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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 maybe mediocre comedy. Leaning towards not very good. I'm Matt Zyrus and each week I'm joined by my residency buddies, Laura Faris and Tim Patton to use our 60 years of combined 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 actually learning something useful. Now, this week we are super excited. We've got sort of dermatitis unspecified type direction we are going to be taking with our special guest, Dr. Amber Atwater, who is a member of the North American Contact Dermatitis Group and previously the residency director at Duke. But first we are going to go ahead and get into our first article and I am going to kick it over to Dr. Ferris.
B
All right, thanks, Matt. So the paper that I picked was published in Nature Scientific Reports. Targeted dual biologic therapy for erythroderma of unknown etiology guided by high parameter peripheral blood immunophenotyping. So that's a lot. This is Cornman et al, but it's Shan Quatra's group. Okay. So, you know, I thought this was really interesting because we all encounter these patients, they're erythrodermic, you're not sure what they have. You biopsy, you can't really tell. You try a B logic, they get better or worse. They methotrexate cyclosporine. So for one patient, this group, they created an immunophenotyping platform. And what they did was they basically did, man, I drew his blood.
A
I think it is, I think it's special when I do a peer review to try and get a biological proof for somebody, let alone create an immunoflow cytometry. Try and figure shit out, man.
B
Exactly. So, yeah, so they looked at pbmc, they compared them to erythodermic patients who had Cesare or prp. And a lot of science in this, but basically what they found was that he had this unique signature of making both IL13 and IL17. He basically had two gamma delta T cell clones that were doing this and sequenced the genome, did whole genome sequencing, found mutations related to IL 417 and you know, also found that the, you know, abnormals and granulocytes specifically increased MRG PRX2, which will mean more to people like you, who love itch and less people like me who do not like itch that much.
A
Now, wait a minute, Paris, I got another question here. First you use the word clone. Does that mean that this guy had like a gamma delta T cell malignancy or these non malignant.
B
It's like, it's a, it's a, it's clone. So they were, you know, restricted by the T cell. This wasn't like a malignant population. It was just an expanded population. That's the way I read it, because that was kind of my first thought, too. Okay, so basically, if you find this person, they make too much, aisle 17. They make too much, know, aisle 13. What are you going to do? You're going to treat them with something with two drugs, Dupixent and cosentix. And basically the guy had to be on like Q2 week Dupixent and Q3 week Cosentix, but he cleared. They got rid of this gamma, this population of pathogenic T cells. And so, you know, I thought this was interesting because, like, this is personalized medicine to the max, right? Like you said, I feel like, wow, I did a peer to peer, you know, and this reminds me of those patients who are like, I want to know the root cause. And you're like, you don't. You're not going to tell. We're not going to tell you the root cause. Right?
A
Well, I'm going to make, I'm going to make one up for them. It may or may not be accurate, but I'm going to make something up.
B
Right? But dang it, if Quatra did not go make us all look bad by actually finding the root cause for this patient and getting them on two different drugs. So it's kind of cool, though, because if you look at the basic immunophenotyping, it's like, draw down some cells, stimulate them, and then look at the cytokines that they're being made by flow cytometry. Something that Patton doesn't know a whole lot about. But, you know, but it's something. It's. It's a test that you could, that you could actually kind of do if you think about, you know, how we do gene profiling on things. So really cool.
A
But it wouldn't. You would have to do because you wouldn't know that these were like, if you did just regular flow cytometry, you would get that these were gamma delta T cells, but you wouldn't know that they were like clonal, you know, IL13 producers or IL17 producers or whatever. Can you tell that they basically get all the.
B
All the. The PBMCs, they stimulated them and then they ran them through a flow cytometer and looked at like, is there a population that's activated in making IL17 or Y interferon gamma? No. IL13. Yes. So that's. It's actually like not the most complicated to do all this. Like, do you have a clonal population? Blah, blah, blah. You'd have to do that. But this is actually a way you could sort of see what's going on in the, you know, in the peripheral blood and actually target a patient. Actually target a patient's very specific pathology.
A
So, Patton, what would you. So normal erythroderma patients, so. Meaning they didn't have preceding psoriasis, they didn't have preceding atopidermatitis, they don't have islands of sparing or any, you know, the nice head to toe progression. Just. You're calling, you know, consulted, you go see him. Four months ago, this rash started. Now it's horrible. What do you.
B
What would you do?
A
What do you do?
B
That's what he's trying to ask you. What would you do?
C
Yeah, so. Right. That's why this paper was a huge waste of time and money. You say that this guy is erythrodermic atopic because you can find some sponge on the biopsy that gets him on the doopie, and then you give them reflumelast to take care of the 17 part there. I just saved you $7 million.
