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Derms on Drugs
Dermatology Fact or Fiction - The Derms on Drugs Find Some Serious Fiction in the Latest Articles in the Literature
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- [00:18]
A
Welcome to Derms on Drugs, a video podcast brought to you by scholars in medicine. Derms on Drugs is where cutting edge derm meets so so comedy. I'm Matt Zyres, and each week I'm joined by my residency buddies Laura Faris and Tim Patton. And we use our 60 years of combined derm experience to discuss, debate and dissect the hottest topics in dermatology. It is everything you need to know to be on the cutting edge of dermatology, and it'll be the most fun you've ever had while learning something useful. New episodes drop every Friday, so make sure you set your calendar and let's go ahead and get into it. This week we've got one of our patented six pack episodes where we're going to talk about six of the coolest articles that we've seen recently in the literature. The same way we would talk about him if we were sitting on Patton's back porch having a six pack of beer. So I don't know if Ferris drinks beer, but she's a little snooty. But Patton and I certainly would be. So, Dr. Faris, I think we have.
- [01:19]
B
In Sauvignon Blanc, but that's okay too.
- [01:23]
A
That sounds right.
- [01:24]
B
Yes. All right, so I'll start with my first paper. So this was in JAMA dermatology, Immune checkpoint inhibition inhibitors in field cancerization and Keratinocyte Cancer Prevention. Cox et al. So this was a clinical trial that was really not an intervention to treat AKs with immune checkpoint inhibitors because that would be a little bit over the top. But what they did was they took 23 adults who were immunocompetent who were starting a PD1 or PD L1 inhibitor for, for another cancer and who happened to also have ak. So these are people who are gonna have it for at least six months. They had to have AKs on their forearms. They couldn't have had like recent topical 5 fu or anything like that. And what they did was they basically did a count of forearm AKS at baseline and then at months 3, 6 and then 12. And so these people were pretty, you know, ake. They started with about 47 mean number at baseline and then it weight went to 14 at 12 months. That was statistically significant. So, you know, AKs, that's nice that they decrease the numbers of AKs. How about keratinocyte carcinomas? So what they did was they looked in the 12 months before they started their checkpoint inhibitor and the 12 months after they started it and their, you know, total Numbers basically decreased from 42 across the 23 people in the 12 months before to 17 in the 12 months after. So the number of SCCs decreased from 16 to 5. These really didn't reach statistical significance. But realize this was 23 patients. So kind of interesting, you know, are we going to start doing this for aks? Like I thought this Kleisseri was an expensive AK treatment. Like I can imagine that a PD1 inhibitor is probably going to be a really expensive AK treatment. Probably not. But like I mean maybe at some point like in those terribly sun damaged, you know, everything's an SCC or an ak. Maybe you only need, you know, maybe you don't need six months, maybe you need a dose or two. You know, these will eventually go biosimilar, this cost will come down. You know, maybe that would make sense. So I thought it was interesting. If you look at the picture, there's a nice photo in the, you know, in the. As a figure, I mean you could see markedly improved AKs.
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A
Did it, did it affect their BCC numbers to the same extent as the SEC? Because like I think of BCCs as pretty non immunogenic. I don't know if that's true, but that's how I think of them.
- [04:07]
B
Yeah, it's interesting. If BCCs, they have a high tumor mutational burden. I think the, the biggest reduction was actually in squamous cell carcinomas. But I have to go back and look at the actual numbers.
- [04:19]
A
The. And did it say anything about if there was any correlation between adverse. So you know I think of with, with imiquimod. Right. Or calcimatriin 5. A few other things that I think of as immunotherapy for aks. I think of it as being the worse their symptoms are, the, the better it works. Or did, did they not really even talk about like did their AKs get inflamed or did they just go away?
- [04:47]
B
They just went away. There wasn't a lot of inflammation. So it sort of looks like it's mechanistically different than what we see, you know, remember in residency because like you don't see a lot of people getting you know, systemic 5 fu anymore. But remember we would see patients who would get put on systemic 5 fu for like head neck cancer. And then they come in and their AKs were all that were all lit up. It seems like it's a little different from that. So um, it looked like in the.
