French Bathhouses, Vitiligo Hacks & the Myth of the ‘Cure’
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The podcast discusses several dermatology topics from recent publications. First, an emerging infection, dermatophilosis, is reported among men who have sex with men in France, presenting as pustular folliculitis in genital and beard areas. This zoonotic infection is normally animal-associated but now shows person-to-person sexual transmission. It responds well to beta-lactam antibiotics like amoxicillin, and clinicians should be aware during summer travel season. Second, acute hemorrhagic edema of infancy (AHEI) is often misdiagnosed as IgA vasculitis. A retrospective study found that age over 30 months, non-blanchable lesions, and pain favor IgA vasculitis, while AHEI typically occurs in happy, chunky infants under 12 months with blanchable, pruritic lesions. Urinalysis can help differentiate. Third, a comparative study shows topical bimatoprost 0.03% solution is as effective as tacrolimus 0.1% ointment for stable vitiligo, supporting combination therapy to both protect and stimulate melanocytes. Finally, a long-term ruxolitinib cream study found that 39% of patients maintained facial repigmentation one year after withdrawal, versus 69% with continued use, emphasizing the need for ongoing treatment to sustain results. The podcast highlights practical clinical pearls for infectious diseases, pediatric dermatology, and vitiligo management.
Welcome to season three of Terms on Drugs and video podcast brought to you by Scholars and Medicine, the best educational platform in dermatology and provided no cosmetic providers. Terms on Drugs is where cutting its dermis, it's a miscommunity. Dr. Matt Zyerson, Dr. Dr. Mottology, in each week, I'm doing a residency buddies, Dr. Laura Ferris from the University of North Carolina, and Dr. Tim Patton from the University of Pittsburgh. And we use our 70 years of combined derm experience to discuss, debate and dissect the hottest topics in dermatology. It is everything you need to know to be under cutting it to derm and you like to have some fun listening. New episodes drop every Friday in Scholars and Medicine, Apple Podcasts, modify another major podcast platforms, and I highly recommend that you download the Scholars and Medicine app to access the full podcast video archive and explore the best derm educational content out there, real, farming independent coverage of all of dermatology supported by an amazing AI clinical consultant called Ask Simon. All right, we are gearing up for a summertime and let's go ahead and get right into it, Dr. Ferris. What do you got? Okay. So my theme today is infectious diseases. Okay. So I am going to start out with this is a little difference, not a paper, but this is something that was just released by the CDC. It's an emerging infection. So the only thing we like better than a known infection is an emerging one. So this just came out in the volume 32 of June 2026 of something called like the dispatch that CDC puts out. So this is called suspected sexual transmission of dermatophilosis among men who have sex with men in Leon and Paris, France 2025 to 2026. Okay. So this is just kind of interesting. This was a series of nine cases of dermatophilus, conglensis, cutaneous infection diagnosed over two month period, men who have sex with men in Leon and Paris. And so they did, you know, genomic studies and showed that they were similar. So it does seem to be like one transmitted strain. So you might be thinking what is dermatophilus, conglensis is, what is it? It is a grand positive, vacillative anaerobic, actinomyces responsible for this cutaneous eruption. So this is normally zooophilic. It is normally just found in animals like cattle sheep, horses, usually in tropical, subtropical climates. And it's usually like a crusted superficial skin lesion. And it can cause particularly mortality in cattle herds. So there have been cases of humans getting this from animals. What is rare is that this is the first time it appears that this has been, you know, implicated in person to person spread. So, you know, first of all, should you see it? How do you treat it? It is, it's not like, oh my gosh, this is a multi drug resistant tinny or something like this. This is actually something that's pretty susceptible to beta lactam. So most of the cases did respond to beta lactam, macrolides, tetracycline. I think a moxasillin was what was used to treat most patients. So, okay, so what's the story here? STI clinics at university hospitals in Leon were the first place that it was described. And these were men who were 22 to 63 median age of 50, no occupational exposure to livestock. And so they kind of presented with these non-specific erythematous. They had some, a lot of, if you look at the photos, there are postules. And then also sort of hyper-charototic or, you know, scaly lesions. Some of these areas looked like folliculitis. They were kind of in the genital area and then in the perioral, like, beard area. And so these were, they said, in areas of sexual contact. There was no