B
I bet this wasn't $7 million.
C
Oh, do you know how much flow cytometers cost? It is a pretty penny, but not.
B
Not for use. I'm teasing him because.
A
No, no, no.
C
The paper. No, the paper was a PhD.
B
I said to Tim, we were reviewing a paper in Journal Club, I said, do you even know how to do flow cytometry? And then, of course, I found out that, like, he spent three years working in this, like, sophisticated flow cytometry lab.
C
Before she saw this poor little do in the derm program and thought I was an idiot. And now she knows me and she knows I'm an idiot.
B
An idiot. I did flow cytometry.
D
So.
C
I did flow cytometry for, like four years. So. No, no, I mean, this is. This is great, right? It's just. It's an amazing amount of work. I the. But don't you think you'd have an easier time. So what would I do with an erythodermic patient? You Know like methotrexate, cyclosporine, if you're going with broad anti inflammatory treatments. I mean, I love dupixent for so much. A lot of these biopsies are sponge derm non specific. If it's not, definitely PRP or psorias.
D
So.
C
So I think dupilumab makes a lot of sense for these people. I, I can't say.
B
But that alone didn't do it. Prednisone didn't do it. Methotrexate and Humira didn't do it. Like.
C
No, I, I get all that. But like it's not unreasonable that you would say this is a, this is just really bad a topic. I'm gonna throw doopie at him.
A
Right. Give them right. Or give them a whole bunch of Rinvoak. Right? I mean, that's right.
C
I would be interested to see where the jacks are and is there a. I was wondering that because they always show those pictures of the jacks connected to these receptors and you know, IL17 binds this receptor and it activates this jack combination. Was there a like a perfect Jack inhibitor that would have hit your, your il 13 and your il 17 together or just like broad jack inhibitor?
A
I think like a broad Jack spends.
B
The most money talking about inhibitors.
C
Yeah, Tofacid it. Give him to sit in it or something.
A
Well, tofa is not that broad. It's actually primarily a Jack 3 inhibitor. I would actually.
C
What am I thinking of? Ruxolitinib.
A
Rux is a 1, 2 and up. Rinvoak is a 1, 2 and then Delga Sit nib, which is the new one coming from Leo is a 1, 2, 3, tick. But that's topical. Rinvoak is probably your best broad spectrum. Ajak.
C
Yeah, that would have been interesting to see.
A
All right, so sticking with that same theme of. Right. Because we're talking about somebody who's got both IL13 and IL17. So we're talking about somebody who's got pathophysiologically and cytokine wise kind of both atopic dermatitis and psoriasis. And so we're next gonna jump in at first. I'm gonna introduce our guest for the week who is the author of the next paper that we're talking about. And we're then gonna go into the deep dive. So Dr. Amber Atwater has been a friend of mine for a long time. A fellow member of the North American contact dermatitis group. We've known each other for a good 10, 15 years. We were Both program directors at the same time. Me at Ohio State University, Amber at Duke University. She then left Duke for a little while, went to work in industry with Lily on Liberkizumab, and now is back taking care of patients again in Northern Virginia. I had a little trouble getting permission to bring her on since she's a former Dukey, but since it's a former Dukey, it was okay. I think if she was still at Duke, I might have had some trouble getting Dr. Ferris to let her on. But Amber, great to have you here.
D
Thank you.
A
So let's get right into this paper. So I couldn't. So the question that I, as a contact dermatitis, atopic dermatitis, rash person get all the time is, oh, what do you do with psoriasiform dermatitis? What do you do with psoriasiform dermatitis? And there's no articles about this. And so this study. Right. So final clinical diagnosis in cases of histopathologic psoriasis form dermatitis, retrospective cross sectional analysis of a southeastern United States population 2004 to 2017. So a 13 year period. And I gotta say, when I first saw this study, I was like, I can't believe somebody actually did this because basically you guys took everybody who had a biopsy that showed psoriasiform dermatitis over many year period at Duke and then literally somebody went through each of their charts to see what the heck happened with them and what was the eventual final diagnosis. Is that about? Right? For what you guys did?
D
Yes. And the reason we did it, Matt, is because when things bother me that there's no data on them that I can't find any information on, that's when it becomes a project. Right. So this is how this became a project. It had been bothering me for about 10 years and I finally had a fellow, Jordan Ward, who's the first author on this paper. And I said, this is what we're going to do. We're going to look at this. And kind of the right way to analyze the data came to us and so we could do it and we did it, but it's because it bothered me. And I think that's how some of the best projects come up.