- [05:15]
C
Photo and maybe I was making this up. Didn't it look like he was Developing vitiligo as time went on. Did they. Did they do any sort of association of. You got a better response. It was probably too small of a study. But did you get a better response if you had like a cutaneous side effect like you do with maybe, you know, like melanoma, things like that?
- [05:34]
B
I don't think that there was. It was powered enough to see that all that. I really. And I have to go back and look at the paper again. But what I kind of noted was like, the adverse event profile looked like every adverse event profile in, you know, PD1 inhibitor studies.
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C
Big drawback to treating AKs. Now you have diabetes and adrenal insufficiency and hypothyroidism, and you may have died.
- [05:59]
A
From colitis, but otherwise it's all good.
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B
Right?
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C
Your skin's not smoother.
- [06:07]
B
Yeah. Yeah. Most. Most common adverse events were rash. So 30% of patients had maculopapular rash. One person actually got bolus pemphigoid in the study. Yeah.
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A
And.
- [06:25]
B
They didn't really correlate it. There was no difference in the clearance of AKs and those with cutaneous versus non cutaneous adverse events. So. That's right. That the outcome that they use was. Did you like. They sort of said, like, good response was greater, 65% or more of a case cleared. You know, not good response was less than 65%. And the people who had cutaneous adverse events weren't more likely to clear their AKs.
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A
All right, I'm about to give you guys a trillion dollar idea here. You ready?
- [06:56]
B
Okay.
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C
Yeah.
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A
Topical PD1 inhibitor could have a tube of that stuff for $24,000.
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C
Yep.
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A
And it would get rid of your AKs.
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C
Yeah.
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B
So I think it would have to be not an antibody that's not going to do well topically, which is what these are. Oh, I didn't really have molecules like you can have inhibit small inhibitory RNAs that could do it.
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C
So maybe we need our cosmetic chemist back.
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A
Okay.
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B
All right, Pat, $100 idea.
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A
Let's. Let's move on to article number two, Pat.
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C
All right, so I did intradermal botox for melasma. It was intradermal botulinum toxin A for melasma. A randomized split phase study trial and invito study and its anti melanogenic effect. It was by than. No, I got this. Thanosar, Nexorn et al and the January 2012 edition of DERM therapy. It had two main parts. In vitro data of ABO botulinum toxins. So this is dysport effects on melanoma cell line and the clinical trial data, details of the in vitro stuff. Basically, it seemed to decrease UVA induced melanin content and tyrosinase activity, and yet it was not cytotoxic for the clinical effects.
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A
12 women, did they have any explanation for how that like I think of both the, but I think of botulinum toxin as so I don't remember what the hell it does. It, it cleaves something.
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C
It's the, yeah, it prevents acetylcholine release from the neuron. So acetylcholine doesn't go and bind to the neuromuscular junct.
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A
Right.
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C
I'm the same way. I, I, I was looking. I mean these cells do have, if, if AI is correct, they do have the capability of releasing acetylcholine. And then I'm like, well, but is that so does the acetylcholine then bind to the cell and make it make melanin? I, I don't think, I don't think they know. Yeah. The mechanism here.
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A
Okay.
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C
I mean, I think they're like, well, maybe Botox has tyrosinase activity like every other thing that can potentially lighten the skin. Or not tyrosinase, but inhibiting tyrosinase. Yeah, that, that, I thought the same thing. I'm like, why would this work? If you put Botox in with a melanoma cell line, why would you expect any effect on these? And I, I, they, they kind of were like, maybe it does this. They didn't really get into it.
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B
Okay, is it like the release of like little granules or something? I don't know. Like, no, I don't know. Transport. All right. Yes.