mucusill involvement. In general, this was skin limited. One patient had some fever and vomiting. I will say that the patients also, like, a couple of them also had other STIs at the same time. So they had secondary syphilis. I think one of them had recurrent syphilis at the same time. And they all had these histories of visiting bath houses, which I guess are a real thing. And they were not all connected to each other, but they did seem to frequent the same bath houses. And just how the mochi pox thing started, isn't it? Yes. So, you know, I thought this was interesting because I think this is like maybe going to be the 2026 inbox. So, you know, just something for us to be aware of. There are photos in here and we can put those up so that people can see what it looks like. You know, they do, some of these did look like pretty prominent postules. Like you could imagine you could think about inbox here, but it's a little more like postual versus pox. So something to be out on the lookout for as, you know, we come into summer travel season. Do you know if it would show up in a regular like this view just all looks like philicolitis and bad philicolitis, but whatever you do it as swab is probably not going to grow on regular culture would be my guess. Yeah, it probably is not, but I mean, well, I acted on my seas, right? Does, doesn't it? I think in the thing they said they cultured it on like blood and chocolate. Blood agar, but I don't know that that's not something that's done in a traditional culture. I have to go back to my micro biology days. And I would imagine the PC if somebody is doing the Vycor PCR is probably not, it's probably is not one that they are. It is, I would doubt that this is on that, you know, PCR. So I think this is a reason why you should have a, you know, maintain a degree of clinical suspicion about this. And I would say, you know, look at the photos. So it does look kind of just like typical philiculitis. You might, philiculitis barbeque that you might expect when you see the face, the cutaneous, you are the ones that are kind of in the, you know, anal general area do look more like pretty impressive postures. So, you know, think about this, particularly, you know, emerging from France was probably going to spread. And fortunately, it seems like treatment of choice at least in Europe was a moxasillin. Okay. If I see a case, I am definitely using my laugh. Oh, you've been to France. Have you not? Yes. You can do that. I don't see how that could possibly go wrong for you. That's a really, really good idea. You know, I think you'll feel kind of that, that good patient rapport that you're not sure what that is. Exactly. One of the community dermatology, it reminded me, and I thought it was the same thing, but she had mentioned, she had seen a couple of patients, same thing, men having sex with men. And it was Klebsiella, erogenes. Have you guys heard of that one? No. Yes. That was, yeah. And it was like, it sounds like erogenous, but it's like AERO. It is. It's not. Yeah. It's not a race. It's not a race. Yeah. That's a good question. That is also another question. It's the same thing. She said, it's like a horrible flaky lightest that responds to antibiotics, but it keeps coming back when she stops them. So that, that's what this reminded me of. So maybe like two new sort of things to be on the lookout for. Yeah. Absolutely. And they did say that just going back, it was cultured on. They said it was non-selectuminous. A blood agar plates, I think are like in chocolate agar are the things that are typically used when you send off aerobic cultures. Okay. So this should actually show up. So yeah, that's a good thing. It's a good thing. It's a good thing. It's a good thing. Yeah. So interesting. Yeah. Very cool. Ferris, what are you doing reading the reports about the infections in French bathhouses? Are you have a trip coming up? Yeah. He has a trip advisor. I was like, I go to this French bathhouse. I'm like, it's not. It's the cheapest, it's the cheapest Airbnb in Pittsburgh or in Paris. Yeah. It's like a Norwegian bathhouse. It's like five bucks a night. Exactly. And I figured nobody will bother me there. Nobody's interested. It's perfect. It's true. That means have a good meal. Let's move on here. Pat, and what do you got? All right. My first six pack papers from the May 2026 edition of pediatric Durham since starting the podcast. I've gotten a ton of emails asking to cover more Pete's term. That's actually not true. I've gotten like, no. I've gotten like three emails and they all ask like, is I was crazy? I'm like, yeah, I was just crazy. But I think we should try to cover more kids stuff from time to time. And we've got, we do for our listeners in the near future. We have Dr. Lisa Swanson coming on. Pediatric dermatologist extraordinaire should be a very good episode there in the near future. Yeah. So my paper is titled acute hemorrhagic edema of infancy, a safe diagnosis or diagnostic challenge question mark, a 15 year retrospective analysis by Suzanne Arnold at all. Intro to the article gives a quick review of AH.