A
One of the first questions I gotta ask you a bit. So. Well, first let's just get to the results. So the results, my main takeaway, right? So if you get, if you, you're out there in practice to see somebody, you're looking at and I don't know, I can't really tell this doesn't look like classic anything. Let's biopsy, see what we get. Comes back psoriasiform epidermal hyperplasia with, you know, minimal to moderate spongiosis and a perivascular lymphocytic infiltrate with a few eosinophils, psoriasiform dermatitis. And then you're still like, I don't know. Okay, great. No help at all. Thanks. Right, but. So what eventually happened to them was about a third of them ended up having psoriasis, about a third of them ended up having dermatitis of some sort. And then about a third of them had whatever. Right. Anything from lichenoid dermatitis to final diagnosis of psoriasis, form dermatitis to ctcl, parasurasis, whatever. And then the dermatitis patients got split into. So you guys did a nice breakout. Half of them had just, quote, chronic dermatitis, which I can't wait to talk more about what the hell chronic dermatitis means. Right. And then you had, you know, 13% of them had allergic contact dermatitis, 13% had atopic dermatitis, some had quote, other dermatitis. So, but about, you know, chronic dermatitis and atopic dermatitis, probably the top two. And then the body area involvement was interesting and useful as well. So the main takeaway was if you had it on your scalp, you probably have psoriasis. If you have it on your face, you probably have dermatitis of some sort. If you've got. In your endogenital area, we're probably never going to figure out what the heck you've got. And other than that, we don't know. None of it's particularly helpful. Is that a reasonable. So a third, a third, a third, a third, psoriasis, third, atopic derm, third, whatever. And then distribution didn't help a whole lot. Is that your takeaway?
D
Yeah. And it's really interesting because this analysis to kind of find if there were any locations that were associated with a diagnosis was the idea of Adam Brist. So I want to give him credit there. We were going through our 700th version of this paper, and. And he said, wouldn't it be. It'd be cool if we did this extra analysis. And I think that's a really important part of the paper now that that really makes it shine a little bit more. So I'm glad we did it.
A
Now I got to ask, why isn't this in a better journal? Right. So it's in the archives of Dermatological Research. This is for. But for practicing dermatologists, this is like, as uber useful as anything could ever get. If there's ever been an article that to me should have been in the, like, did you guys send it to jad? And they were just like, ah, you guys aren't a drug company. You're not advertising. So to hell with your article. Like, what happened? Why is this not in JAD and why is it in Archives of Dermatological Research?
D
Well, you know that this project was 2004 to 2017. We started the project in 2019, and honestly, it was done in 2020. 2021. And at that time, we submitted to six journals.
A
Six.
D
All of them, except for one, just flat out denied it. And the one that didn't deny it tortured me with revisions and then denied it. And so we almost gave up. But interestingly, the paper was a little different then. There's a lot more data, and I had analyzed it a little bit differently. And. And honestly, I learned when I was working with pharma how to write a succinct paper that people care about. And I changed my paper. Not a lot, but a little. I changed it and I shortened it and I cut out some extra data. We had a whole table on what drugs patients were taking. We took a lot out, and I took some of the feedback that we had received. Round one, and I submitted it to one other journal who denied it, which was a journal I had denied it the first time. I think that might just be a vendetta against me personally, but that's a whole nother story. And then I asked one of my friends, Jonathan Silverberg is a friend of mine, and I said to him, can you please look at this paper, because I cannot get it published. And I don't know why. So he read it and he's like, the paper's fine. Submit it to one of these two journals. And I did, and it got accepted. So, like, there's a whole storyline there, right? Like getting advice from others, making revisions when you need. There's so much to. To it. But it was hilarious when Matt emailed me a couple weeks ago and was like, what's the deal with this paper? And I'm like, this is the paper I could never get published.
B
Right.
A
Because it is just so you like. For it is the most common question I get is, what do you do with psoriasiform dermatitis? And there's nothing about it in the literature. Nothing. So, all right, I've been kind of monopolizing, which I usually do. And so I'm going to see Patton. What do you got?
C
I had a question, not specifically about this, the journal article, but you and Matt, you know, you've published a lot on patch testing. So I did patch testing for like a second. And one of the things that I just felt that people did, other dermatologists was they get a patient with dermatitis and they're just like, just you might be allergic to something. They'll do a biopsy. There's some spongiosis with eos and oh, that's got to allergy. And so all these people getting sent to me and it's like you go through their history and they have a family history of asthma and things like that. They, they weren't counseled at all on, you know, maybe trying sensitive things like that. Don't you think that patch testing is, like, way overdone? Like there are things that can be done before those patients are even referred to you, that's just not done, or do you think the referrals are appropriate for the most part?