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C
I didn't want to go into details of that because I didn't know the details. So let's move on. For the clinical effects, 12 women were enrolled and they received dysport on one side of the face and normal saline on the other. Concentration of Dysport was 66.67 units per mil. That seems like the similar dilution for, if they're doing it for fine lines and wrinkles. It was injected intradermally. You would achieve a 2 millimeter wheel and injections were faced 2 millimeter part. So at 3 months they had different measures of melasma. The mazi, the PGA and patient satisfaction scores were all statistically significantly better for the side of the face treated with disport compared to controls. So now. Right. We talked about skin lightening agents for melasma. We have hydroquinone, arbutin, cymene, licorice, tretinoin, vitamin C, koic acid, thiamidol, 4N, butyl, resourcinol, aelaic acid, tranexamic acid. So we have more things to treat melasma than melanoma, and no one should ever have melasma ever again. That was my.
- [10:35]
B
None of them work, like, shockingly well, right? Well, yeah.
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C
I mean.
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B
For, like, facial drooping, right?
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C
Yeah, they. They all scored well. But you look at the pictures and you're like, it's a little bit lighter.
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A
I looked at the pictures and I. It was like, the pictures where you're like. I think that's just blurry. I think it's just blurry.
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C
But they did use, you know, scoring, and people were. The assessors were blinded to treatments. Was I blown away by the pictures?
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A
No.
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C
I mean, given that we have 37 other things to lighten the skin, I think Botox is way down on the list for me because. Right. You will get a droopy face like Ferris when she got her rosacea treated with Botox.
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B
That was a good residency story. I did try half of my face treated with Botox.
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C
Yeah, you didn't have to.
- [11:28]
B
It did not work for the rosacea. I did have facial hemiparesis. The longest acting Botox I've ever had in my life.
- [11:37]
C
When you didn't have to count mice scratching their ears.
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B
I did not.
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C
But yes.
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B
And then I published myself. It was good.
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A
Did anybody make you wear a collar of shame?
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B
No. Fortunately, I couldn't eat a sandwich for, like, six months because I couldn't actually, like, open my. Get my lip up enough to eat.
- [11:57]
C
The food would just fall out of your mouth. Yeah, it was really attractive there.
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B
It was very attractive. Never to be done again.
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A
All right, all right, we're moving on to our. To our next one, which is. I got to say, this is an early contender for worst article of the year. And so title of this article, unmet needs of Effective Advanced Systemic Therapies in Moderate to Severe Atopic Dermatitis Patients in the Target Derm Ad Registry. And the main takeaway for this article is I am going to be ignoring everything that comes out from the Target Derm Ad Registry because this data is just crazy. It's. It's ridiculous. So the takeaway was that that dupixent doesn't work. And so their takeaway was that if. If we look at how good their rash is doing, IGA times, bsa. So Viga times, bsa, multiple Studies have shown that that's a good determinant of efficacy. According to that, half of people did not improve on dupixent. And when I say this is ridiculous data, it is just so different from the clinical trial data and from every single dermatologist who's ever used dupixent's data, who's ever used dupixent. So. And half of them, their. I'm sorry, I got. I actually was looking at the wrong thing. Two thirds of people, their skin did not improve on Botox, on dupy in terms of quality of life. Half of people had lacked improvement in their quality of life whenever they went on dupixent for their moderate to severe atopic dermatitis. When we look at itch, mood and sleep, 85% of people did not improve. Right. We look at depression, 80% of people didn't improve. We look at anxiety, 80% of people didn't improve. Like, it's. I found this so unbelievable that I actually reached out to one of the authors and was like, how do you explain this? This is crazy. And their answer to me was, well, you know, derms are just satisfied with people not having very good results. I was like, let's keep.
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C
I was speechless.
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A
Right?
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B
Speechless.
- [14:21]
C
Patients would come back to us and say, I'm not really much better. And we would say, yes, you are. Like, I mean, that's just, it's. The numbers were just not believable. Is there, Is there a problem with, like, what's the problem? The, the registry, what are they not.
- [14:38]
B
As severe at baseline, so it's harder to measure it because it's like more of a real world setting. Right. So, like, was that what it was? Like, were they not, like, washed out from other drugs? So there wasn't as much room as, like, when you put somebody in a clinical trial and your numbers look really good. Right.
- [14:58]
A
That's kind of what I was hoping for, but it just. It didn't. I can't explain it. And that's what, that's why it makes me say, like, if this is supposed to be a real world registry, this is not real world.