EI, including the fact that's also known as Finkelstein-Cetalmyr vasculitis. Finkelstein disease, that was what I remember. That's right. Oh no. Introduction, author, state that misdiagnosis of AHEI is common up to 40% in one study. And while misclassifying or to carry a viral examinum as AHEI is in a big deal, missing a case of IgA vasculitis could be a big deal. And that was the main point of the study. Are there any clinical factors on initial presentation that should make you think IgA vasculitis instead of AHEI? So as a retrospective study, it's done in the Netherlands, 89 patients initially diagnosed with AHEI. And there were 20 patients whose diagnosis were revised. So 22.5 of patients with revised diagnosis, 13 cases. So almost 15% were considered to be a major revision, nine of which were cases of IgA vasculitis. So 10% of patients overall had their initial diagnosis of AHEI changed to IgA vasculitis. IgA vasculitis patients compared to AHEI patients were older. They had a painful rash and were less likely to have blanchable rash at presentation. So the authors put together this cool little flow chart. We can put it up on the video. And based on patient age, presence of pre-rightus, presence of blanchability, you can kind of poke patients into categories of being more or less likely to actually have IgA vasculitis and not AHEI. So if patients are older, like greater than 30 months old, and if they have non-blanchable lesions or if they have painful lesions, they're more likely to have IgA vasculitis compared to AHEI. So some good maybe clinical screen tools. As someone who doesn't see little babies, I thought this could be helpful. I talked to Ellen Koch, like the pediatric dermatologist extraordinaire in Pittsburgh. And she was kind of like, she's like, you know AHEI, which I'm sure she would, but I thought it was a nice little guide, something to think of when you're examining these kids initially, what sort of factors make me think? All right, I should make sure they don't have IgA vasculitis and not AHEI in this, in this, in that instance. So that's all. So give me the summary again of what should make you, because again, and we're, so Ficklestein's disease is like, basically like LCV, they're going to be fine, no big deal, it'll resolve on its own, like is, and what's the, the things that should make you be like, I better, I better buy up to this. Yeah, so older than 30 months, like, I mean, the flow chart is nice. It's like 12 years, 12 years, 12 months, and less none of those patients had IgA vasculitis. So it's like anyone like that, you just put them aside. If they were a puritic, I think, I mean, to mean, preritic or pureitic, both either or either one of those, and he was a person taking the history. It sounds right to me. It's like when people say February, they don't say February, they say February. And so I, I, I don't pronounce the first R, it's pureitis. That's, that's not right. Whatever, it's, you know what it's the DO pronunciation. My brother-in-law had the best comment. I will be wearing my little badge and he was like, they've left off the R in the K. So yeah, 30 months, if they have non-blanchable lesions, it's more likely, like AHEI can definitely have non-blanchable lesions. But like if you had completely blanchable lesions, that's not, you don't have to worry, that's more AHEI. So age, non-blanchable, and if they were painful, again, AHEI can be painful, but like non-painful lesions, more preridic lesions, that's more AHEI. And so we'll put the flow chart up, but it's kind of pretty straightforward and okay. Do you buy up see all these kids, you know, an adult or me like, buy up see, buy up see. Like you did that, like I asked, I asked Ellen Coat, she was like, no, you never buy up see. She said like, you just know AHEI, she goes in my mind, it's like, and this is, she hadn't read this paper. She was like, it's a little chunky baby that's like all swold up and like really impressive lesions, sometimes like these vialacious lesions, but the kid is just like happy and fine and laughing. She's like, that's AHEI, like IGA Vascularitis, especially when they have the more serious sequela, GI, renal joint, like the kids are sick. And so she says, that's how you kind of separate it. And if you didn't want to do a buy up see, you could do like urinalysis, that's easy enough. And you know, you see blood in the urinary, you're like, okay, this is more IGA Vascularitis. They just do not buy up see these kids. Okay. Did she actually say, swold up? She said chunky. Chunky. Okay. She's like, it's like a little chunky, a demotivist, like happy baby with a pretty impressive rash. Swold up is a Pittsburgh thing. Yeah. Anybody listening, not from Pittsburgh. Yeah. Okay. Swold up. All right. So move a device. First one. So I've got a comparative study in the therapeutic efficacy of topical bimata prost zero point zero three percent of the foul makes solution versus tachyrolime is zero point one percent. Wait, man, unstable bit of LIGO. So basically pre straightforward study. They took a bunch of people with the LIGO who wasn't terrible bit of LIGOs. They'd be over the age of 18 that it'd be stable bit of LIGO less than 5% BSA. No treatment of last three months. And then they gave them either BID tachyrolimeis or BID bimata prost. And right. Okay. It's tachyrolimeis. It's not like