D
Honestly, I think referrals are usually appropriate. I mean, in my experience. So I was at a large academic center where I had everything basically in the state sent to me. Right. Except sometimes they got sent to unc, but usually to me, I do.
A
Clara, those people still have their rashes. They don't. Ferris needs another year to get them all cleaned up.
D
But now I'm in a private practice in Northern Virginia and I'm getting referrals and it's still kind of appropriate. Now, there are many situations where people have been patch tested and they're actually not counseled to avoid their allergens. And they come to me and I'm like, let's try this first. You've already been pat chested. Let's avoid your allergen. But I often think it's appropriate and sometimes it's, you know, wrongdiagnosis.com and that's appropriate too, because I can actually help the patient. Right. Like, I can actually move them towards improving. And that's actually the only thing the patient cares about, right. Is, is. Is. Is clearing their skin. So I usually. I think they're okay.
A
Well, so Amber, if you were, I.
B
Have a question for both of us. Do you think it's just because, like, when you're a patch tester, you become like a dermatitis aficionado expert? Right? Like, I'm wondering if the benefit is truly all the patch testing or if it's more like the, the more thoughtful approach to that Patient. What do you think about that?
D
For sure? For sure. Because not everybody has an allergy. There's a bunch of people that either we don't test because it's not appropriate or we do test and they don't have an allergy or we do test and they have an allergy and they don't get better. But I personally feel it's still my responsibility to help them. And there are all sorts of tricks up my sleeve and I'm sure up Matt's sleeve as well that we can do to help those patients. So it's not always allergy, but there's lots of other. It's multifactorial. Right? So we do all those things.
C
Would you really not patch test? Like that blows me away. I mean it's almost like these patients have been waiting and they have their stack of papers. Would you actually tell somebody like we're not patch testing you? Like, blah, blah, blah, whatever.
D
It's not the rule, it's the exception. But I've had acne sent to me for patch testing. I'm not going to patch test them.
C
Yeah, sorry about that. I got.
D
Psoriasis, DH bullous, pemphigoid. I mean all these things have been sent to me for patch testing. And in those cases I say hold up, we're going to do a biopsy or hold up, we're going to do this first and then we don't patch test those patients.
A
So Amber, the patch testing. So first let me ask a very direct, specific question. So your, let's say you're dermatologist who doesn't do patch testing. There's two or three month wait to get into the good patch tester in town. Maybe it's a 45 minute drive and they're going to take three days off work. Like so it's not trivial, right, to get somebody patch tested. How would you decide? Because right until 2017 like I was still like, just get a patch tested. Because you get a patch. We just need to find out. We don't. If we don't get a patch test, we don't have any good treatments. Now we've got great treatments, right? We've got Doopie and Rinvoak and Eb Glis and Adbri and Sabinko and Nemo and whatever. So how do you decide who to just empirically be like, well let's try treating you for contact for atopic derm and if that doesn't work, we'll send you for patch testing versus first thing we're going to do is send you for patch testing, Right. How do you. Because that's a huge question.
D
So for me, it depends on the story and the distribution. Right. So if it's. There, of course, are cases of contact derm that look like atopic derm, but classic atopic derm. I'm going to treat classic atopic derm first. But, you know, there's certain body parts that are supposedly more consistent with allergy, hands being one of them. I know you guys recently talked about this. Last week or the week before. Eyelids is another one that that might be more likely allergy. So. So, so the answer is it depends, right? It depends on the story. If for me, if there's any chance that it's going to be allergy, I'll patch test because I do not want to put patients on a lifetime of any type of systemic medication if they don't need to be like, that's really important to me to not do that, not just because of money, but because of. That's really annoying to have to do that as a patient. I patch if I need it. That's actually. I wanted to say one thing about the paper, which I think is kind of funny. SEAN has a 2025 version of kind of like my paper. Right. My paper is like the pre DUPY version. So my Data went to December 2017. Dupy wasn't even really available then. And so there's this whole other version. I feel like if we redid the analysis for 2017-2025, we might see something different. Right. Because people are using different drugs to treat their patients. Sometimes people choose the diagnosis based on the drug.