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C
Yeah.
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A
Like, it just, it didn't. And so it, it makes me say, however they designed this registry, like, it's, it's any data that comes out of it, I can't, I can't believe at all. Because it. If it's saying that 80% of people, doopie doesn't help their itch or sleep, that's just ridiculous.
- [15:32]
C
Yeah, I wouldn't. I'm the same Way, like you just put the paper aside and say, I'm never reading another paper coming from this registry because this is clearly not accurate.
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B
Like it's, or the way that they measured that. They looked at data here, didn't give us like the, the, the real view into like what happens. Like we know when you have somebody who starts like a lot of times when you put people in registries, they're your long term patients, you know, you're, they're on their third drug with you. They're not really washed out, treatment naive. You know, they're maybe not that bad when they're switching over to doopie. Right? Like that's, that's kind of was my take on it. Like this is the issue with, you know, with registry data. So if you look at a lot of registers, they registries, like they pick out only those patients who have really severe disease and that like the, you know, kind of clinical, like clinical trial inclusion level severity and then look at how they improve.
- [16:32]
A
But the reason that the people in so is essentially 100% of people who went on advanced systemic therapy were people who went on dupy. And that's because of when they were doing this registry, when they started enrolling people. It was before there were even other drugs available. So it wasn't like these were people who had failed lots of others. I can't understand. Like, I, and I don't also hate to say that I don't know how it's, it's so unbelievable. It's hard to believe it got published. Like, it's, it's just, I just, I don't get it. I don't, I don't understand. So, yeah, that, that's my takeaway though is I'm not going to believe anything from the target derm ad registry.
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C
Me neither, man. I'm with you.
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A
All right. Derms on drugs not approved. All right, let's move on to our next article. Dr. Faris, what do you got?
- [17:27]
B
So this is switching gears. Frequency of androgenic cutaneous adverse events associated with Levo norgestrel IUDs. An analysis of the FDA Event Reporting System database. This is Cassard, which is out of Cleveland Clinic. So this was a paper where what they did. You know, we all think, I know that progesterone IUDs make like acne and hair loss. Like they have hormonal effects. They're like, no, it's just local hormones. But we don't really believe that. We know that they make acne worse. Right. So what they did I thought was kind of clever was that they looked at spontaneous reporting of. Of AES for these progesterone IEDs and for the copper IED, right? So copper has no progesterone in it. And they said, is there a difference? And so what they found was that if you look at odds ratios, if the copper is one, if you look at like Mirena and Kylina and Skyla, they are. They definitely have higher odds of having acne and alopecia and hirsutism. Now, the little, like, kicker like that, the odds were like, you know, sort of aggregating them all, like three times more acne, about six times more alopecia, about 15 times more hirsutism. The kicker of all this was that there was one that didn't seem to show it, which was Liletta. And that is a 52 milligram, you know, IUD levonorgestrel IUD, which is basically like identical to Mirena. And then the other two, Kyleena and Skyla, are 19.5 and 13.5 milligrams. So they're lower and they have it. But for some reason this one, Liletta was not associated with it. So, you know, I was like trying to look up and figure out why is this there. You can measure the rate of, of levonorgestrel from each of these and it's kind of the same. 21 milligrams per day with Mirena. 20, sorry, 21 micrograms per day with Mirena, 20 micrograms per day with, like, Liletta. It shouldn't be that different, you know, So I don't have a really good reason explanation for this. I just thought it was interesting. Maybe there's been, I don't know if one's newer and there's been more, you know, time for reporting. I think they control for those things, but it does answer that question. You know, the OB GYN will be like, nope, there's no increased risk of acne. And it does differ for IEDs. For the. It's not just that you went off an ocp. There is a difference between a copper IED and a levo norgestrel iud.
- [20:22]
C
I know. That was my. That was always my explanation. I thought I was so clever. I'm like, it's not the Mirena, it's that you're not on ocps anymore. And they'd be like, ah, but now I can't say that anymore. I'll. I'll come back to looking as dumb as I've always been.