a great vanilla. I go treatment, but it's okay. You know, if you can't get some pretty good. What's that? I think tachyrolimeis is good. No, okay. All right. Fine, Pat. You go ahead and use it all you want. Well, you have to year in Pittsburgh. You're probably not allowed to use obsulara. Well, that is also true. So they both of them BID for 12 weeks. And the final outcomes were pretty similar. So the bimata prost was basically just as good, maybe a little bit faster than the tachyrolimeis. And so it really supports this idea, right? So I always think of it LIGO as you've got two aspects to treating it. One, you've got to protect the melanocytes. And that's what you think of like obsulara or tachyrolimeis. But then if you constimulate them to actually start to reproduce and migrate, that's going to be ideal. I think the best way to do this, if you know, if I suddenly got BID LIGO on my face or my kids got BID LIGO on their face, or I guess a patient, fine, I would take the best care I could of a patient to. I would do bimata prost I drop twice a day when then with obsulara over it. And you know, nobody's done that study yet, but we've got two studies now showing the bimata prost I drops work pretty well. They're very cheap. And if I couldn't get obsulara, I would do bimata prost plus tachyrolimeis or something like that, one to protect, one to stimulate. I would say it's protect, it's shut down the inflick, the immune response. Yeah, yeah, to protect. Right. So you're like, so address the immune response. Then when you've got viable melanocytes, get them, you know, dividing and producing melanin again. Yeah. Yes, get them moving, right? Yeah, it's hard with new, you know, new drugs, new, indicate like nobody's kind of cared about BID LIGO for a while. So it's like every study is monotherapy. But like, what's the reality? Of course, we're going to use all this stuff. And, you know, together, and this, this was batama prost monotherapy, the madaprost, the madaprost, batana prost, the madaprost is a puritic when you put it on, it is not. And then you put on your eyelashes to get longer eyelashes, the clities. Yeah, yeah, yeah, it's cheap. And it's, you know, see, it comes in a little tiny bottle. So you, they make, like you can't treat a big area, but you just, you know, put a kind of a little drop on and rub it on your little IGO and you just then let it dry for a minute. You have to make it into a gel or a cream. That's right. So a compounding pharmacy should make this actually. Yeah, I mean, like I'd be a great combo of tachyrolinamous and bimataprost and polypodium. And some, how about we also put in some because why not? So, Tofa, yeah, yeah, okay. They say people would be too bad. We're going to give this away. We're going to all be rich. We're not going to have to make the millions podcasting that we make. We're going to make this new little IGO treatment. All right, let's move on, Ferris, which, which your next paper? Well, funny, you should ask because my next paper is also about Vidal IGO. But it is a little bit different. So this is actually a follow up on the Ruxilitinib Vidal IGO studies randomized double blind treatment withdrawal or continuation with Ruxilitinib cream in Vidal IGO. This is from the BJD. This is the long term extension of the true V phase three study. So every time I do a long term extension, I'm like, who cares about the long term extension? But you do care.
because what they're trying to say is, you know, can you withdraw the, can you stop treating in what happens? And so, you know, to what we were just discussing, you know, before, once you have protected the melanocytes, and then you've stimulated them, like, do they stick around? Already have to keep treating. Okay, so what they did was they did a randomized double-blind withdrawal study. So they took patients who had already had a facial, vasy 90. So after using Ruxilitinib cream for a year. So this is like, you know, you really, you're 90% better. Okay, so, they had completed the original study and then they rolled over and they were randomized one-to-one to either keep going with Ruxilitinib cream, BID, or to vehicle BID. And then they could like cross-over, if they had, if they lost their vasy 75 response. So 116 patients, 58 in each arm. And primary endpoint was time to relapse, which was defined as dropping below F-Vase 75. Key secondary was time to maintain F-Vase 90. And then they also looked at patient reported outcomes like DLQI, but also there is a patient reported Vidaligo noticeability scale, which is important right because like, do patients notice it or not? You know, the other thing that's weird about Vidaligo to me is, you can be 50% better and you go from having like smooth depigmentation to blotchy depigmentation. I'm always like, is that better? Like, you know, like, I want it either to be gone or like mostly gone. Like, when it's like, oh, I can see all these little dots in it. I don't know how meaningful that is to patients. That's another thing. Okay. It's like when Pat and always complains about acne studies. And they're like, they got 70% reduction in flammatory lesions in patents, or they, but they don't care. They're about 70%. They want to get rid of all of them. And I, it's, I agree with, right? You got one big pimple left on your cheek like, okay, great. I went from eight to one, but