A
One of the things that I thought was interesting from your paper was that about 30% of people were diagnosed with dermatitis. When all was said and done, about 12% of them were diagnosed with a. With allergic contact dermatitis. So when you get a, you know, based on that group, psoriasis form dermatitis strongly went against allergic contact dermatitis. Right. So about 4%, which is 1 in 25, not none. Yeah, but it was 1 in 25 people with a biopsy that showed psoriasis form dermatitis had a positive patch test and final diagnosis of contact derm. And that's another. So another thing I want to get into. So Peggy Wu is another friend of ours in the NACD just published an article looking at histopathologic features of acd. And basically, so she looked at people had a biopsy and then a patch test. What on the biopsy predicted positive Patch test. And the main takeaway was eosinophils go against allergic contact dermatitis and spongiotic vesicles with Langerhans cells in them go for it. Now, the spongiotic vesicles with Langerhans cells are rare anyways, but so EOS went against contact derm, and that was about it. And they weren't strongly against it. So the takeaway for me was another confirming that biopsies are pretty worthless in terms of determining the cause of dermatitis and what's like, you know, what you should do next, do you? So for all four of us, right? So let's start, right, because patent Ferris, you guys have had plenty of biopsies of, you know, oh, sponge derm, bos, recommend patch testing, might be a drug rash, blah, blah, blah. And I don't know if the dermapath at Pitt would give, you know, recommendations or just, it's dermatitis, period. Did you ever find biopsies helpful in sponge derm patients? Patton, you go first.
C
Just, just to prove that it was sponge derm and, you know, not psoriasis and or other, you know, saw a patient with DM recently that I thought really looked more spongiotic clinically and it came back as a more lichenoid type of inflammation. So just to show that it's SpongeBob. But I never, I mean, I think that's such an odd thing when patients come in because I, I had a couple patients, honestly, in the last month, they came in with sponge derm with EOS and said, my doctor doesn't know what I'm allergic to. He thought maybe you could tell. And like, I'm done patch testing. So it wasn't even a patch test referral. It was just, what am I allergic to? Can you tell me this? And I'm like, I don't like, why do you think, you know, they're like that? That's what my doctor said. I'm allergic to something based on my biopsy. I never did that.
B
No, I think that's passing the buck, I would say. I think, like, looking at your paper, amber, about 8% of those patients ended up having CTCL. So when do I biopsy? When I want to make sure it's not something bad. Right. So particularly, we can go back and forth about does DUPY increase your risk of ctcl. But like, if there's a question, I think a biopsy to rule out ctcl, if that's on your differential, maybe makes sense. And I guess maybe one of the Questions. And also maybe you had very thoughtful pathologists because Ramiel Rohil was your dermatopathologist who now works at unc. So I do think there maybe it was partly because you had a really good thoughtful pathologist. Yes, but. But yeah. So I guess one question like maybe to wrap up the paper and discussion is like, is there a pearl for people like, you know what, this was really more suggestive of ctcl. Or if you see this, maybe a biopsy is more helpful because these are the patients other than the typical, it's on non sun exposed skin, things like that.
D
Well, Matt mentioned psoriasis, scalp, atopic dermatitis, face. And the association for CTCL actually was scattered generalized. So like whole body, which is like all the patients that used to come and do it for patch testing. But to that point, these people with whole body dermatitis for 15 years, we always should think about CTCL anyways. Right? But that's the main marker for ctcl. And I also in the paper mentioned, let me get this number right. In North Carolina, I believe is 35% black or African American. And in our study we had a higher percentage of patients who were black or African American with cutaneous T cell lymphoma. So thinking about psoriasis for derma in black and African American patients, that might be even a stronger marker for ctcl.
B
Great, Interesting.
A
All right, Amber, I got one last question for you. That might be a five minute. Or do you believe. And I like that. I just realized I like that I'm using the term believe in. Do you believe in the diagnosis of dermatitis unspecified. And let me further characterize that by saying in the AAD's DataDerm set, that is the most common inflammatory dermatosis is dermatitis unspecified. Like literally, we diagnose that more than anything else. Do you think it's a real diagnosis?
D
So it's not a real diagnosis. It is a diagnosis that we are forced to choose from ICD10. I guess it is. And many, many of my patients have that diagnosis. That does not mean I think that's the diagnosis. That means that's what I've chosen. It's essentially the equivalent to chronic dermatitis.
A
So why not? So when you look at the AAD 2014 criteria, itchy, chronic spongiotic spares the groin and axilla, that's atopic dermatitis. If it's not contact derm, ctcl, blah blah blah. According to those, you can interpret those criteria to say every single person who's ever been Diagnosed with derma unspecified or chronic dermatitis, has atopic dermatitis.