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B
Just took one brief report it's pretty.
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C
Much story of my life.
- [20:43]
A
Well, what's always interesting to me about these kinds of articles though, is reporting bias, so. Right. Because if, if you got acne or hirsutism or alopecia, you know, we, as the derm, we always ask, well, did you, did you get a new hormone releasing. Oh, it was probably that. And then the patient calls and reports it to the fda. Well, if somebody with got a copper one, I wouldn't be like, oh, I would have been like, well, it wasn't your iud. And then the patient's not gonna, not gonna get online and report it to the fda. It's hard to ferret these out. But these are big numbers. I mean, you know.
- [21:24]
B
No, I, I agree. And the authors did say that was, you know, we, that basically made that exact point. Perhaps we just assume that it's not the IED when it's a copper ied. So there, there is probably some reporting bias.
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A
But, but on the other hand, in, in all the years since these came out, I can't think of a patient I've ever, who's a female, who I've seen and they've been like, oh, I got hormonal acne. And the top of my head like, oh, did you get a Mirena? Like, just because you heard it over and over and over again, never did somebody get a copper IUD before they, you know, got acne onset acne. So it's, it certainly fits. But, you know, I, I don't know. I'm, I'm not, I, I don't want to admit that Patton might be right about the just coming off of the oral contraceptives, but I'm not going to rule it out yet.
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C
Right about the scratching. I'm right about this, man. Just don't, don't disagree with me, Pat.
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A
Next article. Patton, what do you got?
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C
It's my second six pack. Paper was by Amara at Al January 2025, British Journal of Dermatology. It was titled Efficacy of Dupilia for treatment Resistant Grovers a retrospective study single center retrospective chart review. The authors reported on 10 patients diagnosed with Grover's unresponsive to mostly topical therapies and treated them with DUPY standard ad dosing. Did itching improve in everyone? Yes, it completely resolved in six of the ten, improved in two. And was it reported for the other two but their Grovers completely went away. So let's just say that it got the itching completely resolved in 8 of the 10 and improved in 2. Did Grovers go away? And 7 out of 10 it resolved. There was 0% BSA at follow up, which, by the way, that's a weird way to judge Grovers, is it not?
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B
Yes.
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C
I don't even know how you did it.
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B
Smushed together the little.
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C
Yeah, it's like pinpoint.
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B
Yesa. Yeah.
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C
Right. So I wasn't sure. Did they just take a body area? Like, hey, your whole stomach is covered with Grovers. I'm just going to count your whole stomach as being affected. They didn't really go into that, but I thought that was so weird because this is a retrospective chart review. Have you ever. How do you make documented body surfaces?
- [23:46]
B
The grassy. The Grovers area insularity index. I do that all the time on my Grovers.
- [23:52]
C
Did you see?
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A
Are you gonna add that in three.
- [23:58]
C
Of the patients in whom it didn't go away, it got better. Only one patient didn't really have a good response. He went from 15 to 10 BSA, which again, kind of weird. All of the patients with some sort of atop. So maybe they had a history of asthma. One of the patients, I think did have a history of atopic derm. Had resolution of their Grover's. You know, biopsies weren't available for every single one. But man, I mean, I. Grovers is pretty easy to clinically diagnose. So we have DUPY for Grovers. And I think, like, this is doable, right? It's not like this is a disease where you'll be like, I'm never going to be able to get dupy. Because you could easily call this just a manifestation of atopic derm, which I think Grover's like. Like, I always thought of drovers as it was almost an irritant sort of contact dermatitis. And it just had a different morphology than your exematous type of rash. It was just this popular sort of weird, brash. But I. I always thought of it as, yeah, these patients have scanned and this is a reaction.
- [25:01]
A
I'm pretty sure they have now shown that Grover's has some kind of a somatic mutation that affects your follicles. I feel like I read that somewhere a couple years ago. I'll have to look that up and come back.
- [25:19]
B
But the acanth bollysis makes it, I think, harder for me that you see histologically to say it's just like a dermatitis. Right? It's like histologically very distinct lot a fair number of.