I still don't like that. I still worry about that one. Yeah. Yes. Okay. So what happened in the withdrawal arms of the group that came off about 39% of patients maintained at least an F. Vazzy at one year. So the Kaplan Meyer probability of 65% of maintaining an F. Vazzy at a year. And only 21% of them, however, maintain their F. Vazzy of 90. And then in the continuation arm, however, 69%. So 39, if they came off 69% if they stayed on maintained an F. Vazzy of 75 at a year. And the F. Vazzy of 90 was actually 70 was 62%. So 62% maintained the 90 if they stayed on, whereas only 21% did if they came off of it. So, you know, I thought that was kind of interesting. It looks like you do need to continue on the drug to maintain that response. So other, you know, interesting factoids, if the, if they did, you know, in the withdrawal group, if they did go back on their, um, Ruxilett and cream 75% regained F. Vazzy 75 and 69% regained F. Vazzy 90. And it took like three, three and a half months to get that, you know, to sort of be rescued. And, you know, so, and then the other interesting thing was, you know, they asked they did the quality of life in the Biddle I go noticeability scare scales. They were not all that different. They were kind of like not statistically. It wasn't only powerful, but like, they were not really very different between the group who came off and the group who did. So when you measure it with a grid, we're like, oh, you, you lost your response and you did not. But to patients, they're like, yeah, I'm about the same number. We're like, I've got a noticeability, the same noticeability score score safety, nothing new, you know, 36% vehicle and 43% of Ruxilett and Barb had adverse events. The one serious adverse event was a uterine lioma, myoma, which they said was unrelated. And, you know, so, you know, interesting. I thought sort of like, how are we going to do this in the real world? Right? So, you know, this is, and the other, you know, thing is remember, these were only the F-Vase 90 responders. These were like the super high responder population. And this isn't a huge study. And, you know, this is like a BID drug. Like, are people going to continue? How motivated are people going to be to keep doing this BID when they've already repigmented? And then again, like, do we need, there wasn't an arm of like, what if you use it twice a week? What if you do club eight is all once a week in this once a week? Like, are there still many other things? Right. That's why these studies irritated me because I mean, it costs money, but whatever. They're they they're far more they can spend all the money they want. But like, we will figure out this stuff, right? I mean, you'll have a patient who like, I'm a gosh, your Vidal I goes gone. Can I go to twice a week? Can I go to once a day? Yeah, let's see what happens. I think we we we we're not going to pull up this study and be like, well, 39% of blah, like, we'll figure it out. That's what I do. I don't know. Do you really waste with your patients? Yeah. Unless they're furry and boring. I don't get a lot of follow-ups. So yeah, I think it'll be like, you know, what are we going to do in real life with this? I think you could say continue to do it twice a day every day. Like, most patients will not do that. Yes. They'll put an e same twice a day every day. They'll put it on twice a week. That's right. That'd be the Steve Feldman. But they also did like regain the response. Like, it's not like, uh, you lost it. So interesting. Yeah. Okay. Well, I like it. So it's okay. We can tell people if you stop using it, there's a higher chance that your Vidal I go is going to come back. So put it on whenever you remember to. Yes. That's a reason we'll wait to put it. All right. Patent, what do you got? All right. It is the effectiveness of a new drug to treat pancreatic cancer. I mean, what does that have to do with us? Stay keep listening. May 2026 edition of New England Journal Medicine had an article titled Derrach's onresib. Derrach's onresib. Yeah. And previously treated, advanced, rast mutated pancreatic cancer by Brian Wolpen at Al. So Derrach's onresib is an oral multi selective inhibitor of rast, which is part of the map K pathway, map, Chinese pathway, whole growth factor binds to EGFR that activates rast, raff, mech, urk. So we've all seen the EGR EGFR rash acne, form eruptions, suburac distribution, scalp face ears. It can be pretty bad. Apparently this drug turns that rash up to 11. Rashed was seen in close to 90% of patients. This paper was brought to my attention by this oncologist who texted me. He's like, you have to call me, which is usually like some sort of oncodermatologic emergency or like a daughter that has a pimple. When I called him, he just wanted to let me know that like, this came out oncologists are going to be he said handing out this drug like it's water. And this rash is going to be something that we better get ready to see. Senator Ben Sassy from Nebraska. I think he was, he has to present in the University of Florida, but he used to be a senator from Nebraska. Right. So he got diagnosed with metastatic pancreatic cancer and he received this medication and he posted a couple of images and like it's it was like he had a particularly bad case. So pretty bad rash, EGFR rash, maybe worse and Durham should be ready to