D
You read my paper, right? I said that chronic dermatitis might be this AD spectrum disorder, which is essentially AD. And so I would say that my 2017 version of me would say unspecified dermatitis. The now corrupt pharma version of me. That is, I do believe in this AD spectrum disorder. Right. This version of me believes that this is more leaning towards atopic dermatitis. And I'm probably more likely to call it that. Maybe not on day one when somebody walks in with full body dermatitis, I'm like, I don't know, unspecified dermatitis. Right. But when I've had time to work it up, this more chronic dermatitis picture, I am much more likely to call that atopic dermatitis at this point.
A
All right, Patton, do you use dermatitis, unspecified chronic dermatitis dermatitis nos. Do you use any of those or other than as a placeholder to.
C
Yeah, placeholder. Right. Because you, you want to put. Right. I believe in the atopic dermatitis spectrum. You want to get them on dupy, and so you need to call them atopic dermatitis because they'll be like, oh, you never gave them that diagnosis. So it's a placeholder.
A
Okay. Ferris, do you ever use it as a. Because. Right. The patient I'm always thinking about is the 50 year old with dermatitis on their upper back, you know, extensor arms, anterior thighs. Had it for 18 months, had nothing as a child. Their mom is still alive and nope, never had a rash as a kid. It's never been flexural. They have no atopic comorbidities, no family history. They've been patch tested. They didn't get better or even, you know, they didn't have patch tested, but they're using, you know, Dove sensitive skin bar and, you know, low allergenicity moisturizer. Do you, you know, are you in the same bucket as the rest of us? Of, yeah, we should just call all these people atopic derm. Or do you, do you think that it, it's a different thing?
B
It's a good question. I, I guess I, I like to think of it as atopic derm spectrum, knowing it typical, like, you know, yes, early onset. I like the spectrum and I may like it more because then it helps me treat it, but I like it. So I say let's go with it.
A
Okay, Fair. All right, so we're. That is going to conclude our deep dive for the day. So now it's time for us. As I've been getting feedback from my friends and colleagues all over the country, it turns out that everyone's favorite part of the show is Patton's trivia, which he was like, I want to do trivia on the show. I was like, what are. What is. This is supposed to be smart.
C
I know what the people want. They love trivia. Trivia nights at bars. It's all. It's the thing.
A
Okay, all right, all right. So, Pat, we went over the rules with Dr. Atwater before we started, but just to remind our listeners, we're gonna let Dr. Patton finish the question, and then once he finishes the question, we can start blurting out answers. It remains.
C
All right.
A
Ferris is undefeated so far. I have yet to win a week, but this week, I'm feeling good. Feeling good.
C
Well, yeah, because the. The category here is allergens of the year, so.
D
All right, I'm ready.
C
Okay. It's. It. Well, whatever. In the early 1930s, several women developed significant ocular toxicity, including conjunctival edema, corneal ulceration, Corneal Necros, after using Lash Lure, an eyebrow and eyelash cosmetic that was promoted to give women fuller, darker lashes and eyebrows. The tragic outcomes described above occurred because of a severe allergic reaction to what Allergen?
A
Formaldehyde, paraphenylene diamine.
C
It's paraphenylene.
A
No.
C
Yeah.
A
Do you know, I thought I gave.
C
It away with the darker.
D
No, I thought it was the formaldehyde preservative.
A
No. So here.
C
No, it's paraphenylene diamine. So it was one. One woman died. I mean, she. She got eyelid ulceration, and she wound up with an infection, and she died of sepsis. It was one of the catalysts for the passing of the Food, Drug, and cosmetic act in 1938 that gave the FDA the authority to regulate cosmetics. So it's. Pretty soon we're not going to have an fda, so it doesn't matter. But. Yeah, that. That was kind of what, like, FDA is.
D
If.
C
Do I understand this right? FDA banned paraphenylene diamine for use on the skin directly. Right. You can't do that in cosmetics. Or am I misunderstanding that rule?
A
So the. The reason I knew it was PPD was I've done several class action. I've been an expert witness in several class action lawsuits about using PPD for beer to dye. Because. Right. Whenever you're dyeing your beard, you die much more frequently, and you're putting it on your face. And it turns out your scalp is a relatively immuno privileged site. So the stem cells in your follicles do a lot of protecting from allergic contact dermatitis. Susan Netterost taught me that. And it's why you can be allergic to the preservative in your shampoo, but you don't get a rash on your scalp. You only get a rash on your face. Well, beard dyes, the reactions that men get, and the permanent scarring and the permanent dispigmentation and that the companies that make the beard dyes put the exact same warnings that you put on hair dye. And the argument is putting it on your face is totally different from putting it on your scalp. And that becomes part of the argument is you're not even allowed to put it on your skin, but on your. Well, we're telling them to put it on their beard and the blah, blah, blah. But that's the. So I would say that's one of my takeaways of that. I was always like. When I got asked to be an expert witness for that, I was like, fuck, yeah. Because the. Like, I was always like, I can't believe they're allowed to sell beer dye. Like, that seemed crazy to me. And, yeah, so they're very.