- [25:30]
C
Of Grovers. I mean, I think if you biopsy enough little lesions, you'll See, sponge, Derm and EOS on some of those as well.
- [25:38]
A
Now we understand why Patton says it's easy to diagnose clinically because nine out of 10 cases diagnosed by Patton were Sponge, Sponge, Derm. Yeah, it was Grovers. Grover.
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C
Right, right.
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A
So wait, wait. So Emma Gutman is the senior author on this. So she's a very basic, sciency oriented person. I can't think of why. I can think of why doopy would help with the itch, but it's hard for me to think of why it would help with the lesions going away. Did they do any, you know, staining of the biopsies for IL4 and IL? Like, was there any basic sciency stuff in here?
- [26:15]
C
No, this is a very, very short. It was like a one page. It was a pretty lame paper for me to choose. Not that the results were lame, but it just. There wasn't much to it.
- [26:25]
A
That doesn't make it lame. It's useful because these are.
- [26:28]
C
I didn't mean I phrase that wrong. Yeah, but it was pathetic of me to be like, I'm just going to take this paper because it's like two paragraphs after I did that J. I D paper. I needed a break. Will I use doopie for Grovers? Of course. Why not?
- [26:46]
A
Well, and if they're itchy enough, it's. You're right. You know, it's not unreasonable to call people with itch and a rash where you're like, I don't really know why you got this.
- [26:59]
B
All right, so there is a single nucleotide variant, an ATP2A2 gene that is associated with Grover's disease.
- [27:07]
C
That's Dariase.
- [27:09]
B
Yep.
- [27:09]
A
Yeah. So it's like a somatic mutation that for some reason localizes to like hair follicles.
- [27:17]
C
Yeah.
- [27:18]
A
That's why you don't see Grovers in young kids, because you gotta be old to get the mutations.
- [27:23]
C
Sure.
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B
And they were all C to G or G to A, indicating it's potentially UV light induced mutagenesis.
- [27:30]
A
There we go.
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C
Unbelievable what happened today. What was Grover's first name? What was Dr. Grover's first name?
- [27:38]
B
William.
- [27:39]
C
No, Ralph.
- [27:43]
B
Ralph. Ralph Grover. All right.
- [27:47]
C
Oh, you know what, he actually did a follow up study. So his original report was like in 1970, it was like six patients. He did like a follow up report in the 80s where he took 375 patients with Grovers and they did have, I think a statistically significant higher history of like atopic diathesis stuff. So it was like in his paper that did seem to occur like atopic history did seem to occur more frequently in Grovers.
- [28:14]
A
And it was interesting that they, in this article, almost everybody had some kind of an atopic comorbidity.
- [28:20]
C
Yeah.
- [28:21]
B
Okay, maybe those are the people who respond.
- [28:24]
C
They did. I mean, everybody with an atopic diathesis got better. Okay.
- [28:28]
A
All right, let's move on to our last pa, our last paper here. This one was mine. And again, this paper has such a great point. So it's Discrepancies in Patch Testing, Timing and Outcomes. A Retrospective Analysis of the Pediatric Allergic Contact Dermatitis Registry. So the, and this is by Sandler et al. But the senior author's a buddy of mine, Jeff Yu, who's at, I think he's at Harvard. And so they looked at this pediatric allergic contact dermatitis registry from 2018-24, 459 kids in there who had a positive patch test. And so the first, what they were somewhat looking at was how long does it take from getting dermatitis to getting patch tested? And essentially they found out that people with skin of color, it takes longer to get patch test. Okay, I can kind of understand that just because it's a little harder to appreciate the erythema and some of the characteristics and maybe it's partially socioeconomic reasons as well. But what was that? Wasn't the interesting part of the article. The interesting part was this. So there are very, very few studies of outcomes with patch testing. So meaning there's kind of this assumption that, oh, if I send you for patch testing and you're allergic to fragrance and there's fragrance in your body wash, that must be what's causing your rash. Well, there's very, very little data to back that up. And so most of the data, so it's one of the things I've been talking about in lectures recently is that only about 10% of people who have a relevant positive patch test will clear. So about 50% will improve some and 50% won't improve at all. And so if you're diagnosing contact dermatitis based on a positive patch test, you are misdiagnosing half of your patients only partially correctly diagnosing 90%. Right. The gold standard for diagnosing contact derm is people get better whenever they get away from something. Right. So they looked at