treat. So it's kind of a similar to your bathhouse alert, something we should be ready to start managing. Yeah. Well, I think he was on 60 minutes with his rash. He was. And at that point, I think he he he was actually put on hold. Like the drug was put on hold because his rash his face was just a message. What? Oh my god. This looks I just pulled it up. It looks like hamburger face from five FU. Yeah, it's bad. What do you what do you sorry, Pat? And you've been like, well, we've got to be ready to trust. What the hell do you do? I have no idea. So I think it's the EGFR rash. So you know, moisturize things like that. Will they use prophylactic doxie cycle? I'm like, yeah, in a biotic. There was one study that was like this Pan-Canadian study where reactive doxie versus preventative doxie. It was actually comparable. So, you know, you don't have to get doxied all these patients. But with a really, really bad rash like that, is that something that to look at? I loved Isotretinone for this. I actually think Isotretinone is a better drug than doxie. I think it's easier to take. Generally, it was low dose doxie and I'm sorry, low dose Isotretinone. So I think that would be an interesting preventative doxie versus preventative Isotretinone. But you know, that's how I manage these patients. If they weren't on doxie, I put them on doxie. First line. And if they didn't respond to doxie, I would go to Isotretinone. How about Isotretin? Do you think Isotretin works as well? I mean, it's just so much easier to use. Not well. Yeah, but I mean, if it's a male patient and pancreatic cancer, that's not a child bearing sort of potential population. So I think Isotretinone. You're going to the child to the woman who's 30. You're going to be like, we're going to
percent of the size of Trent Noan. You just have to wait a while. Don't worry. You'll be dead before you could get pregnant. Yeah. One of the interesting things that I read about was one of the pathways that was theorized as being activated in at least the EGFR rash was IL-36 pathway. Oh. We're going to see more patients with EGFR rash or I mean this rash, Darock's on-resid rash. We're going to see more patients with that than we're going to see with postular psoriasis. So maybe we'll actually be able to use spedolumab. Yes. And before the interesting thing to also look at. And hey, before anybody gets mad at me for what I just, the insensitive thing I just said about pancreatic cancer, my mom died of pancreatic cancer. So I get free pass. You do. That's a lot. And there's been a lot of chatter on X about this from people who are basically like they've been working. So this is supposed to be an undruggable target. That's what everybody always said. And then they came up with this and it's being heralded. Is this like incredible breakthrough because no, there's never been any treatment that worked at all for pancreatic cancer. Totally untreatable. And yes, this absolutely works, but the average number is it extends lifespan by six months. Yeah. I mean, it's still bad disease. It's still terrible. It's a horrible disease. Terrible disease. And so it's like people are like, oh my god, this is such a huge breakthrough. Like, yeah, it's better than nothing, but it's not like when people like, AI is going to cure all diseases. I'm like, we, we have not cured one disease ever. There's not a single drug that has ever cured any disease, right? And chronic, and chronic infections, yes, that is it, right? You define cure as you take it for a little while, you stop the disease, goes away in pretty much everybody, then you stop taking it and it doesn't come back, right? Isotretinone and acne. Isotretinone is the closest thing we've ever had. And even that, you can make the arguments and infectious disease. Right. We're taking away the sort of substrate for the bacteria to grow in. It's right. You know, it's iffy, it's iffy. But yes, I just tried to know the closest thing we've ever got, but even it only works in 80% of 70% of people, so we don't call it a cure, right? So it is a, there's, we've, in the history of medicine, we've not cured a single disease ever. And so when people are like, we're going to make drugs and it's going to cure stuff, because AI is so smart, I just don't think it's possible. Don't you think immunotherapy, I mean, in the people in whom it works, immunotherapy cures cancer. If it, I would call it that if it worked in like 95% of people. Okay. So we're going to have to have like a consensus statement on what curing disease means. I think when you say to people, oh, we've got a cure for that. They're like, okay, if I get it, I will take that and I will be fine. If you're like, yeah, 50% of people die, I don't call that a cure. I would say if you have, if you are treated, your disease is gone and you can stop the treatment and your disease does not come back, you are cured. Not everybody will be cured, but you are cured. But the, yes, you're cured, but to call something a cure, we have a cure for X Y Z. I think it's got to be at least 90% of people like it works in, right? Because if, you know, otherwise we've got cures for, we've had chemos, been the cure for, we've had the cure for cancer for decades. Because there are some people who could give them chemo, their cancer goes away, right? We don't call that a cure. So there are very few diseases