B
It's a very altruistic motivation. We're really.
A
Shut up. That's right. I didn't get paid except for my $8,000 month. $8,000 hourly fee.
C
Let's. Let's move on here. All right, number two. Bacitracin was the allergen of the year in 2003. Bacitracin was isolated from a bacteria cultured from a compound fracture of a young girl. What was the species of bacteria that produced basitracin, in that case?
B
Bacteroides.
C
No, that's a good guess because of.
A
The name, the girl's name. You told me this is a resident patent. The girl's name was Tracy.
C
That was her last name.
A
That was. And I feel like it was. The name of the bacteria was, like, something subtilis.
C
That's pretty amazing, man.
D
It'd have to be bacillus subtilis.
C
That's it. That goes to Amber. She got it.
A
Damn it.
C
Nice.
D
I have no idea, by the way.
C
It was Bacillus subtilis.
A
Yeah.
C
The name of the young girl with the compound fracture, Margaret Tracy, she got hit by, like, an ice truck, and she had this compound fracture, and they debrided it. And in the lab, the bacteriologist said, something's in here is like killing staph. And they isolated it, and there it was. Basitracin. It's really cute. The sun was kind of bitter because bastracin made a lot of money and the mom never saw any of it. But he finally came around and he told the story of how he would put the basatracin on his daughter's scrapes and cuts and said, this is grandma helping you out?
B
Oh, it's like the healer cell of contact dermatitis.
C
It is the healer story. Yeah.
D
This is in the allergen of the year article from Bessatracin.
C
Say that again.
D
You read this in the allergen of the year article for bassetracin. This story.
C
No, I like, did a rabbit, Patton, spend. I don't get out much. I do.
A
Not ever.
C
That's. That's what I did for Valentine's Day.
A
When you text Patton, if you don't get a response in eight seconds, you're like, what? Are you okay, buddy?
C
All right, Third and final. We got a tie going in. This is exciting. The allergen of the year designation began in the year 2000. Of the 25 allergens of the year, how many are elements?
A
Elements?
D
I thought you're gonna say how many non allergens.
C
No, you only get one guess here.
D
Elements.
C
Sorry. Come on, people.
A
One.
C
No, I could have asked it another way. That might have been more obvious.
D
Well, nickel and cobalt are elements, right? And they have margins of a year, so it has to be. It's not two because Laura said two. That's.
B
Those are the two I was thinking of.
D
I said three. Is it four?
C
What do you want to go with? Final answer.
A
Tie or is at water the winner?
D
Iron. 1. What are the other allergens of the year that are elements? Potassium dichromate. Chromium. 3. I still think it's 3. It's not.
C
It's 4. It's. It's the metals. It's the metals.
A
What's the 4? Gold.
C
Nickel, cobalt.
A
Wait, I'm challenging. I'm challenging. I think gold was one of the non allergens of the year.
C
That was. It was 2001. I don't think you guys got that clever yet. No. 2019 was your only non allergen with the parabens.
D
No, there was another one.
A
Thimerical. Thimerosal was a non allergen of the year, too.
D
Wait, can we hold on? What was the allergen of the year this year? And who is this author?
A
It was. I thought it was lame. One Recent one of the recent Ones was sulfites. Sulfites.
C
Sulfites was last year.
D
This year. Who is the first author? Matt, it's me.
C
Did they announce it?
A
Was it Lanlman?
D
Oh my God, it's me. I was the first author. Ptds. Peritoline Diamond.
A
Yeah, that's right. Ptds. So for those, for, for our listeners, PTDS is peritoluene diamine sulfate. It is used in some PPD free hair dyes in particular. Madison Reed is based sort of around PTDs. But the problem is if you're allergic to PPD, there's a 50, 50 chance you either are or will become allergic to PTDs. So unless you're patch testing to PTTS, you don't want to just say switch over to Madison Reed because it's PPD free.
D
But my paper has a bunch of other alternatives other than Madison Reed. So go read it everybody. Right now.
A
It just came out and it's in the journal. And it's in the journal. Dermatitis, I would assume. And again, the other thing I want to tell everybody. So Amber was the president of the American Contact Dermatitis Society, the camp app. They just re. I think they probably started that it was like a five year process of redoing the camp app and it is so good now. It is. So I don't know how anybody practiced contact derm prior to having camp. It just makes it so easy comparatively.