that. So this was an article where we did have, this is the first ever data I've seen that's follow up data on pediatric patch testing and contact dermatitis. So of the 459 kids who they looked at they stratified by improvement. After allergen avoidance in across the board, if you just look at all the kids, one third had no improvement, a half had partial improvement, and then about 20% had complete improvement. So a little bit better than what some of the data shows in adults. But then if you look specifically at the kids with atopic dermatitis with a known diagnosis of that, numbers were pretty much exactly the same. A third got no better, half got somewhat better, and then 17% got completely better. So first, what you would say there is 17% of them didn't have atopic dermatitis. 17% of them had contact dermatitis. That was misdiagnosed as atopic dermatitis. But then the other really interesting thing. So there's a lot of discussion over the years about, do people with atopic derm, are they more or less likely to have contact dermatitis? So there are a number of studies looking at rates of positive patch tests in people who have atopic dermatitis, and they've been kind of across the board. Some have showed more, some have showed less. But the takeaway here is again, if you're using a positive patch test, you're generally gonna be wrong. Because when you look at the odds ratios, kids with atopic dermatitis versus kids without, if you were allergic to fragrances and you had atopic derm, your odds ratio was only 0.3, so 0.29. So 70% less likely to get better, meaning that probably 70% of the cases were false positive because you had atopic dermatitis and a bad skin barrier with antimicrobials and preservatives, things like formaldehyde. Nice. With isothiazolanones, the odds ratio was 0.44. That was not statistically significant, but still a pretty decent number. But then surfactants, so cocamidoprobal betaine, which has been put out there as that's the one that's more common in kids with atopic dermatitis, your odds ratio was 0.03. So you were 97% less likely to improve than a kid who had a positive patch test who didn't have atopic dermot. And then metals, the odds ratio was 0.26, so 74% less likely to improve. So the takeaway for me was that in kids with atopic derm, sure, it is still reasonable to patch test them and it is still totally reasonable to say, stay away from your allergens, but it really looks like a huge number of these are false positives where the kids are not going to get any better whenever they avoid.
- [33:25]
B
Is that really a false positive or is it just not the whole story?
- [33:29]
A
So that's a great question. So it's a fault. I would describe it like this. It. Well, I would call it a. I think they are false positive irritant reactions. Now, it might be that they are, you're right, only partially getting better because they've also got atopic dermatitis or whatever. But the main takeaway that I want people to have is if you get the kit patch tested and they have a positive relevant patch test, don't be like, oh, avoid this allergen and then come back and oh, you're no better. Well, you know, maybe you missed. And maybe it's the laundry detergent or maybe it's the air freshener or maybe it's the. They're using an air freshener at school and then they come back in three, oh, well, maybe it's this or maybe it's that. And then they come back, well, maybe it's this or may. And so the kid then goes, two years of try avoid this, try and avoid that. Where you just say, okay, we tried avoiding three months, you didn't get any better. Then you treat them with doopie, right? And then if they don't get any better treatment doopie, then you go back and say, okay, maybe there is stuff that we missed, but. So it might be combo contact derm and atopic derm. It might be one or the other. But just don't think that a positive patch test is the end of the story.
- [34:42]
B
So how do we know that some positive patch tests aren't just sort of a, like a worse skin barrier and an irritant reaction. And so it's almost like if you just do IGE or RAS testing for allergies, right? Like you get positive tests to foods that people eat. So it's not necessarily a good test for like things that, for that. For clinically relevant, like clinically relevant result. Is that potentially the case for patch testing too?
- [35:14]
A
So I did. So if you had asked me that in 2016, I would have said, no, no, no, it's a very accurate in the blah, blah, blah, blah, blah. But once we got doopie, which I think works in atopic derm, I think it rarely works in contact derm because there's a lot of people who would get worse and then you'd fight when you put them on duping. Oh, you're allergic to. I think that patch testing is a very non specific Tool. I think that there are lots of people who have a positive patch test, but they don't really have contact derm. They've got atopic derm and a positive patch test.