where we can successfully cure without further treatment and 90% or more of patients. Yes. So like that, the new one that's coming out, the gene therapy for the hyperclustralemia ODL thing, that looks like a cure. Like it's a gene therapy, so I wouldn't really call it a drug, but it looks like it's a cure. Right? It's like you give it to people once, it works as long as it takes, it works in everybody, but it doesn't take, I mean, you give it to them again, like that's a cure, okay? Like, but yes. So I get very annoyed when you hear all these tech people who are like, we're going to, A.I. is just going to cure everyone. We've got proteomics, we've got metabolic omics, we've got, we've left the omics and the epigenomic. It's personalized medicine. That's what it is. And they'll say, like, Dennis Hassabis, the like deep mind Google guy keeps saying, we're going to cure all diseases in 10 years. Yeah, there's no reason we won't. Like you're a moron. Yeah, I don't like we're cure all diseases. He's a Nobel Prize winner, so like, but like, like we're not going to cure anything. We're not. He's no mad Cyrus. That's all I can say. That's exactly right. We're going to get amazing treatments. We are going to get treatments where it's like you take this drug, your disease completely goes away as long as you keep taking it. That's, but like a 98, we're going to get sky reasies for everything, but it's not a cure. It is an amazing treatment. Just don't use the word cure. All right. Get. Get enough my soap. Okay. Take a deep breath. Okay. Feel that. All right. Okay. I'm ready now. Okay. Let's move on here. So I got another, this one's a cute article. I would call it. So this is comparative efficacy of topical and acetylcystine plus doxycycline versus benzoperoxide plus doxycycline in moderate acne, vulgaris and add on double blind randomized control trough because right now, when you look at the data for topicals, people always like to talk about retinoids, first time retinoid, first time. If you only had one topical that you can have for acne, no combos, just one active ingredient, you want benzoperoxide. It is the most effective topic. Now bleaches the hell out of everything, but it is still the single most effective topic. So I saw this was like, oh, is it interesting? No way. It's going to be benzoperoxide. It killed benzoperoxide. So an acetylcystine, I don't ever get down here to like the acne score stuff. It like beat it, but it was almost twice as effective. So like their gag score, which I can never remember what the gag stands for, it started at the same. So 23.67 in the acetylcystine group, 23.5 in the BPO group. Now they all got doxy2, but BPO doxy took it from 23 to 18. Right? I'm sorry, that's the adjust. Yeah, took it for 23 to 18. The an acetylcystine took it from 23 to 9. Right? Like that, it was a big difference. So whenever we look at the average IGA scores went from the see of that, I'm looking at caddy. I know here's IGA. So the average IGA score went from 3.2 to 1.7 versus with doxy or in benzoperoxide went from 3.1 to 2.6. So like dramatically more effective. Now, it wasn't a huge study, right? It was 20 people. But the beauty of this is basically free. So you go online, I take an acetylcystine every day because it's a paddle protective from alcohol. And so you get a big jar of 1,000 milligram capsules. I'm going to give you the recipe right now for how you make this because I worked it all out. Right? Do they make, I'm just going to ask before you dispense pharmacologic advice here. Did they make it or did they like, did they use a commercial product or did they compound it themselves or did they have you go buy some stuff on Amazon and crush it up or what did they do? So let's see, they just says they used an acetylcystine gel to prepare it. We diluted an acetylcystine powder in ethanol and glycerin. The resulting solution was then added to 3% carboxy, methyl cellulose gel. They made it themselves too. They probably did it in a little better conditions than I'm describing, but this works perfectly. So at least it should. Now you haven't actually tried it. You take four acetylcystine, 1,000 milligram capsules and you pour them into a little, you know, a little tougher work container. And then you add one tablespoon of very hot water. Then you mix that up and it should dissolve very well. That's well within the solubility of an acetylcystine and water. So one, and this will be on the slides, one tablespoon of very hot water. You mix it up. And then you add in one quarter cup of the lotion of your choice. So seed of fill, serivie, whatever the hell you want. Yeah, add that in. You mix it all up. Boom. There it is. You got your 5%, it works out, it's like 5.04%. Just make it in your kitchen. It's like, by one jar of the stuff, it's going to last you forever. This might be the biggest breakthrough in acne since acutate. That's. It might be. Yeah. I mean, we can start giving that out as like favors when people come to our live podcast. But you could make it, you know, yeah, I can make labels for it. I can make like a bucket and we can ladle it out. Yeah, we could do that too. I think. I think. Right. But it was a randomized control trial. 20 patients in each arm, but the, but the effect was huge. The effect was huge. Now, I will say. It's not blinded though. It's can't be blinded, right?
