
A
So far. Are you going to be implementing this in the UNC Department of Dermatology?
- [54:42]
B
I don't know if we're going to be doing this for patient responses. We are going to be doing AI scribing, like a lot of academic centers. So. So interested to see how that pans out.
- [54:53]
A
Okay, well, we're gonna have to follow up on that after. When you. When are you guys planning to implement?
- [54:58]
B
Within the next couple months.
- [54:59]
A
Oh, that'll be interesting to see if it saves you because. Right. I don't think it do. People don't think it's going to help patient care. They think it's going to save money. Is that. Is that correct?
- [55:08]
B
Save time. Save time. There's something like an over an hour of pajama time per clinic day, like where you sit and you chart and it saves that and chart closure rate goes up. So there's a lot of interesting data.
- [55:21]
A
Do you gu. Already have scribes?
- [55:23]
B
We have. We have human scribes for some of our encounters.
- [55:26]
A
Right. So that's going to be the question. Is, is it because it. It shouldn't be better than a scribe. I mean, maybe it will be, but it shouldn't be.
- [55:33]
B
We'll see.
- [55:34]
A
We'll see. All right, Patton, what do you got?
- [55:38]
C
I just wanted to bring up two things that I had learned about within, like, the last six months. I didn't want to go into details with the studies. It was two anti perspiration medications. So two medications. Two, two. One device, one medication to treat hyperhidrosis in the axilla. One was soft peronium, something. Something known as Softra. It's basically like topical glycopyrrolate. It's an M3 receptor blocker got approved last year and it just kind of went under my radar completely. It's twelve hundred dollars on GoodRx. I don't see us using a lot of this. The other, the other device was this Brella device. So Brella. I just went to the international Hyperhidrosis Society website and was kind of like, you know, here's all our therapies. And I saw Brella on there. I'm like, I've never heard of Brella. So Brella is this sodium patch that you slap on the skin. The sweat mixes with the sodium, causes heat, and then you kill off the sweat glands and so you don't sweat anymore. Just something, you know, to be aware of. I actually talked to the Brella guy. It's definitely more of a cosmetic sort of way that, that they want to do it. You buy a bunch of these pads for like a hundred bucks and then you charge patients 350 for the treatment. I don't think either one of them are any better than Botox. I don't know how well softer is compared to just topical glycopyrrolate, which you can get a compounding pharmacies. I don't see myself using a lot of, but just something like I had not heard of these and just nice to be aware of.
- [57:18]
A
Do you guys use. So the biggest thing I was surprised about with the soft peronium, like it had a lot of side effects like dry mouth. 14 of people vision blurred, 9% madriasis, which is your pupil doing something with 7%. Like 20, 30% of people had an anticholinergic side effect. Do you, do you use glycopyrrolate or oxybutynin orally for sweating?
- [57:46]
B
Yeah, glycopyrrolate. Yeah, I will. That's the one I use.
- [57:50]
A
Patent you oxybutyne or glycopyrrolate.
- [57:53]
C
Glycopyrrolate. I've switched a couple people to oxybutynin because they, you know, glycopyrly wasn't working.
- [57:58]
A
Yeah, yeah, yeah. I. I more use oxybutynin. I think it works better. But I just saw new data that glycopyrlate does not have a dementia risk and oxybutynin does. So I may be switching back to oxybutynin. So last one was mine. And as somebody who does little to no surgery, I still found this interesting. So. Right. The basic thing they looked at was tearing through. Right. So whatever. You're. So the reason I don't do a whole lot of surgery I'm not a great surgeon, so tearing through was a very common event whenever I was doing surgery on old people. So. Right. It's when you put your suture in and then it pulls through the skin. And the main takeaway was, as you already would have expected, like the bigger the suture, the less tear through there is. But the type of needle you use actually played a big difference. So they compared cutting needle versus reverse cutting needle versus tapered and tapered versus a cutting needle. Reverse cutting needle. Tapered was kind of meaningfully better. So the, the way that I think about this, if you put a stitch through and then you pulled hard enough to lift up a can of Coke, the cutting needle would pull through, but the tapered would not. Before the tapered would pull up, you'd have to put a stitch through and then pull hard enough to lift up a 16 ounce, like a bottle of drinking water. So it was how hard you would pull for a Coke versus to lift a 12 ounce versus how hard you would pull to lift a 16 ounce. So the. I don't know if there's a cost difference between the different needles, but it looks to me like the tapered needles are probably what we ought to be using if we're worried about tear through. What I'm understanding is reverse cutting are probably better if you're worried about maximizing cosmetic outcome. At least that's what I said in the article. But that was just a neat little pearl that I thought might be useful. Any comments?
- [59:57]
C
No. I tried to price it out. I mean, I figured, okay, these tapers must be a lot more expensive. But it didn't seem that way. But pricing gum sutures is kind of goofy to look up online.
- [60:07]
A
Yeah, Ferris, we know you put your people in a bubble for two weeks after surgery. Are. Are you gonna do you do. I didn't even know what needle I used. Like, I was like, I don't even know what the hell we've got in clinic.
- [60:20]
B
We mostly use reverse cutting. That's probably what you're using.
- [60:24]
A
Yeah, yeah, that's what I. Okay. All right. You gonna change what needle you use, Ferris?
- [60:28]
B
I don't know. Maybe I'll try it sometime. But I guess it only matters on like the thin skin, right? So like a 25 year old on the back. I don't have to worry about this.
- [60:36]
C
Yeah. Tearing is not common with the people that I operate on because I probably take the really, really difficult, more likely to have a complication, and I send them to much better surgeons than I am.
- [60:49]
A
Yeah, I hear you. All right. Well, guys, I think that is our last of the day. Now. I, I really want to encourage people to get on for next week's episode. We have such a fascinating discussion coming with our deep dive. So we've got a cosmetic chemist and Dr. John Barbieri from Harvard coming on to talk to us about benzene and benzoyl peroxide. You know, is it, do you need to worry? Is this a real thing? And if you do need to worry, how much do you need to worry? Right. Because and even if you're like, I don't think this is a real, your patients at some point are going to ask you about it because it's out there. So this is, and it, this is going to be a fascinating discussion. You really, you're going to be surprised at what we talk about. So join us next week. Thanks for joining us this week. If you've got questions, comments, ideas for topics you'd like to see us cover, people you'd like to see us have on the show, shoot us an email @questionsrms on drugs.com Again, that's questionsurmsondrugs.com. hope you learned a few things. Hope you laughed once or twice. And mostly, I hope you're going to join us next week. So until then, I'm Matt Zyrus.
- [61:59]
C
I'm Tim Patton.
- [62:00]
B
I'm Laura Farris. And we are Derms on Drugs.