- [35:55]
C
So you've been patch testing forever. 97% of patients. Coca, metopropyl betaine. Is that. Was that sort of your sense of stuff? Would you get these patients that would have that positive reaction? And, like, vast majority of time, they never got better.
- [36:12]
A
I would say that other than facial dermatitis, so face and hands routinely, I would see people like, we'd find something cocomedopropyl betaine, and they'd get better. Like, that was pretty reasonable. But people who had like a widespread dermatitis, really rare, that I would. That they would get better whenever they would avoid the stuff in their body wash or the this or the that or the other.
- [36:43]
C
So the 97 didn't, like, blow you away?
- [36:45]
A
You're like, yeah, it more was like, oh, my God. That's what I thought. But nobody's ever like, I. I'd say the 97 did surprise me, but also, I didn't pass just a ton of kids, right? I. I don't really like seeing kids, okay. So I didn't patch just a ton of them. So I. But it, yeah, it didn't blow me away. I was like, yeah, that makes. Especially now that's only in atopic kids, right? So in kids who don't have atopic derm, it might be that, yeah, when you get a positive, it's really a high probability of getting them better. But that's the kind of. The big takeaway is. Is positive patch tests in people with atopic derm. So take with a huge grain of salt and only call it contact derm once you've seen them get better with avoidance. If they don't get better with avoidance, then try treating them for atopic derm. And then if they don't get better with a top treated for atopic derm, then go back and look for. Did we miss something? Right? Did we. Did we miss an allergen? Did we miss an exposure, Whatever. But that's the. It just drives me nuts when I hear people say that a positive patch test is the gold standard for diagnosing contact dermot. Every time somebody says that, I want to be like, you're a moron. Because if, you know, say you have a positive patch test and you understand, I don't have to go through the whole thing.
- [38:07]
C
But if, yeah, we got it.
- [38:08]
B
You do not have to. Yes, at all.
- [38:11]
A
I Take it.
- [38:12]
B
You don't make a lot of your income on patch testing anymore.
- [38:17]
A
All right. Well, guys, I did want to mention One thing that Dr. Patton brought to our attention. Respegilidusilukin from Nectar Therapeutics was designated as a high priority something by the FDA. It's just a cool thing. It targets the io2 receptor complex and it stimulates T regulatory cells. And so it's. Rather than blocking something, this is one of the first times it's activating something to treat atopic dermatitis. And it may give people a chance for a really long term. If we get your regulatory T cells controlling everything, maybe it really can give people a long term remission. So interesting that that was designated. I can't. What's the designation code? Do you remember?
- [39:15]
C
They asked for a more rapid approval path.
- [39:20]
A
High priority or some.
- [39:22]
C
There was like, yeah, fast track.
- [39:25]
A
Fast track. It was fast track. That's it. It was fast track.
- [39:30]
C
Maybe we should have looked this up before going on. On. On the air and just making up.
- [39:36]
A
Yeah, designated something.
- [39:39]
B
It's designated. It's important.
- [39:41]
A
It's important. That's. It's got a name.
- [39:44]
B
Terms on drugs will be following this carefully, closely. We will keep you updated on any.
- [39:50]
A
Progress on res Pegala dusilukin.
- [39:53]
B
Right. Mostly. If we learn how to pronounce it, that will be the first.
- [39:56]
A
We'll update you on it. All right, so I want to thank everybody for tuning in this week for another great and entertaining hopefully episode. If you've got questions, comments, ideas for stuff you'd like us to cover on the show, shoot us an email @questionsrms on drugs.com Again, that's questions@dermsondrugs.com I hope you learned a few things. I hope you laughed once or twice and hope you're planning to join us next week. Until then, I'm Matt Zyrus.
- [40:27]
C
I'm Tim Patton.
- [40:28]
B
And I'm Laura Faris. And we are derms on drugs.