Let me see here. No, it was double blind double blind. Okay double blind and add on double blind randomized control Try now it was done in Iran So you never know it could have been affected by the war because it was except well It was accepted in September of 2025. So it was pre-war everything was okay Okay, they had the internet to submit it and all that stuff too Right right what journal what journal is in the journal of dermatology practical and conceptual Okay, which I now really like this journal there were like for good articles this I think my other one my other one was from this journal to Bama Prost Versus Takro Limus so it's a journal nobody's ever heard Yes, that has like the highest efficacy of Random Compounded drugs and that is definitely not a red flag Yeah, I'm sure I don't know that you and see Invest in the subscription Way every way shape and for me. So the other one the one with Bama Prost and Takro Limus was from India So apparently you have to be from a country that starts with the letter I And then you can publish in this journal Okay, all right, but I would that's it for for this week. I want to thank everybody for joining us I hope you had a good time. Hope you laughed once or twice. Hope you learned a few things But mostly I hope to plan and to join us next week and until then I'm Mads Iris I'm Tim Patton and I'm Laura Ferris and we are germs on drugs
Podcast Summary
Key Points:
A new emerging infection, dermatophilosis (Dermatophilus congolensis), appears to be spreading through sexual contact among men who have sex with men in France, presenting as pustular folliculitis in genital and beard areas, treatable with beta-lactam antibiotics like amoxicillin.
Acute hemorrhagic edema of infancy (AHEI) is often misdiagnosed as IgA vasculitis; key distinguishing factors include age >30 months, non-blanchable lesions, and pain, which suggest IgA vasculitis, while AHEI typically affects happy, chunky infants under 12 months with blanchable, pruritic lesions.
Topical bimatoprost 0.03% solution is as effective as tacrolimus 0.1% ointment for stable vitiligo, supporting a combination approach of immune modulation (e.g., tacrolimus or ruxolitinib) and melanocyte stimulation (e.g., bimatoprost) for optimal repigmentation.
A long-term extension of the ruxolitinib cream study for vitiligo found that 39% of patients maintained at least F-VASI 75 one year after treatment withdrawal, compared to 69% with continued use, highlighting the need for ongoing therapy to sustain results.
Summary:
The podcast discusses several dermatology topics from recent publications. First, an emerging infection, dermatophilosis, is reported among men who have sex with men in France, presenting as pustular folliculitis in genital and beard areas. This zoonotic infection is normally animal-associated but now shows person-to-person sexual transmission.
It responds well to beta-lactam antibiotics like amoxicillin, and clinicians should be aware during summer travel season. Second, acute hemorrhagic edema of infancy (AHEI) is often misdiagnosed as IgA vasculitis. A retrospective study found that age over 30 months, non-blanchable lesions, and pain favor IgA vasculitis, while AHEI typically occurs in happy, chunky infants under 12 months with blanchable, pruritic lesions.
Urinalysis can help differentiate. 1% ointment for stable vitiligo, supporting combination therapy to both protect and stimulate melanocytes. Finally, a long-term ruxolitinib cream study found that 39% of patients maintained facial repigmentation one year after withdrawal, versus 69% with continued use, emphasizing the need for ongoing treatment to sustain results.
The podcast highlights practical clinical pearls for infectious diseases, pediatric dermatology, and vitiligo management.
FAQs
Dermatophilosis is a cutaneous infection caused by Dermatophilus congolensis, a gram-positive bacterium normally found in animals. It is emerging as a concern because a 2025-2026 CDC report suggests possible sexual transmission among men who have sex with men in France, marking the first suspected person-to-person spread.
Dermatophilosis is susceptible to beta-lactam antibiotics, macrolides, and tetracyclines. In the reported cases, amoxicillin was commonly used and effective.
AHEI presents with impressive purpuric lesions in a chunky, happy infant who is otherwise well. It is typically self-resolving and does not require a biopsy.
IgA vasculitis is more likely in children older than 30 months with non-blanchable, painful lesions, while AHEI is more common in younger infants with blanchable, non-painful lesions. A urinalysis can help if IgA vasculitis is suspected.
Yes, a study showed that bimatoprost 0.03% solution applied twice daily was as effective as tacrolimus 0.1% ointment for stable vitiligo, with possibly faster results. It is a cheap option to stimulate melanocyte repigmentation.
In a withdrawal study, 39% of patients maintained at least a 75% facial improvement one year after stopping ruxolitinib, but only 21% kept a 90% improvement. Continuing treatment led to better maintenance of results.
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