C
Well, Amber was closest on that last question, so I'm giving it to her. So that's an Amber Amber win for Amber.
A
Way to go.
C
Another loss for Matt.
A
Look at Ferris. Looks like she's ready to die over there.
B
She looks so well as a middle aged woman having lots of hair dye allergens. This is all bad news and I've lost. So thanks a lot, Amber.
D
Welcome.
B
Thank you so much, Amber for joining us.
D
Thank you.
C
Thanks for having me.
A
This was great, Amber. Definitely thank you and have a great rest of the week and good luck. And if you are a dermatologist in The Northern Virginia, Dr. Atwater just recently kind of restarted left industry and is now practicing again and is, I promise you, the best patch tester you will ever be able to send a patient to. Hands down.
D
Appreciate that.
A
All right, so thank you everybody for joining us for this week's episode. Really appreciate it. And I hope the deep dive into psoriasiform dermatitis and dermatitis unspecified was helpful. If you got questions, comments, ideas for topics that we should do on the show, shoot us an email@questionsurmsondrugs.com I hope you learned a few things. I hope you laughed once or twice. And mostly I hope you're planning to join us next week. Until then, I'm Matt Cyrus.
C
I'm Tim Patton.
B
I'm Laura Farris. And we are Derms on drugs.
A
It.
Date: February 21, 2025
Hosts: Dr. Matt Zirwas, Dr. Laura Ferris, Dr. Tim Patton
Guest: Dr. Amber Atwater
In this lively episode, the Derms on Drugs crew—Drs. Matt Zirwas, Laura Ferris, and Tim Patton—dive into two particularly challenging and often perplexing areas of clinical dermatology: psoriasiform dermatitis and idiopathic erythroderma. Special guest Dr. Amber Atwater, renowned in the field of contact dermatitis, joins the team to break down recent research, share career anecdotes, and discuss what to do when biopsies and diagnoses aren’t clear.
The episode is a playful, peer-oriented exchange with plenty of laughs, but delivers practical, up-to-date guidance for clinicians navigating these ambiguous dermatologic conditions.
(01:27–09:35)
Notable Quote:
"This is personalized medicine to the max...I did a peer to peer, and this reminds me of those patients who are like, 'I want to know the root cause.' And you're like, 'You don't.'” – Dr. Laura Ferris (03:30)
The group riffs on the realities of clinical practice, with Dr. Patton humorously suggesting,
“You say that this guy is erythrodermic atopic because you can find some sponge on the biopsy. That gets him on the Doopie, then you give them Reflumelast… There, I just saved you $7 million.” (06:37)
They discuss the practical first-line approach—methotrexate, cyclosporine, or dupilumab when “the diagnosis isn’t clear,” and briefly debate JAK inhibitors for broad immunosuppression (08:13–09:35).
(10:44–30:18)
Notable Quote:
“If you have it on your scalp, you probably have psoriasis. If you have it on your face, you probably have dermatitis of some sort…other than that, we don’t know.” – Dr. Matt Zirwas (13:39)
(17:32–23:51)
The hosts and Dr. Atwater debate the value and overuse of patch testing.
Dr. Atwater shares that, in her experience, referrals are usually appropriate:
“I often think it's appropriate and sometimes it's, you know, wrongdiagnosis.com and that's appropriate too, because I can actually help the patient… The only thing the patient cares about…is clearing their skin.” (18:44)
Dr. Ferris wonders: is benefit in patch testing, or the “thoughtful approach to the patient” that comes with being a dermatitis specialist? Dr. Atwater agrees it’s multifactorial.
They discuss practical criteria for referring to patch testing, factoring in disease distribution (e.g., hands and eyelids= higher suspicion for allergy) and the importance of not committing patients to lifelong systemic therapy if avoidable.
(25:57–28:47)
(28:47–32:32)
Notable Quote:
"My 2017 version… would say 'unspecified dermatitis.' The now corrupt pharma version of me… I do believe in this AD spectrum disorder." – Dr. Amber Atwater (30:18)
(32:32–41:39)
Trivia theme: Allergens of the Year, with quirky historical notes and competitive banter.
Dr. Atwater is declared this week’s trivia winner!
If you navigate skin rashes in the trenches, this episode arms you with smart, real-world strategies, and demystifies complicated cases with evidence and expert banter. Whether deciding if a patient truly needs a patch test, wrestling with ambiguous biopsy results, or just enjoying some “derm nerd” trivia, you'll walk away with practical pearls.